RESEARCH ARTICLE


Human Immunodeficiency Virus-Associated Nephropathy (HIVAN) in Indian Children



Prabha Senguttuvan*, Gowtham S, Soundararajan P
Department of Nephrology, Sri Ramachandra Medical University, Chennai, India


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© Senguttuvan et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Department of Nephrology, Sri Ramachandra Medical University, Chennai, India; E-mail: prabha_sen@hotmail.com


Abstract

Human immunodeficiency virus-associated nephropathy (HIVAN) in children has not been reported in India. In a single centre study, we analyzed 8 children diagnosed with HIVAN from 2007 to 2010. There were 6 boys and 2 girls with a male to female ratio of 3:1. Their ages ranged between 5 yrs to 11 yrs with a peak age of 8 years. The routes of HIV transmission were vertical in 5, blood transfusion in 2 and unknown in one. The presentation included generalized edema 100%, hypertension 2/8 (25%) and macroscopic hematuria 1/8 (12.5%). On evaluation by urine dipstick, all children had proteinuria and urine PCR showed nephrotic proteinuria (>3). 5/8 (62.5%) had extra renal involvement: 2 children had hepatosplenomegaly and 3/8 (37.5%) children had pulmonary tuberculosis and were on highly active antiretroviral therapy (HAART) and antituberculous treatment (ATT). Renal disease was the presenting problem in 4/8 (50%) and the remaining 4 (50%) were referred from the HIV clinic. The duration of HIV infection to the development of HIVAN was unknown in 4/8 (50%) nephrotic patients but in those referred from HIV clinic, it ranged between 5 months to 2 yrs. CD4 count ranged from 700 to 2465/mm3. All the children had enlarged kidneys bilaterally, except for one child who had normal sized kidneys with increased echogenicity and loss of corticomedullary distinction. He was not biopsied and he progressed to renal failure. Renal biopsy in other 7 children showed FSGS in 4 (57%) and collapsing FSGS in 2 (28.5%), and early segmental sclerosis with IgA deposits in one child (14.2%). 7/8 who had nephrotic proteinuria were initiated on steroids.

Keywords: Collapsing glomerulopathy, human immunodeficiency virus-associated nephropathy, Indian children, nephrotic syndrome..