Definition

• Oliguria-production of an abnormally small amount of urine (variably described as urine production rate <0.27, <0.5, or <1.0–2.0 mL/kg/h). In euvolemic or hypervolemic patients with good perfusion, urine production <1.0 mL/kg/h = absolute oliguria. Hydrated dogs and cats receiving fluids should produce at least 1.0 mL/kg/h.
• Anuria-limited/no urine formation (urine production rate <0.08 mL/kg/h).

Pathophysiology

• Physiologic (prerenal) oliguria: kidneys limit water loss during episodes of reduced renal perfusion to preserve fluid and electrolyte balance. High plasma osmolality or low circulating fluid volume stimulate ADH synthesis and release. ADH acts on the kidneys to induce formation of small quantities of concentrated urine.
• Pathologic (renal) oliguria: severe renal parenchymal impairment. Factors include: high resistance in afferent glomerular vessels, low glomerular permeability, back leak of filtrate from damaged renal tubules, renal intratubular obstruction, extensive loss of nephrons resulting in marked reduction of glomerular filtrate produced.
• Anuria: may be renal or post-renal origin. Severe renal disease occasionally causes anuria. True anuria is more indicative of urinary obstruction. Mechanisms are the same as for pathologic oliguria (e.g., UTO or excretory pathway rupture).

Systems Affected

• Renal-inability to adequately eliminate wastes and water; hyperkalemia.
• Urologic-obstruction-induced distension of the collecting system.Increased risk of urinary tract infection due to failure to empty the bladder.

Signalment

• Dog and cat.
• Young adult cats: higher incidence of anuria associated with UTO.
• Risk of acute kidney injury increases with age.

Signs

• Reduction in quantity of urine voided.
• Enlarged urinary bladder, straining to void, increased frequency of attempted voiding with urethral obstruction.
• Systemic signs of uremia if oliguria/anuria persists.

Causes

• Physiologic oliguria-renal hypoperfusion (caused by low blood volume or hypotension) or hypertonicity (usually caused by hypernatremia).
• Pathologic oliguria-acute oliguric kidney injury (renal failure), advanced CKD.
• Anuria-complete UTO, urinary excretory pathway rupture, or severe primary kidney disease.

Risk Factors

• Physiologic oliguria-causes include: dehydration, decreased cardiac output, hypotension, ECF volume contraction.
• Pathologic oliguria and anuria: caused by primary kidney disease, preexisting kidney disease, nephrotoxin exposure, dehydration, low cardiac output, hypotension, ECF volume contraction, electrolyte imbalance, acidosis, advanced age, fever, sepsis, liver disease, multiple organ failure, trauma, diabetes mellitus, hypoalbuminemia, hyperviscosity syndrome.
• Anuria-caused by urolithiasis, urinary tract neoplasia, idiopathic feline lower urinary tract disease, functional micturition disorder, trauma, gross hematuria.

Differential Diagnosis

• Physiologic oliguria: poor tissue perfusion (e.g., dehydration; prolonged capillary refill time; pale mucous membranes; weak, rapid, irregular pulse; cool extremities); history of recent fluid loss (vomiting, diarrhea, polyuria, hemorrhage); signs of uremia are typically absent. Oliguria resolves rapidly when renal hypoperfusion is corrected.
• Suspect pathologic oliguria and renal anuria with detection of any of the risk factors; (risk factors are additive). Patients with pathologic oliguria caused by CKD have a history of progressive kidney disease (including long-standing polyuria, polydipsia, poor appetite, weight loss). Patients with CKD are at risk of developing acute kidney injury. Signs of uremia are commonly observed; fluid therapy and other measures to restore adequate renal perfusion often fail to increase urine flow.
• Suspect anuria due to UTO or rupture of the excretory pathway with repeated straining to void but inability to produce urine. Patients may have a history of pollakiuria, dysuria, stranguria, hematuria, urolithiasis, trauma, instrumentation of the urinary tract. Physical exam UTO patient may reveal: enlarged urinary bladder, painful posterior abdomen, masses or uroliths in the urethra or bladder. Physical exam of patients with rupture of the urinary tract may reveal ascites, fluid infiltration in tissues, painful caudal abdomen, masses or uroliths in the bladder or urethra, or evidence of trauma (e.g., pelvic fracture). UTO caused by functional urinary obstruction: suspect in patients with urinary bladder enlargement, increased resistance to manual bladder expression, and neurologic signs affecting the hind limbs and/or tail. Signs of uremia may develop. Restoring urinary flow/correcting rents in the excretory pathway rapidly restores adequate urine flow.

CBC/Biochemistry/Urinalysis

• Serum urea nitrogen/creatinine concentrations: elevated unless onset of oliguria or anuria is very recent.
• Hyperkalemia: common with pathologic oliguria and anuria, less common/less severe in animals with physiologic oliguria (except with hypoadrenocorticism).
• Physiologic oliguria: characterized by high USG (dogs >1.030, cats >1.035). Oliguria associated with lower USG suggests renal parenchymal disease or UTO. Patients with urine-concentrating defects due to other diseases or drugs are the exception to this rule.
• Renal parenchymal anuria is typically characterized by USG <1.030 (dogs) or <1.035 (cats). USG varies in patients with post-renal anuria. Adequate urine-concentrating ability often lost after UTO.

