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Acute Oliguria CURRENT CONCEPTS Current Concepts ops in the hospital usually have had multiple renal injuries. The renal insufficiency is frequently severe, and the prognosis is not as good as it is with acute oliguria that develops outside the hospital.6 In the intensive care setting, acute oliguria occurs late in ACUTE OLIGURIA the clinical course of severe illness with failure of multiple organs.7, 8 SAULO KLAHR, M.D., AND STEVEN B. MILLER, M.D. CAUSES OF ACUTE OLIGURIA The causes of acute oliguria can be grouped into three categories: prerenal, renal or intrinsic, and CUTE oliguria (excretion of less than 400 postrenal (obstructive uropathy) (Table 1). Prompt ml of urine per day) is often the earliest sign identification and treatment of prerenal causes or of impaired renal function and poses a diag- A obstructive uropathy may prevent the development nostic and management challenge to the clinician. of protracted acute renal failure, which is associated Early identification of potentially reversible causes of with high morbidity and mortality rates.9 Assess- acute oliguria and institution of appropriate therapy ment of volume status, hemodynamics, and drug use are crucial, since the therapeutic window is often may uncover potential prerenal causes of oliguria. small.1 Oliguria can have many causes. Some are Invasive monitoring of central venous pressure or overt and apparent, such as septic shock, whereas pulmonary-capillary wedge pressure may be indicat- others are concealed and subtle, such as myoglobu- ed if an accurate assessment of intravascular volume lin release or drug toxicity.2 The main functional de- cannot be obtained by other means — for example, rangement in patients with acute oliguria is a sudden in patients with poor cardiac function. Renal ultra- and severe decrease in the glomerular filtration rate sonography is the study of choice to detect obstruc- (acute renal failure), sufficient to result in increases tive uropathy, which if present is usually manifested in the plasma urea and creatinine concentrations, re- by dilatation of the urinary tract above the obstruc- tention of salt and water, and the development of ac- tion.10 In some instances, despite the presence of ob- idosis and hyperkalemia.3 structive uropathy, dilatation of the urinary tract Patients with acute oliguria that develops outside does not occur for various reasons: malignancy is the the hospital should be expeditiously admitted and cause of the obstruction, the patient is severely de- evaluated for potentially life-threatening complica- hydrated, retroperitoneal fibrosis is present, or there tions such as hyperkalemia, manifested by muscle has been insufficient time for dilatation to occur.10 weakness or paralysis or by electrocardiographic The absence of urinary output suggests that the pa- changes; metabolic acidosis, resulting in Kussmaul’s tient has obstructive uropathy, renal cortical necro- respirations, hypotension, and hyperreflexia; and pul- sis, or necrotizing glomerular disease. Alternating monary edema, ascites, or pleural effusions due to episodes of polyuria and oliguria–anuria strongly salt and water retention. Other complications on ad- suggest the presence of intermittent obstruction of mission to the hospital may include nausea, vomit- the urinary tract.10 ing, drowsiness, pericarditis, confusion, and coma. Once the potentially life-threatening conditions have URINARY SEDIMENT AND INDEXES been ruled out or appropriately treated, a detailed A careful examination of the urinary sediment and history should be obtained, including drugs the pa- the use of urinary indexes can help distinguish pre- tient has taken, occupation, hobbies, recent travel, renal failure from intrinsic acute renal failure. In pre- and previous renal disease. When acute oliguria de- renal failure, hyaline and fine granular casts may be velops outside the hospital, there is usually a single seen; however, coarsely granular and cellular casts are renal cause and a good prognosis.4 Most episodes of unusual. In intrinsic renal failure (acute tubular ne- acute oliguria, however, occur in the hospital and are crosis), brown granular casts and tubular epithelial associated with hypovolemia, decreased cardiac out- cells, singly or in casts, are present in the urine spec- put, the effects of anesthesia or surgery, or the use imens of about 80 percent of patients11 (Fig. 1). of diuretics, nephrotoxic drugs, or radiographic con- Measurements of sodium and creatinine concentra- trast agents.5 Patients with acute oliguria that devel- tions in both plasma and urine may help assess renal tubular function.11,12 In prerenal failure due to a re- duction in the glomerular filtration rate coupled with an increased stimulus for salt and water reabsorption, From