Acute effect of Russell’s viper (Daboia siamensis) venom on renal tubular handling of sodium in isolated rabbit kidney

Abstract

Background:The common complication in cases of poisoning by Russell's viper (Daboia siamensis) venom (RVV) is acute renal failure, but the pathogenesis involved in the alteration of kidney function is still not well understood. Objective: To clarify the role of RVV in the pathogenesis of renal damage, the present study examines the functional short-term alterations acutely induced by RVV in isolated perfused rabbit kidney. Methods: Effects of RVV on renal tubular handling of sodium including mean perfusion pressure (PP), the renal vascular resistance (RVR), the glomerular filtration rate (GFR), the urinary flow (V) and osmolar clearance (Cosm) were studied in two groups of isolated perfused rabbit kidneys; each group had four isolated rabbit kidneys. RVV was added to the perfusion system to obtain the final concentration of 10 g/ml. Results: Immediate decreases in PP and RVR caused by the venom were significantly apparent (p < 0.05) in the first 15 min after RVV administration. A gradual rise in both PP and RVR occurred 15 min after the initial reduction of the first phase, but its remained below pretreatment values. The GFR, V, and Cosm decreased significantly throughout experiments after venom perfusion (p < 0.05). The total fractional sodium excretion increased significantly after venom perfusion throughout experiments, while significant reductions (p < 0.05) of renal tubular handling of sodium were apparent for proximal absolute reabsorption of sodium and proximal fractional reabsorption of sodium including marked reductions of distal absolute reabsorption of sodium and distal fractional reabsorption of sodium of the venom treated kidney. Optical microscopy of treated kidney tissue showed acute tubular necrosis at the end of experiment. Conclusion: The present study suggests that an administration of RVV in the isolated rabbit kidney causes direct acute nephrotoxicity and acute alterations of main functional parameters that are probably mediated by either the direct action of venom components or an indirect effect from vasoactive mediators released from renal cells of the RVV-treated kidney.

Non-neurotoxic activity of Malayan krait (Bungarus candidus) venom from Thailand

“…In the kidneys, the presence of hyaline cast was seen in renal tubules after 3 h venom administration. Similar renal morphologic changes have also been found in tissues exposed to the venoms of some Russell’s vipers, Micrurus species and other terrestrial elapids [ 25 , 30 – 32 ].…”

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

“…Preparation of the rabbit IPK was based on the previously described method ( Chaiyabutr et al, 2014 ). Briefly, adult male white New Zealand rabbits were fasted 24 h before the experiment with access to water ad libitum.…”

“…RVV group: The rabbit IPK was treated with 1 ml of the lyophilized RVV in normal saline (1 mg/ml), added into 100 ml of perfusate of the recirculating system after the 30-min equilibration period as an internal control. This dose was arbitrarily chosen on the basis of an earlier investigation in experimental animals in either dogs or rabbits, where the dosage of crude RVV that caused death in 50% of subjects (LD 50 ) by intravenously injection was 0.5 mg/kg body weight (BW) ( Chaiyabutr et al, 2014 , Tungthanathanich et al, 1986 ). This dosage was equivalent to a concentration of 10 μg/ml plasma, based upon an estimated plasma volume of 5% of the BW.…”

“…These in vivo models do not exclude the influence of a higher order of extrarenal factors, such as the nervous system, blood pressure, coagulation, and other blood borne factors, including corpuscles and hormones. However, few data are available to study the specific mechanisms in responsible for the induction of AKI by RVV and its fractions, although a number of studies have reported the direct effects of RVV on renal tubular and glomerular injury in the isolated perfused kidney (IPK) model ( Ratcliffe et al, 1989 , Willinger et al, 1995 , Chaiyabutr et al, 2014 ).…”

A Study of Acute Kidney Injury in Patients with Snakebite Envenomation

“…Our findings suggested that the renal tubular loss of electrolytes including sodium, potassium and magnesium might be caused by the direct toxicity of snake venom from the Viperidae family. A previous experimental study of Russell's viper venom demonstrated decreased renal tubular absorption of sodium in proximal and distal renal tubules resulting in increased fractional excretion of sodium due to Na + −K + −ATPase activity inhibition of renal tubules in both the renal cortex and medulla [34] .…”