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Development, Prevention, and Potential Reversal of Left Ventricular Hypertrophy in Chronic Kidney Disease

Lawrence P. McMahon^*, Simon D. Roger and Adeera Levin for the SLIMHEART Investigators Group

*Departments of Nephrology, Western and Royal Melbourne Hospitals, Australia; Department of Renal Medicine, Gosford Hospital, Gosford, Australia; and Education and Research Department, St. Paul’s Hospital, Vancouver, British Columbia, Canada

Correspondence to Dr. Lawrence P. McMahon, Departments of Nephrology, Royal Melbourne and Western Hospitals, Melbourne, Victoria 3050, Australia. Phone: 613-9342-8353; Fax: 613-9347-1420; E-mail: lawrence.mcmahon{at}mh.org.au

ABSTRACT. Although a high prevalence of left ventricular (LV) hypertrophy is recognized with increasing severity of chronic kidney disease (CKD), previously neither its progression nor its potential for prevention or reversal has been addressed adequately in this population group. A nested analysis of a 2-yr study involving 155 patients with stage 3/4 CKD, examining effects of hemoglobin change (range, 90 to 130 g/L) on LV mass in patients with (n = 46; 30%) and without (n = 105; 70%) initial LV hypertrophy, is reported. At baseline, the group with LV hypertrophy was older (P < 0.01), had higher BP (P < 0.01), had greater LV wall and cavity dimensions (P < 0.001), and had more prevalent use of antihypertensive agents (P < 0.001) but a lower hemoglobin concentration (P < 0.05) and GFR (P < 0.01). A total of 117 patients were available for assessment at 2 yr. Importantly, 57 (68%) with initial normal LV indices showed no appreciable change with time; however, 27 (32%) developed LV hypertrophy, with growth in both wall and cavity dimensions (P < 0.001). In contrast, 23 (50%) of those with initial LV hypertrophy maintained elevated LV indices, whereas 10 (22%) regressed, through wall but not cavity reduction, to within normal LV indices. Predisposing factors to maintaining or achieving normal LV mass dimensions included relative youth (P < 0.05), a lower pulse pressure (P < 0.05), and a higher GFR (P < 0.05) but not hemoglobin concentration or parathyroid hormone levels. These findings suggest that even at a relatively advanced stage of renal dysfunction, control of BP and volume, together with regulated metabolic and clinical indices, may contribute to the prevention or even reversal of LV hypertrophy in a substantial proportion of patients.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673