the Renal Division, Department of Medicine, Washington Univer- the ratio of urinary to plasma creatinine is usually sity School of Medicine, St. Louis. Address reprint requests to Dr. Klahr at higher and the urinary sodium concentration is lower the Department of Medicine, Barnes–Jewish Hospital, North Campus, 216 S. Kingshighway, St. Louis, MO 63110. than in cases of intrinsic acute renal failure (Table 2). ©1998, Massachusetts Medical Society. The use of urinary indexes is based on the as- Volume 338 Number 10 ؒ 671 The New England Journal of Medicine TABLE 1. PRINCIPAL CAUSES OF ACUTE OLIGURIA. Prerenal events Absolute decrease in effective blood volume due to hemor- rhage, gastrointestinal fluid loss (from diarrhea, vomiting, or nasogastric suction) or pooling of fluid (from pancre- atitis or bowel disease), renal losses (from diuretics or gly- cosuria), trauma, surgery, or burns Relative decrease in effective blood volume due to sepsis, he- patic failure, anaphylaxis, vasodilatory drugs, the nephrotic syndrome, or anesthetic agents Myocardial failure due to myocardial infarction, pulmonary embolism, congestive heart failure, cardiac tamponade, or mechanical ventilation Disruption of renal autoregulation due to the administration of angiotensin-converting–enzyme inhibitors Renal-artery or renal-vein occlusion due to thrombosis, thromboembolism, severe stenosis caused by atherosclero- sis, or dissecting aneurysm Figure 1. Photomicrograph of Urinary Sediment Obtained from Renal or intrinsic events a Patient with Acute Tubular Necrosis (ϫ200). Small-vessel vasculitis or acute glomerulonephritis due to Multiple broad, brown, granular casts are composed of Tamm– connective-tissue disorders (systemic lupus erythematosus Horsfall glycoprotein, cells, remnants of shed brush border, or drug-related disorders), scleroderma, malignant hyper- and other cellular debris. tension, toxemia of pregnancy, microscopic polyarteritis, poststreptococcal glomerulonephritis, rapidly progressive glomerulonephritis, or other disorders Interstitial nephritis related to drugs (e.g., methicillin), infec- tion, or cancer (lymphoma, leukemia, or sarcoidosis) Acute tubular necrosis due to ischemia (mainly as a conse- quence of prerenal events), nephrotoxic antibiotics (e.g., TABLE 2. CHARACTERISTIC URINARY INDEXES IN gentamicin or kanamycin), heavy metals (mercury or cis- PATIENTS WITH ACUTE OLIGURIA DUE TO PRERENAL platin), solvents (carbon tetrachloride or ethylene glycol), OR RENAL (INTRINSIC) CAUSES. radiographic contrast agents, endogenous events, intratu- bular crystals (uric acid or oxalate), or intratubular pig- ments (myoglobinuria) PRERENAL RENAL Postrenal events (obstructive uropathy) INDEX CAUSES CAUSES Upper urinary tract obstruction: ureteral obstruction of one Urinary sodium concentration Ͻ20 Ͼ40 or both kidneys (mmol/liter) Lower urinary tract obstruction: bladder-outlet obstruction Fractional excretion of sodium (%) Ͻ1 Ͼ1 (more common) Ratio of urinary to plasma creatinine Ͼ40 Ͻ20 Ratio of urinary to plasma osmolarity Ͼ1.5 Ͻ1.1 sumption that the ability of the renal tubule to re- present with heme-positive urine, an elevated plasma absorb sodium and water remains intact in prerenal concentration of creatine kinase, and dark urine con- failure, in vascular disease of preglomerular origin, taining dark-brown granular casts. Persistently ab- and in the early stages of glomerulonephritis, where- normal nephrographic findings one or two days after as these functions are impaired in tubulointerstitial a study with radiographic contrast agents suggest disease, later in the course of glomerulonephritis, the possibility of acute renal failure induced by the and in acute tubular necrosis. Interpretation of uri- agents. nary indexes requires caution. Blood and urine spec- imens for these determinations should be collected PREVENTION OF INTRINSIC ACUTE before the use of fluid replacement or the adminis- RENAL FAILURE tration of dopamine, mannitol, or other diuretic Risk factors for intrinsic renal failure include pre- agents. The urine must not contain glucose or radi- existing renal disease and disorders that cause prere- ographic contrast material. Acute renal failure is usu- nal oliguria (Table 1). Prophylaxis should be consid- ally considered to be due to acute tubular necrosis, ered for patients with such risk factors. Appropriate but occasionally, patients have a fractional excretion hydration and optimal preservation of intravascular of sodium of less than 1 percent. This is more com- volume are essential to maintain adequate renal per- mon in patients with pigment nephropathy (myo- fusion. It is also important to maintain adequate car- globinuria) or injury from radiographic contrast diac output and prevent peripheral vasoconstriction.
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