Snakebite-Induced Acute Renal Failure: an Experimental Model

Burdmann, Emmanuel A.; Woronik, Viktoria; Prado, Euthymia B. A.; Abdulkader, Regina C. R. M.; Saldanha, Luiz Balthazar; Barreto, Orlando C. O.; Marcondes, M

doi:10.4269/ajtmh.1993.48.82

Cited by 69 publications

(51 citation statements)

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“…In contrast to the present observations, a decrease in blood pressure and in fractional sodium excretion was reported for rats treated with B. jararaca venom, suggesting indirect renal injury. 6 Burdmann and others 16 observed no significant changes in arterial blood pressure following renal lesions. Acute tubular necrosis (ATN) has not been observed after higher doses of bothropic venoms in experimental models.…”

Section: Discussionmentioning

confidence: 99%

“…15,16 Since B. moojeni venom has a potent coagulant action, 5,37,38 we expected to find fibrin in and around the glomerular capillaries, but did not. Electron microscopic studies are presently being designed to confirm or not these findings and elucidate about ultrastructural changes responsible for glomerular dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…The dose of 0.4 mg/kg was chosen based on an estimate of the volume of venom inoculated in a human snakebite. 16 The venom was dissolved in sterile 0.15 M NaCl immediately before use.…”

Section: Animals and Venommentioning

confidence: 99%

“…4,6,15 Ischemia caused by massive fibrin deposition in the glomerular capillaries as well as intravascular hemolysis appear to have a crucial role in the physiopathology of renal failure. 16 However a direct nephrotoxic action of the venom cannot be excluded.In this work, we studied the pathogenesis of the alterations in renal function and morphology in rats after a single intravenous injection of B. moojeni venom. Experimental protocol.…”

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confidence: 99%

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Histologic and functional renal alterations caused by Bothrops moojeni snake venom in rats.

Bôer¹,

Gontijo²,

Cruz‐Höfling³

1999

The American Journal of Tropical Medicine and Hygiene

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Abstract. Acute renal failure (ARF) is the main cause of death following snake bites by Bothrops species. In this study, we investigated the morphologic and functional renal disturbances caused by Bothrops moojeni venom in rats. Renal function was assessed based on creatinine and lithium clearances and on histologic examination of renal tissue 5 hr after the intravenous administration of 0.2 mg of venom/kg and 5 hr, 16 hr, and 48 hr after 0.4 mg of venom/ kg. A venom dose of 0.4 mg/kg produced renal tubule disturbances, including acute impairment of proximal and post-proximal tubule sodium handling associated with acute tubule necrosis. The glomerular filtration rate (GFR) decreased significantly and was accompanied by severe morphologic disturbances in the renal glomeruli. These functional and morphologic findings were observed in the absence of any change in mean arterial blood pressure. The decrease in GFR was not related to the presence of fibrin deposits in the glomerular capillary loops. These results suggest an early nephrotoxic action of B. moojeni venom involving significant morphologic and functional changes similar to those observed in snakebite-induced ARF in humans. Envenomation following snakebite is a health problem in tropical regions of the world. The genus Bothrops contains many species distributed from Mexico to Argentina. 1 Of the 20,000 snakebite accidents per year in Brazil, about 90% are attributed to the genus Bothrops. 2 Bothrops moojeni is the most common cause of snakebite in central Brazil (Cardoso JLC, unpublished data). In common with other Bothrops venoms, 3-7 B. moojeni venom contains blood-clotting, hemorrhagic, phospholipase A 2 , and proteolytic activities. 8 Envenomation by Bothrops species leads to local and systemic effects that develop simultaneously. The local lesions include edema, pain, erythema, ecchymosis, bullae, cyanosis, necrosis, and cellulitis. The most serious systemic change and primary cause of death is acute renal failure (ARF) secondary to acute tubular necrosis and, occasionally, glomerulonephritis. 3,4,7,[9][10][11][12][13][14] Thus, elucidation of the mechanisms involved in this nephrotoxicity is important. Experimental models used to investigate the pathogenesis of renal lesions caused by bothropic venoms have shown hemodynamic changes and hemolysis prior to renal ischemia. 4,6,15 Ischemia caused by massive fibrin deposition in the glomerular capillaries as well as intravascular hemolysis appear to have a crucial role in the physiopathology of renal failure. 16 However a direct nephrotoxic action of the venom cannot be excluded.In this work, we studied the pathogenesis of the alterations in renal function and morphology in rats after a single intravenous injection of B. moojeni venom. Experimental protocol. One group of rats was injected with venom (V 1 ) and another, which served as the control group, received 0.15 M NaCl solution (S 1 ). The renal function of both groups was evaluated 5 hr (V, n ϭ 7; S, n ϭ 5), 16 hr (V, n ϭ 6; S, n ϭ 4), and 48 hr (V,...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…The dose of 0.4 mg/kg was chosen based on an estimate of the volume of venom inoculated in a human snakebite. 16 The venom was dissolved in sterile 0.15 M NaCl immediately before use.…”

Section: Animals and Venommentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Histologic and functional renal alterations caused by Bothrops moojeni snake venom in rats.

