Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral L-carnitine has been reported to lower the elevated serum myoglobin of renal failure in chronic peritoneal dialysis patients, and intravenous L-carnitine can improve muscle fatigue and cramps in chronic hemodialysis patients. In this study oral L-carnitine, 1.98 g/day, was administered to 6 chronic hemodialysis patients for 8 weeks. Serum levels of myoglobin, creatine kinase, and aldolase, as well as skeletal muscle symptoms (cramps during dialysis, fatigue, and weakness) were monitored biweekly for 12 weeks. Mean baseline serum myoglobin level was 337 +/- 34 ng/mL. By 6 and 8 weeks mean serum myoglobin was 234 +/- 39 and 233 +/- 40 ng/mL, significantly lower by the Friedman test (p < 0.05). Four weeks after carnitine was discontinued, mean serum myoglobin had risen to 320 +/- 118 ng/mL. Serum creatine kinase and aldolase levels were normal throughout the study. All 6 patients noted improvement in muscular symptoms, with maximal effect at 8 weeks, although 2 patients did not improve until 2 to 4 weeks after carnitine was stopped. We conclude that oral L-carnitine may lower serum myoglobin and improve muscle cramps and weakness in hemodialysis patients. The maximal effect of carnitine on myoglobin occurs 2 weeks before the maximal improvement in muscular symptoms.
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PMID:Effect of oral L-carnitine on serum myoglobin in hemodialysis patients. 882 May 5

We report a patient with rhabdomyolysis secondary to hyperosmolar nonketotic diabetic coma (HNKC), who progressed to acute renal failure. A 43-year-old male with diabetes mellitus for three years was admitted to our hospital because of loss of consciousness. The laboratory findings at admission were as follows: serum glucose 1792 mg/dl, serum Na 129 mEq/1, BUN 71 mg/d1, serum creatinine 3.3 mg/d1, CPK 715 IU/1, plasma osmolality 370 mOsm/1, and negative urine ketone bodies. A diagnosis of HNKC was made. On the 2nd day, he had oliguria and the serum creatinine increased despite adequate treatment of HNKC by the administration of intravenous fluid and insulin. On the 4th day, CPK reached 47,300 IU/1, and serum myoglobin was also increased, indicating rhabdomyolysis. His renal function improved gradually and was almost normalized on the 20th day. Renal biopsy on the 23rd day showed myoglobin at the distal renal tubules, which appeared to be involved in the pathogenesis of renal failure by rhabdomyolysis. However, we found little abnormality association with diabetic nephropathy in the renal tissue. Since HNKC is known to induce acute renal failure rarely without diabetic nephropathy, these findings suggested that the acute renal failure was caused mainly by the rhabdomyolysis. Acute renal failure induced by rhabdomyolysis in patients with HNKC is rare, but fatal. The present study showed that the measurement of serum CPK and urine myoglobin was helpful for early diagnosis. Only 12 cases have been reported to have developed renal failure due to rhabdomyolysis among patients with HNKC. To our knowledge, we demonstrated for the first time that myoglobin at the distal renal tubules after renal function was normalized.
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PMID:[Rhabdomyolysis related-acute renal failure in a patient with hyperosmolar nonketotic diabetic coma (HNKC): demonstration of myoglobin casts after normalization of renal function]. 882 59

Myoglobin induces renal injury by mechanisms that remain incompletely defined. In this study, the effects of myoglobin upon renal microcirculation, oxygenation, morphology, and function were investigated in anesthetized rats, and the contribution of coexisting perturbations to myoglobin nephrotoxicity were evaluated. Myoglobin infusion (3.3 mg/min) reduced outer medullary blood flow and Po2, whereas renal blood flow and cortical Po2 were unaffected. Myoglobin infusion (38 mg/100 g weight over 45 min) induced renal failure associated with collecting duct and medullary thick ascending limb dilation and casts, with focal tubular damage, confined mainly to the superficial cortex. Preconditioning with indomethacin, I-N-monomethyl arginine, and theophylline reduced cortical superficial damage but enhanced injury within the inner stripe of the outer medulla and in medullary rays, the zones of lowest O2 supply. In preconditioned animals, tubulorrhexis was primarily observed in collecting ducts transversing the inner stripe, and was remarkably reminiscent of human descriptions (J. Oliver et al., J Clin Invest 1951; 30: 1307-1440). Deterioration in kidney function closely correlated with morphologic features of both tubular obstruction and necrosis. In conclusion, medullary vasoconstriction and intrarenal hypoxia may play a role in myoglobin-induced renal failure. The deterioration in kidney function appears to reflect the combined effects of cortical damage, medullary hypoxic injury, and tubular obstruction.
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PMID:Myoglobinuric acute renal failure in the rat: a role for medullary hypoperfusion, hypoxia, and tubular obstruction. 882 23

We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.
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PMID:Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC. 884 91

