Aims: This study aims to develop and validate a predictive model for Chronic Kidney Disease (CKD) progression in Type 2 Diabetes Mellitus (T2DM).
Methods: We conducted a prospective study on 1582 patients with T2DM from a Diabetes Centre in regional hospital in 2002-2014. CKD progression was defined as deterioration across eGFR categories with ⩾25% drop from baseline. The dataset was randomly split into development (70%) and validation (30%) datasets. Stepwise multivariable logistic regression was used to identify baseline predictors for model development. Model performance in the two datasets was assessed.
Results: During median follow-up of 5.5years, 679 (42.9%) had CKD progression. Progression occurred in 467 (42.2%) and 212 patients (44.6%) in development and validation datasets respectively. Systolic blood pressure, HbA1c, estimated glomerular filtration rate and urinary albumin-to-creatinine ratio were associated with progression. Areas under receiving-operating-characteristics curve for the training and test datasets were 0.80 (95%CI, 0.77-0.83) and 0.83 (95%CI, 0.79-0.87). Observed and predicted probabilities by quintiles were not statistically different with Hosmer-Lemeshow χ 0.65 (p=0.986) and 1.36 (p=0.928) in the two datasets. Sensitivity and specificity were 71.4% and 72.2% in development dataset, and 75.6% and 72.3% in the validation dataset.
Conclusions: A model using routinely available clinical measurements can accurately predict CKD progression in T2DM.
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http://dx.doi.org/10.1016/j.diabres.2016.11.008 | 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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