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Fluid and Renal Physiology > Renal CVT > Flashcards

Renal CVT Flashcards

1
Q

Define PU/PD

A

urine output > 50 ml/kg/day or water consumption > 100 ml/kg/day

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2
Q

Where is ADH synthesized and stored?

A

ADH synthesized in supraoptic and paraventircular nuclei of hypothalamus, stored in pituitary

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3
Q

What is another name for ADH?

A

Anti-diuretic hormone = Vasopressin

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4
Q

What stimulates ADH release?

A

ADH releases when decrease in plasma osmolality, arterial hypotension, fever, pain, nausea, hypoglycemia, exercise, certain drugs

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5
Q

How does ADH work?

A

○ In distal convoluted tubule and collecting duct ADH stimulates passive resorption of solute-free water (without ADH these areas are impermeable to water)
○ ADH binds to V2 receptors leading to insertion of aquaporin-2
○ Channels allow water to flow along osmotic gradient between distal convoluted tubule/collecting duct and the hypertonic renal medulla

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6
Q

What are 3 physiologic processes that allow for concentration of urine?

A

○ Concentration of urine in the presence of ADH
§ PROBLEM: Reduced production of ADH
○ Ability of renal tubules to respond to ADH
§ PROBLEM: Inability to respond to ADH
○ Presence of osmotic gradient btwn hypertonic renal medulla and fluid in distal convoluted tubule and collecting duct
§ PROBLEM: Osmotically active substances in urine filtrate or decreased medullary hypertonicity

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7
Q

Name 6 conditions that can result in primary polydipsia.

A
  1. Behavioral Problem (pyshcogenic)
  2. Hyperthyroidism (cats)
  3. Primary GI disease (dogs)
  4. Hepatic encphalopathy
  5. Hyperadrenocorticism
  6. Fever
  7. Pain
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8
Q

How can serum [Na+] help in determingin primary PU vs primary PD?

A

○ Sometimes can tell from Na+ or measured osmolality
§ [Na+] at or below RR → Primary polydipsia
□ Can also be related to hypovolemia
§ [Na+] above RR → Primary polyuria
□ NOT helpful it normal Na+

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9
Q

What is the percentage of functional renal mass results in loss of concentrating ability?

A

66%

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10
Q

What is the percentage of functional renal mass results in azotemia?

A

75%

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11
Q

What is central diabetes insipidus?

A

§ Deficiency in ADH (may be partial or complete)
□ Trauma, neoplasia, congenital defects, idiopathic
§ Patient cannot produce concentrated urine in response to water deprivation but responds to exogenous ADH

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12
Q

What is primary nephrogenic diabetes insipidus?

A

§ Rare congenital → Renal tubules are unable to respond to ADH
§ Animals cannot concentrate urine in response to water deprivation or administration of exogenous ADH

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13
Q

What is secondary nephrogenic diabetes insipidus?

A

§ Main cause in dogs and cats, usually primary polyuria and secondary polydipsia
§ Acquired inability of renal tubules to respond to ADH (related to loss of medullary gradient or interference of action of ADH)
§ No use for water deprivation test

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14
Q

What are the 4 major mechanisms of secondary nephrogenic diabetes insipidus?

A
  1. Osmotic diuresis
  2. Loss of medullary hypertonicity (medullary washout)
  3. Impaired tubular response to ADH
  4. Downregulation of aquaporin-2
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15
Q

What is renal medulally solute washout?

A

§ Fluid therapy, diuretics, and chronic PU/PD can all lead to this → Lead to impair renal response to ADH

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16
Q

What are the most common causes of PU/PD in dogs?

A

CKD, Hyperadrenocorticism and diabetes mellitus

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17
Q

What are the most common causes of PU/PD in cats?

A

CKD, diabetes mellitus, hyperthyroidism

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18
Q

What are the ranges for minimally concentrated urine?

A

1.013-1.030 (dog) and 1.013-1.040 (cat)

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19
Q

Name 3 methods to assess GFR?

A

iohexol clearance, exogenous creatinine clearance, and nuclear scintigraphy

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20
Q

What is DDAVP?

A

§ Desmopressin (synthetic analog of ADH)
§ When to consider it: All other steps complete and ruled out all causes of secondary NDI, historical information and [Na+] more consistent with CDI, close monitoring and free access to water
□ Look for either drop in water intake or increased USG → CDI
® NOTE: Animals with HAC will also have a positive response!!!

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21
Q

What diseases can result in a positive response to a DDAVP?

A

CDI, and hyperadrenocorticism

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22
Q

What is the mechanism of PU/PD in diabetes mellitus?

A

Secondary NDI

Osmotic diuresis

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23
Q

What is the mechanism of PU/PD in primary renal glucosuria?

A

Secondary NDI

Osmotic diuresis

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24
Q

What is the mechanism of PU/PD in Fanconi syndrome and other tubulopathies?

A

Secondary NDI

Osmotic diuresis

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25
Q

What is the mechanism of PU/PD in Chronic renal failure?

A

Secondary NDI

Osmotic diuresis

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26
Q

What is the mechanism of PU/PD in polyuric acute renal failure?

A

Secondary NDI

Osmotic diuresis

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27
Q

What is the mechanism of PU/PD in postobstructive diuersis?

A

Secondary NDI
Osmotic diuresis
Downregulation of aquaporin-2

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28
Q

What is the mechanism of PU/PD in chronic partial ureteral obstruction?

A

Secondary NDI

Downregulation of aquaporin-2

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29
Q

What is the mechanism of PU/PD in renal medullary solute washout?

A

Secondary NDI

Decreased renal medullary tonicity with loss of osmotic gradient

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30
Q

What is the mechanism of PU/PD in pyelonephritis?

A

Secondary NDI
Bacterial endotoxin reduced tubular sensitivity to ADH
Damaged countercurrent mechanism

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31
Q

What is the mechanism of PU/PD in pyometra?

A

Secondary NDI

Bacterial endotoxin reduced tubular sensitivity to ADH

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32
Q

What is the mechanism of PU/PD in liver failure?

A

Secondary NDI
Loss of medullary hypertonicity (medullary washout)
Impaired hormone metabolism
+/- psychogenic component

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33
Q

What is the mechanism of PU/PD in PSS?

A

Secondary NDI
Loss of medullary hypertonicity (medullary washout)
Impaired GFR
+/- psychogenic component

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34
Q

What is the mechanism of PU/PD in hyperadrenocorticism?

A

Secondary NDI
Impaired tubular response to ADH
Central = Impaired release of ADH
Psychogenic polydipsia

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35
Q

What is the mechanism of PU/PD in hypoadrenocorticism?

A

Secondary NDI

Loss of medullary hypertonicity (medullary washout)

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36
Q

What is the mechanism of PU/PD in hyperthyroidism?

A

Secondary NDI
Loss of medullary hypertonicity (medullary washout)
+/- Psychogenic component

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37
Q

What is the mechanism of PU/PD in acromegaly?

A

Secondary NDI
Osmotic diuresis due to diabetes mellitus
Interference with action of ADH?
Partial CDI (some patients)

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38
Q

What is the mechanism of PU/PD in pheochromocytoma?

A

Secondary NDI

Excessive catecholamines

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39
Q

What is the mechanism of PU/PD in primary hyperaldosteronism?

A

Secondary NDI
Imapired tubular response to ADH
+/- impaired release of ADH = CDI

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40
Q

What is the mechanism of PU/PD in hypercalemia?

A

Secondary NDI

Interferes with action of ADH on renal tubule

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41
Q

What is the mechanism of PU/PD in hypokalemia?

A

Secondary NDI
Downregulation of aquaporin-2
Loss of medullary hyperonicity (medullary washout)

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42
Q

What is the mechanism of PU/PD in hyponatremia?

A

Secondary NDI

Loss of medullary hyperonicity (medullary washout)

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43
Q

What is the mechanism of PU/PD in leiomyosarcoma?

A

Secondary NDI

Impaired tubular response to ADH

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44
Q

What is the mechanism of PU/PD in polycythemia?

A

Secondary NDI
Action of atrial natriuretic peptide
Impaired release of ADH = CDI

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45
Q

What is the mechanism of PU/PD in Leptospirosis?

A

Secondary NDI

Unknown!! But renal failure is not the cause in all cases!!

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46
Q

What are factors that an influence formation of crystalluria?

A
  1. Ion overstauration in urine
  2. Urine volume
  3. Urine pH
  4. Temperature
  5. Inhibitors or promotors of crystal formation
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47
Q

What are 2 crystal inhibitors in the urine?

A

Tamm-Horsfall proteins and nephrocalcin

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48
Q

Does crystalluria mean that uroliths will form?

A

NO!

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49
Q

What are 2 bacteria that are common in struvite formation in dogs?

A

Staph and Proteus (urease producing bacteria)

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50
Q

Can patients have uroliths without crystals?

A

Yes, examples with 50% of patients with CaOx uroliths

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51
Q

What occurs with bilirubin crystals in dogs and cats?

A

Can be normal in concentrated dog urine

ALWAYS abnormal in cats!

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52
Q

What type of crystal is seen with ethylene glycol toxicity?

A

Calcium oxalte monohydrate

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53
Q

Name 3 tx options for CaOx crystalluria.

A
  1. Diet
  2. Potassium cirtate (alkalizing urine and citrate inhibits CaOx formation)
  3. Thiazide diuretics (humans)
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54
Q

How is cysteine handled by the kidneys?

A

○ Cysteine is usually filtered at the glomerulus and resorbed at the proximal tubule, so cysteine crystalluria can occur with defects in resorption at proximal renal tubule

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55
Q

Name 2 ways to treat cysteine crystals?

A
  1. Alkalize urine

2. Break disulfide bond with d-penicillamine or 2-MPG (2-mercaptopropionylglycine)

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56
Q

Name 2 breeds that get uric acid crystals.

A

Dalmatians and English Bulldogs

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57
Q

Name 3 tx options for uric acid crystals.

A
  1. Alkaline urine
  2. Feeding diet low in protein
  3. Allopurinol (xanthine oxidase inhibitor)
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58
Q

What is the MOA of allopurinol?

A

xanthine oxidase inhibitor: Competitively inhibits the conversion of xanthine to uric acid

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59
Q

What breed and treatment in dogs can result in xanthine crystal formation in dogs?

A

Cavalier King Charles Spaniel

Adminstration of allopurinol for uric acid crystals (Dalmatians/English Bulldogs)

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60
Q

What does the urine dipstick detect?

A

Albumin: >30 mg/dl

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61
Q

What does the SSA test detect?

A

sulfasalicylic acid test
Detects albumin, globulins, and Bence Jones proteins
> 5 mg/dl

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62
Q

What is the definition of persistent renal proteinuria?

A

• Proteinuria = positive test results on three or more occasions 2 weeks or more apart

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63
Q

What are the UPC values for albumin of 30 mg/dl in cats and dogs?

A

• UPC of 0.4 (cats) and 0.5 (dogs) correspond with albumin of 30 mg/dl

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64
Q

What is a normal UPC in dogs and cats?

A

• Normal UPC: < 0.2-0.3 (cats/dogs)

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65
Q

What are the most common causes of proteinuria in dogs?

A

• Dogs: neoplasia, infection, polyarthritis, hepatitis, HAC, IMHA, systemic hypertension

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66
Q

What are the most common causes of proteinuria in cats?

A

• Cats: Viral infections, neoplasia, IM disease, polyarthritis, systemic hypertension

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67
Q

At what UPC is treatment for proteinuria recommended in nonazotemic animals?

A

• Treatment when UPC >1.0
○ Low protein diet, n-3 fatty acid supplementation (in renal diets), low dose aspirin, ACEi (Enalapril 0.5-1.0 mg/kg/day PO)

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68
Q

At what UPC is treatment for proteinuria recommended in azotemic animals?

A

• In azotemic animals: treatment when UPC > 0.5

○ Renal diet (n-3 fatty acids), ACEi

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69
Q

What are the NINs?

A

NINs (neoplastic, infectious, noninfectious inflammatory) causes of glomerular disease

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70
Q

What is mebranoproliferative GN?

A

• Immune-mediate disease that if associated with deposition of immune complexes within glomerulus
○ Subendothelial, subepithelial, and/or mesangial
○ Complexes may be circulating and passively get trapped OR may form ““in situ”” when antibody binds to normal glomerular antigen or soluble antigen is localized here

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71
Q

What is the most common GN in dogs?

A

Membranoproliferative GN = 20-60%

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72
Q

What type of Ig is present in membranoproliferative GN?

A

IgG mainly

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73
Q

What is the tx for membranoproliferative GN?

A

Treat NINs and antiplatlet drug

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74
Q

What is the prognosis for membranoproliferative GN?

A

Unknown - studies lacking

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75
Q

What is membranous nephropathy?

A

(Membranous GN) • Results form IgG deposits on the subepithelial aspect of GBM
Result in complement-mediated injury to podocytes and diffuse foot process effacement

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76
Q

What is most common GN in cats?

A

Membranous Nephropathy

In dogs, accounts for 10-45%

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77
Q

What is the tx for membranous nephropathy?

A

Possible immunosuppression, depends on stage of dz (1-4)

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78
Q

What is the prognosis for membranous nephropathy?

A

Progresses slowly, animals can liver out normal lives

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79
Q

What is mesangioprolifetaive GN?

