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PubMed1982

Myoglobinuria in carnitine palmityltransferase deficiency.

An 18-year-old male developed recurrent myoglobinuria after prolonged physical exertion. Histochemical analysis of biopsied muscle revealed complete absence of carnitine palmityltransferase. Significant ultrastructural abnormalities of muscle were present, but these could be the result of the recent episode of rhabdomyolysis. Recurrent myoglobinuria can occur in several disorders of glycogen and lipid metabolism in muscle, and such disorders should be suspected in cases of unexplained recurrent myoglobinuria.

Acyltransferases↗
PubMed1991

Rhabdomyolysis and myoglobinuria associated with violent exercise and alcohol abuse: report of two cases.

Two cases of acute rhabdomyolysis with myoglobinuria and high levels of serum enzyme are presented. The first patient developed acute renal insufficiency in the context of a binge and heavy alcohol drinking lasting several days. He was treated with haemodialysis for three weeks, and survived. The second patient developed rhabdomyolysis and heavy myoglobinuria after playing squash vigorously. Forced mannitol-alkaline diuresis therapy for prophylaxis against hyperkalaemia and metabolic acidosis was performed. He did not develop renal failure. The clinical features, pathology and treatment of rhabdomyolysis and myoglobinuria are summarized.

Acute Kidney Injury↗
PubMed1977

Recurrent myoglobinuria and muscle carnitine palmityltransferase deficiency.

A 16-year-old boy with a two-year history of recurrent attacks of myalgia, muscle cramps without weakness, and myoglobinuria was shown to have a deficiency in muscle carnitine palmityltransferase. Serum concentrations of creatinine phosphokinase, serum glutamic oxalacetic transaminase, and aldolase were elevated. An electromyogram was consistent with a nonspecific myopathy as were microscopic and ultrastructural examinations of biopsied muscle. Venous lactic acid response to ischemic exercise was compatible with paroxysmal idiopathic myoglobinuria. Activities of muscle phosphorylase A and B, phosphofructokinase, muscle palmityl CoA synthetase, carnitine, and serum carnitine were normal as was the glycogen content. Activity of muscle carnitine palmityltransferase (2.7 microM/minute/mg protein), as measured by a spectrophotometric method and by radioactive assay, was significantly reduced when compared to normal control subjects (14.5 microM/minute/mg protein) and ischemic control subjects (13.8 microM/minute/mg protein). Muscle carnitine acetyltransferase (13.4 microM/minute/mg protein) was approximately 50% of normal control values (25.5 microM/minute/mg protein). This is the third reported case of myoglobinuria in a patient associated with a deficiency of muscle carnitine palmityltransferase activity.

Acyltransferases↗
PubMed1979

Myoglobinemia and myoglobinuria in unconscious children.

Myoglobinemia and/or myoglobinuria was demonstrated in 12 of 17 unconscious children studied. Myoglobinemia was noted in patients with serum CPK levels above 200-250 units. Ten of the 12 patients in whom myoglobinemia was present had convulsions. Some degree of renal disturbance was noted in six of seven patients with myoglobinuria. Five patients, including four with renal disturbance, died. In unconscious children with myoglobinuria the possibility of a disturbance of renal function should always be considered.

Blood Urea Nitrogen↗
PubMed2000

Myoglobinuria.

Myoglobinuria refers to an abnormal pathologic state in which an excessive amount of myoglobin is found in the urine, imparting a cola-like hue, usually in association with myonecrosis and a clinical picture of weakness, myalgias, and edema. Myoglobinuria is produced by multiple causes: any condition that accelerates the use or interferes with the availability of oxygen or energy substrates to muscle cells can result in myoglobinuria, as can events that produce direct muscle injury, either mechanical or chemical. Acute renal failure is the most serious complication, which can be prevented by prompt, aggressive treatment. In patients surviving acute attacks, recovery of muscle and renal function is usually complete.

Biopsy↗
PubMed1985

Effects of perinatal asphyxia and myoglobinuria on development of acute, neonatal renal failure.

Thirty four consecutive neonates with birth asphyxia or respiratory problems were examined in the first week of life to clarify the relation between neonatal myoglobinuria and acute renal failure. Investigations included determination of creatinine clearance, fractional sodium excretion, and N-acetyl-beta-D glucosaminidase index as an indicator of tubular injury. The infants' gestational ages ranged from 29 to 41 weeks (mean 36 weeks). Fifteen infants did not have myoglobinuria on the first day of life (group A); myoglobinuria was mild in eight infants (group B) and severe in eleven (group C). Two infants in group B and seven in group C developed acute renal failure (47%). Ten infants in group C (91%) had severe asphyxia, five of whom (45%) also suffered neonatal seizures and intracranial haemorrhage. We suggest that myoglobin derived from muscle breakdown in asphyxiated infants may lead to acute renal failure secondary to a reduction in renal blood flow, or to tubular damage.