Bôer¹,

Gontijo²,

Cruz‐Höfling³

1999

The American Journal of Tropical Medicine and Hygiene

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“…Acute renal failure has been frequently reported after bites of snakes from the Viperidae family (25). Some investigators (5) have reported three possible mechanisms involved in this phenomenon: hemodynamic Macrophages were inoculated with 10 µg/ml venom in the presence or absence of 15 µM thalidomide or 500 µM pentoxifylline for 2 h at 37ºC.…”

Section: Discussionmentioning

confidence: 99%

Thalidomide and pentoxifylline block the renal effects of supernatants of macrophages activated with Crotalus durissus cascavella venom

Martins

Nobre

Almeida

et al. 2004

Braz J Med Biol Res

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Because thalidomide and pentoxifylline inhibit the synthesis and release of tumor necrosis factor-α (TNF-α), we determined the effect of these drugs on the renal damage induced by supernatants of macrophages activated with Crotalus durissus cascavella venom in order to identify the role of TNF-α in the process. Rat peritoneal macrophages were collected with RPMI medium and stimulated in vitro with C.d. cascavella venom (10 µg/ml) in the absence and presence of thalidomide (15 µM) or pentoxifylline (500 µM) for 1 h and washed and kept in culture for 2 h. Supernatant (1 ml) was tested on an isolated perfused rat kidney (N = 6 for each group). The first 30 min of each experiment were used as control. The supernatant was added to the perfusion system. All experiments lasted 120 min. The toxic effect of the preparation of venom-stimulated macrophages on renal parameters was determined. At 120 min, thalidomide (Thalid) and pentoxifylline (Ptx) inhibited (P < 0.05) the increase in perfusion pressure caused by the venom (control = 114.0 ± 1.3; venom = 137.1 ± 1.5; Thalid = 121.0 ± 2.5; Ptx = 121.4 ± 4.0 mmHg), renal vascular resistance (control = 4.5 ± 0.2; venom = 7.3 ± 0.6; Thalid = 4.5 ± 0.9; Ptx = 4.8 ± 0.6 mmHg/ml g -1 min -1 ), urinary flow (control = 0.23 ± 0.001; venom = 0.44 ± 0.01; Thalid = 0.22 ± 0.007; Ptx = 0.21 ± 0.009 ml g -1 min -1 ), glomerular filtration rate (control = 0.72 ± 0.06; venom = 1.91 ± 0.11; Thalid = 0.75 ± 0.04; Ptx = 0.77 ± 0.05 ml g -1 min -1 ) and the decrease in percent tubular sodium transport (control = 77.0 ± 0.9; venom = 73.9 ± 0.66; Thalid = 76.6 ± 1.1; Ptx = 81.8 ± 2.0%), percent tubular chloride transport (control = 77.1 ± 1.2; venom = 71.4 ± 1.1; Thalid = 77.6 ± 1.7; Ptx = 76.8 ± 1.2%), and percent tubular potassium transport (control = 72.7 ± 1.1; venom = 63.0 ± 1.1; Thalid = 72.6 ± 1.0; Ptx = 74.8 ± 1.0%), 30 min before and during the stimulation of macrophages with C.d. cascavella venom. These data suggest the participation of TNF-α in the renal effects induced by supernatant of macrophages activated with C.d. cascavella venom.

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Impairment of the Cell-to-Matrix Adhesion and Cytotoxicity Induced by Bothrops moojeni Snake Venom in Cultured Renal Tubular Epithelia

Collares-Buzato

Sueur

Cruz‐Höfling

2002

Toxicology and Applied Pharmacology

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Snakebite-Induced Acute Renal Failure: an Experimental Model

Cited by 69 publications

References 0 publications

Histologic and functional renal alterations caused by Bothrops moojeni snake venom in rats.

Histologic and functional renal alterations caused by Bothrops moojeni snake venom in rats.

Thalidomide and pentoxifylline block the renal effects of supernatants of macrophages activated with Crotalus durissus cascavella venom

Impairment of the Cell-to-Matrix Adhesion and Cytotoxicity Induced by Bothrops moojeni Snake Venom in Cultured Renal Tubular Epithelia

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