A

• Accounted for 2-16% of dog lesions, expect proteinuria and renal failure, mediated by immune-complex deposition
Characterized by mesangial cell hyperplasia and increased mesangial matrix

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80
Q

What Ig is found in mesangioprolifeative GN?

A

IgA (IgA Nephropathy)

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81
Q

Which disease in dogs have been associated with mesangioproliferative GN?

A

Excessive IgA complexes can be formed by enteric disease or decreased clearance of IgA complexes in association with liver disease

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82
Q

What is different about Shar Peis and Abyssinians with amyloidosis compared to others?

A

§ Familial form = Glomerular (only 64%) and medullary amyloid deposition (ischemia, chronic interstitial fibrosis, papillary necrosis, and nephron loss)
□ Shar Peis as few as 25-43% had proteinuria noted!
More likely to present azotemic than proteinuria

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83
Q

Name the common breeds that get reactive amyloidosis in the glomerulus.

A

• Breeds: Beagles, English foxhounds, collies, and walker hounds

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84
Q

What is glomerulosclerosis?

A

• Nonspecific, End-stage response to glomerular injury or decreased functional renal mass
• Seen on light microscopy as mesangial cell hyperplasia and mesangial expansions of the glomerulus
○ Hyalinosis, adhesions in tuft of Bowman’s capsule

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85
Q

What is minimal change disease?

A

GN with no lesions on LM, but on EM Diffuse foot process effacement
Severe proteinuria and nephrotic syndrome
Uncommon in dogs
Humans respond to steroids

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86
Q

What collagen is affected in hereditary nephritis?

A
  • Inherited defects in structure of type IV (basement membrane) collagen
  • EM: Irregular GBM splitting (Unique to this disease)
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87
Q

How much day to day variation is noted in UPCs in dogs and cats?

A

○ Dogs: Up to 50%

○ Cats: Up to 90%

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88
Q

Why is BUN inferior to creatinine for estimating GRF?

A

BUN is highly influenced by tubular reabsoprtion

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89
Q

Why is there a Nonlinear relationship between GFR and creatinine?

A

early in CKD large drops in GRF produce small increases in creatinine, and the reverse later in disease; occurs because initially when there is a loss of nephrons there is a compensatory hypertrophy of residual nephrons so single nepron GFR may more than double

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90
Q

What is the gold standard for plasma clearance testing to estimate GFR?

A

Inulin Clearance

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91
Q

What is a reliable measure of GFR in dogs and cats currently?

A

Iohexol Clearance (Ominpaque)

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92
Q

What are the 3 core characteristics of CKD?

A
  1. Reduction in kidney function
  2. Proteinuria
  3. Hypertension
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93
Q

What are the 4 parts of conservative management for CKD?

A
  1. Provide adequate nutritional support
  2. Correct deficits and excesses in fluids, acid-base, and electrolytes
  3. Amerliorate CS of CDK
  4. Provide renoprotective therapy to slow the progression of CKD
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94
Q

What are the 3 guidelines for providing adequate nutrition in CKD?

A
  1. Feeding a renal diet (best evidence)
  2. Ensure adrequet nutrition (feeding tube maybe needed)
  3. Provide omega-3 polyunsaturated fatty acids (most in renal diets)
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95
Q

What are the 4 guidelines to correct deficits and excess fluids, acid-base and electrolyte changes in CKD?

A
  1. Maintain Phosphorus
  2. Maintain potassium
  3. Correct metabolic acidosis (bicarbonate)
  4. Maintain hydration
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96
Q

What are the targets for phosphorus levels in CKD?

A

○ Want below 4.5 mg/dl in Stage II, below 5 mg/dl in Stage III, and below 6 mg/dl in Stage IV
Controlled with renal diet and intestinal phosphate binders

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97
Q

Why does metabolic acidosis occur in CKD?

A

○ Metabolic acidosis in CKD primarily from impaired renal ammmoniagenesis, impaired excretion of acid and impaired resorption of bicarbonate may also occur
§ Metabolic acidosis in RTA from impaired bicarbonate resorption (proximal RTA) or impaired urine acidification (distal RTA)

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98
Q

What 2 major clinical effects need to be addressed with CKD?

A
  1. Anemia (Epo supplementation)

2. GI upset (acid blockers, antiemetics, and sucralfate)

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99
Q

What are the 3 renoprotective therapies that are shown to slow the progression of CKD?

A
  1. Reduce proteinuria (ACEi and renal diet)
  2. Control hypertension (cats - amlodipine, dogs - ACEi + amlodipine)
  3. Provide calcitriol (to prevent secondary renal hyperparathyroidism and improve appetite/energy)
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100
Q

What is RIFLE?

A 
Description of AKI
 • Risk
 • Injury
 • Failure
 • Loss
 • End Stage Renal Failure
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101
Q

What are 3 phases of AKI?

A

○ Initiation Phase: This is when injury is occurring
§ Extension phase – during this ischemia, hypoxia, inflammation, and cellular injury continue leading to cellular apoptosis and necrosis
§ This phase is usually < 48 hours
§ May not see any abnormalities
○ Maintenance Phase: characterized by azotemia and may last days to weeks, oliguria (< 1 ml urine/kg/hr) or anuria may occur here
○ Recovery Phase: azotemia improves and renal tubules repair, marked polyuria may occur here (from osmotic diuresis from accumulated solutes

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102
Q

Name 3 drugs that can be used to manage oliguria or anuria in patients.

A
  1. Furosemide
  2. Osmotic diuretic - Mannitol or 20% dextrose
  3. Dopamine CRI
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103
Q

What has proven to work synergistically with dopamine CRI in dog models of AKI?

A

Furosemide

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104
Q

What are the 2 categories of substaging in IRIS CKD?

A
  1. Proteinuria (proteinuria, nonproteinuria, borderline)

2. Hypertension

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105
Q

What has been proven in dogs and cats to lower severity of proteinuria?

A

o Evidence of dietary therapy (n-3 polyunstaurated fatty acids (PUFA)) (Brown et al 1998), and ACE-I in dogs and cats to lower UPC, glomerular filtration pressures, and limiting structural changes in kidneys, and/or slow the decline in GFR
§ Benefit of diet (n-3 PUFA supplementation, and Protein, Na, Phos restrictions): Jacob et al 2002 for dogs and Elliott et al 2000 and Plantinga et al 2005 for cats = Unable to determine precise factors that improved outcome (ie used commercial diets)
§ Benefit of ACE-I (Grauer et al 2000 and King et al 2006)

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106
Q

Name 4 organs that are most prone to end-organ damage from hypertension?

A

Organs most prone to damage from systemic hypertension: 1. Heart, 2. Kidney, 3. Brain, and 4. Eyes

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107
Q

What is the treatment goal for hypertension in CKD?

A

Goal: Reduce systolic BP < 160 mmHg to minimize risk of extrarenal end organ damage

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108
Q

Name the 4 stages of IRIS CKD in dogs.

A

Stage 1: < 1.4 mg/dl
Stage 2: 1.4-2 mg/dl
Stage 3: 2.1-5 mg/dl
Stage 4: >5 mg/dl

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109
Q

Name the 4 stages of IRIS CKD in cats.

A

Stage 1: < 1.6 mg/dl
Stage 2: 1.6-2.8 mg/dl
Stage 3: 2.9-5 mg/dl
Stage 4: >5 mg/dl

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110
Q

Name the ranges of proteinuria for IRIS CKD

A 
Based on UPC
Nonproteinuria (NP) = < 0.2 (dogs and cats)
Borderline proteinuria (BP):  0.2-0.4 (cats), 0.2-0.5 (dogs)
Proteinuria (P):  > 0.4 (cats), > 0.5 (dogs)
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111
Q

Name the ranges of hypertension for IRIS CKD.

A 
Based on systolic BP
Minimal Risk:  < 150 mmHg
Low Risk:  150-159 mmHg
Moderate Risk:  160-170 mmHg
High Risk:  > 180 mmHg
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112
Q

What RBC parameter may indicate aluminum toxicity?

A

Microcytosis

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113
Q

What molecule is releases when iCa is low?

A

Hypocalcemia = ↑ PTH by posttranscriptional mechanism (parathyroid gland membrane Ca-sensing receptor to stabilize PTH ribonucleic acid)

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114
Q

What are the 3 main roles of PTH?

A

↑ PTH →

  1. ↑ Renal Ca reabsorption from ascending Loop of Henle, distal tubule, and collecting tubule
  2. ↑ Ca reabsorption from bone
  3. Enhancing formation of calcitriol (1,25-dihydroxycholecalciferol) from 25-hydroxycholecalciferol by kidneys
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115
Q

What are the main roles of calcitriol?

A

Calcitriol promotes ↑ Ca by:
1. Enhancing absorption of Ca from intestine
2. Facilitating PTH effects on bone (resulting ↑ Ca → ↓ PTH)
® Independent of Ca: Calcitriol inhibits synthesis and storage of PTH by activating Vitamin D receptors (VDR) → ↓ PTH gene transcription

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116
Q

How does calcitriol affect PTH?

A

Independent of Ca: Calcitriol inhibits synthesis and storage of PTH by activating Vitamin D receptors (VDR) → ↓ PTH gene transcription

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117
Q

How do levels of phosphorus influence intestinal Ca and Phos absorption via renal calcitriol production?

A

® Levels of phos influence intestinal Ca and Phos absorption via renal calcitriol production
® ↑ Phosphorus (hyperphosphatemia) inhibits renal 1-a hydroxylase activity (renal conversion of 25-hydroxycholecalciferol to calcitriol (active form of Vit D))
® ↓ Calcitriol → Phos retention and hyperphosphatemia which ↓ phos intestinal absorption
® If ↓ Phos = ↑ Calcitriol → ↑ Intestinal absorption of phosphate

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118
Q

What is the effect of PTH in the proximal tubules in relation to phosphorus?

A

PTH blocks proximal tubule from resorbing phos = phosphaturia

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119
Q

What is the inciting event in renal secondary hyperparathyroidism?

A

Inciting Event = Retention of Phosphorus dt ↓ renal excretion

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120
Q

What are the effects of hyperphosphatemia in development of renal secondayr hyperparathyroidism?

A

o Hyperphosphatemia → ↑ PTH (direct effects of phos on parathyroid gland and ↓ renal production of calcitriol by inhibiting renal 1-a hydroxylase activity
o Hyperphosphatemia may also complex with iCa (thus ↓ iCa) = leading to further ↑ PTH
§ ↑ PTH → phosphaturia (phosphate in serum to normal range)
· Secondary hyperparathyroidism long term is the “trade off” for short term serum control of Phos levels
o As renal dz progresses, capacity to prevent hyperphosphatemia is insufficient and loss of nephrons means less calcitriol produced

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121
Q

What is the “trade - off” hypothesis of renal secondary hyperparathyroidism?

A

Secondary hyperparathyroidism long term is the “trade off” for short term serum control of Phos levels
o As renal dz progresses, capacity to prevent hyperphosphatemia is insufficient and loss of nephrons means less calcitriol produced
§ Persistent calcitriol deficiency may cause parathyroid gland hyperplasia and hypertrophy with sustained automonous PTH secretion (tertiary hyperparathyroidism) = Resistant to conventional medical interventions (may need surgical reduction in renal mass to normalize PTH levels)
§ Thus need to maintain calcitriol in CKD to prevent tertiary hyperparathyroidism, since calcitriol is antiproliferative effects, ↓ PTH gene transcription, and represses parathyroid cell proliferation

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122
Q

What are the 3 main goals of managing divalent ion disorders in CKD?

A
  1. ↓ Hyperphosphatemia and mechanisms underlying phosphate rentention
  2. Restore adequate levels of active Vitamin D (calcitriol)
  3. Normalize serum Ca
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123
Q

What are 3 treatment options for managing divalent ion disorders in CKD?

A
  1. ↓ Dietary Phosphorus (serum phos < 6 mg/dl; ideal 4.5-5.5 mg/dl)
    § CKD diet have 75% less phos = helps to ↓ or normalize PTH levels in most patients with CKD Stage II and many patients with CKD Stage III (diet alone is not sufficient for Stage IV)
    1. Intestinal phosphate binders (Aluminum, Ca, lanthanum): Bind irreversibly to phosphate in intestinal lumen, bound phosphate nonabsorbale, cations are released and may be absorbed
      § Sevelamer hydrochloride (Renagel): Polymer that does not release cations, very expensive and not more effective
    2. Calcitriol (once serum phos < 6 mg/dl)
      § Since Calcitriol ↑ intestinal absorption of BOTH Ca and phos, failure to correct hyperphosphatemia prior can result in an ↑ Ca x Phos product = soft tissue mineralization
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124
Q

Why is it important to ensure that phosphorus is normal (<6 mg/dl) prior to calcitriol treatment?

A

Since Calcitriol ↑ intestinal absorption of BOTH Ca and phos, failure to correct hyperphosphatemia prior can result in an ↑ Ca x Phos product = soft tissue mineralization

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125
Q

What are the main benefits of calcitriol treatment in CKD?

