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Professional Version

Obstructive Uropathy in Small Animals


Scott A. Brown

, VMD, PhD, DACVIM, Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia

Reviewed/Revised Oct 2013 | Modified Oct 2022
Topic Resources

Even though the kidneys would otherwise be able to function normally, obstruction of urine flow at any point below the level of the kidneys leads to accumulation of metabolic wastes and postrenal azotemia/uremia. Obstruction of the urethra by uroliths in dogs and by matrix-crystalline plugs in young male cats and obstruction of a ureter by a urolith in geriatric cats are the three most common causes, although uroliths, tumors, or blood clots may obstruct the ureters (or urethra) in either species.

Hydronephrosis is characterized by dilatation of the renal pelvis as the result of partial or complete obstruction of outflow of urine from one or both kidneys. When the obstruction is acute, complete, and bilateral, morphologic changes in the kidneys are less extensive, because the period of survival is short. In unilateral or partial obstruction, the animal often survives long enough for severe pressure atrophy of the renal parenchyma and cystic enlargement of the affected kidney to develop. Hydroureter commonly develops when the obstruction is located lower in the tract. Increased hydrostatic pressure results in atrophy of functional renal parenchyma. The pseudodiverticula of the renal pelvis disappear first; later, even the cortex may atrophy. The affected kidneys eventually become grossly enlarged, functionless sacs, filled with urine or serous fluid that may harbor bacteria.

Clinical Findings:

Animals with urethral obstruction frequently exhibit pollakiuria, stranguria, and hematuria; abdominal pain may be marked. Signs of uremia develop rapidly and include vomiting, dehydration, hypothermia, and severe depression. The bladder is distended and painful on palpation, and a urethral catheter cannot be readily passed. Bradycardia or cardiac arrhythmias due to hyperkalemia may be present, particularly if plasma potassium is >7 mEq/L. Because compensatory hypertrophy of the nonaffected kidney results in a nonazotemic state, unilateral ureteral obstruction commonly is undiagnosed, unless the animal has accompanying renal disease or the enlarged, hydronephrotic kidney is palpated during physical examination and/or seen on radiologic or ultrasonographic imaging studies.


The history, clinical signs, and physical examination usually provide a straightforward diagnosis of urethral obstruction. Ureteral obstruction should be suspected in any acutely uremic cat, including those with a history of chronic kidney disease. Excretory urography or abdominal ultrasonography are necessary to establish a diagnosis in animals with bilateral or unilateral ureteral obstruction. Serum potassium levels should be determined immediately in animals with cardiac arrhythmias. An ECG can provide presumptive evidence of hyperkalemia (bradycardia; tall, peaked T waves; increased PR interval; widened QRS complex; atrial standstill) if laboratory results are delayed.


The urethral obstruction should be relieved ( see Urolithiasis in Small Animals Urolithiasis in Small Animals Some mineral solutes precipitate to form crystals in urine; these crystals may aggregate and grow to macroscopic size, at which time they are known as uroliths (calculi or stones). Uroliths... read more Urolithiasis in Small Animals ). Fluids given IV improve renal function and correct electrolyte and acid-base abnormalities. Normal saline is preferred but not required in hyperkalemic animals. Unless the animal is markedly hyperkalemic (serum potassium >7 mEq/L), has cardiac arrhythmias, or is known to have preexisting kidney disease, it is often best to avoid overcorrection by allowing plasma potassium and acid-base balance to return toward normal via restoration of renal excretory function for 12 hr before administering therapy specifically intended to correct these abnormalities. In animals with severe hyperkalemia and cardiac arrhythmias, bicarbonate (0.5 mEq/kg, given slowly IV over 5 min) or regular insulin and dextrose infusions can be given to drive potassium intracellularly. Because of a postobstructive diuresis that lasts for 1–5 days, hypokalemia and/or dehydration are often seen within 24–48 hr after correction of urethral obstruction. Plasma electrolytes, body weight, urine output, hematocrit, and plasma total solids should be monitored daily, with the type and quantity of fluid administered adjusted appropriately.

Surgery is often necessary to correct complete ureteral obstruction. When possible, the obstruction should be removed to reestablish urine flow. In some cases, ureteroliths will pass through the ureters, eliminating the need for surgery. This may require partial ureteral resection and reimplantation, particularly in cats, which have very small and friable ureters. In some cases, unilateral nephrectomy may be required, but a kidney should not be removed without clear evidence that the contralateral kidney is capable of sustaining life. Preferred evidence includes the estimation of GFR in the contralateral kidney but could alternatively be based on the following criteria: normal renal size, shape, and consistency on ultrasonography; presence of normal vascular and excretory phases on excretory urography; normal renal ultrasonographic examination; and normal renal biopsy.

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