Aim: To characterize haemoglobin A1c (HbA1c) trajectories and examine their associations with chronic kidney disease (CKD) progression.
Methods: This was a prospective cohort study on 770 patients with type 2 diabetes mellitus (T2DM) attending a diabetes centre in 2002-2017. Group-based trajectory modelling was used to identify HbA1c trajectories. Cox proportional hazards models were used to examine association between the trajectories and CKD progression which was defined as deterioration across the Kidney Disease: Improving Global Outcomes estimated glomerular filtration rate categories with ≥25% drop from baseline.
Results: We identified four HbA1c trajectories: 'near-optimal stable' (49.1%), 'moderate stable' (37.9%), 'moderate-increasing' (6.0%) and 'high-decreasing' (7.0%). Over a median follow-up period of 4.6 years (interquartile range 2.5-5.6), CKD progression occurred in 35.6% of patients. The risk of CKD progression was significantly higher in the moderate-increasing with adjusted hazard ratios (HR) 2.23 (95% confidence interval (CI) 1.09-4.57). After additional adjustment for mean HbA1c, the association between the moderate-increasing subgroup and CKD progression remained significant at HR 3.07 (95% CI 1.08-8.77).
Conclusion: Moderate-increasing HbA1c trajectory is associated with renal disease progression in patients with T2DM, independent of mean HbA1c. The deleterious effects of deteriorating HbA1c trajectory highlight the importance of achieving sustained good glycaemic control in diabetes management.
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http://dx.doi.org/10.1111/nep.13533 | DOI Listing |
Acta Physiol (Oxf)
February 2025
Department of Medicine, Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland.
Aim: Proteinuria is the most robust predictive factors for the progression of chronic kidney disease (CKD), and interventions targeting proteinuria reduction have shown to be the most effective nephroprotective treatments to date. While glomerular dysfunction is the primary source of proteinuria, its consequences extend beyond the glomerulus and have a profound impact on tubular epithelial cells. Indeed, proteinuria induces notable phenotypic changes in tubular epithelial cells and plays a crucial role in driving CKD progression.
View Article and Find Full Text PDFJ Clin Med
January 2025
Hypertension Unit, Division of Clinical Medicine, Department of Medical Sciences, University of Ferrara, 44124 Ferrara, Italy.
An increased renal resistive index (RRI) and proteinuria can predict an estimated glomerular filtration rate (eGFR) decline in patients with chronic kidney disease (CKD) of various causes. This study hypothesized that the RRI and proteinuria interact to determine disease progression in patients with CKDs of unknown origin. : One hundred and fifty six patients (age 76.
View Article and Find Full Text PDFJ Clin Med
December 2024
Department of Nephrology, Hypertension, Transplantation and Internal Medicine, Central University Hospital, Medical University of Lodz, 90-419 Lodz, Poland.
Chronic kidney disease (CKD) is associated with increased annual costs, with the highest costs attributable to renal replacement therapy (RRT). These costs will rise as prevalence increases. Therefore, forecasting the future prevalence and economic burden of CKD, particularly in underdiagnosed populations, may provide valuable insights to policymakers looking at strategies to implement interventions to delay CKD progression.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Physiological Sciences, Interinstitutional Post-Graduate Program of Physiological Sciences, Federal University of São Carlos (UFSCar), São Carlos 13.566-490, SP, Brazil.
Menopause occurs due to the depletion of the ovarian reserve, leading to a progressive decline in estrogen (E2) levels. This decrease in E2 levels increases the risk of developing several diseases and can coexist with chronic kidney disease (CKD). Arterial hypertension (AH) is another condition associated with menopause and may either contribute to or result from CKD.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Medicine, Faculty of Medicine, University of Malaysia (UM), Kuala Lumpur 59100, Malaysia.
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