Inadequate renal perfusion hypovolemia dehydration GI fluid loss hypotension acute blood loss dec CO USG \> 1.025 FCNa \ /= 50% reduction in azotemia w/in 24 hours of fluid therapy \ may be a back door determination

Acute kidney injury: abrupt decrease in GFR Most common cause: Acute tubular necrosis (ATN) vasomotor nephropathy (ischemia) aminoglycoside toxicity NSAIDS Pigment nephropathy lepto

Medularry crest necrosis medulla receives 10-20% Renal blood flow COX inhibitors dec prostaglandin formation PGE2 and PGI2 renal vasodilators, especially when decreased RBF Enhanced by dehydration

Myoglobinuria rhabdomyolysis crush injury heat stroke inc CK, AST serum clear Hemoglobinuria intravascular hemolysis serum pink

Diagnostics (organism or antibody) Serum microscopic agglutination test (MAT) for antibody rise in titer Urine PCR organism in urine sheds more after furosemide Dark field microscopy Culture takes months: clinically useless Immunofluorescence on tissue sample Treatment doxycycline, ampicillin, penicillin, amoxicillin, ceftiofur \ Don't use oxytetracycline \ \ \ nephrotoxic

Rare in adult horses more common in neonatal colts Dysuria, colic Signs neonatal uroabdomen don't rule out even if peeing thru normal hole obstructive urolithiasis bladder necrosis

Clinical signs non-specific Rule out pre-renal and post-renal azotemia Frequently oliguric no urine within 6-12 hours of initiation of fluid therapy Rectal palpation kidney enlarged, painful Ultrasound perirenal edema hypoechogenicity loss of corticomedullary distinction dilation of renal pelvis

Chem inc BUN and Cr ( \< 10:1 ratio) dec Na, Cl, Ca inc K, P Urinalysis hematuria, proteinuria, casts, glucosuria inc UGGT in FCNa, P

LA acute & chronic kidney dz (Reuss) Flashcards by Jessica Fuller

Pre-Renal Azotemia

Inadequate renal perfusion
- hypovolemia
- dehydration
  - GI fluid loss
- hypotension
  - acute blood loss
- dec CO
USG > 1.025
FC_Na< 1%
>/= 50% reduction in azotemia w/in 24 hours of fluid therapy

*may be a back door determination

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After starting IV fluids a patient should urinate in

8-12 hours

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Renal azotemia

Acute kidney injury: abrupt decrease in GFR
- Most common cause: Acute tubular necrosis (ATN)
  - vasomotor nephropathy (ischemia)
  - aminoglycoside toxicity
  - NSAIDS
  - Pigment nephropathy
  - lepto

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Ischemia

‘vasomotor nephropathy’

Continuum of pre-renal azotemia
prolonged marked hypotension
- endotoxemia (toxic line on MM)
Blood loss

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Aminoglycoside toxicity

Bind to brush border of proximal tubule
- pinocytosis
- accumulate in renal cortex
- inhibit phospholipase activity
- impair organelle function
- proximal tubular epithelial cell damange
Renal vasoconstriction
Toxicity Neomycin > Kanamycin > gentamicin > amikacin > streptomycin
Precipitated by concurrent dehydration
Binding saturable: once daily dosing preferred

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Other nephrotoxic antimicrobials

Oxytetracycline
- given to foals with tendon contracture
Polymyxin B
- endotoxemia
Amphotericin B

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NSAIDS

Medularry crest necrosis
- medulla receives 10-20% Renal blood flow
COX inhibitors
- dec prostaglandin formation
PGE₂ and PGI₂
- renal vasodilators, especially when decreased RBF
Enhanced by dehydration

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Pigment nephropathy

Myoglobinuria
- rhabdomyolysis
- crush injury
- heat stroke
- inc CK, AST
- serum clear
Hemoglobinuria
- intravascular hemolysis
- serum pink

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Pigment actions causing tubular necrosis

Pigment
- vasoconstriction
- ischemia
Tubular obstsruction by protein casts
Hydroxyl radicals
Cortex most susceptible d/t inc blood flow

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Leptospira interrogans

Hosts

Exposure

Syndromes

Zoonotic
cause acute kidney injury
horses
- incidental host (except bratislava)
- maintenance hosts: rat, cow, skunk, opossum
Exposure
- urine
- aborted fetus
Clinical syndromes
- AKI, tubulointerstitial nephritis
- Uveitis
- Abortion, stillbirths, neonatal death

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Lepto

Diagnostics

Diagnostics (organism or antibody)
- Serum microscopic agglutination test (MAT) for antibody
  - rise in titer
- Urine PCR
  - organism in urine
  - sheds more after furosemide
- Dark field microscopy
- Culture
  - takes months: clinically useless
- Immunofluorescence on tissue sample
Treatment
- doxycycline, ampicillin, penicillin, amoxicillin, ceftiofur

*Don’t use oxytetracycline ***nephrotoxic

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Acute Glomerulonephritis

Rare in horses
- usually sequela to other diseases
Marked proteinuria, red cell casts
Inciting antigens
- Streptococcus
- EIA
Immune complex deposition
- complement activation
- tissue damage

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Post-Renal azotemia

Rare in adult horses
more common in neonatal colts
Dysuria, colic
Signs
- neonatal uroabdomen
  - don’t rule out even if peeing thru normal hole
- obstructive urolithiasis
- bladder necrosis

