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Determinants of cardiorenal damage progression in normotensive and never-treated hypertensive subjects
Pierre Fesler1, Jean Ribstein, Guilhem du Cailar
1Department of Internal Medicine, Centre Hospitalier Universitaire, Montpellier, France.
Insights
Blood pressure is key to preventing kidney and heart damage. High blood pressure, even in those with normal readings initially, accelerates kidney function decline and increases albuminuria and left ventricular mass.
Area of Science:
- Cardiorenal medicine
- Hypertension research
- Cardiovascular and renal outcomes
Background:
- Investigating cardiorenal damage progression in normotensive and never-treated essential hypertension patients.
- Assessing determinants of disease progression in individuals with varying blood pressure levels.
Purpose of the Study:
- Identify factors influencing cardiorenal damage progression.
- Understand the impact of baseline and follow-up blood pressure on renal function and cardiac structure.
Main Methods:
- Longitudinal study with isotopic techniques and echocardiography.
- Evaluated renal hemodynamics, function, and cardiac morphology over 5.2 years.
- Included 30 normotensive and 33 hypertensive subjects.
Main Results:
- 50% of normotensive subjects became hypertensive during follow-up.
- Age determined systolic blood pressure progression; baseline systolic blood pressure impacted glomerular filtration rate (GFR) decline.
- Increased albuminuria correlated with blood pressure changes in hypertensive subjects; Left Ventricular Mass (LVM) progression linked to aldosterone, uric acid, triglycerides, and systolic blood pressure changes.
Conclusions:
- Baseline and follow-up blood pressure are primary drivers of GFR decline.
- Blood pressure progression significantly influences albuminuria and Left Ventricular Mass (LVM) changes.
- Untreated subjects demonstrate clear links between blood pressure and cardiorenal outcomes.
Background:
In the present longitudinal study, we attempted to identify the determinants of cardiorenal damage progression in normotensive subjects (<140/90 mm Hg) and patients with never-treated essential hypertension.
Methods:
Renal hemodynamics and function and cardiac morphology were evaluated by isotopic techniques and echocardiography at baseline and after a median follow-up period of 5.2 years (range 3 to 13) in 30 normotensive and 33 hypertensive subjects.
Results:
The results are mean +/- SD. Among normotensive subjects at baseline, 50% became hypertensive during follow-up. In the whole population, multivariate analysis showed that age was the main determinant of the progression of systolic blood pressure. The yearly change in glomerular filtration rate (GFR) was exaggerated in hypertensive when compared to normotensive subjects at baseline (-1.22 +/- 2.71 vs. 0.12 +/- 2.08 mL/min/year, respectively) (P= 0.033). In the whole population, only baseline systolic blood pressure remained correlated to the change in GFR, independently of GFR at baseline (model r(2)= 0.44) (P < 0.0001). The observed increase in albuminuria was correlated with change in blood pressure only in hypertensive subjects at baseline. Left ventricular mass (LVM) progression was significant only in men and its determinants were basal plasma aldosterone, serum uric acid, and triglyceride and change in systolic blood pressure (r(2)= 0.71) (P < 0.0001).
Conclusion:
In a population of untreated subjects, baseline blood pressure as well as progression of blood pressure during follow-up are the main determinants of the decline in GFR, progression of albuminuria, and LVM.
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