[Progression of renal disease in patients with reflux nephropathy. Follow-up study]

Abstract

Background: We previously estimated the turning point of reflux nephropathy irreversibly deteriorating to end stage renal disease, mainly based on findings in renal biopsy (Eur. Urol., 26: 153-159, 1994). In this study, we aim to evaluate clinical parameters which may be closely associated with progression of reflux nephropathy to end stage renal disease.

Subjects and methods: Ninety five patients (84 children and 11 adults; 41 men and 54 women) with renal scar and/or reflux (>/ = grade 3), mean aged 9.4 +/- 9.1 years (3 months-53 years) were followed up for 3.7 years +/- 2.7 (6 months-18 years). Vesicoureteral reflux was bilateral in 64 and unilateral in 31; primary in 85 and secondary in 10 patients. Clinical parameters including body weight, height, blood pressure, 24 hour urinary protein excretion, serum creatinine, 99m Tc-DTPA GFR and 99 m Tc-DMSA uptake were monitored over time. All patients underwent antireflux surgery (with or without other reconstructive surgery) and open renal biopsy. Three patients progressing to end stage renal disease underwent subsequent biopsy.

Results: Over-5 year observation period, the prevalence of new scare formation and further extension in scar was significantly higher in the group of renal functional deterioration (35%) than in the group of stable renal function (6.0%). Over the same period DMSA uptake decreased significantly (< 0.05) in the group of scar b (Smellie's classification), suggesting most kidneys of scar b eventually resulting in atrophic kidney (scar c). Proteinuria more than 100 mg/day appeared to be a critical level for predicting irreversible deterioration in renal function. Glomerular hypertrophy was closely related to the increase in urinary protein excretion and serum creatinine, contrary to the decrease in DTPA-GFR. In addition, bilateral renal scar b, glomerular hypertrophy (> 2 SD), proteinuria (> 300 mg/day), low GFR (mean: 49 ml/min), and diastolic hypertension seemed to be implicated in the genesis of ESRD.

Conclusion: Glomerular damage due to either reflux nephropathy or dysplasia may cause proteinuria. Proteinuria of 100 mg/day was significantly (p < 0.01) associated with 2 SD of glomerular hypertrophy on histology and clinical observation (suggesting hyperfiltration). Thereafter, a rapid increase in proteinuria followed by diastolic hypertension appears be significant for predicting ESRD.