Natural History of Heroin-Associated Nephropathy

Tk, Rao; Ad, Nicastri; Ea, Friedman

doi:10.1056/nejm197401032900105

Cited by 152 publications

(40 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…FSGS, with a paucity of focal proliferative changes, was found in 11 of 13 heroin users who underwent biopsies (109). All patients were black men, aged 19 to 34 yr, who admitted to injecting heroin for 1 to 18 yr before the onset of renal disease.…”

Section: Historical Perspective Of Renal Disease and Heroin Usementioning

confidence: 99%

Chronic Nephropathies of Cocaine and Heroin Abuse

Jaffe

Kimmel²

2006

Clinical Journal of the American Society of Nephrology

124

View full text Add to dashboard Cite

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.

show abstract

Section: Historical Perspective Of Renal Disease and Heroin Usementioning

confidence: 99%

Chronic Nephropathies of Cocaine and Heroin Abuse

Jaffe

Kimmel²

2006

Clinical Journal of the American Society of Nephrology

124

View full text Add to dashboard Cite

show abstract

“…Morphine is a metabolite of heroin and opium; progressive glomerulopathy leading to the nephrotic syndrome and renal insufficiency in addicts has been ascribed to heroin toxicity and damage caused by contaminants and other impurities [6,7,8,9,10]. In addition to endothelial cells, mesangial and other cells that play a pivotal role in the maintenance of glomerular integrity express opioid receptors and are modulated by morphine.…”

Section: Introductionmentioning

confidence: 99%

Opioids Induce Renal Abnormalities in Tumor-Bearing Mice

Arerangaiah¹,

Chalasani²,

Udager³

et al. 2007

Nephron Exp Nephrol

View full text Add to dashboard Cite

Background/Aims: The etiology of renal dysfunction in cancer patients is likely to be multifactorial. A large proportion of these patients receive opioid analgesics, but whether opioids contribute to renal dysfunction remains uncertain. In a murine cancer model, we examined the effects of chronic opioid administration on renal function and pathology, and the molecular mechanisms involved. Methods: C3H/HeJ mice implanted with 2472 tumor cells were treated with either morphine or hydromorphone in clinically relevant doses, or PBS (controls). Renal function was assessed by blood and urine chemistry as well as by measuring mean arterial pressure (MAP) and kidney perfusion. Pathological changes in the kidneys were examined by routine histology. Molecular changes were examined by assessing eNOS, iNOS, HO-1 and COX-2 expression in whole-kidney lysates by Western immunoblotting, and cellular colocalization of these enzymes was determined using immunofluorescence microscopy. Results:Three weeks of opioid treatment resulted in increased kidney weight, elevated BUN and proteinuria, and decreased MAP. This was accompanied by histological abnormalities including glomerular enlargement, hypercellularity, peritubular congestion, vasodilatation and tubular casts. The vasoregulatory molecules iNOS, eNOS, HO-1 and COX-2 were upregulated in the kidneys. The NOS inhibitor L-NAME prevented the morphine-induced increase in perfusion and kidney weight. Conclusions: The chronic use of clinically relevant doses of opioidsleads to structural kidney abnormalities, upregulates NOS, COX-2 and HO-1, and results in renal dysfunction in a murine model of cancer.

show abstract

“…Most of our patients with HCV infection had a history of IVDA, which has been reported in association with FSGS and is refered to as heroin nephropathy [9]. Although it is possible that HCV in our patients is simply a marker for IVDA, one of our patients with FSGS and HCV infection did not have a history of IVDA, demonstrating that FSGS can develop in patients infected with HCV in the absence of IVDA.…”

Section: Discussionmentioning

confidence: 72%

“…Like our patients with HCV infection and FSGS, heroin nephropathy occurs primarily in Blacks with a history of IVDA and is associated with a relatively rapid progression to renal failure [6, 9]. Our HCV-infected patients with FSGS could not be distinguished from those with heroin nephropathy by the presence of liver disease as all of our HCV-infected patients had normal liver enzymes and none had clinical signs of liver disease.…”

Section: Discussionmentioning

confidence: 88%

Focal Segmental Glomerular Sclerosis among Patients Infected with Hepatitis C Virus

Stehman‐Breen¹,

Alpers²,

Fleet³

et al. 1999

Nephron

View full text Add to dashboard Cite

This study describes the occurence of hepatitis C virus (HCV) infection in the setting of focal segmental glomerular sclerosis (FSGS). All patients with the pathologic diagnosis of idiopathic FSGS between 1992 and 1996 at the University of Washington Hospitals were examined using a retrospective cohort study design. FSGS was determined by renal biopsy in the absence of secondary causes. Demographic, laboratory, and outcome data were collected in a standardized fashion. Six patients (50%) were infected with HCV. Patients with HCV infection and FSGS were primarily Black (67%), hypertensive (100%), had a history of intravenous drug abuse (83%), and had normal liver enzymes. Those with HCV infection and a history of IVDA appeared clinically and histologically similar to previously described cases of ‘heroin nephropathy’. We demonstrate that there is a high prevalence of HCV infection in our population of patients with idiopathic FSGS. Although this may simply reflect an epiphenomenon, we propose that HCV infection may play a role in the development of FSGS in a predisposed host.

show abstract

Natural History of Heroin-Associated Nephropathy

Cited by 152 publications

References 14 publications

Chronic Nephropathies of Cocaine and Heroin Abuse

Chronic Nephropathies of Cocaine and Heroin Abuse

Opioids Induce Renal Abnormalities in Tumor-Bearing Mice

Focal Segmental Glomerular Sclerosis among Patients Infected with Hepatitis C Virus

Contact Info

Product

Resources

About