A

· Enhanced survival, appetite, activity, alertness, and interactivity with owners
o Improved survival in dogs with Stage III and IV (Polzin et al 2005); unknown in cats
o Failed to confirm benefit of reducing CS of CKD (hard since studies performed in animals with stable disease that were not showing overt CS and phos aggressively managed thus less hyperparathyroidism)
· ↓ PTH secretion
· Systemic Role in direct activation of VDR (humans, Vit D promotes longer survival independent of Ca, Phos, or PTH)
o Dog studies showed little effect of calcitriol on survival and differences in Serum Phos, Ca, PTH levels
o Humans: Paricalcitol (selective activator of VDR), more efficacy to side-effect profile, less morbidity, and better survival

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126
Q

When is calcitriol indicated in dogs and cats with CKD?

A

· Randomized controlled clinical trial – Calcitriol prolonged survival and forestall development of uremic crises with Stage III and early Stage IV
o Rate of progression of CKD was slower in animals getting calcitriol = renoprotective effect (same effects seen in humans)
· Calcitriol INDICATED in dogs with Stage III and early Stage IV
o Should be started even if PTH is not high (hard to manage hyperparathyroidism thus early intervention or prophylaxis)
o Unknown values in dogs with Stage I and II
Cats with CKD
· Insufficient data (1 yr randomized, controlled study for Stage II, III, IV failed to show clinical benefit of calcitriol in cats with CKD

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127
Q

What is the problem long-term with calcitriol and hyperparathyroidism?

A

o Long term hyperparathyroidism with parathyroid hyperplasia = deficiency of VDR on hyperplasic parathyroid cells = hyperparathyroidism that is refractory to calcitriol
· Calcitriol can induce formation of VDR on parathyroid cells, thus if long standing deficiency consider a prolonged calcitriol course or “pulse” therapy

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128
Q

What are the effects of calcitriol on the parathyroid gland and GIT during supplementation?

A

May induce formation of greater numbers of VDR on parathyroid cells, making gland more responsive to action of calcitriol, may also minimize likelihood of inducing hypercalcemia (promoting intestinal Ca absorption) o Actions on newly formed intestinal cells leaving Crypts of Lieberkuhn (ability of cells to absorb Ca dependent on exposure to calcitriol during development)
o Calcitriol has short T1/2 (4-6 hrs), thus less frequency administration means that less cells are exposed to calcitriol and thus less are primed to enhance Ca absorption

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129
Q

What is a potential complication of calcitriol supplementation?

A

Hypercalcemia

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130
Q

What are contraindications for calcitriol suppplementation?

A

hyperphosphatemia, hypercalcemia, ↑ Ca x Phos product

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131
Q

What type of product is used in humans in substitute of calcitriol?

A

Selective VDR activators: paricalcitol (Zemplar) and doxercalciferol = less changes in Ca and phos levels with adequate control of hyperparathyroidism (No reports in dogs or cats)

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132
Q

What monitoring is required during calciltriol treatment and what are the main goals of treatment?

A

· Serum Ca, iCa, phos, and PTH levels MUST be monitored (check q2-4 weeks until dose is stable), then recheck q3-6 months
· Goal of Therapy: Maintain serum phos, Ca, and PTH levels within normal limits

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133
Q

Describe the mechanism of development of renal secondary hyperparathyroidism in CKD?

A

Reduced in GFR initiates development of hyperparathryoidism by promoting phosphorus retenion and hyperphosphatemia
Phosphorus retention suppressess the renal enzyme (1-alpha hydroxylase) - conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol (calcitriol) = Most active form of Vitamin D
Calcitriol deficiency, hypocalcemia, and hyperphosphatemia = contribute to development of hyperparathyroidism and parathyroid gland hyperplasia

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134
Q

What are the 2 types of hemodialysis?

A

Intermittent hemodialysis (IHD) and Continuous Renal Replacement Therapy (CRRT)

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135
Q

What is the general principle behind dialysis?

A

· Removes uremic toxins from blood by diffusion
· Blood from patient carried in disposable tubing (extracorporeal circuit) → Dialyzer (artificial kidney) with porous membrane (Size and charge are major determinants of which particles are filtered) → Blood returned to patient
o Small to middle sized molecules (urea and Crt) diffuse through pores into dialysate solution on other side
o Large molecules (albumin and cells) remain in blood

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136
Q

Why do you need to monitor for hypocalcemia during dialysis?

A

· Citrate via CRI into extracorporeal circuit to bind calcium to prevent coagulation in circuit (thus need to give CaCl centrally in patient to avoid hypocalcemia, also need to check blood Ca to adjust both doses)
o Citrate CONTRAINDICATED with hepatic dysfunction

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137
Q

What are the main indications for dialysis?

A

· Most common = ARF (Goal of ACUTE dialysis: Resolve life threatening disorders (hyperkalemia, pulmonary edema), control uremia (↓ uremic complications), allowing time for renal repair
o Leptosporsis, bacterial pyelonephritis, toxic nephropathy (ethylene glycol, lily ingestion, grapes/raisins, aminoglycosides), renal ischemia, ureteral obstruction (to tx acute uremia syndrome prior to sx; 1-3tx before sx or 2-4 tx prior to renal transplantation)
· CHRONIC Dialysis: Control CS associated with CKD for the rest of patient’s life

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138
Q

What is the indication for dialysis with certain drugs/toxins?

A

· Certain drugs and toxins can be removed (low MW with little protein binding are readily removed)
o IDH with charcoal perfusion cartridge in series with dialyzer (filters blood across microencapsulated charcoal beads to absorb toxic compound)
o Consider that doses of medications may need to be adjusted since they will also be lowered

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139
Q

What is therapeutic plasmaphersis?

A

Therapeutic plasmapheresis (plasmapheresis cartridge = large pores to allow removal of albumin and globulins to separate plasma from cellular components)

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140
Q

Name 4 events that would initiate dialysis?

A

· Anuria or oliguria that does NOT respond to volume expansion and diuretics
o Volume overload (pulmonary edema or pleural effusion dt inappropriate urine output relative to IVF rate)
· Hyperkalemia (start medical management with insulin, dextrose, bicarb, Ca) – Rapid removal of K with IHD
· Severe uremia (BUN> 100 mg/dl, Crt <> 10 mg/dl) or uremia that does not respond to medical management in the first 24 hours
o Humans: Earlier dialysis started in renal failure improves outcome and likelihood of return of renal function
· For CKD: Failure of medical management to control CS of uremia (anorexia, lethargic, vomiting) – Need to place feeding tube
· For toxins: Start ASAP (ex: Antifreeze, get dose of 4-methylpyrazole (dogs) and ethanol (Cats) to slow the metabolism of ethylene glycol

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141
Q

Compared and contrast the different treatment protocols for dialysis?

A

· IHD: Efficient method of solute removal = Good for ARF, CKD, acute toxicities, and fluid removal
o Severe uremia (rapid ↓ urea can lead to untoward effects, first few IHD tx are short, 3-7 short daily tx to gain gradual control, followed by 4-5 hr duration tx 3 times/week, performed until patient regains renal function)
o If severe uremia in unstable patient (first tx long 6-> 24hrs with slow blood flow to gradually control uremia to reduce complications = slow low-efficiency dialysis)
· CRRT: Good for ARF and fluid removal (applied for short duration)
o Blood flow 2-3 ml/kg/min compared to IHD 5-20 mk/kg/min and slow dialysate flow rate (8-34 ml/min compared to 500 ml/min in IHD): Net fluid removal rate based on patient’s hydration (solute cleranace, 0-35ml/kg/min)
o Clinical improvement (increased urine putput, etc) may prompt decreased blood or dialystae flow rate to wean patient off of CRRT

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142
Q

What is dialysis disequilibrium syndrome?

A

Rapid decline in blood osmolality caused by removal of solutes (esp urea) by dialysis · Results in the osmoles are removed from the blood faster than diffuse from the intracellular compartment = intracellular hyperosmolaity = cellular swelling (leading to CNS signs like seizures and mentation changes)
· Higher Risk with: Severe Azotemia, Smaller Blood Volume, preexisiting neurologic signs
· Thus use: Slow, low-efficiency dialysis or CRRT to lower the likelihood of this complication

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143
Q

What is the outcome with Dialysis in AKI?

A

· 40-60% patients with ARF treated with dialysis survive (depending on the etiology)
o Infectious causes of ARF: 60-70% survival rate
o Hemodynamic and metabolic causes: 40-56% survival rate
o Toxic Causes (ethylene glycol): 20-30% survival rate
· Extends time to allow for renal repair and recovery
o Can take 4 weeks to 3-6 months after renal injury

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144
Q

What at the 3 major infectious dz that you should be concerned about in cats undergoing renal transplantation screening?

A
  1. FeLV
  2. FIV
  3. Toxoplasmosis
    Concern since patient will need to undergo immunosupression
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145
Q

When a patient with CKD has a creat < 6 mg/dl is renal transplanation recommended?

A

If moderate azotemia (Crt < 6 mg/dl) consider medial management (G-tube, fluids, dietary, EPO) – survival times parallel renal transplant survival times in these patients

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146
Q

Is tissue typing performed in feline renal transplantation?

A

No!

Screening (FeLV, FIV, IgG/IgM Toxo titers, imaging of kidneys, blood type)

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147
Q

What would need to be be screened to prevent allograft rejection in canine renal transplanations?

A

Dog Lymphocyte Antigen (DLA)

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148
Q

What post-op problem is seen commonly in dogs after renal transplanatation?

A

Enteroplication in DOGS: High incidence in dogs of intussuspection follow allograft implantation, also helps to administer opioids pre-op and intra-op (NOT needed in cats)

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149
Q

What is the mainstay drug for immunosupression to prevent allograft rejection in renal transplanation?

A

Cyclosporine: Calcineurin inhibitor with specific anti-T cell activity
Ketoconazole can be added to dose reduce the cyclosporine

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150
Q

What is the overall outcome of feline renal transplantation?

A

· 80% cats survive perioperative period and discharged; 60% survive to 6 months after sx (Adin et al 2001)
· 42% cats remaining alive at 3 yrs
· Overall median survival 22 months (Matthews and Gregory, 1997)
o Median Crt 8 mg/dl and medical options exhausted
o Improves QOL and duration but not to normal cats lifespan
· Harder to predict in dogs, small number of transplants performed and variation in drugs used
o Survival in experimental dogs exceeds those with naturally occurring renal dz
§ Only about 50% dogs survive first 2 months after kidney transplantation, high rate of opportunistic infections may occur in patients with long term survival (Gregory et al 2006)

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151
Q

What percentage of patients with CKD will have feeding tube stoma site complications?

A

stoma site complications in 46% dogs (may be dt impaired immune function, increased susceptibility to infection, delayed wound healing dt malnutrition and/or uremia)

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152
Q

What percentage of patients will remove their own G-tube?

A

20% dogs will remove their own G-tubes (Elliott et al 2000) = ER situation, peritonitis, new tube needs to be placed ASAP
If tube in for < 7 days, check with radiographic contrast leakage, may need laparotomy

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153
Q

How many dogs and cats get hypertension related to CKD and what is the mechanism?

A

Hypertension in 19.4% felines and 61% canine with renal dz (exact cause unknown – interactions btwn heart, kidney, endothelial signaling, and autonomic NS)

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154
Q

How are the eyes, kidneys, heart, and brain affected by hypertension?

A

o Hypertensive retinopathy/choroidopathy: Retinal edema, tortuous vessels, hemorrhage, retinal detachment (cats come in for acute blindness)
o Some cats, hypertension will precede azotemia with early CKD
o Murmur, arrhythmia, gallop rhythm secondary to hypertension = cardiac muscle hypertrophy
o Hypertensive encephalopathy: Head tilt, ataxia, depression, seizures (hypertension overwhelms cerebral vasculature autoregulatory mechanisms)

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155
Q

What is the initial drug of choice for hypertension in dogs?

A

ACEi

As long as there is no end-organ damage

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156
Q

What is the MOA of angiotensin-converting enzyme (ACE) inhibitor?

A

o Blocks conversion of Ang I to Ang II (powerful vasoconstrictor), systemic vasodilation when blocked
o Ang II directly promotes Na absorption in proximal tubules → IV Expansion
o Ang II stimulates aldosterone release = Na and water reabsoprtion
o Can worsen azotemia therefore check renal values (start at lowest possible dose)

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157
Q

What is the initial drug of choice for hypertension in cats?

A

Since 50% of cats failure to respond to ACEi = Calcium channel blockers (amlodipine)

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158
Q

What is the MOA of calcium channel blockers such as amlodipine?

A

o Blocking influx of Ca needed to cause smooth muscle contraction and thus ↓ systemic vascular resistance (amlodipine: long acting, q24 hr dosing, and gradual effect)

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159
Q

Why should calcium channel blockers such as amlodipine not be used as monotherapy in dogs?

A

§ Humans and dogs: Ca channel blockers may worsen renal dz (paradoxic effect that Ca Channel blockers preferentially dilate the afferent arteriole of glomerulus = glomerular hypertension)
· Therefore DO NOT use in dogs as monotherapy! (Same effect is NOT seen in cats)
§ Cats treated with amlodipine live longer and with fewer hypertensive complications (safe as monotherapy in cats)

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160
Q

What is a potential complication in cats with spironolactone?

A

Horrible facial excoriations

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161
Q

What are potential effects of spironolactone during hypertension?

A

May protect the heart, brain, and kidneys from effects of hypertension, may also help to reduce hypertensive-induced fibrosis of target organ Spironolactone: ↓ Na resorption and K excretion

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162
Q

How does the kidney result in increased preload that can contribute to hypertension?

