Background
Kidney stones are common, frequently occurring worldwide. Some studies have analysed the relationship between dyslipidaemia and kidney stone occurrence but produced inconsistent results due to shortcomings such as small sample sizes, sampling bias, and limited data acquisition. Therefore, correlation studies with sufficient data sources, wide coverage, and strong representation must be carried out.
Methods
Samples used in our study were obtained from the National Health and Nutrition Examination Survey (NHANES) 2007–2016 database. Patients were divided into kidney stone and non-kidney stone groups according to an NHANES standardized question: “Have you ever had kidney stones?” Data on serum total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and the TC/HDL-C ratio were gathered from the two groups. Weighted Mann‒Whitney U tests, weighted chi-square tests, and weighted univariate and multivariable logistic regression analyses were used to analyse the relationship between dyslipidaemia and kidney stone occurrence.
Results
In total, 10,753 participants were included. TG, TC/HDL-C, and the percentage of individuals with abnormal TG or HDL-C were significantly higher in the stone group than in the non-stone group, and HDL-C levels were significantly lower in the stone group than in the non-stone group. Univariate and multivariate weighted logistic regression analyses indicated that TG and HDL-C abnormalities and high TC/HDL-C levels might be related to increased kidney stone risk (all P for trend < 0.05). Subgroup analyses after stratifying the overall data by age group, sex, and BMI showed that the effects of TG abnormality and TC/HDL-C level on kidney stone risk varied by age group and BMI, while the effect of HDL-C abnormality on the risk of kidney stones only varied by age group.
Conclusion
TG, HDL-C, and TC/HDL-C are related to a history of kidney stones in US adults. Dyslipidaemia may increase kidney stone prevalence. Further prospective and mechanistic studies are needed to verify the causal roles and pathogenesis.