Sitagliptin reduces the urine albumin-to-creatinine ratio in type 2 diabetes through decreasing both blood pressure and estimated glomerular filtration rate 西格列汀通过降低2型糖尿病患者的血压以及估算的肾小球滤过率来减少尿白蛋白/肌酐的比值
Background We investigated the change in the urine albumin‐to‐creatinine ratio (ACR) to examine the effect of sitagliptin on diabetic nephropathy. Methods Sitagliptin at a dose of 50 mg was administered to 247 outpatients with type 2 diabetes. Data were collected on the patients' laboratory res...
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Published in | Journal of diabetes Vol. 7; no. 1; pp. 41 - 46 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Blackwell Publishing Ltd
01.01.2015
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Subjects | |
Online Access | Get full text |
ISSN | 1753-0393 1753-0407 |
DOI | 10.1111/1753-0407.12153 |
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Abstract | Background
We investigated the change in the urine albumin‐to‐creatinine ratio (ACR) to examine the effect of sitagliptin on diabetic nephropathy.
Methods
Sitagliptin at a dose of 50 mg was administered to 247 outpatients with type 2 diabetes. Data were collected on the patients' laboratory results (including the ACR), blood pressure, and body weight. Clinical data were compared before and after 3 months' administration of sitagliptin.
Results
The ACR changed from 150.0 ± 538.6 mg/gCre to 148.3 ± 764.6 mg/gCre over 3 months. In the patients with micro‐ and macro‐albuminuria, the ACR after 3 months significantly decreased compared with the baseline (P = 0.04 and P = 0.02, respectively). The subjects whose ACR decreased experienced significantly larger decreases over the 3‐month period in blood pressure and estimated glomerular filtration rate (eGFR) than the other subjects. There was no significant correlation between change in ACR (ΔACR) and change in hemoglobin A1c (ΔHbA1c) during 3 months (r = 0.04, P = 0.59), but there was a significant correlation between change in ΔACR and change in systolic blood pressure (r = 0.16, P = 0.03). Multiple regression analysis revealed that the significant predictors for ΔACR were change in systolic blood pressure (β = 0.21, P = 0.016) and change in eGFR (β = 0.20, P = 0.024) over 3 months (r = 0.35, P = 0.04).
Conclusions
Sitagliptin reduces the ACR through decreasing both blood pressure and eGFR, with no correlation with a decrease in HbA1c over a 3‐month period. These results may reflect the direct action of sitagliptin on the kidneys.
摘要
背景:通过调查尿白蛋白/肌酐比值(ACR)的变化了解西格列汀对糖尿病肾病的影响。
方法:共有247名门诊2型糖尿病患者参加研究,给予西格列汀50 mg/日进行治疗。收集患者的实验室检查结果(包括ACR)、血压以及体重等数据。对比了使用西格列汀治疗前3个月与治疗后3个月的临床数据。
结果:3个月后ACR从150.0 ± 538.6 mg/gCre降至148.3 ± 764.6 mg/gCre。合并微量以及大量蛋白尿的患者治疗3个月后与基线相比较ACR都显著下降(分别P = 0.04与P = 0.02)。3个月后,与其他受试者相比,ACR下降的受试者其血压以及估算的肾小球滤过率(estimated glomerular filtration rate,eGFR)下降程度更大。在3个月期间,ACR的变化(ΔACR)与HbA1c的变化(ΔHbA1c)之间没有显著性的相关性(r = 0.04,P = 0.59),但是ΔACR的变化与收缩压的变化之间具有显著的相关性(r = 0.16,P = 0.03)。3个月后,多元回归分析结果显示,收缩压的变化(β = 0.21,P = 0.016)和eGFR的变化(β = 0.20,P = 0.024)是ΔACR的重要预测因子(r = 0.35,P = 0.04)。
结论:3个月的西格列汀治疗通过降低血压以及eGFR来减少ACR,与HbA1c的下降没有相关性。这些结果可能反映了西格列汀对肾脏具有直接的作用。 |
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AbstractList | Background
We investigated the change in the urine albumin‐to‐creatinine ratio (ACR) to examine the effect of sitagliptin on diabetic nephropathy.
Methods
Sitagliptin at a dose of 50 mg was administered to 247 outpatients with type 2 diabetes. Data were collected on the patients' laboratory results (including the ACR), blood pressure, and body weight. Clinical data were compared before and after 3 months' administration of sitagliptin.
