Reflux nephropathy, or renal parenchymal scarring associated with vesicoureteral reflux (VUR), is an important cause of renal failure. Some studies have shown that in up to 10% of adults and 30% of children requiring renal replacement therapy for end-stage renal disease, reflux nephropathy is the cause of the renal failure. Reflux nephropathy is thought to result from the combination of VUR of infected urine into the kidney by way of an incompetent ureterovesical junction valve mechanism and intrarenal reflux. Acute inflammatory responses to the infection result in renal parenchymal damage and subsequent renal scarring. Loss of functioning renal mass prompt compensatory changes in renal hemodynamics that, over time, are maladaptive and result in glomerular injury and sclerosis.
Clinically, reflux nephropathy may cause hypertension, proteinuria, and decreased renal function when the scarring is extensive. The identification of VUR raises the theoretic possibility of preventing reflux nephropathy. The inheritance pattern of VUR clearly is suggestive of a strong genetic influence. Familial studies of VUR are consistent with autosomal dominant transmission, and linkage to the major histocom-patibility genes has been reported. Identification of infants with reflux detected on the basis of abnormalities seen on prenatal ultrasound examinations before urinary tract infection occurs may provide an opportunity for prevention of reflux nephropathy. In persons with VUR detected at the time of diagnosis of a urinary tract infection, avoidance of further infections may prevent renal injury. Nevertheless, the situation is far from clear. Most children with reflux nephropathy already have renal scars demonstrable at the time of the urinary tract infection that prompts the diagnosis of VUR. Most children found to have VUR do not develop further renal scarring after diagnosis, even after subsequent urinary tract infections. Other children may develop renal scars in the absence of further urinary tract infections. The best treatment of
VUR has not yet been firmly established. No clear advantage has been demonstrated for surgical correction of VUR versus medical therapy with prophylactic antibiotics after 5 years of follow-up examinations. New surgical techniques such as the submucosal injection of bioinert substances may have a role in select cases.
The term obstructive nephropathy is used to describe the functional and pathologic changes in the kidney that result from obstruction to the flow of urine. Obstruction to the flow of urine usually is accompanied by hydronephrosis, an abnormal dilation of the renal pelvis, and calices. However, because hydronephrosis can occur without functional obstruction, the terms obstructive nephropathy and hydronephrosis are not synonymous. Hydronephrosis is found at autopsy in 2% to 4% of cases. Obstructive nephropathy is responsible for approximately 4% of end-stage renal failure. Obstruction to the flow of urine can occur anywhere in the urinary tract and has many different causes.
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