Cocaine use, hypertension, and end-stage renal disease

Norris, Keith C.; Thornhill-Joynes, Monica; Robinson, C. L. N.; Strickland, Tony L.; Alperson, Burton L.; Witana, Sarath C.; Ward, Harry J.

doi:10.1053/ajkd.2001.26845

Cited by 51 publications

(31 citation statements)

References 40 publications

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“…In contrast, cocaine clearly causes deleterious effects on the kidney and can lead to AKI both from rhabdomyolysis and malignant hypertension. 19,20 This study further supports the existence of an association between cocaine use and AKI among persons with HIV/HCV coinfection.…”

Section: Discussionsupporting

confidence: 74%

Incidence and Predictors of Acute Kidney Injury in an Urban Cohort of Subjects with HIV and Hepatitis C Virus Coinfection

Garg

Hoenig

Edwards

et al. 2011

AIDS Patient Care and STDs

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Coinfection with hepatitis C (HCV) significantly increases the risk of acute and chronic renal disease in HIVinfected individuals. However, the burden of acute kidney injury (AKI) directly attributable to HIV among HCV-infected individuals and associated risk factors are not well understood. Within a prospective cohort, AKI episodes were identified by a rise in creatinine of 0.5 mg/dL. Incidence of first AKI events was calculated for HIV/HCV coinfected versus HCV monoinfected subjects, and multivariable analyses using Cox proportional hazards were performed to identify predictors of AKI. Throughout the study period, 35% HIV/HCV coinfected and 17% HCV monoinfected subjects developed AKI, with incidence of 8. (HR 2.06 [1.15, 3.71]) were independently associated with AKI. HCV genotype, HCV viral load, hazardous drinking, and heroin use were not associated with AKI. Study limitations included potential misclassification bias of HCV-infected individuals as serial HIV antibody testing was not routinely performed after study entry, and inability to adjust for tenofovir use in multivariable analysis. In conclusion, among subjects with HCV infection, decompensated cirrhosis, HIV coinfection, and cocaine use are associated with increased risk of AKI. These findings highlight the importance of preventing and treating cirrhosis, controlling HIV coinfection, and reducing cocaine use in HIV/HCV coinfected persons.

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Section: Discussionsupporting

confidence: 74%

Incidence and Predictors of Acute Kidney Injury in an Urban Cohort of Subjects with HIV and Hepatitis C Virus Coinfection

Garg

Hoenig

Edwards

et al. 2011

AIDS Patient Care and STDs

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“…Cocaine use was reported in 28.5% of 193 dialysis patients (92). A history of cocaine use was associated with a diagnosis of hypertension-related ESRD in 89.1% of cocaine users versus 46.4% of nonusers.…”

Section: Pathophysiologic Basis For Renal Diseasementioning

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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“…64 Exclusion criteria for ESRD subjects include clinical diagnosis of ESRD secondary to other (nonhypertensive) causes, such as diabetic nephropathy, glomerulonephritis, polycystic kidney disease, cocaine, or other intravenous drug abuse. 15 Thus, none of these cases had a renal biopsy. All dialysis patients were interviewed regarding their personal and familial medical histories on a single dialysis treatment day, and each patient's age, gender, height, weight, vital signs, and medication list were recorded.…”

Section: Initial Case/control Population: Californiamentioning

confidence: 95%

“…33 Furthermore, in our study, we excluded individuals with other known or potential ESRD risk factors, such as diabetic nephropathy or illicit drug abuse. 15,28 Admixture Another potential pitfall in genetic studies of blacks is the possibility of differential admixture between cases and controls, 69,70 which may lead to artifact conclusions based on comparisons of genetically dissimilar populations. In this study, we estimated admixture for non-ESRD and ESRD patients groups by comparing genotype frequencies at 23 loci outside the genes of interest.…”

Section: Strengths and Limitations Of This Study Diagnosismentioning

confidence: 99%

“…15 In this association analysis, we evaluated allele and genotype frequencies of single nucleotide polymorphisms (SNPs) individually and in combination, in the form of haplotypes at CHGA; we compared such gene and haplotype frequencies in normotensive and hypertensive black controls (with normal renal function) to those in black patients with ESRD as a result of hypertension (HT-ESRD). In addition, we evaluated the impact of CHGA SNPs on a more proximate or "intermediate" biologic phenotype, 16 expression of the catestatin gene product in plasma.…”

mentioning

confidence: 99%

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Chromogranin A Polymorphisms Are Associated With Hypertensive Renal Disease

Salem

Cadman²,

Chen³

et al. 2008

Journal of the American Society of Nephrology

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Chromogranin A is released together with epinephrine and norepinephrine from catecholaminergic cells. Specific endopeptidases cleave chromogranin A into biologically active peptide fragments, including catestatin, which inhibits catecholamine release. Previous studies have suggested that a deficit in this sympathetic "braking" system might be an early event in the pathogenesis of human hypertension. Whether chromogranin A (CHGA) polymorphisms predict end-organ complications of hypertension, such as end-stage renal disease, is unknown. Among blacks, we studied common genetic variants spanning the CHGA locus in 2 independent case-control studies of hypertensive ESRD. Two haplotypes were significantly more frequent among subjects with hypertensive ESRD: 1) in the promoter (5Ј) region, G-462A3T-415C3C-89A, haplotype ATC (adjusted odds ratio ϭ 2.65; P ϭ 0.037), and 2) at the 3Ј-end, C11825T (3Ј-UTR, Cϩ87T)3G12602C, haplotype TC (adjusted odds ratio ϭ 2.73, P ϭ 0.0196). Circulating levels of catestatin were lower among those with hypertensive ESRD than controls, an unexpected finding given that peptide levels are usually elevated in ESRD because of reduced renal elimination. We found that the 3Ј-UTR ϩ 87T variant decreased reporter gene expression, providing a possible mechanistic explanation for diminished catestatin. In summary, common variants in chromogranin A associate with the risk of hypertensive ESRD in blacks.

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Cocaine use, hypertension, and end-stage renal disease

Cited by 51 publications

References 40 publications

Incidence and Predictors of Acute Kidney Injury in an Urban Cohort of Subjects with HIV and Hepatitis C Virus Coinfection

Incidence and Predictors of Acute Kidney Injury in an Urban Cohort of Subjects with HIV and Hepatitis C Virus Coinfection

Chronic Nephropathies of Cocaine and Heroin Abuse

Chromogranin A Polymorphisms Are Associated With Hypertensive Renal Disease

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