Causes of acute renal failure: 1. Hemodynamic causes; 2. Toxic causes; 3. Inflammatory causes.
Renal Components of the Chemistry Panel
1. Creatinine
2. BUN
3. Electrolytes
• Sodium: N to ↓
• Chloride: N to ↓
• Potassium: ↑
• Calcium: acute= ↓ Ca: chronic=↑
• Phosphorus: acute= ↑
• Acid – base parameters: TCO2: ↓
• Anion Gap:↑
Creatinine/BUN: Increase means that GFR has decreased (prerenal,renal) or post-renal disease is present
Renal Disease
• Hyponatremia, hypochloremia
• Hyperkalemia (normal to high)
• Metabolic acidemia (Low TCO2)
o Anion Gap often increases
• Acute Renal Failure
o Hypocalcemia
o Hyperphosphatemia
• Chronic Renal Failure
o Hypercalcemia
o Hypophosphatemia
Causes of acute renal failure: 1. Hemodynamic causes; 2. Toxic causes; 3. Inflammatory causes
1 Hemodynamic causes
• Prolonged hypovolemia
• Coagulopathy Endotoxemia/SIRS
2 Toxic causes
• Phenylbutazone
• Aminoglycosides
• Tetracycline*
• Pigments- hgb, mgb
• Heavy metals
• Blister Beetle
3 Inflammatory causes
• Pyelonephritis
• Leptospirosis
• Neoplasia
• Immune-mediated causes
Glomerulonephritis – Proteinuria
Secondary to Strep equi equi
Prerenal vs Renal Azotemia
• Horses with prerenal azotemia are dehydrated
o Urine is concentrated
o USG > 1.020
• Horses with renal azotemia are isosthenuric regardless of hydration status
o USG: 1.008 – 1.020
Prerenal
A rapid decrease in creatinine is expected with fluid therapy. It should be markedly decreased and close to normal within 24 h if prerenal. Persistent elevation of creatinine in the face of fluids indicates renal disease
Prolonged prerenal azotemia will lead to renal failure if not corrected
Prerenal vs Renal Azotemia
• Fractional Excretion of Sodium
o < 1 % in prerenal cases (Normal FENa is < 1 %)
o 1 % indicates renal dysfunction
• FE reflects tubular reabsorptive capacity
• FENa+ = SerumCr X UrineNa
• UrineCr SerumNa
Case 1: 10-month Paint filly
History: Severe bilateral forelimb contracture
• Unable to fix distal limb
• Upright digit and fetlock joint
• Painful, lies down often, partial anorexia
Historical Treatment
• 0.5 g phenylbutazone PO BID
• Full limb wraps
• Oxytetracycline (44 mg/kg; total 15 g IV twice)
Risk Factors
• Partial anorexia = likely not drinking well > dehydration
• Phenylbutazone: NSAIDS: renal ischemia through inhibition of PGE and PGI
• Oxytetracycline: toxic to tubule epithelium
On day 3 the filly was depressed and Anorexic:
Key Questions:
1. Is it prerenal, renal, post-renal?
Urine Specific Gravity: 1.012
Observed to urinate normal stream
• ANSWER>>>Renal
2. Is it chronic or acute?
Body condition is good
Calcium is normal
Phosphorus is high
No anemia, no dental tartar
• ANSWER>>>Acute
US is helpful – shows enlarged kidneys with perirenal edema
Treatment: Discontinue bute and tetracycline; Opioids for analgesia if pain medication needed
FLUIDS!
Isotonic crystalloids: Initial bolus 30 mL/kg, then 3 mL/kg/h
Maintained on fluids for approximately 5 days
Case 2: 3-Yr old Paint Mare
Key Questions
1. Prerenal, renal, post-renal ?
• Urinary catheter passes easily, normal bladder palpated
USG: 1.010
FE: Scr x UNa
Ucr SNa
FE: 5.1 x 50 = 0.03 = 3 % HIGH ==== ANSWER = RENAL 65 131
Key Questions
Acute or Chronic ?
Weight loss
Mild anemia
Hypercalcemia
Suggest chronic
US is confirmatory
Histopathology is definitive
Biopsy Results
• Severe, Multifocal Chronic Lymphoplasmacytic Interstitial Nephritis With Severe Interstitial Fibrosis And Glomerulosclerosis
Mare euthanized due to biopsy results, marked US changes, and poor clinical response
Case 3: 5 Yr Old QH Gelding
Acute colic: began this morning; nonresponsive to analgesics; HR: 70
• PE: HR: 70
o 8 % dehydrated/hypovolemic
o Moderately painful
o Large colonic distention with tight bands across abdomen on rectal
o US reveals distended colon obscuring liver on right
Right Dorsal Displacement Suspected
Key Findings
• Azotemia
• Mild acidemia
• Increased liver enzymes and BR-Functional indicators are ok
Key Questions
1. Prerenal, renal, or post-renal?
USG: 1.039 – very concentrated
Observed to urinate normally by owners; no ascites
.>>PRERENAL due to hemodynamic causes
Response to fluid therapy confirms this
With fluid diuresis the next day:
• Creatinine has decreased from 3.1 to 2.0
• BUN has decreased from 45 to 27
Liver Enzymes
Liver appeared normal on US and at time of surgery
Enzymes decreased to normal over several days in the post-operative period
Example of transient liver disease secondary to GI causes (endotoxemia or biliary obstruction)
General Guidelines: Therapy of Acute Renal Failure
I. Polyuric Renal Failure
1. IV fluid therapy:
Replace deficits
Then 1.5-2 X maintenance rate
• 4-5 mL/kg/h initially
• As improvement occurs, the rate can be decreased to 2-3 mL/kg/h
• Diuresis should continue until creatinine normalizes or plateaus for 48-72 h
• Avoid nephrotoxic agents such as NSAIDS, Aminoglycosides
2. Nutrition
• If anorexic, add dextrose 1.5-5 %
• Feed low calcium diets in longer term
• Feed lower quantity, but higher quality protein
• Omega 3 fatty acids (flaxseed)
Treatment of Anuria/Oliguria
• Replace fluid deficits
• Diuretics: Furosemide (Lasix): One or two doses of 1 mg/kg boluses IV
If no response, try continuous rate infusion (CRI) at 0.12 mg/kg/h
Mannitol – 0.5 g/kg bolus, do not repeat if no urine is produced; OR 1 mg/kg/min concerned about volume overload
3. Low dose dopamine to make urine flow: - 2 ?g/kg/min for renal afferent arteriolar dilation