Acute Kidney Injury↗
PubMed1990

Myoglobinuria: the importance of reaching a firm diagnosis--a patient with defective fatty acid oxidation.

A 52 year old man presented with myoglobinuria-induced acute renal failure requiring dialysis. Despite renal biopsy, the cause of the myoglobinuria was not established until he re-presented a year later with a milder episode. At this stage investigations, including a muscle biopsy, demonstrated a defect in fatty acid oxidation amenable to dietary and lifestyle advice. This report emphasizes the importance of reaching a definitive diagnosis in myoglobinuria.

Acute Kidney Injury↗
PubMedDate not supplied

Acute renal failure from myoglobinuria secondary to myositis from severe falciparum malaria.

Renal disease is a common complication in malaria infection. In acute falciparum malaria renal involvement is usually mild, but in severe disease acute renal failure is a major problem. Acute renal failure has been attributed to ischaemic tubular necrosis from hypovolaemia resulting from vasodilatation due to endothelial injury. Though myositis is recorded as a common manifestation in falciparum malaria, only 1 case with myositis and myoglobinuria with acute renal failure has been documented; but no renal biopsy was performed in the patient. In the present study we examined the case of a 17-year-old man with severe falciparum malaria with myositis and myoglobinuria who developed acute renal failure requiring dialysis. Muscle biopsy revealed severe myositis with macrophages and T lymphocytes including CD4+ cells. The kidney biopsy showed scanty T cells and macrophages in the glomeruli which were only mildly hypercellular. The renal tubules showed myoglobin casts in the lumen and foci of interstitial inflammatory cells, including macrophages and T lymphocytes but no CD4+ cells. Rhabdomyolysis induced by macrophages and T cells with myoglobinuria and acute renal failure is a problem in severe falciparum malaria infection.

Acute Kidney Injury↗
PubMed1982

Severe dystonia and myoglobinuria.

Myoglobinuria may follow extreme muscular exertion or disorders that cause muscle necrosis. Dystonia has not been implicated previously. We studied an 8-year-old boy of non-Jewish, Mexican-American descent with autosomal-dominant dystonia musculorum deformans who developed rapidly progressive and severe generalized dystonia, hyperpyrexia, myoglobinuria, and renal failure. Curarization was required. Transient improvement was achieved with tetrabenazine and baclofen, but bilateral thalamotomy was then performed. Patients with severe dystonia should be observed for evidence of myoglobinuria.

Child↗
PubMed1996

Sustained myoglobinuria: the presenting manifestation of dermatomyositis.

We describe two patients with sustained myoglobinuria that did not resolve with supportive treatment. After we established a diagnosis of dermatomyositis and started treatment with corticosteroids, there was rapid resolution of the myoglobinuria. Well-documented cases of inflammatory myopathy causing myoglobinuria are rare, but their prompt recognition has important therapeutic implications.

Adult↗
PubMed1976

[Acute myoglobinuria accompanied by renal failure in high febril infection (author's transl)].

A 41 year old man developed a myolysis with myoglobinuria during a period of high fever. The clinical signs were severe myalgia with general muscular weakness without manifest localized paresis. Electromyographically a diffuse generalized floride myopathy was found. Besides the extreme increase of CPK, a myoglobinuria was already macroscopically visible, which caused an acute renal failure. The treatment included corticosteroids and hemodialysis. An illness of several weaks was followed by complete recovery. As other known factors leading to myoglobinuria have been excluded, and the complement fixation reaction for Herpes simplex was more than 1:80, a viral-toxic etiology of this disease might be considered.

Acute Kidney Injury↗
PubMed2003

[Acute alcoholism with myoglobinuria: an autopsy case report].

We report an autopsy case of fatal acute alcoholism showing myoglobinuria and myocardial damage. The victim was a 29-year-old male, who was found drunk at his home. Although he was once brought to a hospital following a police officer's advice, he was taken into custody without effective medical care due to his violent behavior, and died about 16 hours later. Autopsy revealed marked congestion of the viscera and fatty liver. Histologically, skeletal muscle and myocardium showed focal degeneration and necrosis. Immunohistochemical investigation revealed a diffuse myoglobin loss from muscle fibers. Alcohol concentrations were 0.54 mg/ml, 0.79 mg/ml and 2.53 mg/ml in the left, right heart blood and urine, respectively. No other drugs or poisons were detected. The urine was dark brown, showing marked myoglobinuria. Cardiac troponin T, I and CK-MB in the pericardial fluid showed elevated levels even when postmortem influence was taken into consideration. From these observations, the cause of death was determined as myocardial damage from advanced acute alcoholic myopathy accompanied by myoglobinuria, possibly with underlying alcohol abuse. The present case suggests that careful clinical observation and adequate management are essential for an alcoholic patient with neurological symptoms.

Acute Disease↗
PubMed1991

[Myoglobinuria caused by multiple deletions of mitochondrial DNA].

