Urinalysis, Renal ‘Tubular Function, and Urine Flow Rate
A careful urinalysis should be performed to determine the presence or absence of red blood cell casts. The presence of red blood cell casts indicates inflammation of the glomerulus. The presence of red blood cells but not red blood cell casts is less diagnostic and may indicate disease in the kidney itself or in the collecting system. White blood cell casts reflect inflammation (but not necessarily infection) of the renal parenchyma. Polymorphonuclear leukocytes may derive from the kidney and/or the collecting system. The presence of lymphocytes and/or eosinophils may suggest the diagnosis of acute interstitial nephritis. The urinalysis of a patient with obstruction to flow in the collecting system is variable. An important diagnostic point is that the presence of azotemia in the face of a totally normal appearing urinalysis is highly suggestive of obstruction. The presence of red or white blood cells, however, does not rule out the diagnosis of obstruction. The urine of patients with acute tubular necrosis usually contains protein and, on microscopic examination, granular casts. Glucose may be detected in the urine in the absence of hyperglycemia, a finding that reflects the tubular damage. In acute tubular necrosis, the urinalysis is almost always abnormal but nondiagnostic. It is, however, an important test to rule out other etiologies of acute renal insufficiency.
An important diagnostic issue is the determination of tubular function. The most widely used and convenient tests are measurements of the concentration of electrolytes and osmolality of the urine and the calculation of the fractional excretion of sodium. To be of optimal clinical value, such measurements must be obtained prior to the administration of diuretics and considered in concert with other assessments of the state of hydration of the individual. The utility of these urinary indices is highest in patients with oliguria and azotemia. The urine1 indices are not diagnostic in and of themselves. In general, the acute tubular necrosis is characterized by defects in tubular absorptive function as expressed by the findings of a urine concentration of sodium of greater than 40 mEq/L on a spot sample, a fractional excretion of sodium of greater than 1 per cent, and a urine osmolality that approaches that of the serum.
Prerenal azotemia is characterized by a decrease in the glomerular filtration rate as manifest by a rise in the BUN and creatinine and by normal tubular function as evidenced by a low urine concentration of sodium, a high urine osmolality, and a fractional excretion of sodium of less than 1 per cent. Patients with acute renal insufficiency secondary to acute glomerulonephritis may also have well-preserved renal tubular function early in the course of their disease, as may patients with the acute onset of partial urinary tract obstruction.
The major value of determining the urine concentration of sodium and the fractional excretion of sodium is in formulating a differential diagnosis in a patient with decreased renal function. Interpretations of these tests, however, must be made in conjunction with other assessments of the patient. While patients with renal tubular disease frequently have high urine concentrations and fractional excretions of sodium and patients with prerenal disease manifest sodium avidity, there are clinically important exceptions to these generalizations. Certain types of ATN such as radiographic dye-induced renal injury may present with all the clinical characteristics of ATN, but with fractional excretions of sodium of less than 1 per cent. Conversely, a patient with depletion of the extracellular fluid volume may have a high urine concentration and fractional excretion of sodium if diuretics have been administered, during the generation phase of metabolic alkalosis, and when there was pre-existing renal tubular disease with renal salt wasting. In these latter conditions, the urinary excretion of sodium does not reflect the state of hydration of the patient.
Determination of the urine flow rate is not helpful in formulating a differential diagnosis of the etiology of the acute renal insufficiency but is important in clinical management. Oliguria is considered to be present when the urine volume is less than 500 ml/day. Patients with acute tubular necrosis may be oliguric or polyuria The distinction between these two forms may reflect differences in the etiology and/or the severity of the insult. Acute partial obstruction to urine flow may be associated with a decreased or variable urine output. However, the presence of a normal urine volume does not exclude the diagnosis. Obstruction of modest duration may result in loss of concentrating ability by the kidney and, as a consequence, the excretion of an apparently normal volume of urine.
The presence of total anuria provides an important diagnostic clue in the evaluation of a patient with acute renal insufficiency and somewhat reduces the differential diagnostic list. Acute arterial or venous catastrophes, total urinary tract obstruction, severe cortical necrosis, severe acute glomerulonephritis and, occasionally, severe acute tubular necrosis may present with anuria.
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