Resolution of Nephrotic Syndrome and Lack of Progression of Heroin-Associated Renal Amyloidosis

Crowley, Susan T.; Feinfeld, Donald A.; Janis, Rosamond

doi:10.1016/s0272-6386(89)80041-1

Cited by 22 publications

(13 citation statements)

References 8 publications

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“…Indeed, in small series of patients with AL amyloidosis who underwent serial kidney biopsies, the extent of amyloid deposition seemed to be similar in biopsies that were performed before treatment and after treatment-induced resolution of proteinuria (56,57). A lack of biopsy improvement after proteinuria resolution in AA amyloidosis also has been reported (58). Also consistent with a functional effect of amyloidogenic precursor proteins are in vitro demonstrations of specific phenotypic changes in cultured The right side depicts the traditional view that amyloid fibrils accumulate in the extracellular space, causing physical disruption and malfunction of surrounding tissue.…”

Section: How Does Amyloidosis Cause Renal Disease?mentioning

confidence: 83%

Amyloidosis-Associated Kidney Disease

Dember

2006

Journal of the American Society of Nephrology

350

284

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The amyloidoses are a group of disorders in which soluble proteins aggregate and deposit extracellularly in tissues as insoluble fibrils, causing progressive organ dysfunction. The kidney is one of the most frequent sites of amyloid deposition in AL, AA, and several of the hereditary amyloidoses. Amyloid fibril formation begins with the misfolding of an amyloidogenic precursor protein. The misfolded variants self-aggregate in a highly ordered manner, generating protofilaments that interact to form fibrils. The fibrils have a characteristic appearance by electron microscopy and generate birefringence under polarized light when stained with Congo red dye. Advances in elucidating the mechanisms of amyloid fibril formation, tissue deposition, and tissue injury have led to new and more aggressive treatment approaches for these disorders. This article reviews the pathogenesis, diagnosis, clinical manifestations, and treatment of the amyloidoses, focusing heavily on the renal aspects of each of these areas.

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Section: How Does Amyloidosis Cause Renal Disease?mentioning

confidence: 83%

Amyloidosis-Associated Kidney Disease

Dember

2006

Journal of the American Society of Nephrology

350

284

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“…At the time, 38% of heroin abusers in New York State were black (198). Crowley et al (195) speculated that cessation of skin popping and treatment of chronic indolent skin infections may have led to stabilization of renal function in a heroin user who developed renal amyloidosis. Although amyloidosis still was present on a subsequent renal biopsy 6 yr after the diagnosis of disease, proteinuria decreased from 6.8 g to 170 mg/d, and creatinine clearance remained unchanged.…”

Section: Indirect Effects Of Heroin On the Kidneymentioning

confidence: 99%

Chronic Nephropathies of Cocaine and Heroin Abuse

Jaffe

Kimmel²

2006

Clinical Journal of the American Society of Nephrology

124

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Renal disease in cocaine and heroin users is associated with the nephrotic syndrome, acute glomerulonephritis, amyloidosis, interstitial nephritis, and rhabdomyolysis. The pathophysiologic basis of cocaine-related renal injury involves renal hemodynamic changes, glomerular matrix synthesis and degradation, and oxidative stress and induction of renal atherogenesis. Heroin is the most commonly abused opiate in the United States. Previous studies identified a spectrum of renal diseases in heroin users. The predominant renal lesion in black heroin users is focal segmental glomerulosclerosis and in white heroin users is membranoproliferative glomerulonephritis. Although the prevalence of heroin use in the United States has increased, the incidence of "heroin nephropathy" has declined. Because reports of heroin nephropathy predated the surveillance of hepatitis C virus and HIV, the varied findings might be related to the spectrum of viral illnesses that are encountered in injection drug users. Socioeconomic conditions, cultural and behavioral practices, or differences in genetic susceptibilities may be more associated with the development of nephropathy in heroin users than the drug's pharmacologic properties. Administration of cocaine in animal models results in nonspecific glomerular, interstitial, and tubular cell lesions, but there is no animal model of heroin-associated renal disease. The heterogeneity of responses that are associated with heroin is not consistent with a single or simple notion of nephropathogenesis. There are no well-designed, prospective, epidemiologic studies to assess the incidence and the prevalence of renal disease in populations of opiate users and to establish the validity of a syndrome such as heroin nephropathy. It is concluded although there is a paucity of evidence to support a heroinassociated nephropathy, the evidence from in vitro cellular and animal studies to support the existence of cocaine-induced renal changes is more convincing.

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“…Included studies represented studies conducted in eight countries (Table ): 24 were conducted in the United States , 12 in Europe and one in India .…”

Section: Resultsmentioning

confidence: 99%