Normally, the valvelike mechanism at the ureterovesical junction does not permit reflux of urine from the bladder to the upper urinary tract. Cystitis alone, however, as well as anatomic defects, may produce reflux. Vesicoureteral reflux plays a key role in the pathogenesis of renal infection and, more importantly, in the evolution of chronic renal damage associated with infection. The urine gains access to the kidney parenchyma via the ducts of Bellini at the papillary tips and then spreads outward along the collecting tubules. Renal scars caused by chronic pyelonephritis are often associated with such reflux.
Renal infection is focal.
It begins in the pelvis and medulla and extends into the cortex as an enlarging wedge. The infection may arise from several foci, and normal tissue is found between these wedges of infection. Initiation of infection in the medulla is made easier by this site's unique chemical environment, which is characterized by high concentrations of urea and ammonia and high osmolarity and which impairs white blood cell chemotactic and phagocytic functions as well as complement activation. Gross anatomic examination reveals that the acutely infected kidney is swollen, with variable numbers of small abscesses on the subcapsular surface. In some cases of pyelonephritis complicated by diabetes, obstruction, sickle cell disease, analgesic nephropathy, or combinations of these conditions, papillary necrosis may be evident.