Oliguria is the production of an abnormally small amount of urine (urine production rate of < 0.25 ml/kg/hr). Anuria is the formation of essentially no urine (urine production rate of < 0.08 ml/kg/hr).
Physiologic oliguria occurs when the kidneys limit renal water loss during episodes of low renal perfusion to preserve body fluid and electrolyte balance. High plasma osmolality or low effective circulating fluid volume increase antidiuretic hormone (ADH) synthesis and release. ADH acts on the kidneys to induce formation of small quantities of concentrated urine (the hallmark of physiologic oliguria).
Pathologic oliguria results from severe renal parenchymal impairment. Factors include (1) high resistance in afferent glomerular vessels, (2) low glomerular permeability, (3) excessive leakage ("back leak") of filtrate from damaged renal tubules, (4) intratubular obstruction, and (5) extensive loss of nephrons resulting in marked reduction in the quantity of glomerular filtrate produced.
Anuria may be of renal or postrenal origin. Severe renal disease occasionally causes anuria. Mechanisms are the same as for pathologic oliguria. Anuria usually results from postrenal causes (e.g., obstruction of urine flow or rupture of the excretory pathway).
SIGNALMENT Dogs and cats
Physiologic oliguria--renal hypoperfusion (caused by low blood volume or hypotension) or hypertonicity (usually caused by hypernatremia)
Pathologic oliguria--oliguric acute renal failure or end-stage chronic renal failure
Anuria--complete urinary tract obstruction, rupture of the urinary excretory pathway, or severe, primary renal failure
Physiologic oliguria--dehydration, low cardiac output, and hypotension
Pathologic oliguria and anuria caused by primary renal failure (risk factors for acute renal failure)--preexisting renal disease, exposure to nephrotoxins, dehydration, low cardiac output, hypotension, electrolyte imbalance, acidosis, advanced age, fever, sepsis, liver disease, multiple organ failure, trauma, diabetes mellitus, hypoalbuminemia, and hyperviscosity syndrome
Anuria--urolithiasis, urinary tract neoplasia, idiopathic feline lower urinary tract disease (obstruction), micturition disorder, and trauma
Physiologic oliguria is suggested by signs of poor tissue perfusion (e.g., dehydration, slow capillary refill time, pale mucous membranes, weak pulse, rapid or irregular pulse, and cool extremities). Patient may have a history of recent fluid loss (vomiting, diarrhea, polyuria, hemorrhage). Signs of uremia are typically absent and oliguria resolves rapidly when renal hypoperfusion is corrected.
Pathologic oliguria and renal anuria is suspected in patients with any of the risk factors given. The greater the number of these risk factors, the more likely the patient has or will develop acute renal failure. Patients with pathologic oliguria caused by chronic renal failure typically have a history of progressive renal disease (including long-standing polyuria, polydipsia, poor appetite, and weight loss). Patients with chronic renal failure are at risk of developing acute renal failure. Signs of uremia are commonly observed and fluid therapy and other measures designed to restore adequate renal perfusion often fail to increase urine flow.
Anuria caused by urinary obstruction or rupture of the excretory pathway is suspected in patients that repeatedly strain to void but are unable to produce urine flow. They may have a previous history of pollakiuria, dysuria, stranguria, hematuria, urolithiasis, trauma, or instrumentation of the urinary tract. In patients with urinary obstruction, physical examination may reveal a large urinary bladder, painful posterior abdomen, and mass or uroliths in the urethra or bladder. Physical examination of patients with rupture of the urinary tract reveals ascites, fluid infiltration in tissues around the urinary tract, painful caudal abdomen, mass or uroliths in the bladder or urethra, or evidence of trauma (e.g., pelvic fracture). Urinary obstruction caused by disorder of micturition may be suspected in patients with a large urinary bladder, high resistance to manual expression of the bladder, and neurologic signs affecting the hind limbs or tail. Signs of uremia may develop. Restoration of urine flow or correcting rents in the excretory pathway rapidly restores adequate urine flow.
