Role of Aldosterone in Left Ventricular Hypertrophy among African-American Patients with End-Stage Renal Disease on Hemodialysis

Abstract

Aims: Recently, serum aldosterone levels have been reported to play a significant role in cardiac hypertrophy. One study of Japanese patients correlated aldosterone levels with the degree of left ventricular hypertrophy (LVH) in those undergoing hemodialysis. However, the role of aldosterone in LVH in non-Japanese patients with end-stage renal disease (ESRD) has not been established. Materials and Methods: Researchers evaluated 42 [29 African-Americans (69%), 11 Caucasians (26%), and 2 other (5%)] male ESRD patients on dialysis for more than 6 months. Pre- and postdialysis, blood pressures and aldosterone and renin concentrations were measured. Transthoracic echocardiography was performed and left ventricular mass (LVM) index was calculated using the Devereaux formula. Medications were reviewed. Results: There were no differences noted in medications prescribed for African-Americans and for Caucasians. Additionally, data from diabetic patients showed no statistically significant correlation between LVM index and any of the variables, including pre- and postdialysis blood pressure, serum potassium, renin, and aldosterone levels, for African-Americans compared to Caucasians. Data from nondiabetic patients showed a positive correlation between LVM and plasma aldosterone concentration in African-Americans (n = 10). Data from nondiabetic Caucasians were disregarded because only one was studied. Conclusion: LVM and aldosterone correlate in African-American males with ESRD on hemodialysis without diabetes. This has important implications for the etiology of, and therapy for LVH in this population. Larger studies are needed to determine whether the same associations exist in females and Caucasians.

Long-Term Effects of Spironolactone in Peritoneal Dialysis Patients

“…24 Persistent hyperaldosteronemia and/or activation of MR can promote cardiac fibrosis, possibly through generation of signals promoting profibrotic TGF-b production. 1,25,26 In animal models, spironolactone ameliorates cardiac fibrosis in nephrectomized uremic rats. 27,28 We evaluated the effects of adding spironolactone to ACEI or ARB in patients undergoing PD, and we found that LVMI was significantly suppressed in the spironolactone group (Figure 2).…”

Left Ventricular Hypertrophy in Chronic Kidney Disease Patients: From Pathophysiology to Treatment

“…The ones in the first category are represented by an increase in systemic arterial resistance, elevated arterial blood pressure, and reduced large-vessel compliance [17,18,19,20] related in part to aortic ‘calcification', which is typical in CKD patients; all these factors result in myocardial cell thickening and concentric LV remodeling often together with activation of the intracardiac renin-angiotensin system [19,21]. …”

Left Ventricular Mass in Chronic Kidney Disease and ESRD

“…These afterload-related factors result in myocardial cell thickening and concentric LV remodeling. Activation of the intracardiac renin-angiotensin system (RAS) seems to be critically involved in this pathway, but angiotensin II and aldosterone as well can also be involved in myocardial cell hypertrophy and fibrosis, independent of afterload (23,25,26). Non-angiotensin II-dependent pathways for induction of LVH by mechanical stretch have been identified (27).…”

“…Persistent hyperaldosteronemia, consequent to activation of RAS or through non-RAS-dependent factors, can promote cardiac fibrosis, perhaps through generation of signals promoting profibrotic transforming growth factor ␤ production (23,26). Deficiency states, such as iron and/or erythropoietin (with attendant anemia), and perhaps carnitine deficiency as well can promote LVH (49).…”