A

By activating RAAS - Na resorption (water follows)

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163
Q

Name the mechanism of anemia in renal failure.

A
  1. Blood Loss, 2. RBC destruction, 3. Failure of bone marrow to produce RBCs
    o Can have > 1 etiology in CKD (Normally = blood loss and lack of RBC production)
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164
Q

Describe the pathogensis of uremic gastropathy.

A

· Dogs = gastric edema, vasculopathy, glandular atrophy, mineralization, submucosal artertitis, less common (ulceration or necrosis) (Peters et al 2005)
· Can have significant GI bleeding in certain patients: GASTRIN (polypeptide from G cells in stomach, renally excreted)
o Cats with CKD = ↑ Gastrin levels (but relationship btwn gastrin and Crt is not linear) (Goldstein et al 1998)
o Persistent ↑ Gastrin = gastric hyperacidity and mucosal erosions (esp if administering NSAID or steroids)
o Upper GI Bleedings (hematemesis, melena, hematochezia)
· May not see melena if amount of bleeding is very small
· Uremic enterocolitis = Marked large bowel diarrhea with frank blood

165
Q

What is the main mechanism of increased bleeding tendency in uremic patients?

A

Chief Uremic Hemostatic Changes = IMPAIRED platelet FUNCTION

166
Q

Name 4 mechanisms of thrombocytopathy in uremic patients.

A
  1. Defective platelet cyclooxygenase = ↓ thromboxane A2 production
  2. Abnormal concentrations of large multimers of von Willebrand factor (total von Willebrand factor is normal)
  3. Abnormal intracellular cyclic adenosine monophosphate
  4. Abnormal intracellular Ca mobilization
    · All cause impaired subendothelial adhesion of platelets and abnormal platelet aggregation
167
Q

What is erythropoietin and how is it produced?

A

· EPO: Hematopoietic growth factor, stimulates erythrogenesis in anemia, deficiency most common with CKD
· EPO Production: Peritubular interstitial cells of the outer medulla and inner cortex (MAIN), about 10-15% in liver
o Renal hypoxemia (anemia or hypoxia) result in EPO release = Stimulate RBC growth and differentiation of colony-forming unit-erythroid cells of bone marrow (takes about 5 days to see new RBCs in circulation)
o EPO also induced hemoglobulin and RBC membrane protein synthesis and facilities RBC release from bone marrow
o With CDK and reduced renal mass: Less EPO produced (Relative EPO Deficiency)

168
Q

Name 3 other factors that can contribute to anemia in CKD.

A

· Humans with CKD and poor nutrition =
o Vitamin B deficiencies: B12 (cobalamine), folic acid, niacin, B2 (riboflavin), and B6 (pyridoxine)→ All important in erythropoiesis
o Variety of uremic toxins result in poor bone marrow response
§ Not evaluated in dogs or cats
· Protein-calorie malnutrition can contribute to nonregenerative anemias
· Iron deficiency (needs iron therapy, but if anemia of chronic inflammatory disease iron overdose is possible)

169
Q

What are the components on an iron panel?

A
  1. Serum iron (mobile form of iron)
  2. total iron binding capacity (indirect measurement of transferrin, serum carrier molecule of iron)
  3. ferritin (storage form of iron)
170
Q

Describe the differences in iron panels for iron def anemia and chronic inflammation anemia?

A

o Iron def anemia: All results low and decreased iron stores in bone marrow (more invasive test!)
o Chronic Inflammatory Anemia: Serum iron low, transferrin low to normal (iron sequestration), ferritin normal to increased

171
Q

Name the 2 forms of erythropoietin therapy?

A
  1. Recombinant human EPO (r-HuEPO)

2. Darbepoetin

172
Q

What is imperative to supplement when administering EPO?

A

Iron (either oral - ferrous sulfate or IM - iron dextran)

173
Q

What is the major complication of using recombinant human EPO?

A

Produce anti-EPO antibodies!!!
□ 60-100% dogs getting r-HuEPO developed anti-EPO antibodies, clinically significant anemia reported in 20-70% of dogs and cats getting EPO (presumptively related to anti-r-HuEPO antibodies)
® Antibodies develop within first few months, but can have late onset as well
® Antibodies suppress native EPO action on bone marrow precursor cells = profound anemia
◊ Precipitous ↓ PCV following response to treatment (retics will ↓ to zero prior to drop in PCV)
} Stop EPO therapy and consider transfusion
} Antibodies can decline over 2-12 months, anemia secondary to EPO antibodies can be reversed, but patient may be transfusion dependent for weeks to months (anemia that required EPO will persist, thus many animals are euthanized)

174
Q

What is a potential complicaiton with administration of recombinant human EPO in cats?

A

Hypertension (humans and CATS): Noted in 60% of cats, thus check BP

175
Q

What is darbepoetin?

A

Derivative of r-HuEPO with more attached carbohydrates to slow clearance and ↓ freq of administration

176
Q

Why is it thought that darbepoetin is less likely to result in antibody formation?

A

Addition of carbohydrate moieties of darbo may shield protein backbone from immunologic exposure and thus less likely to cause antibody formation (anti-r-HuEPO antibodies are directed against protein component)

177
Q

What happens to the lifespan of RBCs in uremic patients?

A

Life span of transfused RBC SHORTED if patient uremic

178
Q

How does hemoglobin-based oxygen carrier (Oxyglobin) affect creatinine?

A

Color of serum changes (red): Crt underestimated and BUN/electrolytes not affected

179
Q

Describe the pathogenesis of urinary tract infection.

A

· Caused by ascending migration of pathogenic organisms from distal urogenital tract (normally present in distal urogenital tract and host defense is altered to allow colonization)
o Normal micturition
o Normal Anatomy: High pressure zone within urethra, surface characteristics of urothelium, urethral peristalsis, length of urethra, male dogs (prostatic secretions: Ig and antibacterial components), good blood supply and flow, ureterovesical flap valves, ureteral peristalsis
o Mucosal Defense: Antibody production, surface layer of gylcoasminoglycans, intrinsic mucosal antibacterial properties, rapid turnover of urothelial cells
o Urine Properties: Antimicrobial = pH (caution from Vaden), hyperosmolaity, Tamm-Horsfall mucoproteins, high concentration of urea and organic acids

180
Q

Name the 4 most common Gram Negative organisms associated with UTIs?

A

E. coli
Proteus spp
Klebsiella spp
Pseudomonas aeruginosa

181
Q

Name the 3 most common Gram Positive organisms associated with UTIs?

A

Staph spp
Strep spp
Enterococcus spp

182
Q

What are the quantitative urine cultures for the 3 methods of urine collection for UTIs?

A

Cystocentesis: >1000 (dogs/cats)
Catheterization: >10,000 (dog) and > 1000 (cat)
Voiding: >100,000 (dog) and > 10,000 (Cat)

183
Q

What is the MIC?

A

Minimum Inhibitory Concentration = Lowest drug concentration that inhibits microbial growth (NOT all bacteria are killed) o In vitro MIC depends on ability to reach given concentration in the plasma

184
Q

What is the breakpoint for cultures?

A

· Breakpoint = Arbitrary criterion, set at point at which majority of all isolates for that microbe are inhibited (determined by National Committee for Clinical Laboratory Standards)
· The further the MIC for individual organism is from the breakpoint, the more likely a drug is effective

185
Q

What are the general rules of MIC and breakpoints?

A

· General Rule: Avoid choosing a drug when MIC is approaching the breakpoint (“intermediate susceptibility), if selected use dose that his at high end of normal dosing, also consider that if drug excreted through kidney, it may reach higher levels in the urine that may be effective

186
Q

What is the ideal empirical treatment for uncomplicated UTIs?

A

If empirical tx: Board –Spectrum = Cephalosporins (good against E. coli and Staph), TMS
o Avoid fluoroquinolones: Inherent resistance of many gram positive bacteria and development of resistance patterns in gram negative organisms (esp E. coli)

187
Q

What is the difference between a relapse of a UTI and reinfection?

A

o Relapse = UTI caused by same organism that recurs after stopping tx (most occur quickly but can be months, Freitag et al 2006) = · Relapsing Infection = Infection recurs rapidly after stopping tx, with same organism with same sensitivity pattern
o Reinfection = UTI caused by a different organism that recurs at variable intervals after tx stopped

188
Q

What is the likely cause of a relapsing UTI?

A

· Relapsing Infection = Infection recurs rapidly after stopping tx, with same organism with same sensitivity pattern
o Problem: Organism is in deep seated niche within urinary tract and is “protected” (bacteria killed in urine but abx cannot reach bacteria in deep tissue)
§ Sources: Chronic pyelonephritis, prostate, struvite uroliths, any submucosa or location associated with partially obstruction (uretherolith)

189
Q

How can E. coli lead to a relapsing UTI?

A

Experimentally uropathagenic E. coli can enter host bladder epithelial cells and remain quiescent for period time before leaving the cell and replicating again

190
Q

What are underlying potential problems with reinfection UTIs?

A

· Reinfection with a different organism at variable intervals
o Problem: Multiple! Poor systemic immune function (Cushings, immunosuppressive drugs), loss of antimicrobial properties of urine (Glucosuria, poor concentrating ability), anatomic abnormalities (stricture, urolith, previous sx, neoplasa), physiologic predisposition (urine retention from neurologic dx, decreased urethral sphincter tone)

191
Q

What can be frustrating for reinfection UTIs work-ups?

A

o About 30% of dogs, no identifiable underlying reason is noted (esp in females, Sequin et al 2003) – Assumed to be defect in local immunity

192
Q

What is a persistent UTI?

A

· Original causative bacteria continues to be present during therapy that should be effective (based on UC +Sen)
o Diagnosed: ONLY by performing a UC while that patient is receiving the ABX (misconception: that all UC will be negative when a patient is on ABX, only true if drug is effective, not true if organism is resistant)

193
Q

What is a superinfection UTI?

A

· Infection with a different organisms in the face of tx for the original organism
· Diagnosed ONLY by performing UC during therapy (normally associated with indwelling urinary tubes)

194
Q

Name antibiotics that can pentrate renal tissue.

A

§ ABX that penetrate the renal tissue: trimethoprim, chloramphenicol, nitrofurantoin, some quinolones, aminoglycosides (not recommended for long term use dt nephrotoxicity)
· Optimum duration unknown – 4-6 weeks recommended

195
Q

What is suppressive therapy for relapsing UTIs?

A

· Suppressive therapy is used in animals with no underlying abnormalities that can be corrected = low dose long term administration of ABX to assist in UTI control (Sequin et al 2003)
o Single dose of effective ABX once daily (normal dose given, but give at night to help concentrate in the urine)
o Should be started when the infection is under control (negative UC)
o Drugs for Suppressive Therapy: Trimethoprim, nitrofurantoin (neurologic and heaptic toxicity), cephalexin, and enrofloxacin
§ Risks: ABX resistance and/or drug toxicity

196
Q

What is an alternative to suppressive therapy for relapsing UTIs?

A

Not treating unless CS present o Risk: Infection could become systemic

197
Q

Name antibiotics that can pentrate prostatic tissue.

A

ABX with prostatic penetration: Trimthoprim, chloramphenicol, quinolone

198
Q

Name 2 local antiseptics that can be used in the urinary bladder.

A

Local antiseptic (tris-ethylenediaminetetraacetic acid) and urinary antiseptics (methenamine mandelate)

199
Q

What is the normal measurement of kdienys on rads?

A

Rads: 2.5-3.5X length of L2 (dogs); 2.4-3X length of L2 (cats)

200
Q

What is the most common cause of renomegaly in dogs?

A

Primary renal neoplasia

201
Q

What is the most common causes of renomegaly in cats?

A

Renal neoplasia (lymphoma), granulomatous infiltration (due to FIP), perinephric pseudocysts, hydronephrosis, and polycystic kidney disease

202
Q

What is the most common primary renal neoplasia in dogs?

A

Renal Cell Carcinomas

203
Q

Which renal tumor can result in polycythemia?

A

Renal Cell Carcinomas

204
Q

Name the sites of metastasis for renal cell carcinomas.

A

o Site of metastasis: Regional lymph node, liver, and contralateral kidney; CNS (spine, spinal cord, and brain); and lungs (Klein et al., 1988)
o Local Extension: Ipsilateral adrenal gland and abdominal serosal surfaces

205
Q

What are the histologic types of renal cell carcinomas in dogs and cats?

A

Histologic types of RCC → tubular (most common), papillary, tubulopapillary, solid/undifferentiated forms (Henry et al., 1999)

206
Q

What is the treatment for renal cell carcinomas?

A

o Nephrectomy → tx of choice for solitary renal tumors without azotemia or metastasis (partial nephrectomy in humans if not locally extensive)
o No standardized adjuvant chemotherapy protocols → respond poorly to most agents
(doxorubicin, cisplatin, and Interferon-α)

207
Q

What is the biologic behavior of primary renal hemangiosarcomas?

A

o Primary renal hemangiosarcoma may be less aggressive than visceral hemangiosarcoma
§ Slower rate of progression; ¯ frequency of macroscopic metastasis at diagnosis (Locke and Barber, 2006)
§ Mean survival: 278 days (14 dogs); worst outcome hemoperitoneum
§ Chemotherapy: Doxorubicin-based protocol likely is appropriate, others not evaluated

208
Q

What is the most common sarcoma of the kidneys?

