Acute renal failure in leishmaniasis.

Letters Acute renal failure in leishmaniasis Sir, Visceral leishmaniasis (VL) has become a frequent complication of AIDS [1]. When Leishmania and HIV interact, a new broad spectrum of leishmaniasis occurs. Leishmanias can spread to unexpected sites other than the reticulo-endothelial system, such as peripheral blood, normal skin, gastrointes-tinal tract and respiratory tract [2]. Acute renal failure (ARF) has rarely been reported [3]. A 28-year-old Nigerian woman, who had been in Italy for 8 months, attended the hospital because of epistaxis, confusion and anuria. Her temperature was 36.3 C, O 2 saturation 98%, blood pressure 120/70 mmHg and cardiac pulse 125/min. Her physical examination was unremarkable, except for abdominal tenderness. pneumoniae IgG and IgM titres, parvovirus IgM and blood cultures were negative. Parvovirus IgG titre was positive 1/256. The patient received nasal packing and blood transfusions, and dialysis was initiated. She died 2 days later, with unremitting epistaxis. Post-mortem examination showed diffuse alveolar haemorrhage, splenomegaly, lomboaortic lymphoadenopathy and haemorrhagic necrosis of naso-pharynx. Light microscopy examination evidenced striking diffusion of Leishmanias in phagocytic cells and extracellular presence in vascular lumina and connective tissues (kidney, liver, nasopharynx, lung, skin, uterus, ovary, lymph nodes, bone marrow, heart and spleen). Renal changes consisted of the following. (i) Glomerular lesions: as segmental collapse of capillary loops, congestion of capillaries filled by Leishmanias (Figure 1), capsular synechiae, focal and segmental areas of glomerular sclerosis, focal thickening of basement membranes , parasite invasion of mesangial axes (cells and matrix) and focal mesangial and epithelial cell hyperplasia with initial crescent formation. Immunohystochemical examination was negative for immunoglobulins and light chains. (ii) Tubulo-interstitial damage: as acute necrotizing tubulitis, tubular necrosis and hyaline casts, focal infiltration of CD68þ and CD3þ cells, and Leishmanias inside of histiocytes in peritubular areas. (iii) Blood vessel changes as focal leukocytoclastic vasculitis of vasa recta and free Leishmanias in the capillary lumina. Acute glomerulonephritis (GN) [4], proliferative GN [5], collapsing focal segmental glomerulosclerosis [6], acute interstitial nephritis [5] and tubular cell necrosis and tubulitis [7] have all been described in patients with Leishmaniasis. ARF [3], nephrotic syndrome [4] and proteinuria [5] have been reported. The renal damage in our patient was mediated through different mechanisms. Tubular necrosis was secondary to ischaemia, due to small vessel obliteration by Leishmanias, and to haemolysis. Necrotizing tubulitis was due to direct invasion by the parasites and by inflammatory reaction. There was a diffuse invasion of renal structures by Leishmanias. Glomerular …