• Marko Škrtić and David Z I Cherney.
• Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada.
• Curr. Opin. Nephrol. Hypertens. 2015 Jan 1; 24 (1): 96-103.

Purpose Of ReviewRenal hyperfiltration has been used as a surrogate marker for increased intraglomerular pressure in patients with diabetes mellitus. Previous human investigation examining the pathogenesis of hyperfiltration has focused on the role of neurohormones such as the renin-angiotensin-aldosterone system (RAAS). Unfortunately, RAAS blockade does not completely attenuate hyperfiltration or diabetic kidney injury. More recent work has therefore investigated the contribution of renal tubular factors, including the sodium-glucose cotransporter, to the hyperfiltration state, which is the topic of this review.Recent FindingsNovel sodium-glucose cotransporter-2 (SGLT2) inhibitors reduce proximal tubular sodium reabsorption, thereby increasing distal sodium delivery to the macula densa, causing tubuloglomerular feedback, afferent vasoconstriction and decreased hyperfiltration in animals. In humans, SGLT2 inhibition was recently shown to reduce hyperfiltration in normotensive, normoalbuminuric patients with type 1 diabetes. In clinical trials of type 2 diabetes, SGLT2 is associated with significant renal effects, including modest, acute declines in estimated glomerular filtration rate followed by the maintenance of stable renal function, and reduced albuminuria.SummaryExisting data are supportive of a potential renal-protective role for SGLT2 inhibition in patients with diabetes. Dedicated renal outcome trials are ongoing and have the potential to change the clinical practice.

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