Drug-induced oliguria is mainly due to drug-induced changes in urodynamics. In poorly perfused kidneys, on the one hand, prostaglandin secretion increases to improve blood perfusion to the renal unit. On the other hand, angiotensin secretion increases, causing the small outgoing glomerular arteries to contract stronger than the small incoming ones, maintaining the filtration pressure within the glomerulus and ultimately maintaining the glomerular filtration rate. The use of angiotensin inhibitors or non-steroidal anti-inflammatory drugs in this situation predisposes to a decrease in glomerular filtration rate, resulting in nephrogenic oliguria.