Acute Renal Failure Due to Nontraumatic Rhabdomyolysis

Koffler, Alan

doi:10.7326/0003-4819-85-1-23

Cited by 257 publications

(56 citation statements)

References 31 publications

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“…Since then the spectrum of etiologies for rhabdomyolysis, myoglobinuria, and renal failure has been markedly expanded, with both traumatic and, more recently, nontraumatic causes being recognized (2)(3)(4)(5). Rhabdomyolysis may also occur in apparently normal subjects after prolonged strenuous exercise including marathon runners, ice skaters, and football players after competition and in as many as 39% ofthe Marine Corps recruit population (6).…”

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Role of glutathione in an animal model of myoglobinuric acute renal failure.

Abul-Ezz

Walker

Shah

1991

Proc. Natl. Acad. Sci. U.S.A.

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In a previous study we have shown a role for reactive oxygen metabolites in glycerol-induced acute renal failure, a well-established model for myoglobinuric acute renal failure. In the present study we examined the role of glutathione in this model of acute renal failure. Administration of 50% (vol/vol) glycerol at a dose of 10 ml/kg of body weight to rats intramuscularly resulted in significant renal failure associated with depletion of total kidney glutathione (GSH) from 2.6 + 0.1 ,umol/g (mean ± SEM control level) to 1.7 ± 0.1 ,tmol/g after 6 hr (P < 0.001). If GSH were important in glycerol-induced acute renal failure, one would anticipate that exogenously administered GSH should afford protection, while unjury should be potentiated if endogenous GSH is depleted. We examined the effect of i.p. administration of L-buthionine-(S,R)-sulfoximine (BSO) at 2 mmol/kg (which results in depletion of kidney GSH) and the effect of increasing renal GSH by i.v. administration of reduced GSH (2 mmol/kg every 3 hr) on kidney function in glycerol-treated rats. Glycerol-injected rats treated with BSO showed significantly worse renal failure than did rats given glycerol alone, while administration of GSH resulted in significant amelioration of glycerol-induced acute renal failure [glycerol treatment alone, blood urea nitrogen (BUN) = 96 10 and creatinine = 2.5 + 0.4 mg/dl; BSO + glycerol treatment, BUN = 123 +-7 and creatinine = 3.5 + 0.1 mg/dl (n = 9, P < 0.05); GSH + glycerol treatment, BUN = 78 ± 10 and creatinine = 1.25 --0.2 mg/dl (a = 8, P < 0.05)].In separate experiments 1,3-bis(chloroethyl)-1-nitrosourea (BCNU) [which interferes with the enzyme GSH reductase and prevents recycling of oxidized GSH (GSSG) into GSH] resulted in worsening of glycerol-induced acute renal failure similar to that produced by BSO. These functional differences between GSH-depleted and GSH-repleted rats were further substantiated by significant histological differences in tubular injury. Taken together, these results provide evidence for an important role of GSH in glycerol-induced acute renal failure.During the Battle of Britain, Bywaters and Beall (1) described the first causative association of acute renal failure with skeletal muscle injury and the release of muscle cell contents, including myoglobin, into plasma (rhabdomyolysis). Since then the spectrum of etiologies for rhabdomyolysis, myoglobinuria, and renal failure has been markedly expanded, with both traumatic and, more recently, nontraumatic causes being recognized (2-5). Rhabdomyolysis may also occur in apparently normal subjects after prolonged strenuous exercise including marathon runners, ice skaters, and football players after competition and in as many as 39% ofthe Marine Corps recruit population (6). It is estimated that about one-third of the patients with rhabdomyolysis will develop acute renal failure (2) and recent studies show that it is not an infrequent cause of renal failure accounting for 5-7% of all cases of acute renal failure (3).The most widely applied mo...

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confidence: 99%

Role of glutathione in an animal model of myoglobinuric acute renal failure.

Abul-Ezz

Walker

Shah

1991

Proc. Natl. Acad. Sci. U.S.A.

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“…Rhabdomyolysis has been associated with the use of opioids, alcohol and other drugs (10)(11)(12)(13). Rhabdomyolysis can lead to acute renal failure due to direct toxicity of metabolites like ferrihemate (13,14), tubular obstruction due to protein, uric acid crystals, and myoglobin casts, or by reduction in renal blood flow as a result of renal vasoconstriction.…”

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confidence: 99%

Unusual complications of heroin abuse: Transverse myelitis, rhabdomyolysis, compartment syndrome, and ARF

Sahni

Garg

et al. 2008

Clinical Toxicology

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Introduction. Heroin overdose can cause various rare neurological complications like spongiform leukoencephalopathy, seizures, stroke, toxic amblyopia, transverse myelopathy, mononeuropathy, plexopathy, acute inflammatory demyelinating polyradiculoneuropathy, rhabdomyolysis, compartment syndrome, fibrosing myopathy, and acute bacterial myopathy. We report here the simultaneous presentation of multiple complications of heroin toxicity. Case report. A young heroin addict was found unarousable lying in the lotus posture. Examination showed quadriplegia and left leg gangrene. He subsequently developed heroin-induced transverse myelitis, rhabdomyolysis, left leg compartment syndrome, and myoglobin-induced acute renal failure. Discussion. This case leads us to consider a common linked or systemic mechanism of injury rather than a local mechanism when multiple simultaneous organ failure occurs complicating heroin abuse.

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“…Ab b r e v i a t i o n : C P K, c r e a t i n i n e p h o s p h o k i n a s e . such a rare cause of hypertension (2)(3)(4)(5) Table 3 (17,18 (22,(28)(29)(30)(31). Although …”

Section: T a B L E 3 S U Mma R Y F O R Ca S E Re P O R T S O F P R mentioning

confidence: 99%