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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two brothers, 29 and 33 years of age, had recurrent myoglobinuria, renal failure and azotemia, but were otherwise normal, without apparent muscle weakness or exercise intolerance. Ischemic exercise resulted in normal lactate production. Muscle glycogen content and activities of phosphorylase and phosphofructokinase were normal. Plasma triglycerides were elevated (500 mg per deciliter) on a regular diet and rose during fasting. During a 72-hour fast, serum creatine phosphokinase rose more than 10 times, and myoglobin was detected in urine. Plasma ketone production was minimal during fasting, but prompt ketonemia ( a normal response) occurred after ingestion of medium-chain triglycerides. Carnitine palmityl transferase activity was virtually absent in crude muscle extracts and mitochondrial fractions. Lack of this enzyme impairs long-chain fatty acid utilization, reflected in increased content of plasma free fatty acids and plasma triglycerides. Depletion of ATP because of this metabolic block in muscle may account for the attacks of myoglobinuria.
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PMID:A disorder of muscle lipid metabolism and myoglobinuria. Absence of carnitine palmityl transferase. 12 38

Myoglobin is the oxygen-binding protein characteristic of skeletal and cardiac muscle. With muscle disease or dysfunction, myoglobin may enter the circulation, and after renal clearance, it may also appear in the urine. Therefore, the presence of myoglobinemia and myoglobinuria may serve as indicators of the presence and severity of muscle disease. With newly developed methods of detection, myoglobinemia and myoglobinuria are now recognized as complications of trauma, ischemia, surgery, states of exertion and stress, metabolic abnormalities, inherited enzyme disorders, toxin and drug actions, and inflammatory states. Infarction of the heart muscle also can be detected by myoglobin assay. Persistent myoglobinuric states may be complicated by renal failure and electrolyte imbalance. The diagnosis of myoglobinemia and myoglobinuria can be now confirmed with the use of immunoassay techniques. Although not yet widely available, they offer the possibility of the specificity and sensitivity needed for clinical use.
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PMID:Myoglobin: methods and diagnostic uses. 40 72

The quantitation of myoglobin (Mb) in serum and urine is of clinical importance for the differentiation of myocardial infarction from degenerative cardiac disorders as well as for the detection of traumatic and atraumatic rhabdomyolysis, followed frequently by acute kidney failure. A simple method is described to prepare myoglobin from human muscle extract by negative pressure ultrafiltration and dialysis. By a combination of electrophoretic procedures, this preparation was analysed for purity. Saline myoglobin solutions after deep freezing loose rapidly their immunoreactive Mb content. By addition of pure albumin, not containing heme binding proteins, a stable Mb solution was obtained. This has been used as standard (5--50 microgram/ml) in radial immunodiffusion sensitive for detecting 0.2--1 microgram Mb/ml.
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PMID:Human myoglobin: preparation, quantitation and standardization. 41 87

Two chronic alcoholics developed acute renal failure from alcoholic myopathy (acute alcohol-induced rhabdomyolysis). Severe muscle pain developed and was associated with transitory oligo-anuric renal failure, requiring dialysis in one patient. In addition to the typical history and clinical symptoms, excessive elevation of muscle enzymes, especially creatine-kinase, and the appearance of myoglobin in serum are characteristic. Brown discoloration of the urine and a falsely positive test for "blood" due to the presence of myoglobin in urine in the absence of red blood cells are also typical. Definite changes can be demonstrated histologically and electromyographically during the acute stage. It is likely that this condition is more frequent than the sparsity of published reports indicates.
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PMID:[Acute renal failure in alcoholic myopathy (author's transl)]. 44 85

A case of acute renal failure after mercuric chloride poisoning is reported. Laboratory data revealed markedly elevated serum concentrations of aldolase and creatine phosphokinase, and the presence of pigment granular casts and myoglobin in the urine. The patient went into a diuretic phase after 12 days of oliguria and renal function returned to normal during the next 10 days. Besides direct nephrotoxicity, the contributory role of rhabdomyolysis in the pathogenesis of renal failure after mercuric chloride poisoning, has been stressed.
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PMID:Rhabdomyolysis and renal failure in acute mercuric chloride poisoning. 71 32

