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Effect of control of hypertension on progressive renal failure
J P Wight1, C B Brown, A M el Nahas
1Sheffield Kidney Institute, Northern General Hospital, UK.
Insights
Intensified blood pressure control in chronic renal failure (CRF) patients slows disease progression. Reducing mean diastolic blood pressure to 80-85 mmHg significantly improved renal function decline rates.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Clinical Research
Background:
- Chronic renal failure (CRF) is a progressive condition impacting kidney function.
- Blood pressure management is crucial in slowing CRF progression.
- Nephropathies of varying etiology contribute to CRF.
Purpose of the Study:
- To assess the direct impact of varying blood pressure control levels on CRF progression.
- To determine the optimal diastolic blood pressure target for slowing renal function decline.
- To evaluate the efficacy of intensified antihypertensive therapy in CRF patients.
Main Methods:
- Retrospective and prospective study design involving 18 CRF patients.
- Three consecutive phases with varying mean diastolic blood pressure (MDBP) targets.
- Monthly follow-ups and biochemical data analysis to monitor renal function (GFR) and MDBP.
Main Results:
- Reducing MDBP from 89.9 mmHg to 83.9 mmHg significantly slowed renal function decline (from -68.9 to -25.2 1/mol/month).
- Further reduction of MDBP to 77.1 mmHg with nifedipine did not yield additional benefits in slowing renal decline (-53.2 1/mol/month).
- Frequent follow-up and improved blood pressure control demonstrated a clear benefit in preserving renal function.
Conclusions:
- Aggressive blood pressure control, particularly targeting MDBP between 80-85 mmHg, effectively slows CRF progression.
- Intensified monitoring and management are key to achieving beneficial blood pressure targets.
- Lowering diastolic blood pressure below 80-85 mmHg may not provide further renal protection.
Abstract:
This study assesses the direct effect of different degrees of blood pressure control on the progression of chronic renal failure (CRF) in 18 patients with nephropathies of varying etiology (Glomerular filtration rate [GFR]: 14.99 +/- 5.94 ml/min/1.73 m2). The study involves three consecutive phases; Phase 1 consisted of a retrospective analysis of blood pressure and biochemical data: mean diastolic blood pressure (MDBP) was 89.9 +/- 7.9 mmHg and the mean rate of decline in renal function was -68.9 1/mol of creatinine/month. Phase 2 consisted of a 6 months prospective period of frequent (monthly) follow-up and optimization of blood pressure control when MDBP was reduced to 83.9 +/- 6.5 mmHg (p < 0.001 cf phase 1) and the rate of decline in renal function fell to -25.2 1/mol/month (p < 0.05 cf phase 1). Phase 3 consisted of another 6-month period when further reduction of MDBP 77.1 +/- 6.6 mmHg (p < 0.01 cf phase 2) was brought about by the addition of the calcium antagonist nifedipine (10 mg thrice/daily). This was not associated with further improvement in the rate of decline of renal function as in this phase the rate of decline was -53.2 1/mol/month. This study confirms that frequent follow-ups with improved blood pressure control slow the rate of decline in renal function. Further reduction of diastolic blood pressure to below 80-85 mmHg could not be shown to confer additional benefit.