Amyloidosis and infection due to human immunodeficiency virus [letter]

This is a case report of AA amyloidosisassociated with human immunodeficiency virus (HIV). A 32-year old single heterosexual man from Mali was referred to the Department of Nephrology Hopital Bichat Paris France after he was diagnosed with nephrotic syndrome and renal insufficiency. Upon admission his condition was good he was afebrile and his blood pressure was 100/70 mm Hg. However he had lost 6 kg over the past 6 months and presented with a pitting edemaof the lower extremities. He did not belong to any group at risk for HIV. Laboratory results included hemoglobin (10gm/dL) white blood cells (8300/mcL: 50% neutrophils 41% lymphocytes and 5% monocytes) platelets (173000/mcL) erythrocyte sedimentation (90 mm/hour) blood urea nitrogen (36 mg/dL) creatinine (3.2 mg/dL) arterial pH (7.28) and total protein (4.8 gm/dL: .9 gm/dL albumin and 1.75 gm/dL gamma globulin). Serum electrolytelevels (mmol/l) included sodium (134) potassium (3.3) chloride (114) bicarbonate (10) calcium (1.87) and phosphorus (1). Massive proteinuria was present (protein excretion 30 gm/d; 42% albumin and 34% gamma globulin). Polyuriageneralized hyperaminoaciduria high urinary excretions of lysozyme and beta 2 microglobulinand abnormal urinary excretion level of potassium (66mmol/d) and an abnormal urinary pH (6.9) indicated tubular dysfunction in the presence of metabolic acidosisand hypokalemia. The patient had been immunized against hepatitis B virus. Enzyme-linked immunosorbent assay (ELISA) and western blotting were positive for HIV 1 antibodies. Serological syphilis testswere negative. Ultrasonographic examination revealed frankly enlarged hyperechogenic kidneys. Marked mesangial enlargement in diffuse glomerular lesions which was associated with deposits of amorphous eosinophilic acellular material was found in renal tissues. The material was positive upon staining with Congo redand thioflavineT. These deposits were also found in the vascular walls. Scattered inflammatory interstitial infiltrates and large bands of interstitial fibrosis with tubular degeneration were also present. Microcystic tubules were found elsewhere primarily the medulla. Upon immunohistochemical staining the mesangial deposits and the vascular walls reacted strongly with a monoclonal antibody to amyloid protein AA. Immunofluorescence for kappa and lambda chains was negative. Electron microscopy was not performed. No chronic infection or other disorder usually associated with reactive amyloidosiswas found. In view of this it is recommended that the serum concentration of amyloid protein A be monitored in HIV positive patients. Since renal amyloidosismimics HIV associated nephropathydiagnosis must be based on histology.