Fig. 3.

Absence of Na⁺-glucose cotransporter SGLT1 reduced cortical and outer medullary tubular injury during recovery from ischemia-reperfusion (IR). On day 16 after IR, kidneys were harvested for histological analysis and tubular injury quantification by a renal pathologist blinded with regard to study groups. A: representative pictures of cortical and outer medullary tubular injury [periodic acid-Schiff (PAS) staining]. Arrows indicate damaged tubules, some with loss of tubular brush borders and some with dilatation; arrowheads indicate interstitial inflammation. *Tubular casts. B: semiquantitative analysis of cortical and outer medullary tubular injury. Sglt1^−/− sham animals had normal histology features similar to those of WT sham animals. IR injury in WT mice was characterized by interstitial inflammation and patchy tubular injury with some tubular segments containing sloughed cells and/or cell cytoplasm and proteinaceous cast material. Other portions of the tubular parenchyma showed attenuation or loss of proximal tubular brush borders. Sglt1^−/− IR kidneys displayed less severe tubular and tubulointerstitial damage in the cortex and outer medulla compared with WT IR kidneys. The number of medullary tubular casts appeared to be similar in both genotypes after IR. Results are means ± SE; n = 4–6 sham mice/group and 6 IR mice/group. #P < 0.05 vs. sham and *P < 0.05 vs. WT mice using two- way ANOVA and Holm-Sidak post hoc analysis for multiple comparisons.