Aim: To study the natural history and predictors of faster glomerular filtration rate (GFR) decline in a referred population of older patients (aged ≥ 65 years) with type 2 diabetes mellitus.
Methods: A retrospective medical record analysis in an outpatient diabetes clinic for older patients. Baseline characteristics and blood pressure readings for each clinic visit were recorded. All laboratory results were downloaded from the central database of the pathology laboratory. Annual rate of GFR decline was calculated by linear regression analysis as the slope per year for each individual. Patients were then divided into 2 groups on either side of the mean GFR decline. Group 1 had a slower GFR decline (below the mean value) and group 2 had a faster GFR decline (above the mean value). Five variables were investigated as predictors of faster decline in GFR: cardiovascular disease (CVD), hypertension, diabetes control, use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, and albuminuria.
Results: The study included 100 patients with a mean age of 69.5 (standard deviation [SD], 3.9) years on referral, and 54 patients were men. The mean duration of study was 14.4 (SD, 2.0) years. A total of 3908 GFR results were downloaded during the study. The mean annual rate of GFR decline was 1.5 (SD, 1.2) mL/min/1.73 m2. Glomerular filtration rate values were comparable in both groups on first referral. Mean annual rate of GFR decline was 2.6 (SD, 0.9) mL/min/1.73 m2 in group 2 compared with 0.7 (SD, 0.5) mL/min/1.73 m2 (P < 0.001) in group 1. Development of CVD was the only independent predictor of faster renal function decline (odds ratio, 2.9; 95% CI, 1.1-7.6; P = 0.03).
Conclusion: Cardiovascular disease is an independent risk factor for faster decline in GFR in older patients with type 2 diabetes mellitus.
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http://dx.doi.org/10.3810/hp.2012.10.1003 | DOI Listing |
Ann Vasc Surg
January 2025
Division of Vascular and Endovascular Surgery, Massachusetts General Hospital, Boston, MA. Electronic address:
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January 2025
Department of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, 150001, China; Heilongjiang Provincial Key Laboratory of Critical Care Medicine, Harbin, 150001, China; Central Laboratory of the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China. Electronic address:
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View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Nephrology, Carol Davila University of Medicine and Pharmacy, 020021 Bucharest, Romania.
Autophagy and mitophagy are critical cellular processes that maintain homeostasis by removing damaged organelles and promoting cellular survival under stress conditions. In the context of diabetic kidney disease, these mechanisms play essential roles in mitigating cellular damage. This review provides an in-depth analysis of the recent literature on the relationship between autophagy, mitophagy, and diabetic kidney disease, highlighting the current state of knowledge, existing research gaps, and potential areas for future investigations.
View Article and Find Full Text PDFFront Med (Lausanne)
January 2025
Department of Internal Medicine, Texas Tech University Health Sciences Centre, Lubbock, TX, United States.
While changes in glomerular function and structure may herald diabetic kidney disease (DKD), many studies have underscored the significance of tubule-interstitial changes in the progression of DKD. Indeed, tubule-interstitial fibrosis may be the most important determinant of progression of DKD as in many forms of chronic glomerulopathies. The mechanisms underlying the effects of tubular changes on glomerular function in DKD have intrigued many investigators, and therefore, the signaling mechanisms underlying the cross-talk between tubular cells and glomerular cells have been the focus of investigation in many recent studies.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Clinical Physiology, Karolinska University Hospital, Stockholm, Sweden.
Background: The causes of reduced aerobic exercise capacity (ExCap) in chronic kidney disease (CKD) are multifactorial, possibly involving the accumulation of tryptophan (TRP) metabolites such as kynurenine (KYN) and kynurenic acid (KYNA), known as kynurenines. Their relationship to ExCap has yet to be studied in CKD. We hypothesised that aerobic ExCap would be negatively associated with plasma levels of TRP, KYN and KYNA in CKD.
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