Inadequate diagnosis and therapy of arterial hypertension as causes of left ventricular hypertrophy in uremic dialysis patients.

BACKGROUND: Left ventricular hypertrophy (LVH) is highly prevalent in the dialyzed population, possibly because of inadequate diagnosis and therapy of arterial hypertension. The purpose of this study was to ascertain the adequacy of our approach in correctly identifying and treating arterial hypertension in our dialysis center.
METHODS: Fifty-five dialyzed uremics were studied by continuous ambulatory blood pressure (BP) monitoring, which started before a single hemodialysis (HD) session, continued for 24 hours after HD ended, and was repeated for 15 minutes before the beginning of the next HD. Clinical pre-HD and post-HD routine BP measurements taken the month preceding BP monitoring were retrieved, and echocardiography was performed.
RESULTS: LVH was present in 46 out of 55 patients, and clinical pre-HD arterial hypertension was present in 36 out of 55. There were discrepancies between clinical and monitored BPs, mostly concerning diastolic pre-HD BP since BP readings were lower than monitored BP records (P < 0.0002). Although both clinical and monitored BPs bore strong direct correlations with the left ventricular mass (LVM), the closest correlations were those for monitored BP. Four groups of patients were identified by BP monitoring: group A (N = 14), with persistently normal BP, and group D (N = 13), with persistently supranormal BP levels. There were also two other groups (group B, N = 19; and group C, N = 9), whose BP values were high before HD, normalized after HD, and then increased again either soon after HD (group C) or later on following HD (group B). Monthly averaged clinical pre-HD mean BP values differed significantly among the four groups [91 +/- 10 (SD) mm Hg in group A, 101 +/- 7 in group B, 106 +/- 6 in group C, and 106 +/- 7 in group D; P < 0.0001, analysis of variance], as did their corresponding LVMs [132 +/- 27 g/m2 body surface area (BSA), 156 +/- 26, 201 +/- 51, and 200 +/- 36; P < 0.0001]. There were also differences in dialytic age, which was significantly longer in group A patients (109 +/- 54 months), who also tended to have higher, although not significantly higher, Kt/V(urea) values. No differences, however, were detected among the groups as far as type, dosages, and number of antihypertensive drugs given to each individual patient.
CONCLUSIONS: The high prevalence of LVH in the dialysis population might be the result of inadequate diagnosis and therapy of arterial hypertension. Arterial hypertension, in fact, was insufficiently treated in our dialysis center, since patients with varying degrees of severity of both arterial hypertension and LVH were kept on antihypertensive therapy of similar strength. Undertreatment may have resulted from not having recognized and/or from having underestimated the severity of arterial hypertension since some clinical BPs were measured incorrectly. Reluctance to use more aggressive antihypertensive therapy might also result from the deceptive feeling of "normalized" BP that one has following volume unloading with dialysis. This causes both the BP to run out of control between dialyses and LVH to worsen.