Diminished output of urine (oliguria with less than 500 mL of output in 24 hours) and no output of urine (anuria) are best understood using pathophysiology.The causes may be divided into prerenal (where less fluid is delivered to the kidney for filtration), renal (where the kidney is unable to produce urine because of intrinsic disease), and postrenal (where the kidney is obstructed and the urine cannot be excreted).
Anuria and oliguria
Anuria and oliguria
1. Prerenal causes. Anything that reduces the blood flow to the kidney may cause anuria. Thus, shock from hemorrhage, myocardial infarction, dehydration, drugs, or septicemia may be the cause. CHF in which the effective renal plasma flow is reduced is also a possibility. Intestinal obstruction or intense diarrhea may cause the loss of enormous amounts of fluid through vomiting or diarrhea, and the accompanying shock results in anuria. Embolic glomerulonephritis, bilateral renal artery thrombosis, and dissecting aneurysms may cause renal shutdown.
2. Renal causes. These may be analyzed with the mnemonic VINDICATE so that none are missed.
o V—Vascular lesions include embolic glomerulonephritis and dissecting aneurysm; transfusion reactions are considered as well as intravascular hemolysis of any cause.
o I—Inflammatory lesions include pyelonephritis, necrotizing papillitis, and renal tuberculosis.
o N—Neoplasms of the kidney rarely cause anuria because only one kidney is affected at a time.
o D—Degenerative conditions are unlikely to cause anuria.
o I—Intoxication from numerous antibiotics (e.g., gentamicin, sulfa, streptomycin) and from gold, arsenic, chloroform, carbon tetrachloride, or phenol, for example, is a common cause of anuria. Renal calculi and nephrocalcinosis should be considered here.
o C—Congenital disorders include polycystic kidneys and medullary sponge kidneys.
o A—Autoimmune disorders form the largest group of renal causes of anuria. Lupus erythematosus, polyarteritis nodosa, acute glomerulonephritis, amyloidosis, Wegener granulomatosis, and scleroderma are included here.
o T—Trauma includes contusions and lacerations of the kidney for completeness; however, lower nephron nephrosis from crush injury or burns is not unusual.
o E—Endocrine disorders include diabetic glomerulosclerosis, necrotizing papillitis from diabetes, and nephrocalcinosis from hyperparathyroidism and related disorders.
3. Postrenal causes. The mnemonic MINT will help recall this group of disorders that obstruct the kidneys and bladder.
o M—Malformations may cause anuria; they include congenital bands, aberrant vessels over the ureters, horseshoe kidney, and ureteroceles.
o I—Inflammation includes cystitis, urethritis, and prostatitis.
o N—Neoplasms include carcinomas of the bladder obstructing both ureters, prostatic hypertrophy, and carcinomas of the uterus or cervix involving both ureters. N also signifies neurologic disorders such as polio, multiple sclerosis, and acute trauma to the spinal cord that may cause anuria.
o T—Trauma signifies surgical ligation of the ureters, ruptured bladder, and instrumentation of the urinary tract.
Approach to the Diagnosis
The clinical picture will be helpful in determining the cause of anuria. In cases of prerenal azotemia, there will be decreased skin turgor and orthostatic hypotension if the cause is volume depletion. If the cause is CHF, there will be jugular vein distention, hepatomegaly, and pedal edema. Patients with postrenal azotemia may have an enlarged prostate, a distended bladder, and other signs of obstructive uropathy. Patients with renal azotemia may have bilateral flank masses (polycystic kidney), hypertension, peripheral emboli (embolic glomerulonephritis), or a rash (collagen disease, interstitial nephritis).
The initial workup includes a CBC; urinalysis; urine culture and sensitivity; personal examination of the urine for casts, and so forth; chemistry panel; spot urine sodium; serum and urine osmolality; flat plate of the abdomen for kidney size; chest x-ray; and ECG. The bladder is catheterized for residual urine; if this is significant, postrenal azotemia is likely and a urologist is consulted. He will most likely do a cystoscopy and retrograde pyelography after the patient's condition is stabilized. Ultrasonography can be used to determine if there is significant residual urine also.
The laboratory studies will determine whether there is prerenal or renal azotemia. If the sodium concentration in the spot urine is less than 10 meq/L, prerenal azotemia is likely. Also, in prerenal azotemia, the BUN/creatinine ratio is 20:1 or greater and the urine osmolality is 450 mOsm per kilogram of water or greater. The urine sediment will show granular and red cell casts in most cases of renal azotemia, and the BUN/creatinine ratio will be 10:1 or less.
Further workup will depend on what the presumptive diagnosis is. If volume depletion is the cause, intravenous saline and plasma volume expanders are given while carefully monitoring the urine output. If this is ineffective, furosemide and a mannitol drip can be utilized to reestablish urine output. If these measures are ineffective, the patient obviously has a renal cause for his or her anuria, and a urologist should be consulted.
Renal causes can be differentiated by further workup. If intravascular hemolysis is suspected, a serum haptoglobin test should be ordered. If dissecting aneurysm or bilateral renal artery stenosis is suspected, aortography and angiography would be done. If polycystic kidney disease is suspected, ultrasonography or CT scan of the abdomen may be done. Eosinophilia of the blood or urine will be found in drug-induced nephritis. If a collagen disease is suspected, one should order an ANA, double-stranded DNA (dsDNA) antibody titer, or lupus erythematosus cell prep. A renal biopsy may also be necessary in these and many other disorders.
Other Useful Tests
1. Serum protein electrophoresis (multiple myeloma)
2. Anti-streptolysin O (ASO) titer (acute glomerulonephritis)
3. Blood cultures (bacterial endocarditis)
4. Serum complement (acute glomerulonephritis, collagen disease)