VESICOURETERAL REFLUX AND PYELONEPHRITIS IN THE MONKEY - A REVIEW

P-fimbriated Escherichia coli, which cause nonobstructive pyelonephritis, adhere to a specific urothelial glycolipid receptor. In either the presence or absence of reflux (in the area of turbulent urine flow) these bacteria ascend the ureter and cause a decrease in ureteral motility. Endotoxin causes peristalsis to cease, leading to ureteral dilatation and change in papillary shape, thus allowing intrarenal reflux and adherence of the bacteria to renal tubules. Bacterial infection of a refluxing ureter may cause reflux to persist. Once the bacteria reach the kidney rapid effects occur at the cellular level with activation of complement followed by granulocytic aggregation and capillary obstruction, causing renal ischemia and damage during reperfusion. In addition, during phagocytosis the respiratory burst occurs, releasing toxic oxygen molecules, which leads to renal tubular death, invasion of the interstitium, microabscess and renal scar formation, that is chronic pyelonephritis, which equates with reflux nephropathy.