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Q J Med 1988; 67: 343-354
© 1988 Association of Physicians

research-article

Renal Pathology and Proteinuria Determine Progression in Untreated Mild/Moderate Chronic Renal Failure

P. S. WILLIAMS, G. FASS and J. M. BONE

Royal Liverpool Hospital Prescot Street, Liverpool L7 8XP

Address correspondence to Dr. P. S. Williams, M. A.K.R. Research Fellow, 9C Link Unit, Royal Liverpool Hospital, Prescot Street, Liverpool L7 8XP.

Accepted for publication 10 December 1987.

SUMMARY

The progression of renal failure was analysed in 108 patients with mild to moderate renal impairment, none of whom had received any form of dietary protein, phosphate restriction or immunosup pressive treatment. The reciptrocal of plasma creatinine was plotted against time using a minimum of six plasma creatinine values taken over at least six months (mean 13 values over 41 months). Plots indicated there was linear deterioration in 70 patients, non-linear deterioration in 15 and stable renal function in 24. Progressive renal failure was common in patients with glomerulonephritis, diabetic nephropathy, chronic pyelonephritis and polycystic kidney disease. Most patients with hypertensive nephrosclerosis, analgesic nephroapathy and renal impairment following acute renal failure were stable. Among those with progressive impairment the mean rates of deterioration were significantly faster for patients with glomerulonephritis and diabetic nephropathy compared to those with chronic pyelonephritis, polycystic kidney disease and undiagnosed renal disease (p<0. 01). Hence the underlying renal pathological changes appear to be important in determining progression of renal failure and also the subsequent rate of deterioration.

For those with linear progression of renal failure there was a signicficant correlation between 24-h urinary protein excretion and the rate of deterioration. This relationship held for glomerulonephritis and chronic pyelonephritis as separate diagnostic groups only. Proteinuria, therefore, may be a useful prognostic index for the rate of progression of established renal failure.

Calcium phosphate product correlated poorly with the rate of deterioration.

We were unable to demonstrate a relationship between spontaneous protein intake and deterioration of renal function. However, patients prescribed high protein diets were not included in dietary analysis and we cannot, therefore, exclude the possibility that a high dietary protein intake may accelerate renal failure.

Similarly we were unable to show a significant relationship between blood pressure and progression of renal failure although there were weak correlations between mean arterial pressure and rate of deterioration for chronic pyelonephritis and glomerulonephr


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