Rhabdomyolysis is characterized by extensive damage of striated muscle, while the major complication of this disease is the development of acute myoglobinuric renal failure. Although first described more than five decades ago very little has changed with regard to the management of this entity as conventional hemodialysis has not been shown to effect myoglobin elimination. However, continuous arteriovenous hemofiltration (CAVH) offers an alternative to conventional hemodialysis as this procedure is more effective particularly for removing larger molecular weight substances such as myoglobin. We studied the effect of CAVH on myoglobin clearance in an animal model of acute myoglobinuric renal failure. Swine (n = 6) were given 4 grams of equine myoglobin intravenously and underwent the CAVH procedure for six hours each. Once the filtering process was initiated there was a rapid and sustained production of ultrafiltrate. The clearance of myoglobin via the hemofilter was 2.05 +/- 1.48 L/day. The amount of myoglobin excreted in the ultrafiltrate over the six hour filtering period was 410 +/- 234 mg which accounts for 10.27 +/- 5.85 percent of the administered dose. Based on these findings, it appears that the hemofiltration system is a viable option for the removal of myoglobin from the systemic circulation.
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PMID:Evaluation of myoglobin clearance during continuous hemofiltration in a swine model of acute renal failure. 894 33

New clinical requirements for triaging chest pain patients challenge the abilities of the current cardiac markers. Serial measurements of myoglobin, creatine kinase (CK) isoenzyme MB (CKMB) mass, or CK isoforms in emergency rooms help to rapidly rule out acute myocardial infarction (AMI). However, within the first 3 to 4 h from chest pain onset, their sensitivities are too low to contribute significantly to AMI diagnosis during this period. CKMB and lactate dehydrogenase (LDH) isoenzyme 1 are not heart-specific, which hampers reliable diagnosis in patients with concomitant skeletal muscle damage. By contrast, the regulatory proteins troponin I and troponin T are expressed in three different isoforms: one for slow-twitch skeletal muscle fibers, one for fast-twitch skeletal muscle fibers, and one for cardiac muscle (cTnI, cTnT); cardiac-specific cTnI and cTnT assays are already available for routine use. cTnT and cTnI are the most promising markers for risk stratification in patients with unstable angina pectoris. Recent reports on increased cTnT in patients with renal failure or myopathy without evidence of myocardial injury and undetectable cTnI suggest that cTnT could be reexpressed similar to CKMB and LDH-1 in chronically damaged human skeletal muscle. Therefore, cTnI is probably the most heart-specific marker. Among the recently proposed new markers for early AMI diagnosis: glycogen phosphorylase isoenzyme BB (GPBB), fatty acid binding protein, phosphoglyceric acid mutase isoenzyme MB, enolase isoenzyme alpha beta, S100a0, and annexin V, GPBB is the most promising because it increases as early as 1 to 4 h from chest pain onset and its early release appears to be essentially dependent on ischemic myocardial injury.
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PMID:Progress in myocardial damage detection: new biochemical markers for clinicians. 905 56

Acute renal failure (ARF) in burn disease results in a range of phenomena important not only from theoretical, but also from practical point of views, whose causes are manifold. ARF is generally defined as a rapid renal failure resulting in accumulation of protein metabolism degradation products (catabolism). It has been known, for some time, that thermal agents do not produce only local skin damages, but also disturb the integrity of the whole organism producing major functional damages of all organs and systems. Most frequently organs affected by burn disease are the following: the lungs, the heart, the kidney, the liver and blood coagulation systems. There are many factors influencing the renal function during the burns. The most important are: decreased cardiac output, respiratory failure with hypoxia and acidosis, toxaemia and sepsis [1, 4, 6 7, 8-10, 12, 19]. ARF in burn disease may be early due to hypovolaemia and hypoperfusion of the kidneys or late, occurring after a week as a consequence of infection and endotoxaemia. Development of ARF in burn disease is a very unfavorable prognostic sign necessitating a complex evaluation. Anuria in an early phase of burn disease may indicate the development of ARF, particularly if urine findings are positive to haemoglobin, proteins, myoglobin, which is of the utmost importance in deep burns inflicted by high voltage current. The immediate cause of anuria in burn disease may be a reflex transfer and penetration of the large quantities of toxic materials into the circulation form the region affected by burns leading to the spasm of afferent glomerular arteriolae producing sudden discontinuation of glomerular filtration. After burns, sudden increase in the osmotic activity ensues in the affected tissue. Some low molecular links may result, and such particles tend to change the osmotic balance and stimulate the development of oedema, and if not excreted, they increase osmolarity. In 20-30% of the patients with burn disease anuria is absent [2, 5, 11, 14, 18, 20]. The genesis of burn disease-associated anaemias is therefore multifactorial. These factors are the following: haemorrhage, haemolysis and etrythropoiesis level decrease. In massive burns, large amounts of non-specific inflammatory components are produced as well: prostaglandins, histamine, quinines leukocyte phenomena, bacterial toxins, etc. [1, 6, 13-16]. The study based on a years-long treatment of our patients with burn disease included on 100 patients. The youngest of the patients was 14 years old, and the oldest 65 years. The percent of burns-affected body surface ranged from 25% to 75%. In 3/4 of the patients the picture of an early renal failure developed, with oliguria immediately after infliction of the burns with rapid increase of serum urea and creatinine levels, while in 1/4 of the patients ARF occurred on the eighth day following the infliction of the burns. "late form of acute renal failure". Among our series with burn disease, anuria was present in 34.0% of patients and oliguria in 25.0%. ARF (early phase) occurred in 59 patients, 38 patients had no sing of ARF, while late ARF developed only in 3 patients. ARF-associated mortality rate was high among these patients (23%), being 6% among anuric patients with ARF and 17% in patients with ARF with anuria. Seventy-seven percent of the patients survived, and their serum and urine analyses performed upon subsequent out-patient follow-up examinations ranged within normal values. Such high percentage of survival among our patients included in the study is based on an early diagnosis of ARF, understanding of pathophysiology of shock associated with burn disease, adequate therapeutic approaches, including both medicamentous treatment and extracorporeal haemodialysis along with early surgical management (Shema 1, 2). For the time being, haemodialysis is the most effective therapeutical procedure in the treatment of ARF, although the mortality rate of dialyzable patients
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PMID:[Acute renal insufficiency caused by burn injury]. 910 56

