Sodium-glucose linked transporter-2 inhibitors: potential for renoprotection beyond blood glucose lowering?

被引:87
作者
Gilbert, Richard E. [1 ]
机构
[1] Univ Toronto, St Michaels Hosp, Dept Med, Div Endocrinol,Li Ka Shing Knowledge Inst, Toronto, ON MSC 2T2, Canada
关键词
blood pressure; glomerular filtration rate; proximal tubule; sodium-glucose linked cotransporter-2; tubuloglomerular feedback; uric acid; SERUM URIC-ACID; CONVERTING-ENZYME-INHIBITION; GLOMERULAR-FILTRATION-RATE; TYPE-2; DIABETIC-PATIENTS; CHRONIC KIDNEY-DISEASE; RENAL-FUNCTION LOSS; TUBULOGLOMERULAR FEEDBACK; CARDIOVASCULAR RISK; PROXIMAL TUBULE; GENE-EXPRESSION;
D O I
10.1038/ki.2013.451
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
The proximal tubule's sodium-glucose linked transporter-2 (SGLT2) accounts for the vast majority of glucose reabsorption by the kidney. Its selective inhibition, accordingly, leads to substantial glycosuria, lowering blood glucose, and facilitating weight loss in individuals with diabetes. During the past year, two SGLT2 inhibitors, canagliflozin and dapagliflozin, have been approved for the treatment of type 2 diabetes. Beyond their anti-hyperglycemic properties, however, this new class of drugs has several other attributes that provide a theoretical basis for kidney protection. Like agents that block the renin-angiotensin system, SGLT2 inhibitors also reduce single-nephron glomerular filtration rate (SNGFR) in the chronically diseased kidney, though by quite different mechanisms. Additional potentially beneficial effects of SGLT2 inhibition include modest reductions in blood pressure and plasma uric acid. Finally, cell culture studies indicate that glucose uptake from the tubular lumen, as well as from the basolateral compartment, can contribute to proximal tubular production of extracellular matrix proteins. Whether such attributes will translate into reducing the progression of chronic kidney disease will require the undertaking of long-term, dedicated studies.
引用
收藏
页码:693 / 700
页数:8
相关论文
共 76 条
[1]   Role of Sodium-Glucose Cotransporter 2 (SGLT 2) Inhibitors in the Treatment of Type 2 Diabetes [J].
Abdul-Ghani, Muhammad A. ;
Norton, Luke ;
DeFronzo, Ralph A. .
ENDOCRINE REVIEWS, 2011, 32 (04) :515-531
[2]  
Agency EM, 2012, FORX PROD INF
[3]   THERAPEUTIC ADVANTAGE OF CONVERTING ENZYME-INHIBITORS IN ARRESTING PROGRESSIVE RENAL-DISEASE ASSOCIATED WITH SYSTEMIC HYPERTENSION IN THE RAT [J].
ANDERSON, S ;
RENNKE, HG ;
BRENNER, BM .
JOURNAL OF CLINICAL INVESTIGATION, 1986, 77 (06) :1993-2000
[4]  
[Anonymous], 2012, BRENNER RECTORS KIDN, DOI DOI 10.1016/B978-1-4160-6193-9.10003-X
[5]   Improved diabetic syndrome in C57BL/KsJ-db/db mice by oral administration of the Na+-glucose cotransporter inhibitor T-1095 [J].
Arakawa, K ;
Ishihara, T ;
Oku, A ;
Nawano, M ;
Ueta, K ;
Kitamura, K ;
Matsumoto, M ;
Saito, A .
BRITISH JOURNAL OF PHARMACOLOGY, 2001, 132 (02) :578-586
[6]   STRUCTURE AND FUNCTION OF THE KIDNEY IN DIABETIC GLOMERULOSCLEROSIS CORRELATIONS BETWEEN MORPHOLOGICAL AND FUNCTIONAL PARAMETERS [J].
BADER, R ;
BADER, H ;
GRUND, KE ;
MACKENSENHAEN, S ;
CHRIST, H ;
BOHLE, A .
PATHOLOGY RESEARCH AND PRACTICE, 1980, 167 (2-4) :204-216
[7]   Renal sodium-glucose transport: role in diabetes mellitus and potential clinical implications [J].
Bakris, George L. ;
Fonseca, Vivian A. ;
Sharma, Kumar ;
Wright, Ernest M. .
KIDNEY INTERNATIONAL, 2009, 75 (12) :1272-1277
[8]   Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine - Is this a cause for concern? [J].
Bakris, GL ;
Weir, MR .
ARCHIVES OF INTERNAL MEDICINE, 2000, 160 (05) :685-693
[9]   Preserving renal function in adults with hypertension and diabetes: A consensus approach [J].
Bakris, GL ;
Williams, M ;
Dworkin, L ;
Elliott, WJ ;
Epstein, M ;
Toto, R ;
Tuttle, K ;
Douglas, J ;
Hsueh, W ;
Sowers, J .
AMERICAN JOURNAL OF KIDNEY DISEASES, 2000, 36 (03) :646-661
[10]   Renal Transport of Uric Acid: Evolving Concepts and Uncertainties [J].
Bobulescu, Alexandru ;
Moe, Orson W. .
ADVANCES IN CHRONIC KIDNEY DISEASE, 2012, 19 (06) :358-371