Chronic pyelonephritis (reflux nephropathy)
Chronic pyelonephritis is the damage caused to the kidneys by persistent or recurrent infection. The term should largely be replaced by ‘reflux nephropathy’, the most common form.
Accounts for about 15% of cases of end-stage renal failure and is an important cause of hypertension in later life.
The development of chronic pyelonephritis requires there to be infections in a kidney with an underlying anatomical abnormality, such as reflux or stones.
Vesicoureteric reflux (VUR) where urine refluxes back up from the bladder into the ureter, due to an incompetent vesicoureteric junction, is common, affecting 1% of neonates and 30–45% of young children who present with a urinary tract infection (UTI). Reflux due to high pressure can also develop in patients with obstruction due to urethral valves and after spinal cord injury. The severity of the VUR predicts the risk of developing renal damage.
There is a strong familial incidence of VUR, siblings may have a 30–40% risk of also being affected, and infants born to mothers with VUR may have an even higher risk.
In reflux nephropathy, the papillae are damaged, and the calyces become dilated and ‘clubbed’. As areas of the kidney are chronically or recurrently infected, they become scarred, leading to loss of nephrons. As renal function deteriorates, hypertension may follow, which accelerates the renal damage by hypertensive-induced vascular change. Unilateral chronic pyelonephritis does not cause renal impairment, as long as the other kidney is normal an adequate GFR is maintained. However, hypertension may lead to damage to the single functioning kidney.
A single proven UTI in early childhood should be investigated for any underlying congenital abnormality predisposing to reflux, to assess the degree of VUR and any scarring which has already occurred. Recurrent UTI’s in adults should also be investigated. If the diagnosis is missed (often the UTI’s are asymptomatic), then patients present later in life with hypertension, proteinuria and/or renal impairment.
The kidneys are smaller than normal, with an irregular, blunted, distorted pelvicalyceal system and areas of scarring 1–2 cm in size. The poles tend to be more affected.
Areas of interstitial fibrosis with chronic inflammatory cell infiltration. The tubules are atrophic or dilated and the glomeruli show periglomerular fibrosis. Some may be hyalinized in response to damage.
The scarring of reflux nephropathy is best visualised by DMSA scans. Intravenous pyelogram and renal ultra-sound may also identify damaged kidneys (but are less sensitive) and dilated ureters. Infants and young children are screened for VUR following a single UTI, as should siblings, and infants of mothers with proven VUR. Screening may involve renal ultrasound, DMSA scan, micturating cystourogram (MCUG) or MAG3 scan with indirect cystourogram dependant on age.
Patients with chronic renal failure require appropriate treatment (see Chronic Renal Failure page 237). Patients with VUR should be treated with prophylactic antibiotics until reflux is shown to have resolved or puberty. Previously severe reflux was treated with surgical reimplantation of the ureters, this has now been shown to have no additional benefit and risks urinary obstruction.
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