Objectives: HIV-positive patients are at an increased risk for chronic kidney disease. However, these data mainly derive from cohorts with a high percentage of African-American patients, representing a specific ethnical risk group for chronic kidney disease. The aim of this study was to estimate the prevalence and risk factors specifically for early signs of kidney dysfunction in a large, predominantly white cohort of HIV patients.
Design: Cross-sectional study.
Methods: Prevalence of low-grade proteinuria was measured by quantitative analysis of urinary protein-to-creatinine ratio (cutoff >70 mg/g) and further differentiated by assessing α1-microglobulin (tubular proteinuria) and albumin-to-creatinine ratio (glomerular proteinuria) of HIV patients attending the University Hospital in Cologne, Germany. Together with standard and HIV-related laboratory findings and medical history, risk factors for each form of proteinuria were identified using multivariate forward selection.
Results: Of 945 enrolled patients, 55% were identified with low-grade proteinuria, 41% with tubular proteinuria, and 20% with glomerular proteinuria. Older age was a risk factor for all forms of proteinuria in multivariate analysis. Low-grade proteinuria was also associated with concomitant diabetes and exposure to nucleoside reverse transcriptase inhibitor [anytime during HIV infection, not tenofovir (TDF)-specific], whereas tubular proteinuria was linked to current and any exposure to nucleoside reverse transcriptase inhibitor (TDF-specific). Further risk factors for glomerular proteinuria were hypertension and diabetes in this cohort.
Conclusion: Low-grade, glomerular and tubular proteinuria are highly prevalent in this large white HIV cohort. Older age represents a nonmodifiable risk factor for all forms of proteinuria. Glomerular proteinuria is associated with modifiable cardiovascular, but not HIV-related risk factors, whereas tubular proteinuria is linked to TDF exposure.
aDepartment II of Internal Medicine
bDepartment I of Internal Medicine, University Hospital of Cologne
cInstitute of Medical Statistics, Informatics and Epidemiology, University of Cologne
dGerman Centre for Infection Research (DZIF), Partner Site Bonn-Cologne
eCenter for Molecular Medicine Cologne
fCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD)
gSystems Biology of Ageing Cologne, University of Cologne, Cologne, Germany.
*Dr Sophia Gravemann and Dr Paul T. Brinkkoetter contributed equally to the writing of the article.
Correspondence to Sophia Gravemann, MD, Department I of Internal Medicine, University Hospital of Cologne, Kerpener Str. 62, 50937 Cologne, Germany. Tel: +49 221 478 3324; fax: +49 221 478 88646; e-mail: email@example.com
Received 20 January, 2014
Revised 28 April, 2014
Accepted 29 April, 2014
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