A quarter of HIV-infected patients receiving HAART had subclinical tubular damage, which was associated with a near-term decline in eGFR and higher incidence of proteinuria. Periodic monitoring of urinary biomarkers might facilitate the early identification of HAART patients predisposed to significant kidney disease.
Background: Kidney disease has become an important cause of morbidity and mortality in HIV-infected patients in Western countries. Japan is a country with an increasing number of newly infected HIV patients. However, only a few studies have investigated kidney disease in Asian populations infected with HIV. Methods: We studied the prevalence of kidney disease by reviewing the clinical data of 732 HIV-infected Japanese patients. Risk factors for proteinuria, albuminuria, and renal dysfunction were determined using multivariate logistic regression analysis. Results: Microalbuminuria, macroalbuminuria and proteinuria were present in 13.2, 4.55 and 9.52% of patients, respectively. The prevalence of chronic kidney disease of any stage and CKD ≧ stage 3 was 15.4 and 9.70%, respectively. Multivariate analysis showed significant associations between increasing levels of serum creatinine and cholesterol, and the coexistence of diabetes, hypertension and hepatitis C coinfection with either proteinuria or albuminuria, which was significantly related to the presence of renal dysfunction. Lower CD4 cell count was associated with the presence of renal dysfunction, but higher HIV-RNA level was not. Conclusions: Our study has shown the international dimension of the burden of kidney disease in HIV-infected patients. Either proteinuria or albuminuria is likely the most significant factor for renal dysfunction in these patients.
Atazanavir is commonly used as one of the key drugs in combination antiretroviral therapy for human immunodeficiency virus (HIV). However, atazanavir has the potential to yield its crystalline precipitation in urine and renal interstitial tissues, leading to crystalluria, urolithiasis, acute kidney injury (AKI) or chronic kidney disease (CKD). In epidemiological studies, atazanavir/ritonavir alone or in combination with tenofovir has been associated with increased risk of progression to CKD. However, renal biopsies were not provided in these studies. Case reports showing an association between atazanavir use and tubulointerstitial nephritis among HIV-infected individuals provide clues as to the potential causes of atazanavir nephrotoxicity. We now review atazanavir-related kidney disease including urolithiasis, renal dysfunction and interstitial nephritis and illustrate the review with a further case of atazanavir-associated kidney injury with sequential renal biopsies. There are two forms of atazanavir-associated tubulointerstitial nephritis: acute tubulointerstitial nephritis that may develop AKI rapidly (in weeks) after initiation of atazanavir, and chronic tubulointerstitial nephritis that may develop progressive CKD slowly (in years) with granuloma and intrarenal precipitation of atazanavir crystals as well as crystalluria. Caution should be exercised when prescribing atazanavir to patients at high risk of CKD, and therapy should be reevaluated if renal function deteriorates, especially associated with crystalluria and hematuria.
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