Bradykinin related peptides are constituents of venoms of different origins. One of the major effect of envenomation is multiple organ injuries, most commonly kidney injury. Bradykinin is responsible for vasodilation and thus hypotension. I would like to know if bradykinin related peptides (and thus vasodilation/hypotension) can lead to kidney injury.
hypotension: definitely so !!! Prolonged severe hypotension may result in necrosis of the tubular cells [ATN acute tubulus necrosis]. It is seen not infrequently after major reconstructive artery surgery in patients that had a ruptured aneurysma of the abdominal aorta. Sometimes it is due to the direct effects of the aneurysm impeding bloodflow through renal arteries, but sometimes it is due to the hypovolemic/hypotensive shock .
Three points:
1)Prostaglandins are potent renal vasodilators and inhibition of prostaglandins is associated with decreased RBF and can affect the severity of AKI. (acute kidney injury) But ... the precise role of prostaglandins in induction and maintenance of AKI is not established.
2) AKI refers to a complex disorder from multiple causes. The unifying feature of AKI is renal cell injury. Prolonged hypotension definitely may result in ATN and medullary vascular congestion is consistent observation following experimentally induced ischemmic renal injury . Hypoxic/ischemic ATN evolves from prolonged prerenal injury or following severehypoxic insults.
3) Envenomation can result in liberation of endogenous toxins such as myoglobinuria and hemoglobinuria and both can cause ATN that result from injury of tubular epithelial cells.
The ultimate case of renal hypotension [but other mechanisms play a role too] is in kidney transplants. In these patients acute tubular necrosis is a frequent finding.
Considering the low target pressures during cardiopulmonary bypass surgery in the attached paper it seems that hypotension per se does not suffice to induce AKI at least in this clinical setting. In my experience, it often (but certainly not always) takes the combination of two or more factors (e.g., hypoxia, anemia, pre-existing kidney disease, endothelial dysfunction, nephrotoxic drugs etc.) to induce AKI.
http://www.ncbi.nlm.nih.gov/pubmed/21677302
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