High remnant cholesterol as a risk factor for developing chronic kidney disease in patients with prediabetes and type 2 diabetes: a cross-sectional study of a US population.

AIMS: To examine any potential links between remnant cholesterol (RC) and comorbid chronic kidney disease (CKD) in individuals with prediabetes and type 2 diabetes mellitus (T2DM). METHODS: We used data from 2709 American people aged > 20 years from the National Health and Nutrition Examination Survey (NHANES) during 2011-2018. Subjects were categorized according to whether they had comorbid CKD. Logistic regression models and smoothed curve fitting methods were employed to assess the association of RC with comorbid CKD in patients with prediabetes and T2DM. RESULTS: The 2709 participants included 1473 patients with T2DM and 1236 with prediabetes [impaired glucose tolerance (IGT) and impaired fasting glucose (IFG)], of whom 744 (27.46%) had comorbid CKD. In multivariate-adjusted analysis, both RC and triglycerides (TG) were significantly associated with an increased risk of comorbid CKD, and a 1 mmol/L elevation of RC increased the risk by 38.1% [OR (95% CI) 1.636 (1.242, 2.156)], which was higher than the risk associated with a 1 mmol/L increase in TG [1.255 (1.106, 1.424)]. Additionally, those in the highest quartile of RC had a 43.6% higher risk of concomitant renal damage than those in the lowest quartile. RC was linearly and positively associated with the incidence of comorbid CKD in this population. CONCLUSIONS: RC is an independent risk factor for comorbid CKD in patients with prediabetes and T2DM. This finding provides a novel insight into the management and early detection of renal disease in patients with impaired glucose metabolism.

Association of regulatory T cells with renal outcomes in patients with proliferative lupus nephritis.

BACKGROUND: Despite progress in the diagnosis and treatment of proliferative lupus nephritis (PLN), the prognosis remains unfavorable. Previous investigations have suggested that the deficiency of regulatory T cells (Tregs) is involved in the pathogenesis of systemic lupus erythematosus (SLE) and lupus nephritis (LN). But the prognostic value of Tregs in PLN remains controversial. This study aimed to investigate the association of Tregs with renal outcomes in patients with PLN. METHODS: The baseline and follow-up data of patients with biopsy-proven PLN were collected in this study. All patients were divided into two groups according to whether the renal endpoint event occurred. Clinicopathologic features and therapeutic responses were compared between the two groups. Cox regression analyses curve fitting and threshold effect analysis were implemented to investigate the relationship between Tregs level and the long-term renal outcomes. The renal endpoint was defined as end-stage kidney disease (ESKD) or doubling the SCr value. RESULTS: A total of 405 PLN patients were included. After a follow-up of 71.53 (53.13-97.47) months, 42 (10.4%) patients reached the renal endpoint. The Treg cell counts (16/µL) in the renal endpoint group were significantly decreased than that in the non-renal endpoint group (p < 0.001). Univariate and multivariate Cox regression analyses showed that the high level of Tregs was an independent protective factor for the long-term renal prognosis of PLN. Smooth curve fitting of the generalized additive mixed model analysis indicated that the risk of renal endpoint first decreased with Tregs and then slightly increased along with Treg cell levels. The segmented linear model revealed that when Treg cell counts <46/µL, the risk of renal endpoint decreased by 6.8% for every 1 µL increase in Treg levels (p = 0.0029). CONCLUSION: Treg cell counts are closely related to the long-term renal outcomes of patients with PLN, and increasing Treg cell levels may play an important role in improving the prognosis of the kidney, but there may be a turning point (i.e., threshold effect) at the Treg cell counts that leads to directional changes in the renal outcomes.

Relationship between anti-GBM antibodies and kidney outcomes in patients with anti-GBM disease.

INTRODUCTION: Animal experiments have shown that anti-GBM antibodies play a pathogenic role in anti-GBM disease. However, the relationship between anti-GBM antibody levels and kidney outcomes in patients with anti-GBM disease is unclear. METHODS: We performed a retrospective analysis of 110 patients diagnosed with anti-GBM disease. We compared their baseline characteristics stratifying on different anti-GBM antibody levels, and used Cox regression analysis to analyze the correlation between antibody levels and kidney survival. We further selected 69 patients to evaluate the modification of antibody titers over 14 days of treatment, then compared kidney survival of patients in the group with antibody level decrease < 48% to those with antibody decrease ≥ 48%. RESULTS: The 110 patients had a median follow-up of 27.1 (Q1-Q3: 7.9-80.1) months, and among them 90 (81.8%) developed kidney failure. Multivariate analysis suggested that anti-GBM antibody level was an independent risk factor for progression to kidney failure in patients with anti-GBM disease (HR 1.08, 95% CI 1.01-1.16). The patients who reduced the antibodies levels quickly had better kidney survival than those who did not, and multivariate analysis also indicated that antibody decrease rate was related to kidney outcomes. CONCLUSIONS: Anti-GBM antibody level is closely related to kidney outcomes in patients with anti-GBM disease, and short-term reduction of antibodies can be beneficial to improving kidney outcomes.

Relationship Between Serum Complement C3 Levels and Outcomes Among Patients With Anti-GBM Disease.

Background: IgG and complement 3 (C3) are generally found to be deposited along the glomerular basement membrane (GBM) in human anti-GBM disease. The pathogenic role of complement activation in kidney damage of anti-GBM disease has been explored in recent years. Therefore, we investigated the relationship between serum C3 and outcomes among patients with anti-GBM disease in this study. Methods: Ninety-four anti-GBM disease patients between January 2004 and December 2020 at the National Clinical Research Center of Kidney Diseases Jinling Hospital were retrospectively analyzed, and were divided into the low C3 group and the normal C3 group according to serum C3 levels at diagnosis. Fifty-six patients had undergone renal biopsy. We analyzed the clinical manifestations, laboratory tests, kidney pathology, treatment, and outcomes between the two groups. The primary endpoint was kidney failure. Cox regression and smooth curve fitting of generalized additive mixed model analysis were used to explore the correlation between serum C3 and kidney failure. The outcomes of the two groups were compared by the Kaplan-Meier curve. Results: A total of 94 patients (aged 43.6 ± 16.2; male patients, 46%) with anti-GBM disease were enrolled. There were 26 patients with low C3 levels and 68 patients with normal C3 levels. Compared with the normal C3 group, patients in the low C3 group have a higher proportion of glomerular sclerosis progressing to kidney failure. Multivariate Cox regression analysis suggested that C3 is associated with kidney outcomes in patients with anti-GBM disease (HR = 0.782, 95% CI = 0.673-0.907, p = 0.001). Smooth curve fitting of generalized additive mixed model analysis indicated that the level of C3 had a linear relationship with the changing trend of kidney failure. The Kaplan-Meier curve showed that there was a statistical difference between the two groups in terms of kidney failure (p = 0.033). Conclusion: The kidney outcomes of anti-GBM disease in the low C3 group were poorer than those in the normal C3 group. The influence of C3 on the kidney outcomes of patients with anti-GBM disease may be of clinical relevance.