Abstract. Although the nephropathy of visceral leishmaniasis (VL) is known both in humans and dogs, histopathologic alterations have not been thoroughly studied. We examined renal alterations in 55 dogs with naturally acquired VL compared with five noninfected dogs from an endemic area in northeastern Brazil. Glomerulonephritis was found in 55 dogs, interstitial alterations in 53 dogs, and tubular changes in 43 dogs with VL. The glomerular alterations found were minor glomerular abnormalities (n ϭ 8, 14.5%), focal segmental glomerulosclerosis (n ϭ 10, 18.2%), mesangial proliferative glomerulonephritis (n ϭ 17, 32.7%), membranoproliferative glomerulonephritis ,(n ϭ 18, 30.9%), crescentic glomerulonephritis (n ϭ 1, 1.8%), and chronic glomerulonephritis (n ϭ 1, 1.8%). Morphometric and ultrastructural studies complemented the analysis. The five control animals exhibited no glomerular alterations. The glomerular lesions were related to functional alterations. Considering that the alterations of canine and human nephropathy in VL are very similar, the data obtained in this study constitute an important contribution to the understanding of canine and human VL nephropathy.Key words: Dogs; glomerulonephritis; morphometry; renal pathology; ultrastructure; visceral leishmaniasis.Canine visceral leishmaniasis (VL) is a highly prevalent infection encountered throughout the world. In Brazil, VL results from infection by the protozoan Leishmania (Leishmania) chagasi, which occurs in 18 of 27 Brazilian states. 20,22,26 VL is endemic to northeastern Brazil, and in Teresina, in the State of Piaui, some 1,600 dogs presenting naturally acquired VL were known when this study was initiated. At present, VL is also spreading to other urban areas in the southern and southeast regions, where the disease was not previously endemic. 31 In the infectious cycle of VL, the dog is the most important domestic reservoir and exhibits chronic evolution of the disease. 1,8,21 Leishmania is an obligatory intracellular parasite of mononuclear phagocytes. During infection, various host organs are affected including the kidney. Although VL-related nephropathy is known both in humans and dogs, the histopathologic patterns of the lesions present in VL have not been clearly established because most studies are based on very few cases and mainly because well-defined, lesion classification criteria were not used. 3,4,9,10,24,37,38 In human VL, glomerulosclerosis, mesangial cell proliferation, and interstitial nephritis have been reported. 3,9,10,16,18,38 Renal involvement in canine VL is also frequent, and the renal changes are similar to those seen in humans. 2,5,8,23,32 This similarity renders the study of canine VL nephropathy of interest with regard to human pathology. The renal lesion itself does not lead to renal insufficiency. However, when moderate or severe renal lesions are present, VL patients with systemic complications such as secondary infections, sepsis, and hypotension do develop renal insufficiency. 16 Furthermore, glomerular lesions appare...

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Schwann cell disturbance followed by segmental demyelination in the peripheral nervous system occurs in diabetic patients. Since Schwann cell and oligodendrocyte remyelination in the central nervous system is a well-known event in the ethidium bromide (EB) demyelinating model, the aim of this investigation was to determine the behavior of both cell types after local EB injection into the brainstem of streptozotocin diabetic rats. Adult male Wistar rats received a single intravenous injection of streptozotocin (50 mg/kg) and were submitted 10 days later to a single injection of 10 µL 0.1% (w/v) EB or 0.9% saline solution into the cisterna pontis. Ten microliters of 0.1% EB was also injected into non-diabetic rats. The animals were anesthetized and perfused through the heart 7 to 31 days after EB or saline injection and brainstem sections were collected and processed for light and transmission electron microscopy. The final balance of myelin repair in diabetic and non-diabetic rats at 31 days was compared using a semiquantitative method. Diabetic rats presented delayed macrophage activity and lesser remyelination compared to non-diabetic rats. Although oligodendrocytes were the major remyelinating cells in the brainstem, Schwann cells invaded EB-induced lesions, first appearing at 11 days in non-diabetic rats and by 15 days in diabetic rats. Results indicate that short-term streptozotocin-induced diabetes hindered both oligodendrocyte and Schwann cell remyelination (mean remyelination scores of 2.57 ± 0.77 for oligodendrocytes and 0.67 ± 0.5 for Schwann cells) compared to non-diabetic rats (3.27 ± 0.85 and 1.38 ± 0.81, respectively).

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RESUMO -Linfócitos estão presentes nas lesões desmielinizantes induzidas pelo brometo de etídio (BE) no sistema nervoso central (SNC) e a possibilidade de sua participação em eventuais respostas imunomediadas às bainhas de mielina desprendidas não pode ser descartada. Este estudo objetivou investigar as conseqüências da imunossupressão com dexametasona no reparo do SNC após injeção local de BE. Ratos Wistar adultos receberam 10 microlitros de solução de BE a 0,1% na cisterna pontis. Alguns destes foram tratados intraperitonealmente com dexametasona (3 mg/kg/dia, grupo I, n=15) durante o período experimental; outros não foram imunossuprimidos (grupo II, n=15). Animais de ambos os grupos foram perfundidos com solução fixadora de glutaraldeído a 4% aos 7,11,15,21 e 31 dias pós-injeção de BE. Fragmentos do tronco encefálico foram colhidos e processados para estudos de microscopia eletrônica de transmissão. Os ratos do grupo I apresentaram maiores quantidades de membranas derivadas de mielina que os não-imunossuprimidos (grupo II), sugerindo um atraso na atividade macrofágica de retirada dos restos mielínicos. Raros linfócitos foram encontrados. A atividade remielinizante oligodendroglial também mostrou um padrão retardado, com claro predomínio de axônios desmielinizados. PALAVRAS-CHAVE: brometo de etídio, dexametasona, imunossupressão, ratos, remielinização, sistema nervoso central.Ultrastructural study of the remyelinating process following local ethidium bromide injection in the brainstem of dexamethasone-immunosuppressed rats ABSTRACT -Lymphocytes are present within ethidium-bromide (EB)-demyelinated lesions in the central nervous system (CNS) and the possibility of its participation in accidental immune-mediated responses to the detached myelin sheaths can not be ruled out. This study aimed to investigate the consequences of immunosuppression with dexamethasone in CNS repair after local EB injection. Adult Wistar rats received 10 microlitres of 0.1% EB solution into the cisterna pontis. Some were treated intraperitoneally with dexamethasone (3 mg/kg/day, group I, n=15) during the experimental period; others were not immunosuppressed (group II, n=15). Animals from both groups were perfused with 4% glutharaldehyde at 7,11,15,21 and 31 days following EB injection. Brainstem slices were collected and processed for transmission electron microscopy studies. Rats from group I showed greater amounts of myelin-derived membranes than nonimmunosuppressed rats (group II), suggesting a delay in the macrophagic activity of removing myelin debris. Rare lymphocytes were found. Oligodendrocyte remyelinating activity also showed a delayed pattern, with clear predominance of naked axons.KEY WORDS: ethidium bromide, dexamethasone, immunosuppression, rats, remyelination, central nervous system. Acredita-se que a falta de remielinização completa em algumas doenças desmielinizantes do sistema nervoso central (SNC) possa ocorrer devido à presença de fatores inibidores que evitam a expressão plena do reparo mielínico ou pela ausência de...