Results
The ACR changed from 150.0 ± 538.6 mg/gCre to 148.3 ± 764.6 mg/gCre over 3 months. In the patients with micro‐ and macro‐albuminuria, the ACR after 3 months significantly decreased compared with the baseline (P = 0.04 and P = 0.02, respectively). The subjects whose ACR decreased experienced significantly larger decreases over the 3‐month period in blood pressure and estimated glomerular filtration rate (eGFR) than the other subjects. There was no significant correlation between change in ACR (ΔACR) and change in hemoglobin A1c (ΔHbA1c) during 3 months (r = 0.04, P = 0.59), but there was a significant correlation between change in ΔACR and change in systolic blood pressure (r = 0.16, P = 0.03). Multiple regression analysis revealed that the significant predictors for ΔACR were change in systolic blood pressure (β = 0.21, P = 0.016) and change in eGFR (β = 0.20, P = 0.024) over 3 months (r = 0.35, P = 0.04).
Conclusions
Sitagliptin reduces the ACR through decreasing both blood pressure and eGFR, with no correlation with a decrease in HbA1c over a 3‐month period. These results may reflect the direct action of sitagliptin on the kidneys.
摘要
背景:通过调查尿白蛋白/肌酐比值(ACR)的变化了解西格列汀对糖尿病肾病的影响。
方法:共有247名门诊2型糖尿病患者参加研究,给予西格列汀50 mg/日进行治疗。收集患者的实验室检查结果(包括ACR)、血压以及体重等数据。对比了使用西格列汀治疗前3个月与治疗后3个月的临床数据。
结果:3个月后ACR从150.0 ± 538.6 mg/gCre降至148.3 ± 764.6 mg/gCre。合并微量以及大量蛋白尿的患者治疗3个月后与基线相比较ACR都显著下降(分别P = 0.04与P = 0.02)。3个月后,与其他受试者相比,ACR下降的受试者其血压以及估算的肾小球滤过率(estimated glomerular filtration rate,eGFR)下降程度更大。在3个月期间,ACR的变化(ΔACR)与HbA1c的变化(ΔHbA1c)之间没有显著性的相关性(r = 0.04,P = 0.59),但是ΔACR的变化与收缩压的变化之间具有显著的相关性(r = 0.16,P = 0.03)。3个月后,多元回归分析结果显示,收缩压的变化(β = 0.21,P = 0.016)和eGFR的变化(β = 0.20,P = 0.024)是ΔACR的重要预测因子(r = 0.35,P = 0.04)。
结论:3个月的西格列汀治疗通过降低血压以及eGFR来减少ACR,与HbA1c的下降没有相关性。这些结果可能反映了西格列汀对肾脏具有直接的作用。 背景:通过 调查尿白蛋白/肌酐比值(ACR)的变化了解西格列汀对糖尿病肾病的影响。 方法:共有 247名门诊2型糖尿病患者参加研究,给予西格列汀50 mg/日进行治疗。收集患者的实验室检查结果(包括ACR)、血压以及体重等数据。对比了使用西格列汀治疗前3个月与治疗后3个月的临床数据。 结果: 3个月后ACR从150.0 ± 538.6 mg/gCre降至148.3 ± 764.6 mg/gCre。合并微量以及大量蛋白尿的患者治疗3个月后与基线相比较ACR都显著下降(分别 P = 0.04与 P = 0.02)。3个月后,与其他受试者相比,ACR下降的受试者其血压以及估算的肾小球滤过率(estimated glomerular filtration rate,eGFR)下降程度更大。在3个月期间,ACR的变化(ΔACR)与HbA1c的变化(ΔHbA1c)之间没有显著性的相关性( r = 0.04, P = 0.59),但是ΔACR的变化与收缩压的变化之间具有显著的相关性( r = 0.16, P = 0.03)。3个月后,多元回归分析结果显示,收缩压的变化(β = 0.21, P = 0.016)和eGFR的变化(β = 0.20, P = 0.024)是ΔACR的重要预测因子( r = 0.35, P = 0.04)。 结论: 3个月的西格列汀治疗通过降低血压以及eGFR来减少ACR,与HbA1c的下降没有相关性。这些结果可能反映了西格列汀对肾脏具有直接的作用。 |
Author | Yamagami, Keiko Tamai, Anna Yoshida, Yoko Tanaka, Nagaaki Fukumoto, Mariko Kawasaki, Isao Ueno, Hiroki Hosoi, Masayuki Ikuno, Yoshiko Hiura, Yoshikazu Yakusiji, Yosuke Okada, Megumi |
Author_xml | – sequence: 1 givenname: Isao surname: Kawasaki fullname: Kawasaki, Isao email: i-kawasaki@hospital.city.osaka.jp organization: Department of Metabolism and Endocrinology, Osaka City General Hospital, Osaka, Japan – sequence: 2 givenname: Yoshikazu surname: Hiura fullname: Hiura, Yoshikazu organization: Jyuso Municipal Hospital, Osaka, Japan – sequence: 3 givenname: Anna surname: Tamai fullname: Tamai, Anna organization: Department of Metabolism and Endocrinology, Osaka City General Hospital, Osaka, Japan – sequence: 4 givenname: Yoko surname: Yoshida fullname: Yoshida, Yoko organization: Department of Metabolism and Endocrinology, Osaka City General Hospital, Osaka, Japan – sequence: 5 givenname: Yosuke surname: Yakusiji fullname: Yakusiji, Yosuke organization: Department of Metabolism and Endocrinology, Osaka City General Hospital, Osaka, Japan – sequence: 6 givenname: