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

A 50-year-old man developed myoglobinuric renal failure after taking pyrazinamide. Both serum and urine myoglobin levels were elevated and tubulo-interstitial nephropathy was demonstrated on renal biopsy. After pyrazinamide was discontinued, the myoglobin concentrations were normalized and his renal function ameliorated. The rhabdomyolysis was considered to be caused by pyrazinamide. To our knowledge, this is the first reported case of rhabdomyolysis associated with pyrazinamide.
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PMID:A case of pyrazinamide-associated myoglobinuric renal failure. 180 50

Since the demonstration that beta 2-microglobulin (beta 2M) is an amyloidogenic protein in man, the excretion of this low-molecular-weight protein under conditions with normal and reduced renal function has received increased interest. The renal arteriovenous extraction of beta 2M, polyfructosan (an inulin analogue), and a second low-molecular-weight protein, myoglobin, was measured in vivo in 16 human kidneys with normal renal function/gross morphology and in 22 kidneys with reduced function. In kidneys with normal function, the extraction of beta 2M significantly exceeded that of polyfructosan (0.198 +/- 0.037 vs. 0.182 +/- 0.05; p = 0.04), while that of myoglobin (0.177 +/- 0.068) was not different from that of polyfructosan. In kidneys with reduced function, the extraction of polyfructosan or myoglobin was not significantly altered. In contrast, the beta 2M extraction decreased to 0.110 +/- 0.060 (p less than 0.01 vs. extraction of polyfructosan or myoglobin). This decrease was significantly correlated with the decrease of the endogenous creatinine clearance or the total or unilateral 131I-hippuran clearance. These results indicate that in normal renal function the glomerular filtration of beta 2M may be supplemented by a peritubular mode of removal. The mechanism(s) underlying the selective decrease of beta 2M extraction in kidneys with reduced function remain speculative. However, this decrease will lead to a further augmentation of the retention of beta 2M in renal failure.
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PMID:Renal elimination of beta-2-microglobulin and myoglobin in patients with normal and impaired renal function. 220 18

We report a case of lovastatin-induced rhabdomyolysis and resulting life-threatening renal failure. Lovastatin, a hypocholesterolemic agent, decreases endogenous cholesterol synthesis by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase (EC 1.1.1.88). This agent has been implicated in causing rare serious side effects in various clinical settings; however, the mechanism of these adverse reactions is not understood. The clinical course of our patient was characterized by profound muscle weakness with marked increases in serum creatine kinase and myoglobin. Light- and electron-microscopic studies of skeletal muscle of our patient demonstrated a noninflammatory myopathy suggestive of ongoing rhabdomyolysis with vacuolization and focal degeneration of myocytes. The patient's symptoms and the laboratory values referable to rhabdomyolysis resolved after discontinuation of the drug. We speculate that the rhabdomyolysis was due to mitochondrial damage secondary to inadequate synthesis of coenzyme Q and heme A, members of the electron-transport system of the inner mitochondrial membrane.
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PMID:Rhabdomyolysis secondary to lovastatin therapy. 225 72

Proteinaceous cast formation in the distal nephron of the kidney from low molecular weight proteinuria is a significant, but poorly characterized, cause of renal failure. To study this phenomenon, we: (a) microperfused the loop segment (LS) of rats in vivo with artificial tubule fluid (ATF) containing four different low molecular weight proteins, 0.01-50 mg/ml, to detect alterations in LS function, and (b) examined the interaction between several proteins and Tamm-Horsfall glycoprotein (THP) in vitro with turbidity and dynamic light-scattering measurements. Perfusion of the LS for less than 2 min with cast-forming proteins (Bence Jones protein [BJP3] and myoglobin) decreased chloride absorption and elevated early distal tubule fluid (ED) [Cl-], compared with results obtained with control perfusions that used ATF alone. BJP3 decreased chloride absorption in a concentration-dependent fashion. Perfusion with non-cast-forming proteins (albumin and BJP1) enhanced chloride absorption and decreased ED [Cl-]. In vitro, proteins that had isoelectric points (pI) greater than 5.1 aggregated with THP. Aggregation was enhanced with increasing [NaCl] or [CaCl2]. Albumin (pI 4.8) and beta-lactoglobulin (pI 5.1) did not coprecipitate. The molecular size of THP alone increased when [NaCl] greater than 80 mM. Thus, cast-forming proteins aggregated with THP in vitro and caused in vivo LS dysfunction, which elevated ED [Cl-], facilitating aggregation. In contrast, non-cast-forming proteins either did not interact with THP or lowered ED [Cl-], which did not provide an environment for aggregation. Altered LS function and interaction of some proteins with THP were related to different physicochemical properties of the proteins and independently contributed to the formation of proteinaceous casts in the kidney.
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PMID:Mechanisms of intranephronal proteinaceous cast formation by low molecular weight proteins. 229 21

