Diabetic ketoacidosis, sodium glucose transporter-2 inhibitors and the kidney

被引：29

作者：

Palmer, Biff F. ^{[1
]}

Clegg, Deborah J. ^{[2
]}

Taylor, Simeon I. ^{[3
]}

Weir, Matthew R. ^{[4
]}

机构：

[1] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX USA

[2] Cedars Sinai Med Ctr, Biomed Res Dept, Diabet & Obes Res Div, Beverly Hills, CA USA

[3] Univ Maryland, Sch Med, Dept Med, Div Endocrinol Diabet & Nutr, Baltimore, MD USA

[4] Univ Maryland, Sch Med, Dept Med, Div Nephrol, Baltimore, MD 21201 USA

来源：

JOURNAL OF DIABETES AND ITS COMPLICATIONS | 2016年 / 30卷 / 06期

关键词：

Diabetic ketoacidosis; Sodium glucose transporter 2 inhibitors; Kidney; Glucose; Transport maximum; KETONE-BODIES; RENAL AMMONIAGENESIS; SGLT2; INHIBITORS; FATTY-ACIDS; SECRETION; CANAGLIFLOZIN; DAPAGLIFLOZIN; STARVATION; OXIDATION; MELLITUS;

D O I：

10.1016/j.jdiacomp.2016.05.008

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Diabetic ketoacidosis is a serious metabolic condition that may occur in patients with either Type 1 or Type 2 diabetes. The accumulation of ketoacids in the serum is a consequence of insulin deficiency and glucagon excess. Sodium Glucose Transporter 2 (SGLT2) inhibitors are novel therapeutic treatments for improving glucose homeostasis in patients with diabetes. Through reductions in glucose reabsorption by the kidney, they lower serum glucose in patients with Type 2 diabetes and they improve glucose control whether used alone or in combination with other therapies. Mechanistically, these drugs increase serum ketoacids and increase glucagon production, which in some individuals, can lead to formation of diabetic ketoacidosis. This review will first focus in how the kidney normally handles ketoacids, and second will discuss how the SGLT2 inhibitors affect the kidney in such a way so as to enhance the risk for development of ketoacidosis in susceptible individuals. (C) 2016 Elsevier Inc. All rights reserved.

引用

页码：1162 / 1166

页数：5

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