Earlier onset and greater severity of disordered mineral metabolism in diabetic patients with chronic kidney disease.
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2012-05
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Abstract
Disordered mineral metabolism is a common complication of chronic kidney disease (CKD) and a novel risk factor for CKD progression, cardiovascular disease, and mortality. Although diabetes is the leading cause of CKD and is associated with worse clinical outcomes than other etiologies, few studies have evaluated mineral metabolism in CKD according to diabetes status.Using the Chronic Renal Insufficiency Cohort Study, we tested the hypothesis that diabetes is independently associated with lower serum calcium and higher serum phosphate, parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF23).Compared with participants without diabetes (n = 1,936), those with diabetes (n = 1,820) were more likely to have lower estimated glomerular filtration rate (eGFR), lower serum albumin, and higher urinary protein excretion (all P < 0.001). Unadjusted serum phosphate, PTH, and FGF23 levels were higher and calcium was lower among those with compared with those without diabetes (all P < 0.001). After multivariate adjustment, diabetes remained a significant predictor of serum phosphate, PTH, and FGF23 but not calcium. The eGFR cut point at which 50% of participants met criteria for secondary hyperparathyroidism or elevated FGF23 was higher in participants with diabetes compared with those without (PTH: eGFR 30-39 vs. 20-29, P < 0.001; FGF23: eGFR 50-59 vs. 40-49, P < 0.001).Disordered mineral metabolism begins earlier in the course of CKD and is more severe among CKD patients with compared with those without diabetes. Future studies should explore mechanisms for these differences and whether they contribute to excess risks of adverse clinical outcomes among diabetic patients with CKD.
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Wahl, Patricia, Huiliang Xie, Julia Scialla, Cheryl AM Anderson, Keith Bellovich, Carolyn Brecklin, Jing Chen, Harold Feldman, et al. (2012). Earlier onset and greater severity of disordered mineral metabolism in diabetic patients with chronic kidney disease. Diabetes care, 35(5). pp. 994–1001. 10.2337/dc11-2235 Retrieved from https://hdl.handle.net/10161/18487.
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Scholars@Duke
Julia Jarrard Scialla
Dr. Scialla is an Associate Professor of Medicine in Nephrology at Duke University and a faculty member at the Duke Clinical Research Institute. Dr. Scialla trained in Internal Medicine, Nephrology, and Clinical Epidemiology at the Johns Hopkins University School of Medicine and the Johns Hopkins Bloomberg School of Public Health. Her research focuses on chronic kidney disease (CKD) epidemiology and prevention, with an emphasis on the role of metabolic complications and nutrition. Current studies are focused on treatment and prevention of abnormal phosphate homeostasis, acid-base physiology, diabetic and other forms of kidney disease, and outcomes in end-stage kidney disease.
Dr. Scialla’s work engages a number of study designs including prospective cohort studies, observational comparative effectiveness studies, and patient-oriented physiologic studies. She has worked closely with multiple chronic disease cohorts including the Chronic Renal Insufficiency Cohort (CRIC) Study, the African American Study of Kidney Disease and Hypertension (AASK), the Jackson Heart Study (JHS), and secondary analyses in clinical trials. Studies in electronic health records (EHR) and registries have engaged dialysis EHR data, the United States Renal Data System, and public registries, such as the National Health and Nutrition Examination Survey. Physiologic studies include the Acid Base Complication in CKD Study, secondary analyses in the DASH Mechanism Study, and the newly launched MURDOCK Kidney Health Study.
Myles Selig Wolf
The focus of my research is disordered mineral metabolism across the spectrum of chronic kidney disease, including dialysis, kidney transplantation and earlier stages.
My research has been published in leading general medicine and subspecialty journals, including the New England Journal of Medicine, JAMA, the Journal of Clinical Investigation, Circulation, Cell Metabolism, Journal of the American Society of Nephrology, and Kidney International, among others.
My primary contributions have been in the area of hormonal regulation of phosphate homeostasis. I have helped to characterize the physiological role of fibroblast growth factor 23 in health and in chronic kidney disease, and the impact of elevated fibroblast growth factor 23 levels on adverse clinical outcomes in patients with kidney disease.
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