Exertional rhabdomyolysis occurs when exercise, often of the eccentric type, damages myofibrils and sarcolemma, with release of the enzyme creatine kinase and pigmented myoglobin into the serum. Severe muscle soreness and dark urine are the hallmark symptoms, and renal failure may develop. Formerly a disease of military recruits, it is now seen more often in exercisers. Although a genetic trait may predispose, the illness probably can be avoided by common sense behavior such as a gradual increase in exercise intensity, proper hydration before, during, and after exercise, and avoiding exercise in extremely hot or humid environments.
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PMID:When exercise goes awry: exertional rhabdomyolysis. 916 79

Myoglobin induces renal injury by mechanisms that remain incompletely defined. Acidosis has been suggested as an important factor in myoglobinuric renal failure, and urine alkalization is routinely recommended for its prevention. We tested this hypothesis by exploring the effects of acid-base balance upon myoglobin nephrotoxicity in vivo and in vitro. In isolated rat kidneys at normal pH, myoglobin at concentrations of 25-250 mg/dl minimally affected renal perfusion flow, glomerular filtration rate (GFR) and tubular sodium reabsorption (TRNa). By contrast, at pH 7.1 myoglobin induced vasoconstriction, reduced GFR and TRNa and increased hypoxic injury to medullary thick ascending limbs. These changes were largely reproduced by perfusing kidneys with hematin, suggesting its release from myoglobin in acidosis. Chronic alkalosis or acidosis was induced in rats by supplementing drinking water with 0.28 M NaHCO3 or NH4Cl, respectively. Acute renal failure, produced in control animals by myoglobin infusion (38 mg/100 g body weight), was comparably prevented by both chronic alkalosis and acidosis. Acute intravenous or oral acid load provided similar protection. Thus, although acidosis exacerbates myoglobin toxicity in isolated perfused kidneys, acute or chronic exogenous acid load prevents renal damage in vivo. This may underscore the protective properties of solute load, a consequence of preconditioning, and suggests that, in the crush syndrome, endogenous acidosis rather than being an independent risk factor is a marker of tissue hypoperfusion and organism susceptibility to myoglobin renal toxicity.
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PMID:Myoglobinuric acute renal failure in the rat: a role for acidosis? 920 80

The aim of this study was to monitor serum and perfusate levels of myoglobin (MB) and creatine kinase (CK) during isolated limb perfusion (ILP) in order to identify those at risk of renal failure. We investigated the release of MB and CK in 40 patients who underwent ILP for melanoma (n = 15) or sarcoma (n = 25) using rhTNF alpha/melphalan (n = 28) or a triple-drug regimen (n = 12). Serial determinations of CK and MB were performed in both perfusate and systemic circulation during and after ILP and renal function was assessed. A significant increase of MB could be detected in the perfusate during ILP. After ILP, an up to 100-fold increase with a double peak of MB at 4 h and 24 h postoperatively was observed. The maximum elevation of serum activity of CK was at 30 h. The increase for both proteins was highly significant (P < 0.001). ILP with rhTNF alpha/melphalan yielded significantly (P < 0.001) higher serum values of MB and CK and also the impairment of the renal function was more pronounced. The peak values of MB after ILP occur early and allow the patients most at risk of developing renal failure to be identified. Rhabdomyolysis can be detected early by determination of MB from the perfusate. Further measurements twice daily for 2-3 days post ILP from serum samples as well as daily assessment of MB in the urine is helpful for detecting myoglobinuria and imminent renal failure.
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PMID:Rhabdomyolysis and renal function impairment after isolated limb perfusion--comparison between the effects of perfusion with rhTNF alpha and a 'triple-drug' regimen. 927 41


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