CHAPTER 48. Urinary Disorders
Rebecca S. McConnico
ACUTE RENAL FAILURE
I. Abrupt cessation of renal function
A. Results in accumulation of nitrogenous wastes
B. Fluid imbalances
C. Electrolyte imbalances
II. Serum biochemistry abnormalities
A. Elevation in blood urea nitrogen (BUN)
B. Serum creatinine elevation (Cr)
C. Collectively known as azotemia
1. Prerenal azotemia: Decreased kidney perfusion; in strict prerenal azotemia, horses will pass urine > 1.020
2. Renal azotemia: Primary malfunction of the kidneys
3. Postrenal azotemia: Blockage of urine excretion
III. Causes of equine azotemia
A. Most common cause of azotemia in horses is hemodynamic causes such as dehydration
B. Additional causes are acute tubular necrosis (ATN) due to renal toxins
C. Progression of prerenal-induced ischemic tubular damage
D. Reversible if treated appropriately
IV. Causes of prerenal azotemia
A. Acute enteritis: Diarrhea is the clinical sign
B. Colic: Abdominal pain is the clinical sign
C. Prolonged exercise: Exhaustion is the clinical sign
D. Acute blood loss: Pale mucous membranes are a clinical sign
E. Cardiac insufficiency: Weakness and pale membranes are clinical signs
V. Treatment
A. Replacement of plasma volume will correct prerenal azotemia
B. ATN plus prerenal azotemia: Will often result in pulmonary edema or peripheral edema once fluids have been replaced
VI. Cause
A. Tubular obstruction by sloughed cellular debris (Tamm Horsefall mucoproteins or heme proteins)
B. Back leak of the glomerular filtration through the damaged tubular cells
C. Primary reduction in glomerular filtration rate (GFR) through reflex shunting arteriolar circulation away from obstructed nephrons or glomerular capillary permeability decreasing through swelling or mesangial contraction
ACUTE TUBULAR NEPHROSIS
I. Causes
A. Hemodynamic imbalance
B. Toxins
C. Medications
1. Aminoglycosides
2. Certain sulfonamides
3. Polymyxin B
4. Phenylbutazone (and other nonsteroidal antiinflammatory drugs)
5. Menadione sodium bisulfite (vitamin K 3)
D. Endogenous pigments
1. Hemoglobin
2. Myoglobin
E. Plant toxins
1. Oak
2. Wilted red maple leaves
3. Wild onion
4. White snakeroot
F. Heavy metals: Mercury
G. Cantharadin: Blister beetles
II. Postrenal causes
A. Ruptured bladder in newborn foal
B. Uroliths: Adult
III. Pathogenesis: Accumulation of nitrogenous wastes in the blood (elevations in serum creatinine and BUN)
IV. Diagnosis
A. Elevated Cr and BUN
B. Urinalysis
1. Urine specific gravity less than 1.020 in the presence of clinical dehydration suggests intrarenal disease
2. Color of urine: The presence of heme pigments
3. Sediment analysis
a. Normal reveals considerable mucus and calcium carbonate crystals
b. Casts are easily overlooked because they dissolve easily
C. Renal ultrasound: Cyst or structural changes
D. Nuclear medicine techniques: GFR
E. Renal biopsy: Perform only when there is the necessity to know prognosis because of complications of severe hemorrhage
V. Treatment
A. Correction of fluid, electrolyte, and acid-base disorders
C. Oral fluids
1. Well tolerated
2. Water
3. Isotonic fluid
4. Balanced electrolyte fluid
D. Intravenous therapy: Indicated for animals with gastrointestinal disease