HDCN Article Review/Hyperlink

Tucker B, Fabbian F, Giles M, Thuraisingham RC, Raine AEG, Baker LRI

Left ventricular hypertrophy and ambulatory blood pressure monitoring in chronic renal failure

Nephrol Dial Transplant (Apr) 12:724-728 1997

This paper analyzes in detail the association between hypertension and LVH in patients with mild (CrCl>30ml/min) to moderate (CrCl<30 ml/min.) CRF. Eighty-five clinically stable patients (64 on antihypertensive medications) selected from 120 non-diabetic patients in an academic clinical center participated in the study. Patients with known cardiovascular complications or poorly compliant with the antihypertensive treatment were excluded from the study.

Hypertension (24h Syst >140 mmHg, 24hDiastolic >90 mmHg) was present in the 26% of patients with mild CRF and in the 46% of those with severe CRF (notwithstanding antihypertensive treatment). There was a high prevalence of non-dippers (40% in the first group and 52% in the second group). Interestingly, the loss of the nocturnal BP fall was confined to hypertensive patients. LVH and LV dilatation increased with progression of chronic renal failure being more prevalent in the group with severe CRF (LVH 38%, LV dilat. 17%) than in that with mild CRF (LVH 16%, LV dilat. 9%). Systolic function (FS<25%) was present only in one patient with severe CRF. In the combined analysis of the two groups, 24h systolic pressure was the stronger univariate predictor of LVMI (r=0.52). On separate analysis of the two groups, daytime systolic pressure (group I) and night- time systolic pressure (group II) were the most important determinant of LVM. On multivariate analysis arterial pressure remained a significant independent predictor of LVM. The correlations between LVM and clinic BP were less strong than those between LVM and 24h BP.

Comment: This paper confirms the importance of echocardiography for early detection of LVH in patients with renal diseases. LVH (which identifies patients at risk of cardiac death and stroke) and LV dilatation increase with progression of renal failure. Thus even in stable, compliant patients without clinical evidence of cardiac disease, arterial hypertension contributes to LVH. This study extends recent observations made in "normotensive" patients with chronic glomerulonephritis and normal GFR. Ambulatory BP in these patients is distinctly higher than in normotensive controls and is associated with increased LVM [Gebert S. JASN 1995(6):388 abstr.] Intervention studies will establish whether strict BP control can allow the reversion of LVH in patients with mild to moderate CRF. (Carmine Zoccali, M.D., Reggio Calabria, Italy).

The abstract of this paper is available from Oxford Press at this site.