Renal Changes Induced by Envenomation with Africanized Bee Venom in Female Wistar Rats

Abstract

Human envenomation caused by bee or wasp stings has been reported to cause acute renal failure (ARF), usually due to acute tubular necrosis (ATN), as a frequent complication. The pathogenetic mechanisms of ATN occurring in these accidents are still unclear. In the present study, female Wistar rats weighing 150-200 g were injected intravenously with Africanized bee venom at a dose of 0.4 µl/l00 g body weight and used in functional and light microscopy studies. The animals were divided into two groups: the early group was studied 3-8 h after inoculation, and the late group was studied 24-30 h thereafter. The animals showed ARF characterized by reduction of glomerular filtration rate with increasing levels of plasma creatinine. They also showed increased fractional sodium and potassium excretions, suggesting changes in the proximal portion of the nephron. The water transport through collecting tubules was reduced, with consequent diuresis, indicating functional changes in the distal portion of the nephron. These functional changes were more marked in the early group, with recovery tending to occur after 24 h. Albuminuria was also observed in this group. Light microscopy showed ATN mainly in cortex and outer medulla, with isolated necrosis in cells or small groups of cells and cast formation in the distal and collecting tubules. After 24 h frequent mitotic figures were found in the tubular epithelium. The observed ARF was due to ATN which in turn was probably caused by multiple effects, mainly hemodynamic changes secondary to cardiotoxicity and systemic vasodilation caused by the venom, myohemoglobinuria, and the direct action of the venom on tubular cells.

Effect of Bee Venom and Its Melittin on Apical Transporters of Renal Proximal Tubule Cells

“…Victims may die due to renal failure or cardiac complications [14]. Nonsensitized persons that survive a massive attack may develop acute renal failure, as a consequence of the acute renal tubular necrosis, severe hemolysis, rhabdomyolysis, and shock [5,6,15]. In the present study, 1 µg/ml bee venom significantly decreased the viability of PTCs over 30 min.…”

Acute Kidney Injury Induced by Snake and Arthropod Venoms

“…On the other hand, the mechanisms of bee venom-induced AKI have been more explored in experimental models in vivo and in vitro. In the case of bee envenomation, the experimental injection of venom in rats caused a significant and early reduction in glomerular filtration rate and diuresis and an increase in plasma creatinine levels (dos Reis et al, 1997;Grisotto et al, 2006). Tubular alterations such as increased fractional sodium and potassium excretions and a reduced water transport through collecting tubules, were also described (dos Reis et al, 1997).…”

“…In the case of bee envenomation, the experimental injection of venom in rats caused a significant and early reduction in glomerular filtration rate and diuresis and an increase in plasma creatinine levels (dos Reis et al, 1997;Grisotto et al, 2006). Tubular alterations such as increased fractional sodium and potassium excretions and a reduced water transport through collecting tubules, were also described (dos Reis et al, 1997). The early glomerular filtration rate reduction was concomitant with marked cortical and medullary renal blood flow decrease (Grisotto et al, 2006).…”

“…Neither hypertension and hypotension nor intravascular hemolysis were detected in experimental models. Despite of the absence of hemolysis, rhabdomyolysis was present with massive myoglobin deposition in the lumen of the tubules as well as into the tubular cells (dos Reis et al, 1997;Grisotto et al, 2006). The injection of purified melittin or phospholipase A2 also induced rhabdomyolysis, due to their capacity to disrupt the membranes of myocytes (Ownby et al, 1997).…”

The Water-Soluble Fraction (<10 kD) of Bee Venom <i>(Apis mellifera)</i> Produces Inhibitory Effect on Apical Transporters in Renal Proximal Tubule Cells

“…Only a few of these individual components of BV have been tested to date for their possible biochemical effects [6,7]. Several lines of evidence demonstrated that envenomated animals cause acute renal failure which is usually due to acute tubular necrosis or reduction of the glomerular filtration rate [8]. They also show increased fractional sodium and potassium excretions, suggesting the significant effects in the proximal portion of the nephron.…”