Figure 2.

Hemodynamic changes in diabetic kidney disease (DKD).

Notes: Early in the course of diabetes mellitus (DM), there is volume expansion and an increase in sodium (Na) reabsorption from the proximal tubule (PT) mediated by increased insulin production, and the augmented sodium–glucose cotransport leading to increased tubuloglomerular feedback (TGF) mediated afferent arteriolar (AA) dilatation and increased flow rate. This is accompanied by an increased production of local angiotensin II (AngII) augmenting the dilatory effects of TGF on AA. Increased local AngII will cause mesangial cell constriction and efferent arteriolar (EA) vasoconstriction, causing along with the increased flow rate an increased intraglomerular pressure (IGP). This will increase sheer stress and chronically worsens kidney damage.