THESIS: M. A. Reis submitted this thesis for the degree of Doctor of Philosophy publicly examined at the Department of Pathology, School of Medicine of Ribeirão Preto of the University of São Paulo, Ribeirão Preto, SP, Brazil in 1995.
Advisor: Professor Roberto Silva Costa
Co-advisor: Terezila Machado Coimbra
ABSTRACT. Reports of human envenomations caused by bee or wasp stings have shown that among the systematic changes acute renal failure (ARF), usually due to acute tubular necrosis (ATN), is a frequent complication. Pathogenetic mechanisms of ATN that occur in these envenomations are not well known yet. We used 38 female Wistar rats weighing 150 to 200 g in the present work. They received intravenous Africanized bee venom, in a dose of 0.4µl/100g of body weight, which corresponds to half of the average lethal dose (LD50). The following functional and morphological studies were conducted: light microscopy, immunohistochemistry and electron microscopy. The animals were divided into two groups: a) the Early group, with studies being conducted 3 to 8 hours after inoculation; b) the Late group , with studies being conducted 24 to 30 hours after inoculation. 1) The animals showed ARF characterized by a reduction of glomerular filtration rate, with increased levels of plasma creatinine. They also showed an increase of fractional excretion of sodium and potassium, which suggested changes on the proximal portion of the nephron. There was also a reduction of water transport through the collecting tubules. This promoted hydric diuresis, pointing to functional changes in the distal portion of the nephron. The functional tests were more enhanced in the Early group, recovering after 24 hours. Albuminuria was also observed in this group. 2) Morphological study at light microscopy showed acute tubular necrosis, with isolated necrosis in cells or small groups and cast formation. Frequent mitoses were found in the tubular epithelium. Immunohistochemical studies revealed the presence of myoglobin and muscular actin in tubular casts, suggesting that those substances participate in tubular cell aggregation. 3) Changes mainly in segments of proximal tubules and thick ascending limb of Henles group could be observed at electron microscopy. These changes were characterized by hydropic degeneration with attenuation of the brush border and the basolateral infolding. 4) The resulting ARF was due to ATN, which is likely to have multiple causes, mainly hemodynamic changes secondary to cardiotoxicity and systemic vasodilation caused by the venom, myoglobinuria and the direct action of the venom on tubular cells.
CORRESPONDENCE TO:
M. A. REIS - Disciplina de Patologia Geral, Faculdade de Medicina do Triângulo Mineiro, FMTM, Praça Manoel Terra, s/nº, CEP 38015-050, Uberaba, MG, Brasil.
Publication Dates
-
Publication in this collection
08 Jan 1999 -
Date of issue
1996