A

o NCSU: 24% primary renal tumors (dogs) → hemangiosarcomas

209
Q

Which renal tumor arises from undifferentiated embryonic elements?

A

Nephroblastoma
Called Wilm’s tumor (humans)
o Nephrectomy may be curative, + adjunctive chemotherapy when histology suggests a less differentiated, more aggressive tumor
o Sites of mets: Spinal cord (most common)

210
Q

What is the most common site of mets for nephroblastomas?

A

Spinal cord

211
Q

What breed of dogs gets multifocal renal cystadenocarcinoma and nodular dermatofibrosis?

A

GSD

212
Q

What renal disease is seen in related families of GSDs?

A

syndrome of bilateral multifocal renal cystadenocarcinomas, nodular dermatofibrosis, and uterine leiomyomas
o Affected dogs have mutation in 1 allele of folliculin (protein of unknown function)
· Long term prognosis is POOR, due to metastatic disease and renal failure (common), mean age at death 9 yrs
· Treament
o Nephrectomy = contraindicated → both kidneys affected
o Chemotherapy possible, but no successful reports (paclitaxel and pirfenidone)

213
Q

What is the chief compliant for GSD with multifocal renal cystadenocarcinoma and nodular dermatofibrosis?

A

Evaluation of diffuse skin nodules (mean age 8 yrs)

214
Q

What is the most common renal tumor in cats?

A

Renal Lymphoma

215
Q

What is the chief compliant in cats with renal lymphoma?

A

Acute renal failure (up to 80%)

216
Q

What is the chief compliant in cats with renal lymphoma?

A

Acute renal failure (up to 80%)
What virus is strongly associated with development of renal lymphoma in cats? FeLV strongly associated with development of renal lymphoma (50% affected cats are FeLV +)

217
Q

What is the treatment protocol for renal lymphoma?

A

CHOP
§ About 60% achieve complete remission → mean duration of remission 372 days (median 127 days), mean survival 408 days (median 169 days) (Mooney et al., 1987)
§ Nephrectomy is not recommended → both kidneys invariably are affected
§ Azotemia improves dramatically with tx of lymphoma, so renal failure is not cause of death in most, but residual renal damage may persist

218
Q

Name 3 negative prognostic factors in renal lymphoma?

A
  1. involvement of other organ systems (particularly CNS)
  2. FeLV infection
  3. Severity of renal failure
    (Mooney et al., 1987)
219
Q

Why is nephrectomy possible in dogs with unilateral renal lymphoma?

A

primary renal lymphoma, RARELY have involvement of other organs
o Nephrectomy is possible in dogs if unilateral (only if azotemia and urine concentrating is ok), followed with chemotherapy

220
Q

Which renal tumor accounts for 20-30% of primary renal tumors in dogs/cats but is not of renal origin?

A

Transitional Cell Carcinomas

o Not renal origin, but they invade renal parenchyma

221
Q

What type of extrarenal neoplasm is likely to met to the kidney?

A

Carcnimoas

Renal Blood Flow = 15% of total CO

222
Q

Name 4 paraneoplastic syndromes of renal tumors.

A
  1. Polycythemia → secondary to excess production of erythropoietin → most common paraneoplastic syndrome
  2. Extreme leukocytosis → Excess production of granulocyte-macrophage colony-stimulating factor
  3. Hypertrophic osteropathy Palpable firm swelling of distal long bones (most prominent in metaphyseal regions) can be VERY painful § May occur with extreme leukocytosis
  4. Hepatopathy: ↑ ALP, GGT (no ↑ bilirubin), common in humans, reports in dog with sarcomatoid RCC
223
Q

What is the pathogenesis of polycythemia as a paraneoplastic process?

A

· Polycythemia → secondary to excess production of erythropoietin → most common paraneoplastic syndrome
o Not true paraneoplastic syndrome, as it may results from renal tumors ¯ O2 levels → excessive EPO production by nonneoplastic renal epithelial cells
o Could be incidental finding or patient presents with epistaxis or CNS signs (disorientation, seizures)
o Measure serum erythropoietin (question value!), since erythrocytosis and renal mass are enough for dx
o Reports with renal carcinomas, fibrosarcoma, and lymphoma; cats: renal carcinoma
o Nephrectomy can resolve polycythemia but mets of functional cells may prevent resolution

224
Q

What extra-renal paraneoplastic process is most common?

A

· Azotemia → Paraneoplastic hypercalcemia, secrete PTHrp or other humoral factors that ↑ calcium release from bones and promote calcium absorption from GIT
o Hypercalcemia of malignancy: Higher serum calcium and phosphorus → more likely to develop kidney dz than those with hyperparathyroidism
o Kidney damage from mineralized tubular basement membranes, dysregulated renal tubular cell mitochondrial function, dehydration 2nd to hypercalcemia-induced polyuria, changes in GFR

225
Q

What treatment options can be considered for paraneoplastic hypercalcemia?

A
  1. Diuresis (0.9% NaCl)
  2. Loop diuretics (Lasix): ↑ renal Ca excretion (once hydrated)
  3. Bisphosphonate drugs: Inhibit osteoclast function and↓ mobilization of Ca stores from bone
    □ Pamidronate is highly effective
  4. Prednisone: Promote calciuresis (may worsen long-term prognosis)
226
Q

What type of cancer can lead to damage to the kidneys by a product that they secrete?

A

· Kidney disease high in humans with monocolonal gammopathies 2nd to multiple myeloma or B-cell lymphoma
o Obstruction of renal tubules by light chains, toxicity to renal tubules dt resorption of proteins, deposition of Ig light chains within renal parenchyma; ¯ renal perfusion by hyperviscosity, tumor infiltration into kidney
o Cast nephropathy (obstruction of renal tubules and tubular cell toxicity): Not definitively described in dogs/cats
§ Humans: Light chains lead to amyloidosis and fibrillary nephropathy
□ Rare reports of light chain associated amyloidosis in dogs/cats
§ Humans with multiple myeloma: Fanconi syndrome (not reports in dogs/cats)

227
Q

Name neoplasias that are associated with glomerulonephritis (PLN).

A

§ Leiomyosarcoma
§ Adrenal adenocarcinoma
§ Parathyroid adenoma (membranoproliferative glomerulonephritis)
§ Hemangiosarcoma
§ Osteosarcoma (microalbuminuria)
§ Mast cell tumor (membranous glomerulopathy)
§ Mammary tumors and Sertoli cell tumor (reactive amyloidosis)
§ TCC
§ Bronchogenic adenocarcinoma
§ Lymphoma (microalbuminuria)

228
Q

What is tumor lysis syndrome and how can it result in renal failure?

A

· Tumor Lysis Syndrome: Secondary to massive release of intracellular content (phosphorus, uric acid, potassium): After chemo for lymphoma is a rare cause of renal failure
o Humans: Precipitation of uric acid, calcium phosphate, or hypoxanthine in renal tubules, cytokine-induced perturbations in renal blood flow → rapid renal failure, often death
§ TX: Rehydration (to improve renal perfusion), alkalinization of urine (inhibit uric acid precipitation) and tx hyperkalemia and hypocalcemia

229
Q

Name 3 chemo drugs that can result in renal tubular necrosis.

A 
Platinum compounds (primarily cisplatin)
Streptozotocin
Methotrexate (dogs - uncommon)
230
Q

Which chemo drug can result in renal disease in cats?

A

Doxorubicin (unknown mechanism)

231
Q

Which chemo drug can result in idiosyncratic acute renal failure?

A

Lomustine (CCNU) - VERY rare

232
Q

What 2 cat breeds are at an increased risk of forming ureteroliths?

A

Hiamalyan and Persian

233
Q

What 2 ureteroliths are on the rise in cats?

A
  1. CaOx

2. Dried Solidified Blood Calculi

234
Q

Discuss the the sensitivity of AXR and AUS in identifying ureteroliths in cats?

A

o Sensitivity of abdominal rads for dx of ureterolithiasis: 81% (Kyles et al., 2005a)
§ AUS: Sensitivity for dx ureterolithiasis: 77% (Kyles et al., 2005a)
§ Combo of Abdominal Rads + AUS: Sensitivity of 90%

235
Q

Discuss the medial management of feline ureteroliths.

A

o Fluid diuresis (+/- diuretics; furosemide, mannitol)
§ Humans: IV Glucagon: Relaxation of ureteral smooth muscle = Promotes passage of calculi
□ NO effect in cats (0.1mg per cat IV)
§ Humans: α-adrenergic antagonists (prazosin, tamsulosin), amitriptyline (a tricyclic antidepressant), and calcium channel blockers
□ No reports in dogs and cats (??? But there is a report of 8 cats with amitriptyline)

236
Q

What is the 12 month survival rate for feline ureteroliths with medical management?

A

12 month survival 66% (dying related to chronic renal insufficiency or recurrent ureterolithiasis (Kyles et al., 2005b)

237
Q

Discuss the recovery of renal function about removal of obstruction.

A

§ Recovery of renal function about removal: Duration and extent of obstruction
o Research dogs: Almost completely recovered after 4 days of relief, 46% GFR returned after 14 days of obstruction, almost NO GRF returned after 40 days of obstruction
o Optimal time has not been determined in cats; reported median interval btwn dx and sx = 3 days (Kyles et al., 2005b)

238
Q

What is the 12 month survival rate for feline ureteroliths with surgical management?

A

§ 12 month survival was 91% (many dying from chronic renal insuffuicency, recurrent ureterolithiasis, or nonregenerative anemia)

239
Q

What is a risk factor in humans for forming CaOx stones?

A

Hypocitraturia (risk factor for CaOx stones since citrate is chelated to calcium – more soluble salt) o Citrate supplementation helpful in humans; No studies in cats
Potassium citrate

240
Q

Name several diets that are used to prevent formation of CaOx stones?

A

Hill’s feline x/d
Purina NF
RC: Feline SO

241
Q

Define lithotripsy.

A

Crushing/fragmenting uroliths by shock waves or laser energy

242
Q

What are the 3 types of lithotripsy?

A

Extracorporeal shock wave llithotripsy (SWL), electrohydraulic lithotripsy, laser lithotripsy ○ SWL: Neprholiths, ureteroliths (Adams and Senior, 1999)
○ Electrohydraulic lithotripsy: Urocystoliths in larger females = REPLACED with safer methods
○ Laser lithotripsy: Using rigid or flexible endoscope
§ Humans: Holmium: YAG (Ho:YAG) laser for intracorporeal lithotripsy
§ Percutaneous nephrolithotomy → Procedure of choice for large staghorn nephroliths
§ Ho:YAG can efficiently fragment uroliths from dogs regardless of chemical composition (Wynn et al., 2003)
§ Implanted urethroliths in male dogs safely fragmented by Ho:YAG laser (Davidson et al., 2004)
§ Successful removal of bladder and uretheral calculi in dogs with laser lithotripsy fragmentation (Adams and Lulich, 2006)

243
Q

What were the success rates for tranurethral cystoscopy and laser lithotripsy in males and females?

A

Transurethral cystoscopy and laser lithotripsy → stone-free status in 80% male dogs and 100% female dogs (Adams and Lulich, 2006)

244
Q

What are advanatages of laser lithotripsy?

A

· Minimally invasive stone removal = Reduced postprocedureal dysuria and hematuria
· Shorter than sx
· Owner preference
· If recurrent uroliths: Can be performed repeatedly to avoid cystostomy

245
Q

What are contraindications to laser lithotripsy?

A

· Presence of ACTIVE urinary tract infection
o ↑ intravesicular pressure during voiding urohydropropulsion may induce vesicoureteral reflux = ascending pyelonephritis
o Small perforations of bladder wall = spread of microbes into abdominal cavity
o Perioperative ABX given to animals that have current UTI or prior UTI → fragmentation of infected uroliths may liberate viable bacteria from inner layers of uroliths
· Coagulopathy: Intraluminal or periurethral hemorrhage
· Obstruction of urinary outflow distal to urolith (urethral stricture): Hard to pass cystoscope and remove fragments

246
Q

What is laser fragmentation for laser lithotripsy?

A

· Laser fragmentation: Photothermal mechanism that can induce chemical alterations in stone composition (Chan et al., 1999)
o Not clinically relevant in most stone types
o Converts uric acid uroliths into small quantities of cyanide (can be absorbed into systemic circulation) but risk of clinical toxicity is VERY low (Teichman et al., 1998)
§ Unable to detect cyanide in fluids during procedure, but still need constant irrigation of saline and frequent evacuation of bladder to prevent cyanide from accumulating

247
Q

What can occur when uric acid uroliths undergo laser lithotripsy?

A

Laser Fragmentation
o Converts uric acid uroliths into small quantities of cyanide (can be absorbed into systemic circulation) but risk of clinical toxicity is VERY low (Teichman et al., 1998)
§ Unable to detect cyanide in fluids during procedure, but still need constant irrigation of saline and frequent evacuation of bladder to prevent cyanide from accumulating

248
Q

What are other names for feline nonobstructive idiopathic cystitis?

A

Classified as idiopathic feline lower urinary tract disease, idiopathic cystitis, or interstitial cystitis

249
Q

What is the biological behavior of feline nonobstructive idiopathic cystitis?

