To the editor: Collapsing focal glomerulonephritis (CFG) is found in 2-10% of all HIV-infected patients.1 It is the most common form of renal disease in HIV patients, appearing in over 60% of the renal biopsies made.2 The presence of proteinuria and/or impaired renal function are associated with increased patient morbidity-mortality.3 The management of nephropathy associated to HIV infection (NAHIV) has not been established, and most patients require renal replacement treatment a few months after the appearance of nephrotic syndrome.4



A 41-year-old black male with type 1 HIV infection not subjected to antiretroviral therapy was admitted with generalized edema and proteinuria in the nephrotic range. Upon admission, the blood pressure was 140/90 mmHg,

and edema with fovea was seen to ankle level. The laboratory tests showed normocytic and normochromic anemia with an erythrocyte sedimentation rate of 157 mm in the first hour, normal kidney function (plasma creatinine 1.1 mg/dl and plasma clearance calculated by the MDRD equation 78.41 ml/min), proteinuria 5.83 g/day without Bence-Jones proteinuria, plasma albumin 1.6 g /dl with polyclonal band in gamma region 7.7 g/dl (IgG 9860 mg/dl, IgA 151 mg/dl, IgM 643 mg/dl), and a CD4+ count of 314 cells/mm3. HBV, HCV and herpes group serology proved negative. A myelogram revealed reactive plasmacytosis, while a bone cylinder specimen showed intense polyclonal

lymphoplasmacytosis. Renal ultrasound showed symmetrical kidney enlargement, with preserved corticomedullary

differentiation but with a diffuse increase in echogenicity. The Doppler study proved normal. The kidney biopsy revealed collapsing glomerulopathy with preserved tubules and an interstitial lymphocytic and polyclonal infiltrate. Antiretroviral treatment was started with efavirenz, stavudine and lamivudine, together with furosemide and enalapril. At discharge the blood pressure was 130/80, with proteinuria 300 mg/day. The patient posteriorly returned to his country of origin and reappeared 14 months later, without any reported opportunistic processes or nephrotic manifestations. While in his country, the patient continued treatment with enalapril and started nevirapine, zidovudine as lamivudine as antiretroviral therapy. The patient was found to have normal blood pressure, with no edemas, and showed normocytic and normochromic anemia, with normal kidney function (plasma creatinine 0.98 ml/dl), proteinuria 3 g/day and plasma albumin 2.6 g/dl. The CD4+ count was 350 cells/mm3.



Collapsing focal glomerulonephritis (CFG) is found in 2-10% of all HIV-infected patients,1 and is the most common form of kidney involvement in black HIV-infected individuals.2,6,7 CFG is characterized by glomerular collapse and severe tubulointerstitial alterations. The underlying pathogenesis appears to be related to viral infection ¿ HIV infection being the most common example. NAHIV is characterized by proteinuria in the nephrotic range, with rapid deterioration of renal function. In this context, proteinuria and increased plasma creatinine are regarded as indicative of a poor prognosis.3 At present there is no effective treatment for NAHIV, and most patients require renal replacement therapy on a chronic basis.4 Some studies suggest that treatment with antiproteinuric agents and highly active antiretroviral therapy (HAART) can delay the progression of renal failure8 and even reduce the incidence of NAHIV5 ¿ emphasis being placed on the importance of an early biopsy in these patients.5 In our case it can be affirmed that combined HAART and angiotensin-converting enzyme inhibitor (ACEI) treatment avoided the

deterioration of renal function, reducing proteinuria and resolving the nephrotic syndrome, in a black patient with NAHIV.