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Clinical Eval of AKI

Clinical signs non-specific
Rule out pre-renal and post-renal azotemia
Frequently oliguric
- no urine within 6-12 hours of initiation of fluid therapy
Rectal palpation
- kidney enlarged, painful
Ultrasound
- perirenal edema
- hypoechogenicity
- loss of corticomedullary distinction
- dilation of renal pelvis

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Clin path AKI

Chem
- inc BUN and Cr ( < 10:1 ratio)
- dec Na, Cl, Ca
- inc K, P
Urinalysis
- hematuria, proteinuria, casts, glucosuria
- inc U_GGT
- in FC_{Na, P}

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Treatment of AKI

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d/c nephrotoxic drugs
treat concurrent dz
correct volume def and establish diuresis
- balanced electrolyte solution
- deficit = % dehydration x BW
- maintenance = 40-60 ml/kg/day
monitor closely for urination or development of edema

TX of hyperkalemia in AKI

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0.9% NaCl fluids
5% dextrose
Calcium gluconate
Sodium bicarbonate
Insulin

Other treatments AKI

establishing diuresis

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Furosemide
- loop diuretic: blocks Na/K/2Cl co-transporter
- depends on GFR
Mannitol - NOT REALLY USED
Dopamine - NOT REALLY USED
Peritoneal dialysis
Hemodialysis: brutus the tiny cow

Prognosis for AKI

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Varies with underlying cause
if oliguria persists > 72 hours, prognosis guarded
secondary complications: laminitis
polyuria
- transient
- permanent

Chronic kidney disease

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irreversible
variable rate of decline
‘end stage kidney dz’

Causes CKD

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Acquired
- glomerular dz
  - glomerulonephritis
  - amyloidosis => more common in cattle
- tubulointerstitial dz
  - chronic interstitial nephritis
    - incomplete recovery from ATN
    - pyelonephritis
    - obstructive dz
Congenital (dx with rectal, ultrasound, bx)
- suspect if < 5 yo with CKD
  - renal agenesis
  - hypoplasia
  - dysplasia
  - PKD

Clinical signs of CKD

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Uremia: clinical manifestation of azotemia
Chronic weight loss
- uremic toxins: appetite supp, oral and GI ulcers
- Gastrin half-life prolonged
- inc catabolic state
Rough hair coat
Poor athletic performance
- anemia: dec EPO; dec RBC survival time
PU/PD
- degree not correlated
- collecting tubule can’t compensate for excess glom filtrate
Ventral edema
Uremic halitosis
urea exretion in sweat
dental tartar, gingivitis, oral ulcers

Uremia

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Uremia: clinical manifestation of azotemia
- effects of uremic toxins on cell metabolism and function
  - BUN, other nitrogenous compounds
  - Cr and other guanidino compounds
  - products of intestinal bacterial metabolism
  - middle molecules
  - abnormal metabolism of hormones and trace minerals

*correlation btwn magnitude of azotemia and degree of uremic syndrome is poor

Ventral edema

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dec oncotic pressure
- PLE
- glomerular protein loss
inc vascular permeability
- uremic toxins
inc hydrostatic pressure
- renin release

four mechanisms of edema

1. dec oncotic pressure 2. inc vascular permeability 3. inc hydrostatic pressure 4. dec lymphatic return

Clinical evaluation of CKD

* Azotemia * BUN: Cr \> 10:1 * \> 15:1 = excessive protein intake * BUN actually helpful here * Electrolytes * **hyperCa, hypoP** * HypoNa, Cl * +/- K * metabolic alkalosis or neutral until terminal * metabolic acidosis late * hypoalbuminemia * hyperlipidemia * hematology * non-regenerative anemia * Urinalysis * isosthenuria (1.008-1.014) * develops before azotemia * enzymuria, proteinuria, glucosuria * pyuria, bacteruria * FC_Na \> 1 % * Rectal: small firm kidney * U/S: small, hyperechoic * BX: end stage kidney dz, congenital dz, immunfluor, EM

CKD prognosis

* Grave * 75% renal function loss if azotemic * doubling of Cr = 50% decline in GFR * Cr \< 5 mg/dl =\> may manage for months - years * Cr \> 10-12 mg/dl =\> marked compromise * Cr \> 15 mg/dl =\> grave

CKD prognosis GFR measuring

* Measure GFR * endogenous creatinine clearance * Requires timed collections * tubular creatinine secretion possible * plasma dissapearance of * exogenous creatinine sulfanilate * technicium 99 tag \***not done clinically**

acute exacerbation tx

* treat like AKI * judicious fluid therapy * antimicrobials if pyelonephritis * discontinue nephrotoxic drugs

CKD management

* d/c alfalfa, legumes * use good grass instead * maintain normal protein intake (about 10%, not higher, deficiency can inc morbidity/mortality) * maintain BUN:Cr 10:1 - 15:1 * maintain BCS * Only if necessary * NaCl * NaHCO3 * omega-3 fatty acids * flaxseed oil

AKI vs CKD AKI signs

1. Good BCS 2. normal hematocrit 3. kidney consistency normal to soft 4. recent association with disease, drugs 5. US: normal echogenicity or hypoechoic with loss of renal architecture 6. BUN:Cr \< 10:1 7. HypoCa, hyperPh

AKI vs CKD CKD signs

1. Poor BCS, weight loss 2. Anemia 3. Kidney size normal to decreased 4. Kidney consistency normal to firm 5. No recent history of other dz 6. US: hyperechoic 7. BUN:Cr \> 10:1 8. HyperCa, HypoPh

LA acute & chronic kidney dz (Reuss) Flashcards

(32 cards)