Cardiovascular disease and chronic kidney disease (CKD) are intimately linked, with left ventricular hypertrophy (LVH) frequently demonstrated in patients with these conditions. The likelihood of having LVH appears to be related to the stage of CKD. However, it is less clear if patients with preserved kidney function or early stage CKD (eGFR >60 mL/min) maintain this relationship between eGFR and LVH. In a recent AJKD, Bansal et al examined the association of eGFR using cystatin C with the CKD-EPI equation (eGFRcys) in adults with eGFRcys >60 mL/min and a rapid decline in eGFR with subsequent LV mass index (LVMI). The cohort comprised 2410 subjects from the CARDIA (Coronary Artery Risk Development in Young Adults) study, a US multicenter study of young adults aged 18 – 30 years at recruitment between 1985 and 1986. Analyses performed were the association of year 15 eGFRcys and rapid decline in eGFRcys between years 15 and 20 (defined as >3% decline per year), with year 25 LVMI.
Patient characteristics included mean age of 40 +/- 4 years, 58% were women, and 43% were African American. Unsurprisingly, LVMI was higher in those with lower eGFRcys at baseline despite adjusting for potential confounders. In the multi-factorial model including demographics, cardiovascular risk factors, and albuminuria, eGFRcys of 60 – 75 mL/min (compared to eGFRcys >90 mL/min) was significantly associated with higher LVMI 10 years later. Cumulative 10-year systolic BP exposure was also included in the model.
In the analysis of change in eGFRcys between year 15 and 20, every 1% decline in eGFRcys was associated with a 0.40 g/m2.7 increase in LVMI at year 25. This was not significant in the multi-factorial model. However, the 379 participants who had a rapid decline in eGFRcys over the 5 years had a significantly higher mean LVMI at year 25. The effect was partially attenuated with adjustment for systolic BP exposure, but remained significant.
This study suggests that mild decreases in kidney function may be associated years later with the subsequent development of cardiovascular disease, or at least higher LVMI. The potential mechanisms for this remain speculative and may include alterations in the renin-angiotensin-aldosterone system or vitamin D-PTH-fibroblast growth factor 23 axis, to name a few. The observational nature of the study and the abrogation of the effect with adjustment for covariates lead to a potential for residual confounding. However, the study does highlight the possible cardiovascular significance of early CKD in young adults and the decline in eGFR in those with “preserved” kidney function. The next question is: what do we do about it?
Dr. Paul Phelan
AJKD Blog Contributor