A

· CS subside within 5-7 days (without tx) in up to 92% of cats with acute nonobstructive idiopathic cystitis (Barsanti et al., 1982, Kruger et al., 2003; Osborne et al., 1996)
· CS may recur and again subside without tx: 40-50% of cats with acute idiopathic cystitis experience recurrence of CS within 1-2 yrs (Barsanti et al., 1982; Kruger et al., 2003)

250
Q

How many cats with acute idopathic cystitis will develop chronic forms?

A

· Subset of cats that CS persist for weeks to months or recur frequently → chronic idiopathic cystitis
o Spectrum of clinical manifestations associated with similar etiologic factors or entirely different mechanism of disease
· Fewer than 15% of cats with acute idiopathic cystitis will develop chronic forms

251
Q

Discuss the use of antibiotics in feline nonobstructive idiopathic cystitis?

A

· Empirical tx for hematuria, dysuria, and pollakiuria – BUT only 1-3% have bacteria noted at onset of CS of lower urinary tract disorders in young-middle aged cats
· USELESSNESS for ABX in abacteriuric cats with lower urinary tract disease have been documents (Barsanti et al., 1982)
· Tx with ABX has been perpetuated by misinterpretiation of “pseudobacteria” in unstained urine sediment and failure to perform UC
○ 89% of unstained feline urine sediments reported as + bacteruria by light microscopy were sterile on UC → Reduce false-positive bacteruria using a modified Wright-stain (Diff Quik)

252
Q

Discuss the use of amitripytline in feline nonobstructive idiopathic cystitis?

A

· Amitriptyline hydrochloride (Elavil): tricyclic antidepressant drug with anticholinergic, antihistaminic, sympatholytic, analgesic, and antiinflammatory properties
o Humans: Months for antidepressant actions to be evident, BUT rapid onset of other properties
§ Used in humans with interstitial cystitis (randomized placebo controlled, double masked study found that 63% on amitriptyline for 4 months rated good or excellent compared to 4% of placebo group)
o Uncontrolled study in cats (severe recurrent idiopathic cystitis): CS ↓ in 60% (9/15) cats treated with amitriptyline for 6 months (Chew et al., 1998)
o Randomized double-masked, placebo-controlled clinical trial in short term (7day) amitriptyline in 31 cats with acute nonobstructive idiopathic cystitis, amitriptyline did NOT reduce duration of pollakiuria and hematuria (Kruger et al., 2003)
§ CS recurred sooner and with higher frequency in amitriptyline treated cats than placebo
§ Adverse events: Urinary tract infection, sedation, hyperbilirubinemia, ↑ ALT
o Placebo-controlled study in cats: No difference in severity of CS after short-term (7 days) with amitriptyline and amoxicillin compared to placebo and amoxicillin (Kraijer, Fink-Gremmels, and Nickel, 2003)
o Thus short term tx may not work; but it is unknown if the long-term use may be helpful (studies needed)
o Use amitriptyline in cats with severe chronic idiopathic cystitis that are not responding to other tx
§ If no change in CS in 2-4 months, taper over few weeks and then stop this medication
□ Humans: Abrupt discontinuation = Withdrawal syndrome (GI somatic, neurologic, and psychiatric disturbances)

253
Q

Discuss the use of anti-inflammatories in feline nonobstructive idiopathic cystitis?

A

Glucocorticoids
· Small, double-blind, placebo-controlled study: Antiinflammatory prednisolone (1 mg/kg PO q12hrs for 10 days) = NO benefit in ¯ CS or duration of CS in affected cats (Osborne et al., 1996)
Nonsteroidal Antiinflammatory Drugs
· NSAIDs more effective when inflammation has causes sensitization of pain receptors to normally painless mechanical and chemical stimuli
Studies in cats needed

254
Q

Discuss the use of opioids in feline nonobstructive idiopathic cystitis?

A

For 24-72 hrs may be beneficial in alleviate acute “flare-ups”
Studies in cats needed

255
Q

Discuss the use of anti-cholinergics in feline nonobstructive idiopathic cystitis?

A

· Pollakiuria may be associated with pain, bladder fullness, urgency → Related to inflammation induced stimulation of bladder sacral sensory afferent nerves → sensation of pain or fullness/urgency → premature micturition reflex = inappropriate or involuntary voiding of small quantities of urine
o Detrusor contraction: Cholinergic parasympathetic efferents → anticholinergics agents may help with pollakiuria and urge incontinence
· Propantheline (Pro-Banthine): potent nonselective muscarinic antagonist = ¯ force and frequency of uncontrolled detrusor contractions = No benefit in cats
· Oxybutynin chloride (Ditropan) / Tolterodine (Detrol): synthetic tertiary amine muscarinic receptor antagonists
o Humans: Used for overactive bladder and urge incontinence
No studies in cats

256
Q

Discuss the use of glycosaminoglycans in feline nonobstructive idiopathic cystitis?

A

· Transitional epithelium of bladder covered by glycocalyx composed of hydrated glycoconjugates (glycoproteins and glycosaminoglycans (GAGs)
o Urothelial GAGs minimize adherence of microorganisms and crystals to bladder urothelium and limit movement of urine proteins and other solutes from bladder lumen to other surrounding tissue
· Defects in surface GAGs leading to ↑ urothelial permeability hypothesized as causative factors in pathogenesis of feline idiopathic cystitis (Human interstitial cystitis)

· Pentosan Polysulfate (Elmiron)
o Oral and intravesicular of GAG (humans): Reduced transitional cell injury
= May benefit SOME cats ( no studies in cats)
· Glucosamine and Chondroitin Sulfate
o Glucosamine: Amino sugar made in body (important intermediate in formation of GAGs)
o Chondroitin Sulfate: Most abundant GAG in bladder surface GAG layer
§ 6 month randomized placebo controlled study with oral glucosamine: NO difference in CS (Gunn-Moore and Shenoy, 2004)
o Combination of glucosamine and chondroitin has NOT been evaluated (potential synergism)

257
Q

Name 3 other important management strategies in feline nonobstructive idiopathic cystitis?

A
  1. Dietary management - more canned food (increased water intake)
  2. Stress management
  3. Environmental Enrichment
258
Q

Does feline facial pheromone work in feline nonobstructive idiopathic cystitis?

A

· Feline facial pheromone fraction F3 (Feliway): Synthetic pheromone
o Application to living environment as adjunctive therapy
o Randomized double-blind, placebo-controlled, crossover study (9 cats): NO significant difference in CS, behavior, or overall health (Gunn-Moore and Cameron, 2004)

259
Q

What are the 2 most common causes of feline urethral obstruction?

A

Mucous or mucocrystalline plug secondary to feline lower urinary tract disease OR CaOx stones

260
Q

Name potential life-threatening complications that can occur with urethral obstruction.

A

Cardiovascular compromise (check MM, CRT, pulse quality, rate) o Slow HR → Hyperkalemia → Check ECG and serum potassium
§ NOTE: In cats hyperkalemia can have normal to rapid HR
o Metabolic Acidosis
o Ionized Hypocalcemia

261
Q

Discuss the ECG findings with hyperkalemia.

A

Hyperkalemic induced cardiac conduction changes (tall positive or large negative T-waves, diminished or absent p-waves, prolonged, P-R intervals, widened QRS complex, since waves (end-stage when QRS and T waves merge) – Association of increasing K levels with abnormalities is inconsistent o NOTE: Can see ventricular tachycardia with hyperkalemia (or sinoventricular rhythm with intraventircular conduction delay)

262
Q

How do we treat hyperkalemia?

A

Driving potassium intracellularly or by removal of K from body = Effect is transient o Calcium gluconate: Direct antagonism of cardiac effects of hyperkalemia (50-100 mg/kg IV over 2-3 mins with ECG monitoring, since Ca can induce arrhythmias)
§ Effects are immediate (lasting 20-30 mins)
§ SHOULD be the FIRST drug in hyperkalemic cats
o Regular Insulin: Promotes intracellular movement of K (0.1-0.25U/kg IV bolus, followed by slow bolus of 1-2 g of 25% glucose per unit insulin to prevent hypoglycemia)
§ Effects within mins to 1 hour (monitor BG for several hours after administration of insulin)
o Sodium Bicarbonate: Lower K by raising pH and driving K into cells
§ Effects within 30-60 mins, persists for hours

263
Q

What can exacerbates the effects of hyperkalemia on membrane excitability?

A

Hypocalcemia

264
Q

What is a complication that are occur 24-48hrs after relieving a uretheral obstruction?

A

· Post-obstructive diuresis is profound (esp 24-48 hrs later) – May exceed 120 ml/hr in some cats

265
Q

What can be considered if multiple ureteral obstructions occur and what are complications of this procedure?

A

· If multiple obstructive events → perineal urethrostomy

o Complications: Stricture formation, recurrent UTIs, does NOT eliminate underlying cause

266
Q

What physical features of the urethra aid in closure?

A

urethral folds, moist epithelial seal, primary smooth muscle

· Urethral outlet resistance maintained by smooth and striated muscle components of urethra

267
Q

What drugs can result in Contraction of smooth muscle in urinary bladder neck and urethra?

A

Activation of terminal α-adrenergic receptors

Non-selective agent = Phenoxybenzamine (dog); Prazosin: Potent (dogs/cats)
Uroselective α1-antagonists (terazosin, doxazosin, tamsulosin) – Humans

268
Q

What drugs can result in Striated muscle relaxation urethra?

A

Benzodiazepine (diazepam, alprazolam)

269
Q

What drug can be given if urinary bladder contraction is weak?

A 
Enhance by activating terminal receptors for parasympathetic input or antagonizing the (sympathetic) adrenergic input on β-receptors in detrusor muscle 
 o Bethanechol (parasympathomimetic agent):  Primary tx for detrusor atopy or dysfunction
270
Q

What is the most common urethral incompetence in dogs?

A

primary sphincter mechanism incompetence

271
Q

Why is combined reproductive hormone and α-agonists recommended in urinary incontinence in dogs?

A

Combined reproductive hormone and α-agonists to see synergistic effects (allows estrogen to “prime” the urethral receptors for α-agonist treatment – both drugs can be reduced over time

272
Q

What reproductive hormones can be used for urinary incontinence and how do they work?

A

§ Estrogen diethylstilbestrol (DES), stilbestrol, estriol, and conjugated estrogens (Premarin) improve urethral resistance by increasing α-adrenergic receptor responsiveness and improving urethral vascularity and other mucosal epithelial characteristics
□ Can be used with phenylpropanolamine (PPA) = May be synergistic when combined
□ Improves 60-80% of treated dogs
® BM suppression unlikely but owners should be warned
§ Gonadotropin-releasing hormone (GnRH) analogs – Suppress sex hormone release
□ Theory: Chronically unsuppressed FSH and LH release (because of lack of negative feedback) in spayed dogs may contribute to urinary incontinence
® GnRH analogs = Reduced FSH and LH over time
□ Leuprolide, buserelin, and deslorelin (Reichler et al 2003)

273
Q

What type of drug is PPA?

A

· α-agonists (sympathomimetic drugs)
o Phenylpropanolamine, phenylephrine, and pseudoephedrine
o SE: restlessness, tachycardia, systemic hypertension, anorexia, GI side effects, and aggression and other behavioral changes

274
Q

Name underlying etiologies that may be related to urinary incontience.

A

o Urethral tone, smooth muscle (MAJOR component)
o Mucosal integrity, vasculature, and connective tissue surrounding the urethra
o Healthy urothelium
o Surface tension from glandular secretions
o Pliability of the mucosa
o Bladder position
o Exposure to vesicourethral junction and proximal urethra to intraabdominal pressure
§ Studies have linked urethral position/length and vesicourethral angle to incontinence (Gregory, 1994; Gregory et al., 1996)
§ Incontinence: Short urethra and intrapelvic bladders
o Hormone Status
§ 20% of neutered females will develop a degree of urinary incontinence (75% within 3 yrs of neutering)
□ Decreased estrogen (woman) associated with loss of uretheral muscle tone, urethral vascular atrophy, decreased glandular secretions
® Increasing FSH and LH may play a role, but mechanism is unknown (Reichler et al., 2005)
o Other factors: breed, body weight, tail docking

275
Q

What breeds are prone to urinary incontinence?

A

§ Old English sheepdogs, Doberman pinschers, GSD, boxers, weimeraners, rotties, Irish setters
□ Labs have a decreased risk (Holt and Thrusfield, 1993)
□ Large and giant breed dogs (Over 20kg), small breed are at decreased risk

276
Q

What percentage of FS dogs will develop urinary incontinence?

A

§ 20% of neutered females will develop a degree of urinary incontinence (75% within 3 yrs of neutering)
□ Decreased estrogen (woman) associated with loss of uretheral muscle tone, urethral vascular atrophy, decreased glandular secretions

277
Q

In dogs, what are the 4 mainstays of treatment for urinary incontinence?

A

Lympathomimetic drugs, estrogens, periurethral injections, and colposuspension

278
Q

What is the response to collagen injections in dogs with urinary incontinence?

