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. 2012 Mar;22(2):108-15.
doi: 10.4103/0971-4065.97126.

Retarding the progression of chronic kidney disease with renin angiotensin system blockade

Affiliations

Retarding the progression of chronic kidney disease with renin angiotensin system blockade

M Limesh et al. Indian J Nephrol. 2012 Mar.

Abstract

We assessed the effect of renin angiotensin system blockade (RASB) in chronic kidney disease (CKD) of diverse etiology. Two hundred and sixty-five consecutive CKD patients attending our renal clinic, with estimated glomerular filtration rate (eGFR) of 20-70 ml/min/1.73m(2) at baseline and a minimal follow-up of 1 year, were studied retrospectively. We devised a scoring system to quantify RASB, wherein the maximum dose of an agent recommended for control of hypertension was scored as 1. The renal endpoints studied were the rate of change in eGFR (ΔeGFR) and decline of eGFR>50%. The mean age was 48 ± 11.2 years and 69% were male. The mean duration of follow-up was 4 ± 2.7 years. The rate of ΔeGFR was -1.5 ± 5.0 ml/min/1.73 m(2) per year in patients who received RASB (N=168) and -6.0 ± 5.4 in those who did not (N=97) (P<0.001). The incidence of decline of eGFR >50% was 11.3% with RASB and 24.7% without (P=0.003). In a subgroup of patients who received RASB, the incidence of decline of eGFR >50% was 17.8% in the low-dose RASB group (N=84, RASB score 0.63 ± 0.38) and 4.8% in the high-dose group (N=84, RASB score 2.5 ± 0.7) (P=0.001). RASB was associated with significantly better renoprotection in CKD of diverse etiology, even in nonproteinuric diseases. This effect appeared to be dose-dependent, with higher supramaximal doses exhibiting better renoprotection than the lower conventional doses. Our results make a strong case for use of aggressive RASB in all CKD patients to postpone end-stage renal disease.

Keywords: Chronic kidney disease; progression of nephropathy; renin angiotensin system blockade.

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Conflict of interest statement

Conflict of Interest: None declared.

Figures

Figure 1
Figure 1
Scatter plot showing the change in GFR over a period of time in RAS blockade and no RAS blockade
Figure 2
Figure 2
Scatter plot with cubic regression line, showing the relationship between RASB score and the rate of ΔeGFR
Figure 3
Figure 3
The graph depicting the interaction between degree of RAS blockade and blood pressure control on renal outcome on decline in eGFR >50% (RASB, rennin angiotensin system blockade; SBP, systolic blood pressure at last follow up; Bars represent incidence in percent, of renal outcome of decline in eGFR >50%)

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