Yoshiko surname: Ikuno fullname: Ikuno, Yoshiko organization: Department of Metabolism and Endocrinology, Osaka City General Hospital, Osaka, Japan – sequence: 7 givenname: Megumi surname: Okada fullname: Okada, Megumi organization: Department of Metabolism and Endocrinology, Osaka City General Hospital, Osaka, Japan – sequence: 8 givenname: Hiroki surname: Ueno fullname: Ueno, Hiroki organization: Department of Metabolism and Endocrinology, Osaka City General Hospital, Osaka, Japan – sequence: 9 givenname: Nagaaki surname: Tanaka fullname: Tanaka, Nagaaki organization: Jyuso Municipal Hospital, Osaka, Japan – sequence: 10 givenname: Keiko surname: Yamagami fullname: Yamagami, Keiko organization: Department of Metabolism and Endocrinology, Osaka City General Hospital, Osaka, Japan – sequence: 11 givenname: Mariko surname: Fukumoto fullname: Fukumoto, Mariko organization: Department of Metabolism and Endocrinology, Osaka City General Hospital, Osaka, Japan – sequence: 12 givenname: Masayuki surname: Hosoi fullname: Hosoi, Masayuki organization: Department of Metabolism and Endocrinology, Osaka City General Hospital, Osaka, Japan |
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References | Pala L, Mannucci E, Pezzatini A et al. Dipeptidyl peptidase-IV expression and activity in human glomerular endothelial cells. Biochem Biophys Res Commun. 2003; 310: 28-31. Ogawa S, Ishiki M, Nako K et al. Sitagliptin, a dipeptidyl peptidase-4 inhibitor, decreases systolic blood pressure in Japanese hypertensive patients with type 2 diabetes. Tohoku J Exp Med. 2011; 223: 133-135. Gutzwiller JP, Tschopp S, Bock A et al. Glucagon-like peptide 1 induces natriuresis in healthy subjects and insulin-resistant obese men. J Clin Endocrinol Metab. 2004; 89: 3055-3061. Augustyns K, Bal G, Thonus G et al. The unique properties of dipeptidyl-peptidase IV (DPP IV/CD26) and the therapeutic potential of DPP IV inhibitors. Curr Med Chem. 1999; 6: 311-327. Hattori S. Sitagliptin reduces albuminuria in patients with type 2 diabetes. Endocr J. 2011; 58: 69-73. Mogensen CE, Christensen CK. Predicting diabetic nephropathy in insulin-dependent patients. N Engl J Med. 1984; 311: 89-93. Schmieder RE, Mann JF, Schumacher H et al. ONTARGET Investigators. Changes in albuminuria predict mortality and morbidity in patients with vascular disease. J Am Soc Nephrol. 2011; 22: 1353-1364. Seino Y, Nanjo K, Tajima N et al. Report of the committee on the classification and diagnostic criteria of diabetes mellitus. J Diabetes Invest. 2010; 1: 212-228. Kirino Y, Sato Y, Kamimoto T, Kawazoe K, Minakuchi K, Nakahori Y. Interrelation of dipeptidyl peptidase IV (DPP4) with the development of diabetes, dyslipidaemia and nephropathy: A streptozotocin-induced model using wild-type and DPP4-deficient rats. J Endocrinol. 2008; 200: 53-61. Mega C, de Lemos ET, Vala H et al. Diabetic nephropathy amelioration by a low-dose sitagliptin in an animal model of type 2 diabetes (Zucker Diabetic Fatty Rat). Exp Diabetes Res. 2011; 2011: 1-12. Kashiwagi A, Kasuga M, Araki E et al. International clinical harmonization of glycated hemoglobin in Japan: From Japan Diabetes Society to National Glycohemoglobin Standardization Program values. J Diabetes Invest. 2012; 3: 39-40. Mistry GC, Maes AL, Lasseter KC et al. Effect of sitagliptin, a dipeptidyl peptidase-4 inhibitor, on blood pressure in nondiabetic patients with mild to moderate hypertension. J Clin Pharmacol. 