A

· 32 FS dogs refractory to PPA, tx with periurethral collagen injection (Arnold et al., 1996)
o 52% were continent after 1 or 2 injection w/o PPA
o 75% if PPA added
o No complications observed
o 19% (6) continent for longer than 30 months after 1st injection
· 40 dogs over 7 yrs(Barth et al., 2005)
o 68% dogs were continent for mean of 17 months (1-64 months) after injection
o Additional 25% with 60% continent after addition of α-agonist therapy
o Side effects in 15% (stranguria, hematuria, vaginitis)
· 29 FS dogs (34 collagen injecitons) (Byron et al., 2005)
o 6 had ectopic ureters (6 had corrective sx)
o 66% complete continence immediately after the injection, additional 32% were improved
o 55% achieved full continence after additional of medical tx
o Mean duration of continence = 12.1 months w/o other tx
o Client satisfaction 88%, 76% were 100% satisfied
· Repeated injection of collagen: Enhancing the previously placed blebs or additional of new blebs = Improved response and reinduction of continence

279
Q

In which breed dose cutaneous and renal glomerular vasculopathy occur?

A

Greyhound
AkaGreenetrack Disease or Alabama Rot
Syndrome of skin ulcerations, edema, and renal dysfunction

280
Q

What disease in children is similar to the cutaneous and renal glomerular vasculopathy seen in greyhounds?

A

Hemolytic-uremic syndrome (HUS)

281
Q

What form of hemoglobin can be used to differentiate AKI from CKD?

A

Carbamoylared Hb
High levels of CaHb in humans and dogs with CKD
urea exists in equilibrium with cyanate which can react with valine groups on Hb

282
Q

What crazy body part can be used to differentiate AKI from CKD?

A

TOENAIL creatinine!!

283
Q

What are some DDX for renomegaly?

A

compensatory hypertrophy, acute inflammatory renal diseases (interstitial nephritis or glomerulonephritis), metabolic nephropathies, portosystemic shunt, toxic insult, and diffuse infiltrative neoplasia (LSA)

284
Q

What are the 3 parameters that define AKI?

A

reduction in kidney function within 48 hours defined by the occurrence of at least one of the following:

(1) an absolute increase in serum creatinine concentration of at least 0.3 mg/dl (26.4 mmol/L),
(2) an increase in serum creatinine concentration of more than 50% of baseline,
(3) oliguria of less than 0.5 ml/kg/hr for more than 6 hours

285
Q

What is AKIN?

A

Acute Kidney Injury Network

286
Q

What have studies with RIFLE and AKIN shown?

A

Significant association btwn increasing severity of AKI and mortality, even with minimal increases in creatinine concentration that previously were not considered important.

287
Q

What is the suggested incidence of hospital acquired AKI in dogs and cats?

A

Based on 2 retrospectives: 10-17%

For cats - 20-21.3%

288
Q

What are risk factors for HA-AKI?

A 
preexisting renal disease** 
dehydration and volume depletion
decreased CO **Heart dz**
advanced age** (>7)
fever
hypotension
hypertension, hypoalbuminemia
sepsis
electrolyte imbalances acidosis
 hyperviscosity syndromes
 liver disease
administration of nephrotoxic drugs**
administration of radiocontrast media pancreatitis
diabetes mellitus
 anesthesia**
surgery
(Humans: decreased renal perfusion)
289
Q

What is the low molecular weight protein that is a biomarker of AKI?

A

Retinol-binding protein (URBP) - Freely infiltered by reabsorbed in proximal tubular (if increased = Proximal tubular damage)

In SIRS dogs: increased URBP to UC compared with healthy
=>presence of increased quantities of URBP could occur from direct tubular damage as an indication of AKI or from competition with other HMWPs for tubular binding sites

290
Q

What are 2 renal proximal tubular cellular enzymes that are used as biomarkers for AKI?

A

N-acetyl-β-d-glucosaminidase (NAG)

γ-glutamyl transpeptidase

291
Q

What is the outcome of HA-AKI in dogs and cats?

A

Decrease in survival was significant with both mild and severe changes in creatinine concentration
ion (dogs: 38-46% compared to 84%; cats 48% compared to 85% - but more significant for cats with more severe AKI)

About 50% that survive will develop CKD!

292
Q

Are there reports of hetastarch and AKI in dogs/cats?

A

NO reports of HA-AKI

But there are reported in humans with sepsis (blackbox warning)

293
Q

What are the tests for proteinuria in dogs and cats?

A
  1. Dipstick colorimetric

2. Sulfosalicylic acid (SSA) precipitation test = Turbidity

294
Q

What do the dipstick and SSA test detect and what are their limits of detection?

A

Dipstick: Mainly albumin;

30 mg/dl

D: 81%/48%
C: 90%/11%

SSA: Albumin
Globulins
Bence Jones Proteins

5 mg/dl

D: 73%, 64%
C: 58%, 25%

295
Q

What are result in false positives on the SSA test?

A

Radiographic contrast agents
Penicillin, cephalosporins, sulfisoxazole
Thymol (a urine preservative)
Unknown Reasons

296
Q

What is the problem with feline urine samples and dipsticks and SSA tests?

A

Performed Poorly = High # false positive results
NEITHER USEFUL for albuminuria in cats = NEED to use species specific ELISA

NOTE: Cats with CKD the accuracy of dipstick and SSA improved (likely dt high amount of proteinuria)

297
Q

What is the definition of microalbuminemia?

A

Microalbuminuria is defined as concentrations of albumin in the urine that are higher than normal (>1.0 mg/dl) but below the limit of detection using conventional urine dipstick tests (<30 mg/dl).

298
Q

What is concerning about decreasing proteinuria with increasing creat?

A

Suggests dz progression

299
Q

What are the 2 sources of renal proteinuria?

A
  1. increased glomerular filtration of plasma proteins associated with intraglomerular hypertension, structural abnormalities of the glomerular capillary wall, or the presence of immune complexes or vascular inflammation in the glomerular capillaries.
  2. Decreased reabsorption of filtered plasma proteins due to tubulointerstitial disease
300
Q

What is considered borderline proteinuria in dogs/cats?

A

Dogs: 0.2-0.5
Cats: 0.2-0.4

301
Q

What UPC is strongly suggestive of glomerular dz?

A

UPC >2.0

302
Q

Why is UPC not recommended as rountine screening test for urine albumin in dogs and cats?

A

the cutoff value of 0.2 for UP/C ratio resulted in an unacceptable number of false-negative results.

303
Q

What are the common causes of renal proteinuria in dogs?

A

Neoplasia, infection, polyarthritis, hepatitis, hyperadrenocorticism, immune-mediated hemolytic anemia, and systemic hypertension are common concurrent medical problems

304
Q

What are the common causes of renal proteinuria in cats?

A

iral diseases, neoplasia, immune-mediated disease, polyarthritis, and systemic hypertension

305
Q

What is the difference in tx recommendations for nonazotemic and azotemic animals?

A

Nonazotemic: TX if UPC 1-2
Azotemic: Tx if UPC >0.5 dogs or >0.4 cats

306
Q

What is the tx for proteinuria?

A

Reduction in dietary protein (renal diet)
Omega-3 FA (found in most renal diets)
ACEi
If higher magnitude - Aspirin
Supportive care: Control hypertension, edema, and thrombolic potential

307
Q

What are the 3 nonspecific management recommendations for animals with glomerular dz?

A

(1) monitoring for and treatment of underlying NIN disorders,
(2) reduction of proteinuria, and
(3) management of uremia and other complications of renal failure

308
Q

What is the primary determinant of net protein movement across the glomerular filtration barrier?

A

Intraglomerular hydrostatic pressure

309
Q

What has been shown in dogs with glomerular dz to significantly reduce proteinuria and delay onset or progression of azotemia?

A

ACEi (ENALAPRIL) - Considered standard of care for glomerular dz in dogs

310
Q

Is there a difference btwn enalapril and benazepril in dogs/cats?

A

no evidence that one ACE inhibitor is pharmacokinetically superior to others in either dogs or cats

311
Q

What is aldosterone escape?

A

Serum aldosterone concentrations increase over time in people treated with maximal dosages of ACEi or Angiotensin II receptor blockers

312
Q

What are potential tx for hyperkalemia in dogs with kidney dz from RAAS inhbition?

A

Reducing the dosage of ACE inhibitor, ARB, or spironolactone; feeding a reduced-potassium diet; or administering a gastrointestinal potassium binder (e.g., Kayexalate)

313
Q

On average how much to ACEi and AIIRB reduce hypertension?

A

WEAK, only 10-15 mmHg

314
Q

What is the potential negative of using amlodipine alone to control hypertension?

A

induce preferential dilation of the afferent glomerular arteriole, thereby increasing intraglomerular hydrostatic pressure, as well as RAAS activation in dogs and potentially also cats (based on Atkins work)
THUS, some recommend that in dogs/cats with CKD that you need a ACEi as well

315
Q

What is the “permeability factor” that may be related to nephrotic syndrome?

A

increases net fluid extravasation from vascular beds (edema) and simultaneously widens glomerular endothelial pore size (proteinuria)

316
Q

What are options for nephrotic syndrome animals that are accumulating fluid?

A

Remove some of it (QOL)

Lasix initially and then spironolactone

317
Q

Why are pooled UPC readings recommended?

A

Day-to-day UP/C variations of up to 50% in dogs and 90% in cats have been described, and therefore averaging results of two to four UP/C ratios measured over a 3- to 5-day period is ideal for estimating the severity of proteinuria in an individual patient.

318
Q

What is a negative prognostic indicator of glomerular disease and what is the prognosis?

A 
Variable prognosis (dead to years!)
Concurrent azotemia - negative prognostic indicator

605 days in nonazotemic nonnephrotic dogs with glomerular dz

45 days in azotemic nonnephrotic dogs with glomerular dz

319
Q

What is the at risk stage in IRIS staging of CKD?

A

HX that suggests animal is at increased risk of CKD = Expsoure to nephrotoxin, breed, high prevalence of infectious dz, or old age)

320
Q

What is the IRIS classification at this patient: nonproteinuric cat (UP/C ratio of 0.12) with a systolic blood pressure of 210 mm Hg, retinal detachment, and blood creatinine concentration of 2.0 mg/dl (176 µmol/L)?

A

IRIS CKD Stage 2-NP-AP3(c), where NP indicates absence of proteinuria and AP3(c) denotes arterial blood pressure associated with a high risk of target-organ damage and evidence of complications secondary to high blood pressure present at initial staging

321
Q

What is the IRIS classification at this patient:dog with borderline proteinuria (UP/C value of 0.35) and blood creatinine concentration of 5.4 mg/dl (475 µmol/L) that did not undergo blood pressure assessment ?

A

IRIS CKD Stage 4-BP-RND, where BP denotes borderline proteinuria and RND indicates that the risk of target-organ damage associated with arterial blood pressure was not determined

322
Q

What is the IRIS classification at this patient:proteinuric dog (UP/C ratio of 0.7) with a systolic pressure of 120 mm Hg and blood creatinine concentration of 3.4 mg/dl (300 µmol/L)?

A

IRIS CKD Stage 3-P-AP0(nc), where P denotes proteinuria and AP0(nc) designates an arterial pressure status associated with minimal or no risk of target-organ damage accompanied by no evidence of hypertensive complications

323
Q

How do you denote treatment on the staging and substaging in IRIS staging?

A

(T)

324
Q

At what stage in IRIS is feeding a renal diet recommended?

A

Late IRSI CKD Stage 2
Dog: 1.4- 2.0
Cat: 1.6-2.8

325
Q

At what albumin level is aspirin recommended for CKD dogs and cats?

A

Albumin <2

326
Q

What are IRIS steps for hypertension in cats?

A

1.Restrict dietary sodium
2. Calcium channel blocker (amlodipine)
3. Icrease dose of amlodipine
Add ACEi to CCB tx

327
Q

What are IRIS steps for hypertension in dogs?

A
  1. Restrict dietary sodium,
  2. Start ACE inhibitor therapy at the standard dosage.
  3. Double the dose of ACE inhibitor (this will improve antihypertensive efficacy in some patients).
  4. Combine the ACE inhibitor with a CCB (e.g., amlodipine). Caution: see step 4 earlier for cats.

5.Add hydralazine to combined ACE inhibitor and CCB treatment.

328
Q

When does renal secondary hyperparathyroidism develop in CKD?

A

early in the course of CKD, and many cats with IRIS CKD Stage 2 disease already have increased blood parathyroid hormone (PTH) concentrations even when blood phosphate concentrations remain within reference limits

329
Q

What is helpful for renal parahyperparathyroidism?

A

Reducing phosphorus intake may be benficial

330
Q

When should calcitriol be considered in CKD?

A

For dogs with IRIS CKD Stage 3 or 4 there is evidence that judicious use of calcitriol prolongs survival when phosphate is controlled and ionized calcium and PTH are monitored

331
Q

What medications can be given for CKD animals with metabolic acidosis?

A 
Na Bicarbonate
K citrate (esp if hypokalemic)
332
Q

Which species gets hypokalemia with CKD?

A

CATS!

Consider potassium gluconate

333
Q

What are the 3 cyclooxygenase Isoenzymes?

A
  1. COX-1: Housekeeper
  2. COX-2, inducible form in inflammation and other dz states
  3. COX-3 or splice variant of COX-1 - Poorly understood
334
Q

Which COX isoenzyme may be upregaulated in CKD in dogs/cats?

A

COX-2

335
Q

What is important about the COX isoenzymes in the kidney?

A

Both isoenzymes (COX-1 and COX-2) are constitutive and inducible in the kidney and both contribute to the control of renal blood flow, GFR, renin release, and cytoprotection
NOT a big deal in normal animals
BIG deal in at risk patients!

