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Ettinger > Renal disease > Flashcards

Renal disease Flashcards

1
Q

What is considered the gold standard for assessment of GFR?

A

Urine inulin clearance

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2
Q

Why is plasma inulin clearance nor recommended in dogs?

A

40% inulin is cleared from the plasma by non-renal routes

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3
Q

Which breed of cat is associated with elevated sCr?

A

Birman

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4
Q

What is cystatin C?

A

Protease inhibitor

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5
Q

How is cystatin C handled in the kidneys?

A

Freely filtered
Reabsorbed by megalin-mediated endocytosis

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6
Q

What does increased urinary cystatin C indicate?

A

Tubular dysfunction

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7
Q

How and where are filtered proteins reabsorbed in the kidney?

A

Megalin- and cubulin- mediated endocytosis in proximal tubular cells

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8
Q

What can cause false positive/negative results on a urine protein dipstick?

A

Positive - cats, alkaline/concentrated urine, pyuria/haematuria
Negative - acidic/dilute urine, BJ proteinuria

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9
Q

What stain is used to highlight the basement membrane in renal biopsies?

A

Jones methenamine silver

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10
Q

Can serum albumin / AT III be used to guide thromboprophylaxis in dogs with PLN?

A

No - magnitude of hypoalbuminaemia, AT concentration or UPCR are not predictive of thromboembolic complications

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11
Q

What is USG?

A

The weight of a volume of fluid compared to the weight of an equal volume of distilled water

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12
Q

Where is filtered glucose reabsorbed?

A

Mostly SGLT 2 (SGLT 1 to lesser extent) in proximal tubule

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13
Q

What is the function of different regions of the renal tubule with regards to pH regulation?

A

PT - main site of H+ and HCO3- reabsorption
DT - regulation of H+ secretion

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14
Q

What are hyaline casts composed of? What is their significance?

A

Proteinaceous material
Marked proteinuria

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15
Q

What are epithelial casts composed of? What is their significance?

A

Proteinaceous material and epithelial cells
Direct tubular cellular damage

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16
Q

What are granular casts composed of? What is their significance?

A

Partial degradation of a cast
Renal tubular insult

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17
Q

What are waxy casts composed of? What is their significance?

A

Complete cellular degradation
Protracted tubular stasis

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18
Q

What condition should be considered in a cat with a marked increase in renal cortical echogenicity?

A

EG toxicity

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19
Q

Ddx AKI

A

Haemodynamic (pre-renal)
Intrinsic renal - vascular
- acute glomerulonephritis
- acute interstitial nephritis
- acute tubular necrosis
Post renal

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20
Q

What GI complication has been reported in dogs with AKI?

A

Intussusception

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21
Q

What are the 4 stages of AKI?

A

Initiation
Extension
Maintenance
Polyuric

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22
Q

What test can be used to distinguish haemodynamic from intrinsic renal azotaemia?

A

FE-Na
<1% expected if haemodynamic

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23
Q

Do a) norepinephrine and b) vasopressin preferentially constrict the afferent or efferent arteriole?

A

a) Afferent
b) Efferent

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24
Q

What features of aminoglycosides make them associated with AKI?

A

Not metabolised
LMW
Water soluble
Ionise to cationic complexes which bind to anionic sited on PT epithelium - internalised and concentrate

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25
Q

How do NSAIDs cause AKI?

A

Renal function more dependent on prostaglandin synthesis in situations of low blood flow
Predominant renal prostaglandin causes afferent arteriolar dilation - maintains RBF during systemic vasoconstriction

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26
Q

MOA fenoldopam

A

Selective DA-1 agonist

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27
Q

What are the hypothetical benefits of mannitol in AKI?

A

Inhibits renin => inhibits NA reabsorption
Increases tubular flow
Decreases vascular resistance and cellular swelling
Increases RBF, GFR and solute excretion
Induces intrarenal prostaglandin production and vasodilation
Induces ANP release
May blunt Ca influx into mitochondria

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28
Q

What is the evidence for mannitol in AKI?

A

No evidence of benefit in people or healthy cats

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29
Q

When is mannitol contraindicated in AKI?

A

Dehydration
Overhydration
May worsen pulmonary oedema

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30
Q

What are the theoretical benefits of frusemide in AKI?

A

By inhibiting Na/Cl/K pump, NaK pump becomes unnecessary - medullary oxygen consumption reduces
Renal vasodilatory effects

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31
Q

What is a proven benefit of frusemide in AKI?

A

Reduced structural damage in thick ascending LOH

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32
Q

What are established indications for frusemide in AKI?

A

Hyperkalaemia
Overhydration

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33
Q

When is frusemide contraindicated in AKI?

