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Early increase in blood pressure and diastolic left ventricular malfunction in patients with glomerulonephritis
A Stefanski1, K G Schmidt, R Waldherr
1Department Internal Medicine, Ruperto Carola University, Heidelberg, Germany.
Insights
Patients with glomerulonephritis show elevated blood pressure within normal ranges, alongside early heart damage. This suggests early intervention may be beneficial for managing kidney disease progression.
Area of Science:
- Nephrology
- Cardiology
- Hypertension Research
Background:
- Diabetic nephropathy shows progressive blood pressure increase before exceeding 140/90 mm Hg.
- Limited data exists on blood pressure trends in primary chronic glomerulonephritis (GN).
Purpose of the Study:
- To investigate ambulatory blood pressure and cardiac changes in untreated patients with primary chronic glomerulonephritis (GN) and normal GFR.
- To determine if blood pressure elevates within normotensive ranges in early GN.
Main Methods:
- Ambulatory 24-hour blood pressure monitoring in 20 GN patients and matched controls.
- Echocardiography to assess left ventricular structure and diastolic function.
- Measurement of glomerular filtration rate (GFR), urinary sodium, plasma renin activity (PRA), and insulin levels.
Main Results:
- Significantly higher mean 24-hour, daytime, and nocturnal blood pressure in GN patients compared to controls.
- Evidence of left ventricular hypertrophy (increased posterior wall and septal thickness) in GN patients.
- Impaired left ventricular diastolic function (lower E/A ratio) observed in GN patients.
Conclusions:
- Primary chronic glomerulonephritis patients exhibit elevated ambulatory blood pressure within normotensive limits.
- Associated cardiac structural and functional changes indicate early target organ damage.
- Findings support considering early antihypertensive intervention in GN, pending further clinical trials.
Abstract:
In patients with diabetic nephropathy blood pressure increases progressively before the conventional threshold of normal blood pressure (140/90 mm Hg) is transgressed. In patients with glomerulonephritis, no information on this point is available. To clarify this issue we sequentially examined 20 untreated patients with biopsy-proven primary chronic glomerulonephritis (GN) who had casual blood pressure below 140/90 mm Hg and normal GFR by inulin clearance. Patients were compared with normotensive healthy controls who were matched for BMI, gender and age. We measured ambulatory 24-hour blood pressure (SpaceLab system), echocardiography (ASE criteria, Acuson 128 XP 10), CIn and CPAH, urinary Na excretion, PRA and insulin concentration. In patients with GN, the median 24 hour (P < 0.0005), daytime (P < 0.001) and nocturnal sleeping time (P < 0.0001) MAP values were significantly higher than in matched controls (daytime, mean 97 mm Hg, 85 to 106 GN vs. 89 controls range 82 to 102; nocturnal sleeping time, mean 80.3 mm Hg, 71 to 89.5 GN vs. 73 controls, range 63 to 84). Echocardiographic examination showed significantly greater posterior wall thickness (P < 0.01) and ventricular septal thickness (P < 0.003). In addition the early diastolic to late diastolic (E/A) ratio of mitral valve peak inflow velocity was significantly (P < 0.0008) lower in patients. The data point to left ventricular wall thickening accompanied by LV diastolic malfunction. The study documents elevated ambulatory blood pressure in patients with primary chronic glomerulonephritis despite normal body weight and normal GFR. This is associated with evidence of target organ damage in the heart. The findings suggest that in patients with glomerulonephritis blood pressure increases initially within the normotensive range. This observation in conjunction with evidence of early target organ changes provides an argument for early antihypertensive intervention, but controlled trials to test efficacy and safety of this proposal are necessary.