336
Q

What are the 2 general syndromes of NSAID nephrotoxicity?

A
  1. Acute cortical nephrotoxicity (acute hemodyanmic insult)

2. Chronic meduallary cytotoxicity (chronic cytotoxic insult)

337
Q

What is the type of syndromes of NSAID nephrotoxicity most common in vet med?

A

Hemodynamically mediated acute cortical nephrotoxicity = Classical AKI

338
Q

What are the risk factors for NSAID acute cortical nephrotoxicity?

A 
ECF depletion (dehydration)
Systemic hypotension
General anesthesia
Dietary salt restriction
Diuretic use
Administeration of antihypertensive drugs
Higher NSAID dose
Hypoalbuminemia
Genetic factors?
339
Q

What is the toxic effect of NSAID acute cortical nephrotoxicity?

A

Loss of renoprotective effects of vasodilatory prostaglandins

Primary effects: Decreased renal blood flow and GFR

340
Q

What isoenzyme is involved in NSAID acute cortical nephrotoxicity?

A

Inhibition of COX-1 more important than inhibitor of COX-2

341
Q

What are the early, intermiediate, and late CS with NSAID acute cortical nephrotoxicity?

A

Early: Renal cells and casts in sediment, renal enzymuria, proteinuria, microalbuminuria

Intermediate: Serum electrolyte changes, reduced urine concentration

Late: Rising creatinine!!

342
Q

What are the interspecies difference in susceptibility with NSAID acute cortical nephrotoxicity?

A

Dogs are more susceptible than people

Cat unknown

343
Q

What are the risk factors for NSAID chronic medullary cytotoxicity?

A 
Chronic dehydration
Chronic hypotension or multiple acute bouts of hypotension
Administration of antihypertensive drugs
Higher NSAID dose
Hypoalbuminemia
Genetic factors?
344
Q

What is the toxic effect of NSAID chronic medullary cytotoxicity?

A

Loss of cytoprotective effects of prostanoids

Effect - Necrosis of medullary interstitial and tubular cells (papillary necrosis)

345
Q

What isoezyme is involved in NSAID chronic medullary cytotoxicity?

A

Inhibition of COX-2 more important than inhibition of COX-1

346
Q

What are the early, intermediate, and late CS associated with NSAID chronic medullary cytotoxicity?

A

Early: NONE!!!

Intermediate: Renal enzymuria, decreased concentrating ability

Late: Electrolyte abnormalities, acid-base changes, rising creatinine

347
Q

What are the interspecies difference in susceptibility with NSAID chronic medullary cytotoxicity?

A

Dogs are more susceptible than people

Cat unknown

348
Q

Which dog breed may be more susecptible to NSAID nephrotoxicity?

A

GSD

349
Q

Why are COX-2 selective agents preferred when NSAIDs are indicated in CKD patients?

A

Dt potential for GI toxicity

350
Q

What are the 4 stages of AKI?

A
  1. Initiation
  2. Extension (ishcemia, hypoxemia, inflammation, cellular injury)
  3. Maintenance (urine production variable)
  4. Recovery (marked polyruia possible, tubular repair, can take ks to months)
351
Q

Why are animal polyuric during the recovery phase?

A

Partial restoration of renal tubular function and osmotic diuresis of accumulated solutes

352
Q

Which medication is no effective in people to increase urine production and thus is NOT recommended for oliguria or anuria in AKI in dogs and cats?

A

Dopamine infusion

353
Q

After Lasix and mannitol are considered, which dog is not for patients that have oliguria or anuria AKI?

A

Fenoldapam (selective dopamine D1 receptor agonist)
Renoprotective in humans
Few studies in normal dogs and cats - Beneficial effects on GFR and urine volume

354
Q

What is a major consequence of polyuria with electrolytes?

A

hyponatremia and hypokalemia

355
Q

Which antihypertensive drug can be dissolved in a small amount of saline and administered rectally?

A

Amlodipine

356
Q

What are other poor prognostic indicators in AKI?

A
  1. Severe azotemia (creat >10)
  2. Lack of improvement or worsening with IVF and supportive care
  3. Concurrent dz (pancreatitis or sepsis)
357
Q

What is the primary benefit of convection in dialysis?

A

Ability to remove larger molecules from blood than can diffusion
HARD since ultrafiltrate must be calculated and replaced

358
Q

What is Slow continuous ultrafiltration (SCUF)?

A

Purely convection

positive transmembrane pressure forces fluid (ultrafiltrate) out of the blood, hemoconcentrated blood returned

359
Q

What is Continuous venovenous hemofiltration (CVVH)?

A

Purely convection
positive transmembrane pressure forces fluid (ultrafiltrate) out of the blood, ultrafiltrate is replaced with a sterile balanced electrolyte solution

360
Q

What is Continuous venovenous hemodialysis (CVVHD)?

A

Diffusion therapy
Blood enters the dialyzer, where it is divided into thousands of strawlike semipermeable membranes that are bathed in dialysate
Movement of molecules is based on their relative concentrations in dialysate

361
Q

What is Continuous venovenous hemodiafiltration (CVVHDF)?

A

diffusive aspects of CVVHD with the convective aspects of CVVH

Blood flowing through the dialyzer’s semipermeable membranes are bathed in dialysis solution and exposed to a positive transmembrane pressure so that both diffusion and ultrafiltration guides the movement of solutes

362
Q

What are the 2 most commonly employed anticoagulant methods in CRRT?

A

Systemic heparinization

Regional citrate infusion

363
Q

What is known about exogenous and endogenous steroids as a risk factor for UTIs?

A

39% dogs UTI (no CS) with chronic skin dz that got steroids compared to 18% w/o steroids

IVDD sx dogs that got dexSP = 11.4X more likely to have +UC than w/o dex sp

HAC: 46% found to have UTI, CS rare

364
Q

What is known about diabetes mellitus as a risk factor for UTIs?

A

Dogs: UTI in 24-37% (few had CS)
Cats: 12-13% UTIs (CS in 14-445)

365
Q

What is complication of UTI in diabetics?

A

Emphysematous cytitis - E.coli

366
Q

What % of cats with hyperthyroidism has + UC?

A

12% (none had CS)

367
Q

What % of parvo dogs developed subclinical UTI?

A

23%

368
Q

What factor was associated with a 7.5X greater risk of asymptomatic UTI in dogs?

A

Morbidly obese dogs (>45% body fat)

369
Q

What is known regarding indwelling U caths in dogs with UTIs?

A

45% dogs with U cath develop UTI

Increased with age (by 20% with each year), duration of catheterization (27% each day), and antimicrobial use (by 454%)

370
Q

In which dz are UC recommended?

A

CKD (twice yearly)

DM and HAC

371
Q

What has been shown about the culture or uroliths and bladder mucosa compared to urine culture?

A

Culture of uroliths and bladder mucosa may be more sensitive!

372
Q

What other factors could be considered when differentiateing begnin bacteriuria and clinical UTI?

A

Bacterial virulence factors

Host muscoal response (cytokine production)

373
Q

What is UPEC?

A

Uropathogenic E. coli (35-50% UTIs)

Posses genes and virulence factors that allow colonization and persisitence in urinary tract

374
Q

How does UPEC involve urothelial cells?

A

Cell entry: Pili (fimbriae) = Type 1 pilia (tip of adhesin, FimH = binds to monomannose molecules)

Disrupt and increased host cell mobilization

= = Penetrate deeper layers, permits bacterial persistence despite host defenses and ABX

375
Q

When you have a MDR E. coil, even if resistant to clavamox, what can you consider?

A

High dose Clavamox (25 mg/kg PO q8hrs) BEFORE carbapenems

376
Q

When is prophylatic antimicrobials therapy recommended?

A

Used to prevent reinfection in an animal documented to develop UTIs three or four times per year or more

Bedtime dosing (max bladder contact time) at 30-50% daily therapeutic dose

377
Q

What is cranberry extract?

A

Proanthocyanidins - UPEC antiadhesion effects
Abstract in dog urine (similar effects)
No in vivo studies!

378
Q

What is considered an urinary antisepctic?

A

methenamine hippurate = Dissociated to formaldehydrate = Bactericidial

379
Q

What has been shown in FIC cats to reduce CS and restore antiadhesive properties of bladders of mucin def rabbits?

A

Polysulfated glycosaminoglycans (Elmiron) - Though that bladder urothelium is protected by a glycosaminoglycan layer that accounts in part for its capacity to tolerate constant contact with urine and also helps prevent bacterial adhesion

380
Q

What is a cell wall active bactericidal drug that has demonstrated effectiveness against UPEC and MDR E. coli?

A

Fosfomycin (Monurol) - Similar B-lactams, BUT is NOT inactivated by ANY class of B-lactamases

381
Q

What is the idea of induction of asymptomatic bacteriuria used for?

A

Deliberate induction of asymptomatic bacteriuria with a specific E. coli strain (that cannot express primary adhesins but has superior biofilm-forming capacity) has been shown in murine models and in humans to successfully prevent establishment of a range of UPEC strains in the bladder
NOT shown in dogs

382
Q

What can be used to kill a wide variety of UPEC strains?

A

Bacteriophages, noted to work in dog and cat urine, but no in vivo studies

383
Q

What has been found in regards to concurrent bacterial infection in dogs and cats with ureterolithiasis?

A

Cats: 1/3
Dogs: 2/3 (65-70%(
will have concurrent UTI

384
Q

Which stones will be missed on radiographs?

A

dried solidified blood calculi, mucus plugs, and radiolucent uroliths

385
Q

In dogs with struvite nephroliths how long are ABX needed?

A

Up to 2-3 months

386
Q

T/F: Dogs can have negative UC but positive cultures from upper urinary tract if urolithiasis present.

A

TRUE

387
Q

Which tricyclic antidepressant has been used in cats to modulate pain and ureteral relaxation?

A

Amitripytline

388
Q

What pancreatic hormone has been used for ureteral dilation and relief of pain in humans with ureteral obstruction?

A

Glucagon

No shown in vet med

389
Q

Why is morphine NOT recommended in ureteral obstruction in dogs?

A

one in vitro canine ureteral study morphine was found to have spasmogenic effects (even after naloxone given)

390
Q

What should be avoided in a dogs with ureteral obstruction?

A

H2receptor blockers

391
Q

what drugs have shown benefit in dog models of unilateral ureteral obstruction to assist in recovery of renal function following obstruction?

A

ACEi

Angiotensin receptor blocker = Losartan

392
Q

In which spp has hyperoxaluria been reported?

A

Cats

393
Q

What are potential urine inhibitors of CaOX formation?

A 
Mg
Citrate
Pyrophosphate
Nephrocalcin
Tamm-Horsfall glycoproteins
394
Q

What are potential urine promotors of CaOX formation?

A 
Uric acid (seen in min Schnauzers)
Foreign material
395
Q

Besides diet, what medications can be used for CaOX stones?

A

Potassium citrate (alkalinzing agent, and provide citrate to inhibit formation of CaOX)

Thiazide diuretics (inhibit Na/Cl cotransporter, Ca reabsorption promoted)

396
Q

How does urine pH vary throughout the day?

A

Lowest at night

Highest during the day

397
Q

What does it indicate when urate crystalluria is seen a “treated” animal?

A

insufficient dietary purine (protein) reduction, insufficient urine alkalization, insufficient urine dilution, insufficient allopurinol administration

398
Q

What does it indicate when xanthine crystalluria is seen a “treated” animal?

A

excessive allopurinol administration in relation to insufficient dietary purine (protein) reduction, insufficient urine alkalization, or insufficient urine dilution

399
Q

What procedure has a shorter recovery time then a conventional cystotomy?

A

Minilaparotomy-assisted cystotomy

400
Q

What is a SMARTR plan?

A

Specific, Measurable, Action oriented, Realistic, Time-driven/Timely, and Rewarded
For cat environmental enrichment

401
Q

What is used in sclerotherapy?

A

For idiopathic renal hematuria

silver nitrate and povidone-iodine = flush into renal pelvis

402
Q

What does SUB stand for?

A

Subcutaneous Ureteral Bypass device

403
Q

What is the stone size for the use of baskets?

A

<5mm in female dogs and 3mm in male dogs or cats

404
Q

Is there a synergetic effect with sympathomimetic agents and estrogens for urinary incontinence?

A

NOT proven, but some people think so, you can try it in refractory cases

405
Q

What is the reason for use of oxybutynin, propantheline, imipramine, duloxetine?

A

When bladder overactivity is a cause or consequence of incontinence in dogs

406
Q

What 3 medications can be used for urethral hypertonicity (component of detrusoe-uretheral dyssynergia or urethrospasms)?

A

Phenoxybenzamine - Nonslective a-antagonist

Prazosin - Selective a1-antagonist

Tamsulosin - Uroselective a1 antagonist in male prostate

Dantrolene - Relaxant of striated muscle (important in cat urethra)

407
Q

What is the mainstay for bladder atony in vet med?

A

Bethanechol - Parasympathomimetic

408
Q

If bethanechol is not working for bladder atony what can be considered?

A

cholinesterase inhibitors (pyridostigmine), β-blocking agents, dopaminergic antagonists, prostaglandins, and prokinetic agents (cisapride and metoclopramide)

Fluid and Renal Physiology (4 decks)

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