The most common is an ascending bacterial infection, usually of P-fimbriated E. coli which adhere to the mucosa. The initial colonization of the walls of the ureter is in areas of turbulent flow which leads to paralysis of peristalsis. Dilation and functional obstruction result, with subsequent pyelonephritis. Second, some cases are secondary to direct reflux of bacteria. In these cases, P-fimbriated E. coli aren't necessary.
Hematogenous spread is the third pathophysiology.
Gram positive cocci are usually the organisms. This has become less prevalent since the advent of rapid use of antibiotics. The histology is tubulointerstitial nephritis. White cells migrate from the interstitium into the tubules and destroy them by releasing enzymes. This takes only about 48-72 hours.