Renal Impairement in HIV Patients

About author
IGBOH*, N. M, NNAMAH, N.K, ONWUBIKO, D.,CHIGBU, L.N., AGOMUO,E.N., IHEANACHO,K,M.E. ONYESOM,C.A, MADUAGWUN,C.A, EMUCHEY,C.I.
College of Medicine and Health Sciences, Abia State University Uturu. Nigeria.
Department of chemical pathology, College of Medicine and Health Sciences, Nnamdi Azikwe University Teaching Hospital, Nnewi. Nigeria.
Department of Biochemistry, Faculty of Sciences. Imo State University, Owerri, Nigeria.
Department of Medical Biochemistry Delta State University, Abraka, Nigeria.
Department of Pharmacology, College of Medicine and Health Sciences, Abia State University Uturu. Nigeria
Department of Biochemistry, Faculty of Sciences. Federal University of Technology Owerri, Nigeria.
E-mail: [email protected]

Abstract
Renal impairment in HIV patients on drugs and those not on antiretroviral drugs was assessed using biochemical markers such as Uric acid, Urea, Creatinine and Phosphate. A total of one hundred individuals were used for the study and they were within the age of 35±7.1 years consisting of 50 HIV positive individuals on antiretroviral therapy, 30 HIV positive individuals not on antiretroviral therapy and 20 HIV sero negative individuals (control) all within Aba Metropolitan. HIV patients were on antiretroviral drugs (triviro-LNS-Lamivudine, Nevirapine and Starvudine) 1-2 pills daily depending on the CD4 count.  Moreso, have been on the drug for the duration of 2- 3 years. The investigations were done with serum. The biochemical parameters were assayed using fortress diagnostic kit based on calorimetric method. The results were subjected to statistical analysis. The results of the study revealed that there was a significant increase in   the serum levels of Uric Acid and Urea in HIV positive individuals not on drugs compared to HIV sero negative subjects( Uric acid level control (mg/dL). 5.61 ± 2. 31 vs 7.16 ± 2.42, Urea -control (Mmol/L)   4.7 ±1.58 vs   7.82. ±3.8 (P<0.05 ).Inaddition, there was remarkable decrease in   Phosphate  levels in HIV patients not on drugs compared to control and HIV infected subjects on antiretroviral drugs (phosphate level Mmol/L Control 1.07± 0.27 vs 0.79 ± 0.19). Equally indicated was that HIV positive subjects  not on drugs   exhibited slight increase in  Creatinine levels compared to the other two groups (control mg/L; 0.90 ± 0.50vs 1.90 ± 1.20P<0.05). The use of antiretroviral drugs is helping in alleviating the HIV associated metabolic abnormalities. This not withstanding, attention needs to be paid to hyperuricaemia which is common with patients on antiretroviral drugs. Prevention of hypophosphataemia is also vital.
Key words:  Uric acid, Urea, Phosphate, Bicarbonate, HIV, AIDS
Introduction
HIV/AIDS is a major health problem in many parts of the world, and is considered a pandemic.  Incidentally, Nigeria is not left out. As of 2010, approximately 34 million people have HIV globally, of these, approximately 16.8 million are women and 3.4 million are less than 15 years old. HIV/AIDS resulted in about 1.8 million deaths in 2010, down from 3.1 million in 2001. Unfortunately, approximately 220,000 people died from AIDS in Nigeria in 2009. More awareness concerning this deadly disease is still necessary, moreso when, 80-95 percent of HIV infections in Nigeria are as a result of heterosexual sex and some youths till this moment do not believe in its existence. The advent of highly active antiretroviral therapy in conjunction with improved standard antiviral and antibiotic regimens has dramatically changed the clinical course of HIV infection, resulting in prolonged survival  Hyperuricemia has been associated with HIV disease progression especially those with low CD4⁺ and co-infection with either hepatitis B or C virus. But when considering the potentials pathophysiological mechanism of the frequent occurrence of Hyperuricemia in HIV infected patients, it was suggested that it may result from multiple metabolic, immunologic and pathological abnormalities which characterized the disease progression from asymptomic infection to terminal illness. Infact, abnormal serum  urate levels have been observed  in a broad spectrum of pathologic situations often complicating the course of HIV disease such as prolong fever due to infections, neoplastic or autoimmune disorders, hypercatabolic states associated with fasting or cathexia, viremia and possibly HIV related loss of mononuclear cells. Hypouricemia has also be attributed to increased renotubular loss , 1990).Aside from HIV infection itself, serum urate levels could potentially be altered by antiretroviral drugs. However the use of Didanosine and Stavudine or the combination of the two drugs was associated with hyperuricemia . Respiratory chain failure causes ATP depletion which increases urate production in the purine nucleotide cycle. Mitochondrial dysfunction may increase the formation of lactate which competes with urate for tubular excretion in the kidney. This mechanism is the basis for the hyperuricemia and other metabolic myopathies. And, may also provide an explanation, for the association between dideoxynucleoside analogues (Stavudine and Didanosine) and elevated urate. Therefore hyperuricemia is multi factorial origin in HIV patients. More recently, tubular disorders have been related to ARV drug toxicity. Acyclic nucleotide reverse transcriptase inhibitor and more particularly tenofovir despoil fumarate (TDF) has been involved in tubulopathy leading to Fanconi or Fanconi-like syndrome with or without acute renal failure .An impairment of renal proximal tubular function is characterized by decreased  tubular handling of phosphate leading to  hypophosphatemia and their relation  to tubular reabsorption  disorder in tenofovir treated patients remain uncertain. In this study, we aimed at determining the Serum levels of Uric acid, urea, creatinine and Phosphate in HIV positive individuals and those on Antiretroviral Drugs to enable us assess possible variation in biochemical parameters among the groups studied.