Mechanisms of Renal Damage in Chronic Pyelonephritis (Reflux Nephropathy)

Abstract

The relation between vesicoureteral reflux and pyelonephritis was first pointed out in a study of patients with neurogenic bladder (HUtch 1952). Almost 10 years later, studies done by HOdson and EDwards (1960) indicated the importance of intrarenal reflux in the pathogenesis of chronic pyelonephritis. Further studies by HOdson et al. (1975), using the pig as an experimental animal, showed that sterile reflux could produce renal scars in the areas of intrarenal reflux. His model, however, required bladder neck obstruction and a high voiding pressure in order to produce the high-grade reflux. While Hodson felt that sterile reflux damages the kidney, RANSLEY and RISDON’S study (1978) in the same model did not confirm Hodson’s work, and they showed that scarring from sterile reflux would occur only if the bladder neck obstruction was severe enough to cause high-pressure reflux. This has been confirmed in another pig model of obstructive reflux (JOrgeson 1986). We also confirmed these latter studies in the monkey, showing that after bladder neck obstruction, increased voiding and resting bladder pressure as well as peristaltic failure of the ureter led to transmission of these high pressures to the kidney with renal damage and interstitial nephritis (MEndoza and ROberts 1983). Neurogenic sphincteric dysfunction such as that which occurs in myelodysplasia may also cause high-pressure voiding, which will cause renal damage whether reflux is present or not, as shown in studies of myelodysplastic patients (MCGUIRE et al. 1981). The studies of Allen (1977), HInman (1973), KOff and MUrtagh (1984), and VAn Gool (1979) all showed that the dysfunctional voiding which can occur in neurologically normal children, may cause not only reflux, but also renal damage from voiding pressures as high as 150 cm of water.

Supported by USPHS grant RR00164 and DK14681