Serum urea nitrogen and creatinine concentrations are typically high unless the onset of oliguria or anuria is very recent.
Hyperkalemia is common in animals with pathologic oliguria and anuria, less common and less severe in animals with physiologic oliguria (except in those with hypoadrenocorticism).
Physiologic oliguria is characterized by urine specific gravity values > 1.030 in dogs and > 1.035 in cats. Oliguria associated with urine specific gravity values below these values suggests primary renal failure. Patients with urine concentrating defects from other diseases or drugs are the exception to this rule.
Renal anuria and anuria resulting from postrenal causes often is characterized by urine specific gravity values < 1.030 (dogs) or 1.035 (cats). Adequate urine concentrating ability often is lost after urinary obstruction, but may persist with rupture of the excretory pathway.
OTHER LABORATORY TESTS N/A
Abdominal radiographs and ultrasound are useful to rule out urinary obstruction and rupture of the excretory pathway. Distension of any portion of the excretory pathway or observation of uroliths within the excretory pathway suggests urinary obstruction.
Detection of fluid within the peritoneal cavity or adjacent to the urinary tract supports a diagnosis of rupture of the excretory pathway.
Excretory urography, retrograde urethrocystography, and vaginourethrocystography may provide definitive proof of urinary obstruction or rupture of the excretory pathway.
OTHER DIAGNOSTIC PROCEDURES
Electrocardiography may be used to quickly establish whether patient has clinically important hyperkalemia. Hyperkalemic cardiotoxicity is characterized (in order of progressing hyperkalemia) by: tall, peaked T waves with a narrow base; prolongation of the P-R interval and QRS complex; decreased amplitude and increased width of P waves; bradycardia; atrial standstill; QRS-T fusion causing a wide-complex, idioventricular rhythm; ventricular fibrillation or asystole.
Urethrocystoscopy may provide evidence of obstruction or rupture of the urinary tract.
Placing a urinary catheter may provide information concerning the integrity of the lower urinary tract, but this approach is not recommended as a diagnostic procedure because it may be misleading, it may induce additional trauma to the urinary tract, and it may introduce bacteria.
Oliguria and anuria are medical emergencies. If untreated, they may lead to death within hours to days. Death typically results from uremia, hyperkalemia, or sepsis (in patients with urinary tract infection).
Persistent renal hypoperfusion may lead to acute ischemic renal injury and therefore must be rapidly corrected.
Treatment for primary renal oliguria and anuria is usually limited to symptomatic and supportive care, designed to allow the patient to survive long enough for some recovery of renal function to occur spontaneously. Elimination of etiologic factors may slow or stop further renal injury (eg, terminating aminoglycoside administration, correcting hypercalcemia, and restoring adequate renal perfusion). However, once oliguria or anuria have developed, few if any renal diseases will be amenable to specific treatment.
Postrenal causes for anuria may be corrected by nonsurgical or surgical methods. Nonsurgical methods include hydropropulsion of uroliths or urethral plugs or placement of urinary catheters to restore low-pressure urine flow. Surgical methods include removal of uroliths, polyps, or neoplastic tissue and surgical correction of rents, strictures, or malposition of the excretory pathway.
DRUGS AND FLUIDS
Renal hypoperfusion should be corrected by intravenous administration of normal saline or lactated Ringer's solution. In selected animals, other fluids may be more appropriate (eg, blood to correct hypoperfusion resulting from hemorrhage).
In patients with renal oliguria, diuretics are usually indicted after correcting renal hypoperfusion. However, diuretics may not improve renal function, and diuretic-induced increase in urine flow rate does not necessarily indicate improved renal function. Nonetheless, diuretics are indicated because converting oliguria to nonoliguria facilitates managing the patient by fluid and electrolyte administration. Increase in urine flow after diuretic administration suggests a more favorable prognosis.