2008; 48: 592-598. Viberti GC, Hill RD, Jarrett RJ et al. Microalbuminuria as a predictor of clinical nephropathy in insulin-dependent diabetes mellitus. Lancet. 1982; 1: 1430-1432. Adler AI, Stevens RJ, Manley SE, Bilous RW, Cull CA, Holman RR, UKPDS Group. Development and progression of nephropathy in type 2 diabetes: The United Kingdom Prospective Diabetes Study (UKPDS 64). Kidney Int. 2003; 63: 225-232. Araki S, Haneda M, Koya D et al. Reduction in microalbuminuria as an integrated indicator for renal and cardiovascular risk reduction in patients with type 2 diabetes. Diabetes. 2007; 56: 1727-1730. 2011; 2011 2011; 223 2012; 3 2010; 1 1982; 1 1984; 311 2004; 89 2008; 48 2011; 22 2011; 58 2008; 200 1999; 6 2007; 56 2003; 63 2003; 310 e_1_2_7_6_1 e_1_2_7_5_1 e_1_2_7_4_1 e_1_2_7_3_1 e_1_2_7_9_1 e_1_2_7_8_1 Augustyns K (e_1_2_7_7_1) 1999; 6 e_1_2_7_16_1 e_1_2_7_2_1 e_1_2_7_15_1 e_1_2_7_14_1 e_1_2_7_13_1 e_1_2_7_12_1 e_1_2_7_11_1 e_1_2_7_10_1 |
References_xml | – reference: Augustyns K, Bal G, Thonus G et al. The unique properties of dipeptidyl-peptidase IV (DPP IV/CD26) and the therapeutic potential of DPP IV inhibitors. Curr Med Chem. 1999; 6: 311-327. – reference: Kirino Y, Sato Y, Kamimoto T, Kawazoe K, Minakuchi K, Nakahori Y. Interrelation of dipeptidyl peptidase IV (DPP4) with the development of diabetes, dyslipidaemia and nephropathy: A streptozotocin-induced model using wild-type and DPP4-deficient rats. J Endocrinol. 2008; 200: 53-61. – reference: Hattori S. Sitagliptin reduces albuminuria in patients with type 2 diabetes. Endocr J. 2011; 58: 69-73. – reference: Mogensen CE, Christensen CK. Predicting diabetic nephropathy in insulin-dependent patients. N Engl J Med. 1984; 311: 89-93. – reference: Pala L, Mannucci E, Pezzatini A et al. Dipeptidyl peptidase-IV expression and activity in human glomerular endothelial cells. Biochem Biophys Res Commun. 2003; 310: 28-31. – reference: Schmieder RE, Mann JF, Schumacher H et al. ONTARGET Investigators. Changes in albuminuria predict mortality and morbidity in patients with vascular disease. J Am Soc Nephrol. 2011; 22: 1353-1364. – reference: Gutzwiller JP, Tschopp S, Bock A et al. Glucagon-like peptide 1 induces natriuresis in healthy subjects and insulin-resistant obese men. J Clin Endocrinol Metab. 2004; 89: 3055-3061. – reference: Adler AI, Stevens RJ, Manley SE, Bilous RW, Cull CA, Holman RR, UKPDS Group. Development and progression of nephropathy in type 2 diabetes: The United Kingdom Prospective Diabetes Study (UKPDS 64). Kidney Int. 2003; 63: 225-232. – reference: Mega C, de Lemos ET, Vala H et al. Diabetic nephropathy amelioration by a low-dose sitagliptin in an animal model of type 2 diabetes (Zucker Diabetic Fatty Rat). Exp Diabetes Res. 2011; 2011: 1-12. – reference: Araki S, Haneda M, Koya D et al. 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Snippet | Background
We investigated the change in the urine albumin‐to‐creatinine ratio (ACR) to examine the effect of sitagliptin on diabetic nephropathy.
Methods... 背景:通过 调查尿白蛋白/肌酐比值(ACR)的变化了解西格列汀对糖尿病肾病的影响。 方法:共有 247名门诊2型糖尿病患者参加研究,给予西格列汀50 mg/日进行治疗。收集患者的实验室检查结果(包括ACR)、血压以及体重等数据。对比了使用西格列汀治疗前3个月与治疗后3个月的临床数据。 结果:... |
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SubjectTerms | albumin-to-creatinine ratio diabetic nephropathy sitagliptin 关键词:白蛋白/肌酐比值,糖尿病肾病,西格列汀 |
Title | Sitagliptin reduces the urine albumin-to-creatinine ratio in type 2 diabetes through decreasing both blood pressure and estimated glomerular filtration rate 西格列汀通过降低2型糖尿病患者的血压以及估算的肾小球滤过率来减少尿白蛋白/肌酐的比值 |
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