Oliguria and Anuria
Marcia W. Funderburk
Oliguria and anuria are important clinical signs that should be recognized quickly so that the cause can be identified and treatment initiated promptly to preserve renal function and prevent life-threatening complications.
Approach
The amount of urine output must first be established (most reliably measured using an indwelling catheter). Oliguria is defined as urine volume less than 500 ml/24 h or less than 20 ml/h (in small children, less than 0.8 ml/kg/h). Anuria is strictly defined as the total absence of urine; in the clinical setting, however, a urine output of less than 50 to 100 ml/24 h is often considered anuria (1).
A. Oliguria. It is helpful to think of oliguria as being either (a) prerenal, (b) renal, or (c) postrenal.
1. Prerenal disorders are characterized by decreased renal perfusion, leading to decreased glomerular filtration rate such that the daily endogenous load of nitrogenous wastes cannot be excreted, thus the term prerenal azotemia.
2. Renal disorders are characterized by pathology within the kidney parenchyma itself, which can be the end result of prolonged decreased renal perfusion.
3. Postrenal disorders causing oliguria are characterized by partial obstruction of the urinary tract at an anatomic position distal to the kidney. This can be confusing because these disorders can also cause polyuria.
B. Anuria results from total obstruction of the urinary tract or as an end result of the prerenal and renal causes of oliguria. A sudden cause of anuria, especially in the elderly, is bilateral renal artery occlusion (or unilateral occlusion in a single kidney) typically caused by embolism. Early recognition of this entity is imperative to restore blood flow to the ischemic kidney(s).
History
A. Pertinent present history. A patient may complain of decreased urine output in some clinical situations. More often, however, the clinical situation and pertinent history should lead to an evaluation of the presence of oliguria or anuria.
1. Are there symptoms of illness or trauma leading to hypotension?
a. Hypovolemia (e.g., hemorrhage, diuretic overuse, gastrointestinal fluid loss, skin fluid loss owing to burns or heat exposure, third spacing, secondary to burns, peritonitis, pancreatitis, or trauma)?
b. Decreased cardiac output (e.g., congestive heart failure, myocardial infarction, pericardial tamponade, or acute pulmonary embolus)?
c. Peripheral vasodilatation (e.g., septic shock, anaphylactic shock)?
2. Are there symptoms of vascular disease? Consider bilateral renal vascular obstruction due to severe renal artery stenosis, thrombosis, or embolism.
3. Is there any history consistent with renal parenchymal injury [e.g., recent radiocontrast agent, nephrotoxin exposure such as ethylene glycol, nonsteroidal antiinflammatory drug overdose, acute nephritis, acute vasculitis, pyelonephritis (in the elderly), papillary necrosis (in diabetic patients), or prolonged hypotension with hypoperfusion of the kidney]?
4. Is there any history consistent with urinary tract obstruction?
a. Bladder neck obstruction (e.g., benign prostatic hypertrophy, prostate cancer, bladder cancer, or functional obstruction due to drug side effects)?
b. Obstruction of the urethra or bilateral ureters—internally (2° blood clots, stones, sulfonamide or uric acid crystals, pyogenic debris, necrotizing papillitis or edema), or externally (2° tumor, periureteral fibrosis, accidental ureteral ligation during pelvic surgery, ascites, pregnancy, pelvic abscess, or hematoma).
5. Medication use must be considered—diuretics, antihypertensives, anticholinergics, aminogycosides, amphotericin B, or chemotherapeutic drugs.
B. Other pertinent past history. Is there a history of cancer, recent surgery, kidney stones, neurologic disorder, vascular disease, chronic liver disease (hepatorenal syndrome), or kidney transplant?
Physical examination
A. Focused physical examination (PE). This should include vital signs (notably blood pressure, pulse, and temperature). Orthostatic blood pressure and pulse may be necessary. Signs of hypovolemia, hypotension, and dehydration should be noted—skin turgor and color, mucous membranes, capillary refill, warmth of extremities.
B. Additional PE. Depending on the history (e.g., skin rash, cardiac examination, bruits over kidneys) palpate for a distended bladder; if a cancer or outlet obstruction is suspected, perform a rectal or pelvic examination.
Testing
A. An indwelling urinary catheter serves as a diagnostic tool (if obstruction has occurred at the bladder neck or urethra) and for accurate urine volume measurement. Urine output and blood pressure monitoring can often lead to expedient correction of prerenal causes, thus avoiding further complications.
B. Urinalysis is often normal in prerenal causes of oliguria or anuria, except being highly concentrated with possible qualitative proteinuria because of the high concentration. Microscopic analysis is usually unremarkable (or reveals few hyaline or granular casts) in prerenal causes; whereas proteinuria, casts, and hematuria can point to renal causes.
C. Urine osmolality is typically high in prerenal causes (>500 mOsm/kg H2O) versus impaired in renal causes (<350 mOsm/kg H2Ο) (2).
D. Urine sodium is typically less than 20 mEq/L in prerenal causes (unless diuretics have been used) versus more than 40 mEq/L in renal causes (2).
E. Blood urea nitrogen and creatinine levels are elevated. The ratio must be interpreted considering the entire clinical situation. Urine:plasma creatinine ratio (U:P Cr) is calculated to help differentiate between prerenal (U:P Cr >40) and renal (U:P Cr <20) causes (2).
F. Diagnostic imaging, which may be necessary in some cases, is guided by the history and PE findings [e.g., ultrasound (US), computed tomography (CT), retrograde pyelogram, renal biopsy].
Diagnostic assessment
The key to a diagnosis of oliguria or anuria is to actively anticipate when it is likely to manifest and accurately measure using an indwelling catheter. Once recognized and a cause is suggested, (a) prerenal causes can be assessed further by measuring hemodynamic status and administering fluids; (b) renal causes can be assessed further with urinalysis (qualitative and quantitative), renal US, or renal biopsy; and (c) postrenal causes can be assessed further using US, CT, or retrograde pyelography.
References
1. Eliahou HE. Oliguria and anuria. In: Massry SG, Glassock RJ, eds. Massry and Glassock’s textbook of nephrology, 3rd ed. Baltimore: Williams & Wilkins, 1995:543–546.
2. Lake EW, Humes HD. Acute renal failure including cortical necrosis. In: Massry SG, Glassock RJ, eds. Massry and Glassock’s textbook of nephrology, 3rd ed. Baltimore: Williams & Wilkins, 1995:984–987.>>
Book Source Details
- Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
- Author(s): Robert B. Taylor (editor)
- Year of Publication: 2000
- Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.
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Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2008 Williams & Wilkins.
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