Urine chemistry

The kidney responds to hypoperfusion by avidly retaining salt and water with production of urine that may reach a specific gravity of 1.030. Measurement of the specific gravity may be included as part of the standard urinalysis. Specific gravity is a convenient and rapidly obtained indicator of urine osmolality. It can be measured accurately with a refractometer or a hygrometer. The normal range is 1.003 to 1.030, but values fall with age as the kidney's ability to concentrate urine decreases. Specific gravity can be used to obtain a crude estimate of how the concentration of other urine constituents may reflect their total excretion because it correlates inversely with 24-h urine volume (M.c.Co.rm..a.c.k.. etai 19.91).

In acute intrinsic renal failure, when the kidney is unable to concentrate or dilute the urine, specific gravity is 1.010 (like that of serum). A prerenal cause of failure will give rise to high specific gravity values. There are a few other tests that help to distinguish prerenal from renal conditions ( Table... ..1). Urine osmolality is a reliable index of concentrating ability; values greater than 500 mosmol/l suggest prerenal causes, while values less than 350 mosmol/l point to a parenchymal origin of renal failure. Urinary sodium concentrations below 10 mmol/l are typical of prerenal azotemia. In order to enhance the sensitivity of diagnostic tests, urine-to-plasma ratios have been developed. For example, the urine-to-plasma ratio for creatinine concentrations is a useful diagnostic index. In practice, however, some patients may have intermediate values and the diagnosis cannot be made on the basis of this index alone.

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Table 1 Urine indices used in the differential diagnosis of prerenal and intrinsic renal azotemia

The fractional excretion of sodium (FENa) is the most sensitive index for distinguishing between prerenal and parenchymal causes of renal failure ( Es£inelJ976). This index relates sodium clearance to creatinine clearance:

Sodium is reabsorbed avidly from glomerular filtrate in patients with prerenal azotemia as a consequence of suppression of atrial natriuretic peptide secretion, activation of renal nerves and the renin-angiotensin-aldosterone axis, and local changes in peritubular hemodynamics. In contrast, sodium reabsorption is inhibited in acute tubular necrosis as a result of tubule cell injury. Creatinine is reabsorbed to a much smaller extent than sodium in both conditions. Consequently, FE Na is typically less than 1 per cent in patients with prerenal azotemia, whereas it is usually greater than 1 per cent in those with ischemic or nephrotoxic acute renal failure.

However, this diagnostic index is also of limited discriminatory value. It is frequently greater than 1 per cent in patients with prerenal azotemia who are receiving diuretics or have bicarbonaturia or adrenal insufficiency. In contrast, FE Na below 1 per cent is found in 15 per cent of patients with non-oliguric ischemic or nephrotoxic acute renal failure. This has been described in patients with renal failure of a variety of causes, including ischemia, aminoglycosides, radiocontrast agents, rhabdomyolysis, hemolysis, burns, sepsis, and hepotorenal syndrome.

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