A

Aminoglycoside-induced AKI

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34
Q

What are potential complications with dialysis?

A

Dialysis disequilibrium syndrome - rapid decline in osmolality - CNS signs
Hypotension
Haemorrhage
Hypocalcaemia
Catheter thrombosis

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35
Q

What treatment is recommended for Aminoglycoside toxicity?

A

Ticarcillin and carbenicillin - complex aminoglycosides and prevent uptake

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36
Q

What treatment is recommended for sulphonamide toxicosis?

A

Urinary alkalisation +/- high-volume fluid therapy/mannitol

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37
Q

What treatment is recommended for pigment nephropathy?

A

Urinary alkalisation +/- high-volume fluid therapy/mannitol

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38
Q

What ECG findings are reported with hyperkalaemia?

A

Bradycardia, tall spiked T waves, shortened QT interval, wide QRS complex with small/absent P wave

39
Q

What ECG findings are associated with SEVERE hyperkalaemia?

A

Sinoventricular rhythm, VF, ventricular standstill

40
Q

What effect does metabolic acidosis have on calcium?

A

Increases ionised fraction

41
Q

What is the mechanism of hypercalcaemia in AKI?

A

v GFR = ^P
Ca decreases by law of mass action

42
Q

When should hypomagnasaemia be suspected in AKI?

A

Refractory hypokalaemia, normally in PU phase

43
Q

What are the most common histopathological findings in dogs with CKD?

A

58% tubulointerstitial nephritis
28% glomerulonephropathy
6% amyloidosis

44
Q

What are the most common histopathological findings in cats with CKD?

A

70% tubulointerstitial nephritis
15% glomerulonephropathy
11% lymphoma
2% amyloidosis

45
Q

In cats with CKD, what 2 baseline parameters are associated with survival?

A

Creatinine and phosphorus

46
Q

What are the mechanisms of PUPD in CKD?

A

Increased solute load per nephron
Impaired renal responsiveness to ADH
Impaired genesis of hypertonic gradient of medulla

47
Q

What RBC morphological abnormalities are recognised inCKD?

A

Burr cells or echinocytes

48
Q

Do CKD patients have relative or absolute EPO deficiency?

A

Relative (higher than normal but nor proportional for degree of anaemia)

49
Q

What changes in plasma aldosterone and PRA are seen in azotaemic hypertensive cats?

A

Elevated aldosterone with reduced renin

50
Q

What are the 3 layers of the filtration barrier?

A

Fenestrated endothelium
Glomerular basement membrane
Visceral epithelial cells (podocytes)

51
Q

What CBC finding is common in dogs with glomerular disease?

A

Thrombocytosis

52
Q

What are the hallmarks of nephrotic syndrome?

A

Hypoalbuminaemia, proteinuria, hypercholesterolaemia, oedema

53
Q

What stains are used for evaluating renal biopsies and what do the stain?

A

PAS - glycoprotein, interstitial and glomerular scarring and assessment of GBM
Methenamine silver - GBM
Trichrome - mesangium and immunoglobulin
Congo red - amyloid

54
Q

What breed is associated with a familial membranoproliferazive glomerulonephritis?

A

Bernes Mountain dogs

55
Q

What infectious disease is associated with a rapidly progressive form of membranoproliferazive glomerulonephritis?

A

Borrelia

56
Q

What is the pathogenesis of membranoproliferazive glomerulonephritis?

A

Immune complex deposition - cytokine-mediated complement activation, expansion of the mesangium and inflow of leukocytes

57
Q

What are the histo findings of membranoproliferazive glomerulonephritis?

A

Thickened capillary loops and mesangial hypercellularity

58
Q

What is the recommended treatment of membranoproliferazive glomerulonephritis?

A

Identification and treatment of underlying disease
Immunosuppression if severe/progressive
Anti-platelet medication

59
Q

What is the most common glomerular disease in cats?

A

Membranous nephropathy

60
Q

What is the pathogenesis of membranous nephropathy?

A

Antibodies bind to supepithelial (urinary) side of GBM
Primary - ICGN
Secondary - circulating immune complexes
Complement and formation of MAC

61
Q

What are the histo findings of membranous nephropathy?

A

Uniform thickening of GBM
Irregular thickening of capillary walls
Immune deposits +/- engulfment by GBM on TEM

62
Q

What specific treatment is recommended for membranous nephropathy? What is the prognosis?

A

Identification and treatment of underlying disease
Immunosuppression
Can be slow to progress, spontaneous remission reported
Worse if higher grade

63
Q

What is the pathogenesis of proliferative glomerulonephritis

A

ICGN causing endocapillary or mesangial proliferation

64
Q

What are the histo findings in proliferative glomerulonephritis?