Imaging

• Abdominal radiographs and ultrasound are useful to rule out UTO/excretory pathway rupture.
• Excretory urography, retrograde urethrocystography, pyelography, or vaginourethrocystography may provide definitive proof of UTO/excretory pathway rupture.
• Distension of the excretory pathway or detection of uroliths in the ureters, bladder neck, urethra suggest UTO.
• Detection of fluid within the peritoneum supports a diagnosis of excretory pathway rupture. Contrast media leakage confirms a rupture.

Diagnostic Procedures

• Electrocardiography: to identify significant hyperkalemia (see Hyperkalemia).
• Urethrocystoscopy: may provide evidence for UTO/urinary tract rupture.
• Urinary catheterization: may provide information about the integrity of the lower urinary tract. Not recommended as a diagnostic procedure because it may be misleading and may cause additional trauma, iatrogenic UTI.

Drug(s)

• Diuretics: indicated after establishing euvolemia in patients with renal oliguria. Diuretic-induced increased urine production facilitates fluid and electrolyte therapy and implies less severe kidney injury.
• Administration of diuretics before restoring adequate renal perfusion is counterproductive and may promote renal injury.
• Avoid diuretic-induced dehydration.
• Furosemide (2–4 mg/kg IV): often used first in patients with renal oliguria. Urinary flow should increase within 1 hour if not, repeat at the same or double dosage. If diuresis ensues, administer CRI of furosemide to sustain diuresis (0.25–1 mg/kg/h or 2–4 mg/kg IV q8h). Bolus injection followed by CRI may be most effective.
• Mannitol (0.25–1 g/kg IV) can be given as a 10% or 20% solution over 15–20 minutes. Urinary flow should increase within 1 hour. Do not repeat if diuresis does not ensue; may cause excessive volume expansion. If diuresis ensues, mannitol may be continued as CRI (1–2 mg/kg/h) or intermittent IV doses (0.25–0.5 g/kg every 4–6 hours) to sustain diuresis. Avoid mannitol when overhydration, pulmonary edema, congestive heart failure present.
• Dogs, dopamine (0.5–3 µg/kg/min) may increase urine flow by increasing renal blood flow, glomerular filtration, renal sodium excretion. Higher doses may cause renal vasoconstriction, tachycardia, and cardiac arrhythmias and are contraindicated in AKI. Dopamine is generally administered concurrent with furosemide. Diuresis should ensue within 1–2 hours. If diuresis ensues, dopamine should be continued until fluid and electrolyte balance can be maintained without further drug therapy. If urine flow does not increase within 2 hours, discontinue dopamine. Dopamine has not been established to be an effective treatment for oliguria in dogs. Dopamine is not appropriate for oliguric cats.
• Fenoldopam (0.1–0.6 µg/kg/min), a selective dopamine A1 receptor antagonist, promotes a delayed (4- to 6-hour) diuresis in normal cats; however, its effectiveness in oliguric cats has not been established.

Contraindications

Nephrotoxic drugs

Precautions

• Administer fluids carefully to patients that are persistently oliguric or anuric to avoid overhydration. Do not continue to administer fluids to oliguric/anuric patients after their fluid volume deficit has been restored absent a plan to prevent development of overhydration. In patients with unresponsive renal oliguria; peritoneal dialysis/hemodialysis may be required to correct iatrogenic fluid-induced volume overexpansion.
• Failure to correct fluid deficits before initiating diuretic administration may cause further renal hypoperfusion and ischemic renal injury.
• Use drugs requiring renal excretion with caution.
• Avoid electrolyte solutions containing more than 4 mEq of potassium per liter in most animals. However, some hypokalemic patients may require cautious administration of higher doses of potassium.
• Dopamine can cause cardiac arrhythmias, particularly in animals with hyperkalemia. ECG monitoring is recommended when high dosages are used and in animals with hyperkalemia.

Possible Interactions

Furosemide may promote the nephrotoxicity associated with aminoglycoside antibiotics.

Patient Monitoring

• Urinary flow rate-determine early during the course of case management. When unclear, consider transurethral catheterization to accurately determine urine production. Place catheters using aseptic technique. Intermittent catheterization is less likely to cause UTI than indwelling catheter. Short catheter indwelling time lowers the risk of UTI. Properly placed/managed indwelling catheters are usually safe for at least 48 hours. Use a closed, sterile drainage system.
• Creatinine, serum urea nitrogen, and potassium concentrations should be reevaluated after 12–24 hours; patients with severe hyperkalemia may need more frequent monitoring.
• ECG should be performed at appropriate intervals to assess cardiac effects of drugs and hyperkalemia and to monitor response to therapy.

Prevention/Avoidance

• Avoid nephrotoxic drugs and substances.
• Avoid dehydration and volume contraction.

Possible Complications

• Hyperkalemia and associated cardiotoxicity
• Uremia leading to death
• Dehydration
• Overhydration
• Bacterial UTI and sepsis

Expected Course and Prognosis

• Oliguria and anuria are poor prognostic signs in acute or CKD; unless urine outflow can be corrected, survival is not expected.
• Anuria associated with UTO is often reversible if urethral patency is restored.

See Also

• Azotemia and Uremia
• Hyperkalemia
• Nephrotoxicity, Drug-Induced
• Renal Failure, Acute
• Renal Failure, Chronic
• Urinary Tract Obstruction

Abbreviations

• ADH = antidiuretic hormone
• AKI = acute kidney injury
• CKD = chronic kidney disease
• CRI = constant rate infusion
• ECG = electrocardiogram
• USG = urine specific gravity
• UTI = urinary tract infection
• UTO = urinary tract obstruction

Author David J. Polzin

Consulting Editor Carl A. Osborne