RESUMO
Acute kidney injury (AKI) is prevalent and is associated with high morbidity and mortality globally. The epidemiology differs remarkably between developing and developed economies. Infections, diarrheal illnesses, obstetric causes and nephrotoxins are very rampant in the tropics. Even though the etiologies are different, the final common pathway in the pathogenesis is similar - tubular damage or necrosis, tubular blockage, and back leak of glomerular filtrate. The mechanism of AKI in infections could be through ischemic insult consequent to hypovolemia and/or hemoglobinuria, as seen in malaria and viral hemorrhagic fevers, interstitial inflammation, or nephrotoxicity. On the contrary, the mechanism of nephrotoxin-induced AKI includes direct toxic effect on the renal tubules, intratubular precipitation of substances like djenkolic and oxalic acids (crystalluria) as well as intratubular obstruction and AKI. Toxicity could also be indirect by interacting with the pharmacokinetic profile of other coadministered medications. Bites and envenomation as well as obstetric complications also induce AKI through hypovolemia, interstitial nephritis, and other unclear mechanisms in eclampsia and preeclampsia. Outcome is variable and dependent on etiology. Prognosis appears to be significantly better in hypovolemic or prerenal and/or obstructive AKI compared to intrarenal or intrinsic AKI.