We report two brothers with inherited recurrent myoglobinuria associated with distinct morphological abnormalities of muscle mitochondria and multiple deletions of muscle mitochondrial DNA. Patient 1 (26 years old) and Patient 2 (21 years old) had recurrent episodes of myoglobinuria provoked by strenuous exercise or alcohol intake. Histochemistry of their biopsied limb muscles showed ragged-red fibers and cytochrome c oxidase-negative fibers as well as degenerating and regenerating fibers. Electron microscopy showed a pronounced accumulation of abnormal mitochondria containing paracrystalline inclusions and moderate increases of glycogen particles. Southern blot analysis revealed multiple deletions of mitochondrial DNA, some of which were common to both patients. By the primer shift polymerase chain reaction method, we detected multiple abnormal fragments indicating mitochondrial DNA deletions. Nucleotide sequencing of the deleted regions disclosed directly repeated sequences of 1 to 12 bp on each side of the deletions. Since the end points of mitochondrial DNA deletions were within 20 bp of the major non-coding region, probable mutations in this region contribute to the pathogenesis of multiple mitochondrial DNA deletions found in these patients. We propose that a defect of the mitochondrial energy-transducing system due to multiple mitochondrial DNA deletions is a novel genetic cause of inherited recurrent myoglobinuria.

Base Sequence↗
PubMed1990

Carnitine palmitoyltransferase deficiency: a common cause of recurrent myoglobinuria.

Six patients with carnitine palmitoyltransferase (CPT) deficiency were diagnosed. Five were males aged 12-48 years and one was a 7-year-old girl. Severe myoglobinuria with renal shut-down led to the diagnosis in four, the main cause of myoglobinuria being prolonged exertion. Other precipitating factors included febrile illnesses, fasting and sleep deprivation. Between attacks, EMG, serum creatine kinase (CK) activity and the response of serum lactate to ischemic exercise were normal in all patients. The diagnosis of CPT deficiency was based on assay of the enzyme by the isotope exchange assay in leukocyte, muscle or cultured skin fibroblast homogenates. CPT activity assayed by the forward assay under standard conditions was normal. CPT deficiency seems to be a common cause of exercise-induced myoglobinuria. Prompt diagnosis can lead to avoidance of risk factors and prevention of rhabdomyolysis and its consequences.

Adult↗
PubMed1975

Low molecular weight proteinuria in association with paroxysmal myoglobinuria.

A patient with paroxysmal myoglobinuria presented with low molecular weight (LMW) proteinuria in association with an episode of exertional myoglobinuria. Since no signs of acute renal failure were present, the cause was probably competition between myoglobin and other LMW proteins for proximal tubular reabsorption. Agarose gel electrophoresis was found to be an excellent method for the investigation of myoglobinuria since this technique not only allowed the separation of myoglobin from hemoglobin but also myoglobin from metmyoglobin.

Adult↗
PubMed1982

Polymicrobial septicemia associated with rhabdomyolysis, myoglobinuria, and acute renal failure.

Myoglobinuria and renal failure resulting from bacterial infection have only rarely been reported. To our knowledge, we describe the first reported case of polymicrobial septicemia resulting in rhabdomyolysis and myoglobinuric renal failure. Renal failure secondary to myoglobinuria has an excellent prognosis; in our patient, recovery was complete. The frequency of rhabdomyolysis, myoglobinuria, and renal failure in septicemia is unknown and can only be determined by an increased awareness of this potential complication of septicemia.

Acute Kidney Injury↗
PubMed1981

[Creatininphosphokinase isoenzymes in anaesthesia-induced myoglobinuria (AIM) (author's transl)].

During a three year period, pediatric patients 4 to 16 years old were post-operatively screened for anaesthesia-induced myoglobinuria. All investigated cases had general anaesthesia and received succinylcholine prior to intubation. Anaesthetics were predominantly performed for tonsillectomies and/or adenoidectomies. Of a total of 1704 anaesthetics, 7 (0.4%) resulted in postoperative myoglobinuria without hyperthermia. Anaesthesia-induced myoglobinuria occurs more often than previously presented. This abnormal reaction to succinylcholine is not harmless in all cases. The possible genetic influence on total CPK and its isoenzymes is discussed.

Anesthesia, General↗
PubMed1978

Myoglobinuria, rhabdomyolysis and marathon running.

Rhabdomyolysis, secondary to exertion is known to result in myoglobinuria and is occasionally associated with acute renal failure. In this study myoglobinaemia occurred in 25 of 44 runners completing a 99 km marathon. A marked rise in the values of myoglobin, lactate and the enzymes creatine kinase (CPK), aspartate transaminase (AST) and lactic dehydrogenase (LDH) was noted. A linear correlation was demonstrated between the level of serum myoglobin and the serum concentrations of urate, CPK, AST and LDH. Both the myoglobin itself and the increased concentration of urate may contribute to the acute renal failure. The pathophysiology of rhabdomyolysis during exertion is discussed in the context of other causes of myoglobinuria. A classification of rhabdomyolysis and myoglobinuria is suggested.

Acute Kidney Injury↗