A prospective study of urine and serum myoglobin levels in patients with acute rhabdomyolysis.

Serum and urine myoglobin levels, measured by radioimmunoassay, were determined prospectively in eight patients with acute rhabdomyolysis, within 24 hours of admission. Five patients had urine myoglobin concentrations greater than 1,000 ng/ml (normal < 5 ng/ml); four of these patients subsequently developed acute renal failure. In three patients whose urinary myoglobin levels ranged from 19 to 275 ng/ml, acute renal failure did not occur. This difference in the occurrence of acute renal failure between the two patient groups was statistically significant (p < 0.05). Mean peak serum creatinine was significantly higher in the patients with high urine myoglobin (6.4 +/- 1.3 mg/dl) compared to those with low urine myoglobin (2.2 +/- 0.3 mg/dl), p < 0.02. There was no statistical correlation between level of serum creatine phosphokinase and serum or urine myoglobin, although the serum and urine myoglobin levels correlated well with each other. These findings suggests that among other factors, urine myoglobin may need to reach a critical level in order for myoglobinuric renal failure to ensue.

Serum myoglobin in patients on intermittent and continuous ambulatory peritoneal dialysis.

Serum myoglobin levels were determined in patients maintained on chronic peritoneal dialysis. Eleven intermittent peritoneal dialysis patients had a mean serum myoglobin of 174 +/- 29 ng/ml. In 7 patients tested serially, there was no consistent change in serum myoglobin: the mean level was 154 +/- 36 ng/ml pre-dialysis and 170 +/- 20 ng/ml post-dialysis. Seventeen patients on continuous ambulatory peritoneal dialysis had a mean serum myoglobin of 215 +/- 18 ng/ml. Two patients given oral carnitine supplements had a substantial decrease in their serum myoglobin levels. Patients on peritoneal dialysis, like those on hemodialysis, tend to have elevated serum myoglobin levels, and neither form of dialysis affects serum myoglobin concentration. This hypermyoglobinemia may be due to metabolic changes in muscle.

Erythrocyte sodium and potassium in patients on peritoneal dialysis.

Intracellular sodium and potassium concentrations were determined on erythrocytes obtained, before and after treatment, from patients with end-stage renal disease undergoing 48-hour intermittent peritoneal dialysis. Erythrocyte sodium increased from 7.5 +/- 0.3 to 8.6 +/- 0.4 mmol/L cells with a mean of 1.1 +/- 0.1 mmol/L cells (P less than .001), but erythrocyte potassium and cellular water content were virtually unchanged. Plasma potassium decreased during dialysis from 4.2 +/- 0.2 to 3.3 +/- 0.1 mEq/L (P less than .001). The increase in red-cell sodium correlated with this decrease in plasma potassium (r = .51, P less than .01). In contrast, erythrocyte sodium and potassium in undialyzed control patients with chronic renal failure did not change over a similar period, and plasma potassium was unchanged (4.3 +/- 0.1 mEq/L before and 4.3 +/- 0.2 mEq/L after 48 hours). Incubation of postdialysis erythrocytes from the dialysis patients in their own plasma at varying potassium concentrations showed that the rise in cell sodium was blunted as the plasma potassium was increased from 3.2 +/- 0.1 to 4.5 +/- 0.2 mEq/L. These results suggest that unlike hemodialysis, which is not associated with short-term changes in red-cell electrolytes, intermittent peritoneal dialysis results in a reversible increase in erythrocyte sodium. This change appears to be causally related to the decrease in extracellular potassium concentration.

Myoglobinuria in chronic renal failure.

Serum and urine myoglobin levels were determined on 14 patients with stable chronic renal failure. Serum myoglobin ranged from 38 to 350 ng/mL. Eleven patients had myoglobinuria between 15 and 250 ng/mL; none developed myoglobinuric renal failure. Fractional excretion of myoglobin in the myoglobinuric patients increased as creatinine clearance decreased, although there was no correlation between filtered load and excretion rate of myoglobin. This confirms that renal failure leads to hypermyoglobinemia and usually to myoglobinuria. Surviving nephrons tend to reabsorb less of the filtered load of myoglobin as renal function diminishes.

The effect of renal failure and hemodialysis on serum and urine myoglobin.

In 33 patients with chronic renal disease, the concentration of myoglobin in serum and urine was found to be significantly elevated over that of normal controls. Hemodialysis had no statistically significant effect in lowering the serum myoglobin of patients with end stage renal disease. Similarly, no difference was found in serum myoglobin in blood entering and leaving the dialysis coil. Since myoglobin was not detectable in the dialyzate, these data illustrate that myoglobin is not appreciably dialyzable. The association between chronic renal failure and high concentration of serum and urine myoglobin was confirmed. These abnormally high levels of myoglobin in serum and urine do not necessarily lead to myoglobinuric renal failure.