The association between monocyte to high-density lipoprotein cholesterol ratio and chronic kidney disease in a Chinese adult population: a cross-sectional study.

BACKGROUND: Monocyte to high-density lipoprotein cholesterol ratio (MHR) was confirmed as a novel inflammatory marker and strongly associated with the risk of several diseases. This study aimed to investigate the relationship between MHR and chronic kidney disease (CKD) in a Chinese adult population. METHODS: In this cross-sectional study, 232,775 community-dwelling adults in Binhai who completed health checkups in 2021 were enrolled. Participants were categorized based on the MHR quartiles. Clinical characteristics of participants across different groups were compared using one-way ANOVA, Kruskal-Wallis h-test, and Chi-squared test as appropriate. Univariate and multivariable logistic regression analyses were taken to assess the relationship between MHR and the presence of CKD, as well as its association with low estimated glomerular filtration rate (eGFR) and proteinuria. Subgroup analyses were further executed to confirm the reliability of this relationship. RESULTS: A total of 21,014 (9.0%) individuals were diagnosed with CKD. Characteristic indicators including waist circumference, body mass index (BMI), blood pressure (BP), serum uric acid (SUA), triglyceride, and fasting blood glucose (FBG) showed a gradual increase with higher MHR quartiles, whereas parameters such as age, total cholesterol, high-density lipoprotein cholesterol (HDL-C), and eGFR decreased (p < .001). In the multivariable logistic regression analysis, we observed independent associations between MHR (per 1 SD increase) and CKD, as well as low eGFR and proteinuria, with odds ratio (ORs) and 95% confidence intervals (95%CIs) of 1.206 (1.186-1.225), 1.289 (1.260-1.319), and 1.150 (1.129-1.171), respectively (p < .001). Similar conclusions were confirmed in subgroup analysis stratified by gender, age, BMI, central obesity, hypertension, and diabetes mellitus, after justification for confounding factors. CONCLUSION: Elevated MHR level was independently associated with the presence of CKD, suggesting that it might serve as a useful clinical tool for risk stratification, offering valuable insights to inform preventive and therapeutic approaches for clinicians in their routine medical practice.

Impaired orthostatic blood pressure stabilization and reduced hemoglobin in chronic kidney disease.

Impaired orthostatic blood pressure (BP) stabilization is prevalent in patients with chronic kidney disease (CKD) and is associated with adverse outcomes. We aimed to test the hypothesis that reduced hemoglobin is an important contributor to orthostatic intolerance in CKD in the present study. This study included 262 patients with non-dialysis-dependent CKD. Seated and standing BP was measured, and orthostatic BP reduction was calculated for both systolic BP (∆ SBP) and diastolic BP (∆ DBP). The association between orthostatic BP reduction and hemoglobin was determined by multiple linear regression models. We also performed mediation analysis to test to what extent the effect of renal dysfunction on impaired orthostatic BP stabilization can be explained by reduced hemoglobin. The mean age of the patients was 57.7 (±14.5) years, and 61.5% were male. Both ∆ SBP and ∆ DBP correlated negatively with estimated glomerular filtration rate (eGFR). With adjustment for age and sex, hemoglobin level was negatively associated with ∆ SBP (ß = -1.4, SE = 0.4, P < .001) and ∆ DBP (ß = -0.6, SE = 0.2, P = .009). The associations remained significant with further adjustment for additional covariates. When eGFR was introduced as a covariate, it did not eliminate the significance (both P < .05). The associations remained essentially unchanged in a sensitivity analysis excluding those with concurrent erythropoietin use. Mediation analysis demonstrated that reduced hemoglobin accounted for 35.4% (P = .004) of the effect of eGFR on ∆ SBP and 47.7% (P = .032) on ∆ DBP. Our study suggests that reduced hemoglobin is a potentially important contributor to the development of orthostatic hypotension in CKD.

Circulatory mitochondrial DNA is a pro-inflammatory agent in maintenance hemodialysis patients.

Chronic inflammation is highly prevalent in maintenance hemodialysis (MHD) patients, and it has been shown to be a strong predictor of morbidity and mortality. Mitochondrial DNA (mtDNA) released into circulation after cell damage can promote inflammation in patients and animal models. However, the role and mechanisms of circulatory mtDNA in chronic inflammation in MHD patients remain unknown. Sixty MHD patients and 20 health controls were enrolled in this study. The circulatory mtDNA was detected by quantitative real-time PCR assay. Plasma interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) were quantitated by ELISA assay. Dialysis systems in MHD patients and in vitro were used to evaluate the effect of different dialysis patterns on circulatory mtDNA. Circulatory mtDNA was elevated in MHD patients comparing to that of health control. Regression analysis demonstrated that plasma mtDNA was positively associated with TNF-α and the product of serum calcium and phosphorus, while negatively associated with hemoglobin and serum albumin in MHD patients. MtDNA induced the secretion of IL-6 and TNF-α in the THP-1 cells. Single high-flux hemodialysis (HF-HD) and on line hemodiafiltration (OL-HDF) but not low-flux hemodialysis (LF-HD) could partially reduce plasma mtDNA in MHD patients. In vitro, both HD and hemofiltration (HF) could fractional remove mtDNA. Collectively, circulatory mtDNA is elevated and its level is closely correlated with chronic inflammation in MHD patients. HF-HD and HDF can partially reduce circulatory mtDNA in MHD patients.