A

Mesangial or endocapillary hyperplasia with deposits of IgG or IgM

65
Q

What is the pathogenesis of IgA nephropathy? Why are dogs more prone than people?

A

IgA non-specifically trapped in GBM
Dog IgA is polymeric, so more likely to be trapped n GBM than monomeric IgA

66
Q

What are the light microscopy findings in IgA nephropathy?

A

Mesangial proliferative glomerulonephritis

67
Q

What diseases are most associated with IgA nephropathy?

A

Hepatic/GI

68
Q

What breeds are associated with amyloidosis? In which is there a pattern to amyloid deposition?

A

Chinese Shar-Pei - medulla
Beagles/English Fox hounds - glomeruli
Abysinninans - medulla
Siamese

69
Q

How is reactive amyloidosis confirmed on histo?

A

Stains red with Congo Red
Discoloured by potassium permanganate oxidation

70
Q

MOA colchicine?

A

Inhibits release of SAA from hepatocytes by binding microtubules

71
Q

What breeds are affected by hereditary nephritis and what is the method of inheritance?

A

English cocker - autosomal recessive
English springer - autosomal recessive
Bull terrier - autosomal dominant
Dalmatian - autosomal dominant

72
Q

What is the pathogenesis of hereditary nephritis?

A

Mutation/deletion of type IV collagen - premature deterioration of the GBM

73
Q

What are the histo findings of minimal change disease?

A

Light microscopy - minimal
TEM - podocyte foot process effacement

74
Q

What is the treatment for minimally change disease?

A

Steroids

75
Q

Where do defects associated with cystinuria occur?

A

Proximal tubule

76
Q

What is the mechanism of inheritance of cystinuria? Give examples of affected breeds

A

Type 1 - autosomal recessive. Labrador, Newfoundland, Australian Cattle dog
Type 2 - autosomal dominant

77
Q

What genes are abnormal in cystinuria?

A

Slc3a1 and Slc7a9

78
Q

What treatment is recommended to avoid calculi in cystinuria?

A

Reduced protein
Urine alkalisation
Diuresis

+/- 2-MPG and D-penicillamine

79
Q

What is a consequence of carnitinuria?

A

DCM

80
Q

What condition is carnitinuria commonly associated with?

A

Cystinuria

81
Q

How is the purine portion of amino acids metabolised?

A

To hypoxanthine and xanthine, oxidised to uric acid by xanthine oxidase
Uric acid metabolised to allantoin by hepatic uricase

82
Q

What diseases increase excretion of xanthine?

A

HAC, neoplasia, CKD

83
Q

What breeds are associated with hyperuricosuria?

A

Dalmatian, English Bulldog, Black Russian Terrier

84
Q

What are the differences in purine metabolism in Dalmatians? What gene is involved?

A

Abnormal uric acid transport across hepatic membrane, unable to transport uric acid to uricase
Less proximal reabsorption of uric acid
Increased tubular secretion of uric acid

Slc2a9

85
Q

How is hyperuricosuria treated? What is the rationale for each treatment?

A

XO inhibitors - reduce uric acid production
Purine restricted diet - to prevent xanthine calculi
Urine alkalisation - reduced proximal tubular ammonia production - reduces ammonium ions that complex with urate to form calculi

86
Q

What breed is Fanconi syndrome reported in? What is it’s prevalence?

A

Basenji’s
10-30%

87
Q

What medication has been associated with acquired Fanconi syndrome in a) dogs and b) cats

A

a) Gentamicin
b) Chlorambucil

88
Q

What acid-base abnormality is associated with Fanconi syndrome?

A

Hyperchloraemic metabolic acidosis

89
Q

Which breeds are overrepresented for renal a genesis?

A

Beagle, Doberman, Shetland Sheepdog

90
Q

What breed is affected by podocytopathy? What is the typical age of presentation?

A

Soft coated Wheaten Terrier
6y

91
Q

What gene is involved in PKD?

A

Polycystin-1 (PKD-1)

92
Q

Which dog breeds are affected by PKD?
What is the mechanism of inheritance?

A

Bull Terrier - autosomal dominant
Cairn Terrier - autosomal recessive
WHWT - autosomal recessive

93
Q

What is the mechanism of inheritance of PKD in Persian cats?

A

Autosomal dominant

94
Q

What is the proposed mechanism for hyperlipidaemina in glomerular disease?

A

Hypoalbumoinaemia stimulating hepatic protein synthesis leading to production of lipoproteins
Glomerular loss of orosomucoid, leads to reduced hepatic production of heparin - cofactor for normal lipoprotein lipase function

Ettinger (13 decks)

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