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The quantitative relationship between treated blood pressure and progression of diabetic renal disease
1Department of Medicine, Ohio State University, Columbus.
Insights
Higher diastolic blood pressure is linked to faster kidney function decline in diabetic nephropathy patients. Controlling blood pressure is crucial for slowing kidney disease progression.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
Background:
- Diabetic nephropathy is a leading cause of chronic kidney disease.
- Antihypertensive therapy is standard but optimal blood pressure targets remain unclear.
- Understanding blood pressure's impact on kidney function decline is vital.
Purpose of the Study:
- To quantitatively analyze the relationship between treated blood pressure and the rate of glomerular filtration rate (GFR) decline.
- To identify the optimal blood pressure for slowing GFR loss in diabetic nephropathy.
Main Methods:
- Retrospective analysis of 59 patients with diabetic nephropathy and treated hypertension.
- Weighted univariate and multivariate regression models were used.
- GFR was calculated using the Cockcroft and Gault formula.
Main Results:
- Higher diastolic blood pressure showed the strongest correlation with faster GFR decline (r = 0.70, P < 0.0001).
- Each mmHg increase in diastolic pressure correlated with a 0.69 mL/min/yr GFR decrease.
- This association persisted even when excluding patients with diastolic pressures >90 mmHg.
Conclusions:
- Diastolic blood pressure is a significant predictor of GFR decline in diabetic nephropathy.
- Current antihypertensive strategies may need refinement to optimize diastolic pressure control.
- Further research is needed to establish definitive blood pressure targets for kidney protection.
Abstract:
Antihypertensive therapy reduces the rate at which glomerular filtration rate (GFR) declines (delta GFR) in diabetic nephropathy; however, the optimal blood pressure is unknown. The quantitative relationship between treated blood pressure and delta GFR was analyzed retrospectively in 59 patients with established diabetic nephropathy and treated hypertension using weighted univariate and weighted multivariate regression. The GFR was calculated using the Cockcroft and Gault formula. More rapid GFR loss correlated most strongly with higher diastolic blood pressures (r = 0.70; P < 0.0001); for each millimeter of mercury of diastolic blood pressure, the GFR decreased by 0.69 mL/min/yr. This relationship remained present if those individuals with diastolic pressures greater than 90 mm Hg were eliminated from the study (r = 0.50; P < 0.001). The correlation for systolic blood pressure was weaker (r = 0.30; P < 0.05) and explained completely by covariance between systolic and diastolic blood pressures. The correlation for mean blood pressure (r = 0.59; P < 0.0001) fell between the correlations for diastolic and systolic blood pressures. Proteinuria, serum albumin concentration, and serum cholesterol concentration also correlated with delta GFR. In multivariate analysis, neither these indices of disease severity nor the initial GFR explained the correlation between delta GFR and diastolic blood pressure. Age, sex, race, type of diabetes, and percentage of glycosylated hemoglobin did not correlate with delta GFR.