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Poisonous animals
Cnidarians (Jellyfish, Corals and Anemones)
Venomous fish
Hymenopterans (Bees, Wasps and Ants)
Sea snakes
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Renal venom/poison effects

Definition: Effects that arise due to the direct action of venom/poison on renal tissue, i.e. on the glomeruli and tubules.


Signs and symptoms:

  • Oliguria (<400 ml of urine every 24 h), anuria, polyuria,
  • flank pain, renal bed sensitive to percussion,
  • laboratory findings: elevated urea, creatinine and potassium.


The development of renal dysfunction and lesions has multifactorial causes (Chugh 1989, Sitprija and Boonpucknavig 1980) (Fig. 5.6).



Figure 5.6 Venom/poison effects on the kidneys



This makes it difficult or even impossible to characterise the primary renal effects of venoms/poisons.

Based on the available data it is difficult to evaluate the significance of the direct effect of venom/poison on the kidneys, but it is probably small compared to that of the indirect effects.

The direct action of venom/poison on the kidneys appears to primarily cause glomerulonephritis. It is not yet possible to determine with certainty to what extent this action is also responsible for tubulo-interstitial damage.


In the following cases a direct renal effect in humans is proposed on the basis of the histopathology of renal biopsies:

  • terrestrial snakes
    proliferative glomerulonephritis
    Bitis arietans (Seedat et al. 1974)
    Daboia russelli (Sitprija and Boonpucknavig 1980).


Ratcliffe et al. (1985) and others also demonstrated a direct nephrotoxic effect of Daboia russelli venom in experiments with isolated rat kidneys.

In most cases acute renal failure is caused by indirect effects of envenoming/poisoning due to animal venoms/poisons.

These effects consist almost exclusively of tubular necrosis and renal cortical necrosis. In contrast, glomerulonephritis occurs only rarely and is suggested to be associated with immunological reactions, among other factors.

Tubular necrosis is primarily the result of hypovolaemia and arterial hypotension, while renal cortical necrosis, on the other hand, is caused by ischaemia due to microthrombosis.

The prognosis of diffuse renal cortical necrosis is poor, but that of acute tubular necrosis is good, as long as the dysfunction, which usually only lasts a few days, can be bridged by means of dialysis.


The following venom/poison effects damage the kidneys indirectly:


Autopharmacological venom/poison effects

  • Immune complex formation;
  • arterial hypotension as a result of autopharmacological venom/poison effects and the release of autacoids (histamine, bradykinin etc.) with a direct effect on peripheral blood pressure regulation;
  • hypovolaemia and arterial hypotension due to autopharmacological reactions, which lead to an increase in vessel permeability and thus to generalised fluid sequestration.


Local venom/poison effects

  • Hypovolaemia and arterial hypotension as a result of local venom/poison effects with extensive swelling of the subcutaneous tissue and possibly also muscle tissue due to regional fluid sequestration;
  • hypovolaemia and arterial hypotension as a result of local venom/poison effects in the gastrointestinal tract with vomiting and diarrhoea.


Haemostatic/haemolytic venom/poison effects

  • Hypovolaemia and arterial hypotension as a result of bleeding in cases of envenoming due to haemostatically active venoms;
  • microthrombosis and ischaemia as a result of blood clotting defects, in particular DIC;
  • haemoglobinuria as a result of haemolytic venom/poison effects.


Neurological venom/poison effects

  • Hypoxia as a result of paralysis of the respiratory musculature with respiratory insufficiency.


Muscular venom/poison effects

  • Myoglobinuria as a result of venom/poison-induced rhabdomyolysis.


Cardiac venom/poison effects

  • Arterial hypotension as a result of myocardial insufficiency.