African Americans with left ventricular hypertrophy and chronic kidney disease: what should we do?

Patients with chronic kidney disease (CKD) have an exceedingly high incidence of cardiovascular diseases including heart failure. Cardiac morphological abnormalities such as left ventricular hypertrophy (LVH) are associated with an increased incidence of heart failure, ventricular arrhythmias and death [1, 2]. Seventy-four percent of patients with CKD have LVH, which in part explains their high incidence of cardiovascular diseases, hospitalization and death [3, 4]. African Americans are disproportionately affected by both heart failure and CKD [5]. This is partly explained by the increased prevalence of hypertension, hyperparathyroidism, elevated fibroblast growth factor 23 and vitamin D deficiency as well as a decrease in preventive strategies and access to care [6]. Furthermore, African Americans respond differently to salt reduction and pharmacologic therapies such as angiotensin-converting enzyme inhibitors and diuretics [7, 8]. Despite their elevated cardiovascular risk, African Americans have been under represented in all major trials evaluating heart failure and cardiac morphological abnormalities in patients with CKD. Bansal et al. [9] report the largest population-based cohort of African Americans to date, where they found an adjusted mean increase in left ventricular mass of ∼8 g in patients with proteinuria (albumin:creatinine ratio >30 g/mg) compared with those patients without proteinuria. Similarly, there was an adjusted ∼2-fold increase in heart failure hospitalizations over the course of 3 years of follow-up, independent of baseline left ventricular mass. These findings suggest a similar or related pathophysiology between proteinuria and LVH (i.e. NF-κB, TGF-β, collagens, etc.). However, the study did not find an association between left ventricular ejection fraction and renal function parameters. There was a similar association between the estimated glomerular filtration rate, left ventricular mass and heart failure hospitalizations. Translating the results of this robust study into clinical practice remains a challenge. We cannot compare the incidence or degree of LVH in African Americans relative to White individuals with a similar degree of renal dysfunction, which would help determine if differences in biologic pathway activation between African Americans and White individuals exist. More importantly, although the results of this study are interesting, they do not provide any evidence that screening for LVH or modifying lifestyle or medical regimen would change outcomes over time (LVH, heart failure hospitalizations, etc.). Future studies need to focus on longitudinal follow-up of LVH and heart failure with different therapeutic regimens, enabling application of these findings in the clinic. None declared. (See related article by Bansal et al. Markers of kidney disease and risk of subclinical and clinical heart failure in African Americans: the Jackson Heart Study. Nephrol Dial Transplant 2016; 31: 2057–2064)