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Discussion on a Case of HIV Associated Nephropathy

Introduction

HIV-associated nephropathy (HIVAN) is one of the leading causes of end-stage renal disease (ESRD) among HIV-infected patients. HIVAN is characterized by heavy proteinuria and impairment of renal function, this is seen in my patient who had proteinuria of +++ and subsequently developed acute on chronic kidney disease. HIVAN could be an early and first manifestation of HIV infection in an otherwise asymptomatic patient. This is classical in my patient who had never had any symptoms of HIV prior to time of presenting with symptoms of Nephrotic syndrome. The term HIVAN is reserved for the characteristic light microscopic pattern of focal segmental glomerulosclerosis (FSGS) with collapsing feature and related mesangiopathies [1].

 

Aetiology

The mechanisms of renal cell injury are still being defined. Human immunodeficiency Virus (HIV) infection is associated with protein manifestations, with the kidney being a common target.   Viral DNA has been demonstrated in the renal epithelia of HIV-infected patients with or without nephropathy, suggesting that pathogenic factors, other than the infection of cells, are required for the induction of disease [1,2]. The development of HIVAN is not associated with any particular mode of transmission. In my patient, both parents tested negative. The only suspected mode of transmission was through sharing of clippers at barbers’ salon.

 

Epidemiology

HIVAN is the most common form of chronic kidney disease resulting directly from HIV infection As seen in my patient, proteinuria serves as its first sign. The true prevalence of HIVAN in Africa is unknown, largely due to lack of surveillance and reporting of kidney disease in HIV positive patients. This is particularly so in children since in many paediatric centres, renal biopsies are not performed regularly in HIV–infected patients even with persistent proteinuria. In the USA, Strauss et al and others reported a prevalence of childhood HIVAN of approximately 10-15% with over 95% being African American children. There is strong predilection for HIVAN among male black HIV-infected patients. The black:white ratio among patients with HIVAN is 12:1.4. Blacks are also more likely to have more severe clinical renal disease with heavier proteinuria and higher incidence of nephrotic syndrome and associated renal insufficiency [1]. Studies in Southern and Western Nigeria have reported the prevalence of proteinuria among HIV-infected children to be 18.8% and 20.5% respectively [2] especially children between age 1 and 5. This is in correlation with my patient who is 5 ½ year old who had being having complains of scrotal and peri-orbital swelling for months before presenting.

 

Diagnosis

Although the definitive diagnosis of HIVAN requires a histological examination of renal tissues, clinical criteria can strongly suggest HIVAN in children, persistent proteinuria with renal ultrasound changes can be used as the basis for diagnosis. In my patient, a black male child, a persistent Nephritic- Nephrotic picture with HIV Rapid Diagnostic Tested positive on 3 occasions. Abdominal USS showed Grade 2 renal parenchymal disease: Both kidneys are normal in position and outline. They are enlarged measuring:   

                                                 Right kidney = 9.9 x 4.2cm

                                                 Left kidney   = 10.4 x 4.7cm

Both kidneys showed increased parenchymal echogenicity more than the liver and spleen with preservation of their cortico-medullary differentiation. No pelvicalyceal or ureteric dilatation seen. A renal biopsy was done, the tubules appeared unremarkable. There was mild infiltration of the interstitium by chronic inflammatory cells comprising mainly lymphocytes. The vessels seen were thin walled and congested. Biopsy was inadequate for interpretation of glomerular pathology due to absence of glomeruli. There is no consistent correlation between the stage of HIV and the development of HIVAN with regards to CD4 count and viral load[1]. In my patient CD4 count of 636 (23.59%) and Viral load of 149,726 copies/ml was detected.

 

Treatment / prognosis

HIVAN progresses to end-stage renal disease (ESRD) at a rapid rate, varying from weeks to months. A fulminant course is seen in children compared with adults. Highly active anti-retroviral therapy (HAART) a combination of two nucleoside reverse transcriptase inhibitors (Lamivudine and Zidovudine) and one nonnucleoside reverse transcriptase inhibitor (Nevirapine) is used. Other therapeutic measures include use of angiotensin converting enzyme (ACE) inhibitors and steroids in patients with ESRD. [2]. In my patient, abacavir (ABC), lamivudine (3TC)and Efavirenz (EFV) was used with anti TB drugs (Isoniazide, Rifampicin, Ethambutol and pyrazinamide) due to opportunistic TB infection.

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