Chutatip Limkunakul1, Ian H de Boer2, Bryan R Kestenbaum2, Jonathan Himmelfarb2, T Alp Ikizler3, Cassianne Robinson-Cohen4. 1. Department of Medicine, Srinakharinwirot University, Thailand. 2. Kidney Research Institute, Division of Nephrology, Department of Medicine, University of Washington, Seattle, WA, United States. 3. Division of Nephrology, Vanderbilt University Medical Center, Nashville, TN, United States. 4. Division of Nephrology, Vanderbilt University Medical Center, Nashville, TN, United States. Electronic address: cassianne.robinson-cohen@vumc.org.
Abstract
CONTEXT: Diabetic kidney disease (DKD) is the leading cause of end stage kidney disease (ESKD) and is associated with a considerably shortened lifespan. While glucose-lowering therapy targeting glycated hemoglobin (HbA1c) <7% is proven to reduce the risk of developing DKD, its effects on complications of DKD are unclear. OBJECTIVE: We examined the associations of HbA1c with risks of progression to ESKD and death within a clinic-based study of CKD. We hypothesized that higher HbA1c concentrations would be associated with increased risks of ESKD and death. DESIGN AND SETTING: We studied 618 participants from the Seattle Kidney Study (mean eGFR 42 ml/min), 308 of whom had diabetes, and tested associations of baseline HbA1c with time to a composite outcome of initiation of renal replacement therapy or death. RESULTS: During a median follow-up of 4.2 years, there were 343 instances of the composite outcome (11.5 per 100 person-years). Among participants with diabetes, in both crude and adjusted analyses, higher HbA1c levels (examined continuously or categorically) were not associated with the risk of the composite outcome (HR (95% CI): 0.99 (0.88, 1.10) per 1% additional HbA1c, p = 0.79). HbA1c was not associated with ESKD or mortality when the outcomes were examined separately, nor when stratified between insulin users and non-users. CONCLUSION: In a referred population of established DKD, higher HbA1c was not associated with higher risk of ESKD or death. These data support current recommendations to be conservative with glycemic control among patients with advanced diabetes complications, such as CKD.
CONTEXT: Diabetic kidney disease (DKD) is the leading cause of end stage kidney disease (ESKD) and is associated with a considerably shortened lifespan. While glucose-lowering therapy targeting glycated hemoglobin (HbA1c) <7% is proven to reduce the risk of developing DKD, its effects on complications of DKD are unclear. OBJECTIVE: We examined the associations of HbA1c with risks of progression to ESKD and death within a clinic-based study of CKD. We hypothesized that higher HbA1c concentrations would be associated with increased risks of ESKD and death. DESIGN AND SETTING: We studied 618 participants from the Seattle Kidney Study (mean eGFR 42 ml/min), 308 of whom had diabetes, and tested associations of baseline HbA1c with time to a composite outcome of initiation of renal replacement therapy or death. RESULTS: During a median follow-up of 4.2 years, there were 343 instances of the composite outcome (11.5 per 100 person-years). Among participants with diabetes, in both crude and adjusted analyses, higher HbA1c levels (examined continuously or categorically) were not associated with the risk of the composite outcome (HR (95% CI): 0.99 (0.88, 1.10) per 1% additional HbA1c, p = 0.79). HbA1c was not associated with ESKD or mortality when the outcomes were examined separately, nor when stratified between insulin users and non-users. CONCLUSION: In a referred population of established DKD, higher HbA1c was not associated with higher risk of ESKD or death. These data support current recommendations to be conservative with glycemic control among patients with advanced diabetes complications, such as CKD.
Authors: Aram V Chobanian; George L Bakris; Henry R Black; William C Cushman; Lee A Green; Joseph L Izzo; Daniel W Jones; Barry J Materson; Suzanne Oparil; Jackson T Wright; Edward J Roccella Journal: JAMA Date: 2003-05-14 Impact factor: 56.272
Authors: Robert T C E Robinson; Nigel D Harris; Robert H Ireland; Stuart Lee; Christopher Newman; Simon R Heller Journal: Diabetes Date: 2003-06 Impact factor: 9.461