In a mortal case of ophidism, in an individual 15 years old, bitten by a snake (Bothrops jararaca) on the external face of his right leg and who died 26 days after the accident, the AA. describe the pathologic-anatomical changes met with and the modifications of the metabolism put into evidence through chemical blood examinations. The main changes there existing are located in the kidneys, which present changes of diffused glomerulonephritis and the typic features of symmetrical cortical necrosis. Among the changes of greater significance there are, moreover, observed vascular injuries of great intensity and essentially constituted by a process of productive endoarteritis. The necrosis of the cortex renis, in view of the intensive vascular changes (productive endoarteritis) conveying the obliteration of the arteries, is considered as a direct consequence of such vascular changes. The renal vessels, which are the seat of the inflammatory process, are the interlobar, arciform and interlobular arteries, but mainly the arteriolary ramifications of the cortical layer. The process of endoarteritis always assumes a progressive character so that the vascular lumen, little by little, is getting obstructed. In opposition to what has been observed in the cases, quoted in the literature, of symmetrical necrosis of the cortex, in which the parenchymatous changes are consecutive to thrombosis of the renal vessels, in the present case this appearance was not verified, there being observed only the existence of obliterating productive endoarteritis. The AA. consider the kidney changes in their case as resulting from the slow and prolongated action of the snake venom on the renal structures, on the strength of the following facts already known and agreed to: elimination of snake venom through the kidneys; capability of the same venom of determining diffused glomerulonephritis, and action of snake venom on vascular endothelium, turned essentially easier by the specific function of the organ. The modifications of metabolism were shown by urine and blood changes. Urine was eliminated in very small quantities (50 cc. in 24 hours); yet, absolute anuria was not observed. Hyaline and granular casts, as well as white blood cells and kidney cells along with albuminuria, were present. Hematologic examination revealed 11% of hemoglobin; 960.000 red blood cells per cmm., and 5.200 leukocytes per cmm.; differential blood count revealed increase of neutrophil leukocytes along with 74% of segmentated ones. The rate between serum and clot was 9 x 3 cc. Wassermann's test in blood serum was negative. The chemical blood examinations revealed: Total proteins 7.61 grs per 100 cc.; Albumin 2.39 grs. per 100 cc.; Globulin 5.22 grs. per 100 cc.; Urca 6.42 grs. per 100 cc.; Fibrinogen 0.324 grs. per 100 cc.; Indican +++; Plasmal cl. 339 mgrs. in 100 cc.; Globular cl. 170 mgrs. in 100 cc.; Cholesterol 163 mgrs. in 100 cc.; Creatinin 260 mgrs. in 100 cc.; Inorganic phosph. 13.4 mgrs. in 100 cc.; Calcium 10.3 mgrs. in 100 cc.; Potassium 28 mgrs. in 100 cc.; Sodium 328 mgrs. in 100 cc.. The renal insufficiency in the case studied was shown by humoral modifications, particularly by increased azotemia, by the increase of creatinin, inorganic phosphorus and indican. In opposition to the existence of such modifications, the patient did not present the clinical evidence observed in cases in which azotemia is at a high degree, a fact which reproduces the clinical aspect as described for the symmetrical necrosis of cortex renis.