Further Observations of Renal Insufficiency in Snakebite

Sitprija, Visith; Benyajati, C.; Boonpucknavig, Vijitr

doi:10.1159/000180416

Cited by 29 publications

(9 citation statements)

References 6 publications

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“…Acute tubular necrosis (ATN) has not been observed after higher doses of bothropic venoms in experimental models. 6,15,18 In contrast, ATN has been described in humans following snakebite by various species, 4,10,12,[19][20][21][22][23] including Bothrops spp. 3,4,9,11,24 In this study, a dose of 0.4 mg of B. moojeni venom/kg produced ATN and functional abnormalities that peaked 5 hr and 16 hr after envenomation.…”

Section: Discussionmentioning

confidence: 99%

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%

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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“…Segmental necrotizing arteritis of the interlobular arteries has been described in Russell’s viper bite 9,43 . The lesion could have been missed if the renal biopsy was superficial.…”

Section: Renal Pathologymentioning

confidence: 99%

“…The lesion could have been missed if the renal biopsy was superficial. Segmental thrombophlebitis of the arcuate vein and its tributaries has been reported in both Russell’s viper bite and green pit viper bite 9,43 . Deposition of C3 without immunoglobulins in the wall of necrotizing arteries is demonstrable.…”

Section: Renal Pathologymentioning

confidence: 99%

Snakebite nephropathy (Review Article)

2006

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SUMMARY:There is a broad clinical spectrum of renal involvement in snakebite. Besides the local and systemic symptoms, clinical renal manifestations vary from mild proteinuria, haematuria, pigmenturia to acute renal failure. Bites by haemotoxic snakes and myotoxic snakes are the common causes of renal involvement especially acute renal failure. Therefore, renal failure is often associated with haemorrhagic diathesis, intravascular haemolysis and rhabdomyolysis. Renal pathological changes include mesangiolysis, glomerulonephritis, vasculitis, tubular necrosis, interstitial nephritis and cortical necrosis. Tubular necrosis is an important pathological counterpart of acute renal failure. Haemodynamic alterations induced by cytokines and vasoactive mediators leading to renal ischaemia are important in the pathogenesis of acute renal failure. Haemolysis, intravascular coagulation and rhabdomyolysis are important contributing factors. Direct nephrotoxicity can be induced by the venom through metalloproteases and phosphilipase A 2. Immunologic mechanism plays a minor role in the pathogenesis of the renal lesion.

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“…The mechanisms acting within the body to induce AKI during envenomation are uncertain. The pathogenetic mechanisms underlying acute renal failure (ARF) may include renal vascular obstruction by disseminated intravascular coagulation (DIC), ischemia or hypoperfusion due to the fall in blood pressure, and some extent of intravascular hemolysis lead to pigment nephropathy ( Sitprija et al, 1974 ). This manifestation does not exclude the presence of proteolytic enzymes and vasoactive substances, which could promote, or even potentiate, the coagulant process in renal sites.…”

Section: Introductionmentioning

confidence: 99%

The pathophysiological effects of Russell's viper (Daboia siamensis) venom and its fractions in the isolated perfused rabbit kidney model: A potential role for platelet activating factor

et al. 2020

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The pathophysiological effects of Russell's viper venom (RVV) and its fractions, including phospholipase A 2 (RvPLA 2 ), metalloprotease (RvMP), L-amino acid oxidase (RvLAAO), and phosphodiesterase (RvPDE) on renal functions were investigated using the isolated perfused rabbit kidney (IPK) model. Moreover, whether their effects on renal alterations were promoted by platelet activating factor (PAF) was tested using the PAF receptor antagonist, WEB 2086. There was a marked reduction in the perfusion pressure (PP) and renal vascular resistance (RVR) 10 min after RVV administration (1.0 mg/100 ml of perfusate), thereafter both PP and RVR gradually increased and approached the control level within 90 min. These effects were abolished by pretreatment with WEB2086 (2 μg/μl). Administration with RvPLA 2 (280 μg/ml), RvMP (280 μg/ml), or RvLAAO (135 μg/ml) alone increased both the PP and RVR, whereas RvPDE (100 μg/ml) reduced both the PP and RVR. Pretreatment with WEB 2086 completely abolished the effects induced by RvMP, but not the other fractions. The RVV also caused a marked decrease in the glomerular ﬁltration rate (GFR), urinary ﬂow rate (UF), and osmolar clearance (Cosm), and these effects were not inhibited by pretreatment with WEB2086. Each RVV fraction also increased, to varying extents, the GFR, UF, and Cosm, and these effects induced by RvPLA 2 or RvMP, but not the other fractions, were completely blocked by WEB 2086. Changes in percent filtered Na + and K + excreted in the IPK by RVV, RvPDE, and RvMP were abolished by pretreatment with WEB 2086. Histological evaluation proﬁled mainly tubulonephrosis in the treated kidney. These results reveal that the alterations in renal functions induced by RVV and its fractions are due to the synergistic action of the different components of snake venom, instead of the action of a single component. The effects of RVV and its fractions in rabbit IPK are mediated at least in part by PAF.

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Further Observations of Renal Insufficiency in Snakebite

Cited by 29 publications

References 6 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.

Snakebite nephropathy (Review Article)

The pathophysiological effects of Russell's viper (Daboia siamensis) venom and its fractions in the isolated perfused rabbit kidney model: A potential role for platelet activating factor

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