Yu-Feng Lin1,2, Shuei-Liong Lin2,3, Tao-Min Huang2,4, Shao-Yu Yang2, Tai-Shuan Lai2, Likwang Chen5, Vin-Cent Wu6, Tzong-Shinn Chu2, Kwan-Dun Wu2. 1. Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan. 2. Division of Nephrology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan. 3. Graduate Institute of Physiology, National Taiwan University College of Medicine, Taipei, Taiwan. 4. Graduate Institute of Epidemiology and Preventive Medicine, National Taiwan University College of Medicine, Taipei, Taiwan. 5. Institute of Population Health Sciences, National Health Research Institutes, Zhunan, Taiwan. 6. Division of Nephrology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan q91421028@ntu.edu.tw.
Abstract
OBJECTIVE: Acute kidney injury (AKI) is related to a high prevalence of insulin resistance. However, information is lacking on the sequelae of further metabolic change among AKI requiring dialysis in patients who could be weaned off dialysis (acute kidney disease [AKD]). RESEARCH DESIGN AND METHODS: Using the National Health Insurance Research Database from 2000 to 2010, with the exclusion of those with diabetes at the start, we identified 3,307 subjects with AKD and 9,921 matched control subjects from 963,037 hospitalized patients for the comparison of the outcomes, including new-onset diabetes and all-cause mortality. RESULTS: Within the median follow-up period of 5.99 years, AKD patients had a higher incidence of new-onset diabetes than the matched control patients (5.16% vs. 4.17% per person-year, P = 0.001). AKD patients were at higher risk of mortality than control patients (adjusted hazard ratio [aHR] 1.27 [95% CI 1.18-1.36], P < 0.001). With mortality as a competing risk, a Cox proportional hazards analysis showed that AKD patients had a higher risk of subsequent diabetes (subhazard ratio [sHR] 1.18 [95% CI 1.07-1.30], P < 0.001) compared with the matched control patients. Subgroup analysis showed that patients with baseline hypertension (aHR 1.15 [95% CI 1.04-1.28]), hyperlipidemia (aHR 1.23 [95% CI 1.02-1.48]), and gout (aHR 1.23 [95% CI 1.03-1.46]) had increased odds of developing new-onset diabetes during follow-up. CONCLUSIONS: Patients who experienced AKI had a higher incidence of developing new-onset diabetes and mortality. This observation adds evidence regarding potential metabolic dysregulation after AKI.
OBJECTIVE:Acute kidney injury (AKI) is related to a high prevalence of insulin resistance. However, information is lacking on the sequelae of further metabolic change among AKI requiring dialysis in patients who could be weaned off dialysis (acute kidney disease [AKD]). RESEARCH DESIGN AND METHODS: Using the National Health Insurance Research Database from 2000 to 2010, with the exclusion of those with diabetes at the start, we identified 3,307 subjects with AKD and 9,921 matched control subjects from 963,037 hospitalized patients for the comparison of the outcomes, including new-onset diabetes and all-cause mortality. RESULTS: Within the median follow-up period of 5.99 years, AKD patients had a higher incidence of new-onset diabetes than the matched control patients (5.16% vs. 4.17% per person-year, P = 0.001). AKD patients were at higher risk of mortality than control patients (adjusted hazard ratio [aHR] 1.27 [95% CI 1.18-1.36], P < 0.001). With mortality as a competing risk, a Cox proportional hazards analysis showed that AKD patients had a higher risk of subsequent diabetes (subhazard ratio [sHR] 1.18 [95% CI 1.07-1.30], P < 0.001) compared with the matched control patients. Subgroup analysis showed that patients with baseline hypertension (aHR 1.15 [95% CI 1.04-1.28]), hyperlipidemia (aHR 1.23 [95% CI 1.02-1.48]), and gout (aHR 1.23 [95% CI 1.03-1.46]) had increased odds of developing new-onset diabetes during follow-up. CONCLUSIONS:Patients who experienced AKI had a higher incidence of developing new-onset diabetes and mortality. This observation adds evidence regarding potential metabolic dysregulation after AKI.