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Abstract: FR-PO940

The Association Between Mean Blood Pressure and the Rate of Progression of CKD Is Dependent on the Underlying Disease

Session Information

Category: CKD (Non-Dialysis)

  • 2201 CKD (Non-Dialysis): Epidemiology‚ Risk Factors‚ and Prevention

Authors

  • Kondo, Tatsuo, Saitama Ika Daigaku, Iruma-gun, Saitama, Japan
  • Inoue, Tsutomu, Saitama Ika Daigaku, Iruma-gun, Saitama, Japan
  • Fukaya, Daichi, Saitama Ika Daigaku, Iruma-gun, Saitama, Japan
  • Amano, Hiroaki, Saitama Ika Daigaku, Iruma-gun, Saitama, Japan
  • Watanabe, Yusuke, Saitama Ika Daigaku, Iruma-gun, Saitama, Japan
  • Tomori, Koji, Saitama Ika Daigaku, Iruma-gun, Saitama, Japan
  • Okada, Hirokazu, Saitama Ika Daigaku, Iruma-gun, Saitama, Japan
Background

The correction of intraglomerular pressure suppresses glomerulosclerosis thereby retarding CKD progression in animal models whereas the degree of increase in intraglomerular pressure in the human kidney in patients with CKD is assumed to vary with etiology. In this study, we examined the association between mean blood pressure (mBP) and the rate of progression of CKD, with a focus on different etiologies.

Methods

We recruited patients with chronic glomerulonephritis (CGN), diabetic kidney disease (DKD), or nephrosclerosis (HNS). The progression rate was defined as the SLOPE: ΔeGFRcre/year (ml/min/1.73m2 per year). Regression coefficients for predicting the SLOPE using each risk factor were examined using Bayesian analysis. A model with linear combination of each explanatory variable was assumed.

Results

A total of 167 patients (37.7% female; mean observation period, 3.17 years; eGFR, 43.89±23.54; urinary protein (UP), 1.54±2.01 g/gCr; mBP, 96.90±9.58 mmHg) with CGN (n=64), DKD (n=26), or HNS (n=77) were included. The mean SLOPE values for CGN, DKD, and HNS were -3.15, -5.19, and -1.91, respectively, and ANOVA showed significant differences among groups (p<0.01). Multiple regression analysis using age, gender, and known risk factors revealed that UP and mBP were significant explanatory variables for the SLOPE. In addition, the interaction was also significant for mBP (age*etiology, p=0.08; UP*etiology, p=0.05; mBP*etiology, p=0.01). After adjusting for age and UP, the coefficient of mBP was estimated for each etiology. Model: SLOPE∼normal (intercept+age+UP+mBP*etiology, σ2), prior distribution Normal (0, 100), σ∼iγ (0.01, 0.01), iter=12500, burn-in=2500, chains=4. All MCMC sampling results were well-converged. The mean values [95% Cred. Inter.] for the MCMC samples of CGN, DKD, and HNS were -0.063 [-0.113, -0.013], -0.020 [-0.035, -0.005], and -0.003 [-0.016, 0.010], respectively. The mBP did not affect the SLOPE in HNS

Conclusion

Unlike UP, the association between mBP and SLOPE is dependent on the underlying disease/etiology of CKD. Factors associated with decreased renal function differ depending on the primary disease, and careful consideration is needed to construct a renoprotective strategy with antihypertensive therapy, particularly for patients with HNS.