The frequency of myoglobinuric renal failure is estimated between 8 and 20%. Despite early onset of therapy often the use of renal substitution by hemodialysis or hemofiltration is required. This study of the clinical course of nine patients with myoglobinuric acute renal failure reveals continuous arterio-venous hemofiltration (CAVH) to have an effective clearance for myoglobin. Thus, the time until recovery of renal function as well as the frequency of secondary complications in rhabdomyolysis induced acute renal failure can be distinctly reduced.
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PMID:Hemofiltration in myoglobinuric acute renal failure. 234 54

A 47-year-old man developed progressive renal impairment after a series of seven generalised tonic-clonic seizures. The patient did not become oliguric and because recovery of renal function was rapid, dialysis was not required. The diagnosis of myoglobin-induced renal failure was made on the basis of markedly elevated muscle enzyme values, and myoglobin in the urine.
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PMID:Myoglobinuric renal failure after generalised tonic-clonic seizures. A case report. 341 14

The prophylactic effectiveness of a small "self-taming" dose of succinylcholine (0.1 mg X kg-1), of d-tubocurarine (0.05 mg X kg-1), and of pancuronium (0.02 mg X kg-1) on succinylcholine-induced fasciculations and myoglobinaemia was studied in 64 healthy children (ages two to nine years), anaesthetized with halothane, nitrous oxide and oxygen. Serum myoglobin was analyzed by radioimmunoassay and taken as a tracer of muscle damage. No correlation was found between the serum levels of myoglobin and the incidence of muscle fasciculations. Self-taming with succinylcholine decreased the incidence of fasciculations (p = 0.001) but did not decrease the succinylcholine-induced myoglobinaemia (p = 0.224). D-tubocurarine (0.05 mg X kg-1) and pancuronium (0.02 mg X kg-1) both significantly reduced the myoglobinaemia and the fasciculations produced by succinylcholine. The pancuronium pretreated group presented less variable values of serum myoglobin which, when compared to the control group, had a more significant p value (p less than 0.001) than for d-tubocurarine pretreated group (p = 0.003). Muscle fasciculations and increased myoglobin levels were observed in children less than four years old who received succinylcholine. The prophylaxis of acute rhabdomyolytic renal failure due to succinylcholine (seven cases reported in the medical literature) is considered.
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PMID:Succinylcholine, fasciculations and myoglobinaemia. 369 14

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.
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PMID:Myoglobinuria in chronic renal failure. 374 57

A case is presented in which decerebrate posturing after a head injury led to rhabdomyolysis and renal failure. Exertional rhabdomyolysis is caused by an energy deficient state in overworked musculature that leads to a loss of integrity of the muscle cell. The resultant myoglobin in serum leads to acute renal failure. This condition should be suspected in a comatose patient with fever, brown discoloration of the urine, and edema of the extremities. Laboratory results will show orthotoluidine positive urine with a clear serum, elevated serum creatine phosphokinase, and serum creatinine elevation out of proportion to blood urea nitrogen. Management consists of fluids and diuretics with dialysis if necessary. Rhabdomyolysis with head injury and decerebracy may occur more frequently than has been previously reported.
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PMID:Exertional rhabdomyolysis associated with decerebrate posturing. 374 64

Two patients, brother and sister, aged 19 and 16, with combined, partial deficiency of carnitine palmityltransferase (CPT) are reported. Both patients had recurrent exercise-related myoglobinuria. The brother had also experienced an episode of transient renal failure associated with myoglobinuria. Both had elevated CK and myoglobin in plasma between attacks. There was a normal production of lactate in ischaemic forearm exercise, but elevated levels of NH3, resulting in an increased NH3/lactate ratio; 48-h fasting caused no significant changes in cholesterol, triglycerides or glucose, no rise of CK, and a normal ketogenic response, indicating no hepatic enzyme deficiency. Muscle biopsy showed slight changes of myopathy in both patients, with scattered atrophic fibres, but no lipid accumulation or other specific changes. Biochemical analysis of muscle tissue revealed a reduction of carnitine to 48% and 40% and a reduction of CPT to 55% and 59% of normal values, which is similar to the findings in the only previous report of combined partial carnitine and CPT deficiency. The heterogeneity of the laboratory findings in CPT deficiencies and the value of the various diagnostic procedures in metabolic myopathies are discussed.
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PMID:Familial combined deficiency of muscle carnitine and carnitine palmityl transferase (CPT). 382 3


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