Although obstruction from stones, clots, and strictures usually leads to acute renal failure, such obstructions can also produce chronic tubulointerstitial damage to the kidney. The pathophysiology of obstructive nephropathy involves increased intratubular pressure, local ischemia, and, often, associated infection, which combine to produce tubulointerstitial damage. The pathologic findings consist of dilatation of the collecting ducts and distal tubules, along with chronic tubular atrophy with little glomerular damage. The diagnosis of obstructive nephropathy is typically based on evidence of renal dysfunction and blockage of urine outflow in the absence of other causes of renal damage. Ultrasonography usually shows dilatation of the urinary collecting system and hydronephrosis.
Treatment consists of relieving obstruction.
Various anatomic factors appear to play a role in incompetence at the vesicoureteral junction. In each case, the incompetent vesicoureteral junction allows urine to reflux into the ureters and collecting system of the kidneys. The reflux may be unilateral or bilateral, and the severity is variable. When infection is present, even low-pressure refluxed urine that reaches the kidney can produce chronic interstitial inflammation and scarring. However, it is unclear whether repeated episodes of high-pressure sterile reflux alone can damage the kidney.