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Pharmacology

SGLT2 inhibitors: renal mechanism, cardiorenal benefit and euglycaemic ketoacidosis

How blocking proximal tubular glucose reabsorption lowers glucose in proportion to filtered load, why tubuloglomerular feedback causes the expected eGFR dip and slows CKD, the heart failure and kidney trials with worked NNTs, and the physiology of euglycaemic ketoacidosis and perioperative withholding.

Tier 1Medical sciences concept

Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made

3 questions8 flashcards

At a glance

  • SGLT2 inhibitors (empagliflozin, dapagliflozin; canagliflozin and ertugliflozin overseas) block sodium-glucose cotransporter 2 in the proximal tubule.
  • Glucose lowering is modest (HbA1c 0.5 to 0.8%) and depends on GFR. The heart failure and kidney benefits don't depend on glucose and persist at low eGFR.
  • Paper 1 tests the transporter physiology, the haemodynamic eGFR dip, the mechanism of euglycaemic ketoacidosis, and trial numbers.

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Last updated
14 November 2026
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