Reflux nephropathy : the glomerular lesion and progression of renal failure

Reflux nephropathy is the cause of 5%-10% of dialysed end-stage renal failure. Once scarring has occurred, the prognosis depends on the severity of initial damage and the presence of proteinuria, which reflects the development of glomerulosclerosis. It is independent of ongoing reflux or infection....

Full description

Saved in:
Bibliographic Details
Published in:Pediatric nephrology (Berlin, West) West), 1993-08, Vol.7 (4), p.365-369
Main Authors: BECKER, G. J, KINCAID-SMITH, P
Format: Article
Language:English
Subjects:
Age Factors
Animals
Biological and medical sciences
Female
Humans
Kidney Failure, Chronic - etiology
Kidney Failure, Chronic - prevention & control
Kidney Glomerulus - pathology
Male
Medical sciences
Nephritis, Interstitial - pathology
Nephrology. Urinary tract diseases
Prognosis
Pyelonephritis - complications
Pyelonephritis - etiology
Pyelonephritis - prevention & control
Sclerosis
Urinary system involvement in other diseases. Miscellaneous
Urinary tract. Prostate gland
Vesico-Ureteral Reflux - complications
Vesico-Ureteral Reflux - prevention & control
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Reflux nephropathy is the cause of 5%-10% of dialysed end-stage renal failure. Once scarring has occurred, the prognosis depends on the severity of initial damage and the presence of proteinuria, which reflects the development of glomerulosclerosis. It is independent of ongoing reflux or infection. Histological appearances highly suggestive of reflux nephropathy can occur in radiologically normal kidneys. Duplex Doppler scans of ureteric orifices suggest these patients may have lateral insertion, suggesting past reflux. Glomerular hypertrophy correlates well with reduced renal function and severe renal scarring, but poorly with focal and segmental glomerulosclerosis, which correlates with proteinuria. Increasing attention is being paid to the tubulo-interstitium and the relationships between the cellular infiltrates (mainly T4 cells) and glomerular, tubular and vascular damage. Control of hypertension, hyperphosphataemia and a low-protein diet are the only currently widely accepted treatments for slowing progression.
ISSN:0931-041X
1432-198X
DOI:10.1007/BF00857540