Association of Uric Acid to High-Density Lipoprotein Cholesterol Ratio with Left Ventricular Hypertrophy in Chronic Kidney Disease.

INTRODUCTION

Chronic kidney disease (CKD) is associated with a high prevalence of cardiovascular complications, including left ventricular hypertrophy (LVH), which significantly increases morbidity and mortality. LVH in CKD results from a complex interplay of hemodynamic, neurohormonal, and metabolic factors. The uric acid-to-high density lipoprotein cholesterol ratio (UHR) has recently been proposed as a potential marker for cardiovascular outcomes, combining the effects of uric acid and HDL-C on inflammation and cardiovascular risk. However, the relationship between UHR and LVH in CKD patients remains unexplored. This study aimed to investigate the association between UHR and LVH in patients with CKD.

METHODS

This cross-sectional study included CKD patients admitted to the Division of Nephrology between April 2019 and October 2019. CKD was staged according to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines. LVH was assessed using transthoracic echocardiography, and left ventricular mass index (LVMI) was calculated. LVH was defined as an LVMI >115 g/m2 for men and >95 g/m2 for women. UHR was calculated by dividing serum uric acid levels (µmol/L) by HDL-C levels (mmol/L). Multivariable logistic regression models were used to assess the association between UHR and LVH, adjusting for covariates including age, gender, BMI, and other relevant clinical factors.

RESULTS

A total of 466 patients were included, of whom 56 had LVH. Patients with LVH had significantly higher UHR levels compared to those without LVH. In multivariable regression analysis, the natural logarithm of UHR (LnUHR) was significantly associated with an increased risk of LVH (OR: 2.04, 95% CI: 1.05-4.12, p = 0.035) after full adjustment for confounders. Further analysis using restricted cubic splines revealed a non-linear relationship between UHR and LVH, with an inflection point at UHR = 0.60. Below this threshold, each increase of one standard deviation in UHR was associated with a 2.11-fold increase in LVH risk (OR: 2.11, 95% CI: 1.51-3.03, p < 0.001), while above this threshold, the association was not significant (OR: 0.82, 95% CI: 0.39-1.47, p = 0.54).

CONCLUSION

This study provides the first evidence of an association between UHR and LVH in CKD patients, particularly at lower UHR levels. The findings suggest that UHR could serve as a novel marker for cardiovascular risk stratification in CKD, reflecting the balance between pro-inflammatory and protective cardiovascular factors. These results highlight the potential of UHR as a cost-effective tool for identifying CKD patients at increased risk of LVH, warranting further investigation in longitudinal studies to establish causality and explore targeted interventions.