A study was carried out to document the occurrence of rhabdomyolysis and renal complications in patients undergoing vascular reconstruction. Indices of muscle damage and renal function were monitored before, during and for up to 10 days after vascular reconstruction for a variety of conditions ranging from intermittent claudication to acute ischaemia. Seven patients with acute limb ischaemia (group 1) and nine with intermittent claudication (group 2) were studied prospectively. In group 1, median creatine kinase (CK) and myoglobin levels were markedly raised 24-48 h after surgery (CK, 29,370 units/l; myoglobin, 8.17 mg/l). Myoglobin reached its peak concentration and declined more quickly than CK, but both indices gave similar information about the extent of muscle damage. In contrast, patients undergoing elective surgery for claudication showed no significant departure from reference values for myoglobin or CK. All patients in group 1 underwent fasciotomy to relieve raised compartmental pressures and five were treated with alkali and mannitol to produce diuresis. Despite these measures, two patients suffered renal failure (peak creatinine levels 611 and 590 mumol/l) after successful revascularization and subsequently required haemodialysis; these patients did not have diuresis. One of these patients died following a stroke 8 days after surgery; the other survived and was discharged with a normal limb and restored renal function. There was no evidence of muscle damage or renal complications in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reperfusion injury in skeletal muscle: a prospective study in patients with acute limb ischaemia and claudicants treated by revascularization. 847 68

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.
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PMID:A prospective study of urine and serum myoglobin levels in patients with acute rhabdomyolysis. 142 5

Heme proteins such as myoglobin or hemoglobin, when released into the extracellular space, can instigate tissue toxicity. Myoglobin is directly implicated in the pathogenesis of renal failure in rhabdomyolysis. In the glycerol model of this syndrome, we demonstrate that the kidney responds to such inordinate amounts of heme proteins by inducing the heme-degradative enzyme, heme oxygenase, as well as increasing the synthesis of ferritin, the major cellular repository for iron. Prior recruitment of this response with a single preinfusion of hemoglobin prevents kidney failure and drastically reduces mortality (from 100% to 14%). Conversely, ablating this response with a competitive inhibitor of heme oxygenase exacerbates kidney dysfunction. We provide the first in vivo evidence that induction of heme oxygenase coupled to ferritin synthesis is a rapid, protective antioxidant response. Our findings suggest a therapeutic strategy for populations at a high risk for rhabdomyolysis.
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PMID:Induction of heme oxygenase is a rapid, protective response in rhabdomyolysis in the rat. 163 13

There have been recent reports of rhabdomyolysis associated with cocaine abuse. The pathologic findings from these cases have not been described. Pathologic abnormalities in two fatalities with cocaine-associated rhabdomyolysis, including one with hyperpyrexia, acute renal failure, and disseminated intravascular coagulation, are discussed in detail. Skeletal muscle in both cases showed necrosis without evidence of vasculitis, polarizable foreign crystals, or other specific lesions. The individual with renal failure showed acute tubular necrosis with granular myoglobin casts in tubules. The mechanism of cocaine-associated rhabdomyolysis is unclear, but potentially includes ischemia due to vasoconstriction, direct toxicity, hyperpyrexia, and increased muscle activity from agitation or seizure. Adulterants may also play a role. In unexplained cases of rhabdomyolysis, toxicologic evidence of cocaine should be sought. In those cases of rhabdomyolysis associated with acute renal failure, the presence of cocaine in blood may be prolonged because of impaired renal clearance.
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PMID:Rhabdomyolysis associated with cocaine abuse. 174 98

Since myoglobin is a low molecular weight proteins and most serum myoglobin is usually excreted into the urine, but serum myoglobin is elevated in patients with renal failure. This elevation hampers diagnosis of muscular damage in patients with renal failure. We studied the influence of renal function on serum myoglobin level and estimated corrected myoglobin levels. We first examined the correlation of serum myoglobin level with levels of serum creatinine and serum beta 2 microglobulin in patients without muscular damage. Creatinine level was more highly correlated with serum myoglobin level than with beta 2 microglobulin level. Measured myoglobin level was corrected using the regression line obtained from the correlation between levels of myoglobin and creatinine, and the corrected myoglobin levels thus obtained were within a reasonable range. The influence of renal failure was compensated for by this correction. We then measured myoglobin level and creatine kinase activity in patients with various heart muscle or skeletal muscle diseases, with or without renal failure, and compared measured myoglobin levels with the corrected ones. In these patients, myoglobin level changed faster than such muscle enzymes as creatine kinase. Thereafter, we found that the stage and degree of muscular damage could be estimated from both corrected myoglobin level and creatine kinase activity, even in patients with renal failure. In conclusion, corrected serum myoglobin level might be a useful diagnostic marker of muscle damage even in patients with renal failure.
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PMID:[Evaluation of serum myoglobin level in patients with muscular disorder and renal failure]. 176 98


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