Furosemide (2 mg/kg IV q8h) is often used initially in patients with oliguric acute renal failure. Urine flow should increase within 1 hour. If diuresis does not ensue within an hour, dosage may be increased to 4 to 6 mg/kg/IV. Infusion of mannitol or infusion of dopamine with furosemide appears to be more effective than furosemide alone.
Dopamine (1 to 5 µg/kg/minute) is generally administered concurrently with furosemide. Diuresis should ensue within 1 to 2 hours. If urine flow does not increase within 2 hours, discontinue dopamine.
Mannitol (0.5 to 1.0 gm/kg/IV) can be given as a 10 or 20% solution over 15 to 20 minutes. Urine flow should increase within 1 hour. Administration of mannitol should not be repeated if diuresis does not ensue because it may cause excessive volume expansion.
A safer but possibly less effective alternative to mannitol is infusion of 10-20% dextrose solution (25 to 50 ml/kg/IV q8h-q12h) over 1-2 hours. Because dextrose is metabolized, the potential for volume expansion is minimized.
Administer fluids judiciously to patients that are persistently oliguric or anuric to avoid overhydration. In patients with unresponsive renal oliguria, peritoneal dialysis or hemodialysis may be the only means of correcting severe volume over expansion.
Correct fluid deficits before initiating diuretic administration. Otherwise, renal hypoperfusion and ischemic renal injury may be exacerbated.
Drugs requiring renal excretion should be used with caution. If resolution of oliguria or anuria can reasonably be expected within minutes to a few hours (eg, physiologic oliguria and anuria caused by urinary obstruction), standard dosages of drugs requiring
renal excretion can be used.
Avoid electrolyte solutions containing more than 4 mEq/L of potassium in most animals.
Dopamine can cause cardiac arrhythmias, particularly in animals with hyperkalemia. ECG monitoring is recommended when high dosages are used and in animals with hyperkalemia.
Furosemide may promote the nephrotoxicity associated with aminoglycoside antibiotics.
Mannitol can be used in preference to furosemide in patients with aminoglycoside-induced, oliguric acute renal failure.
Urine flow rate: Urinary catheterization may be necessary for accurate determination of urine volume. However, urinary catheterization can induce bacterial urinary tract infection, an important cause of morbidity and mortality in patients with acute renal failure. Catheters must be placed by aseptic technique. Intermittent catheterization is less likely to cause urinary tract infection than an indwelling catheter. The shorter the interval that a catheter is left indwelling, the lower the risk of urinary tract infection. Indwelling catheters should be attached to a closed, sterile, urinary drainage system.
Creatinine, serum urea nitrogen and potassium concentrations after 12 to 24 hours. More frequent monitoring of serum potassium concentration may be indicated in animals with severe hyperkalemia.
ECG monitoring to assess cardiac effects of dopamine, hyperkalemia, and response to treatment.
Hyperkalemia and associated cardiotoxicity
Uremia leading to death
Dehydration caused by vomiting, diarrhea, and respiratory losses
Overhydration caused by excessive fluid intake or administration leading to pulmonary edema
Bacterial urinary tract infection
ASSOCIATED CONDITIONS N/A
AGE-RELATED FACTORS N/A
ZOONOTIC POTENTIAL N/A
Creatinine and Blood Urea Nitrogen (BUN) Azotemia and Uremia
Nephrotoxicity, Drug Induced
Renal Failure, Acute
Renal Failure, Chronic
Urinary Tract Obstruction
ADH = antidiuretic hormone
Grauer GF, Lane IF. Acute renal failure. In: Ettinger SJ, Feldman EC, eds. Textbook of veterinary internal medicine. Philadelphia: WB Saunders, 1995:1720-1733.
DiBartola S. Clinical approach and laboratory evaluation of renal disease. In Textbook of Veterinary Internal Medicine. Ettinger SJ,Feldman EC, editor. Philadelphia, WB Saunders. 1995:1706-1719.
Author David J. Polzin
Consulting Editors Larry Adams and Carl Osborne