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Abstract: FR-PO418

Renin Producing Cells in the Diabetic Kidney

Session Information

Category: Diabetic Kidney Disease

  • 601 Diabetic Kidney Disease: Basic


  • Tang, Jeannette, Northwestern University, Chicago, Illinois, United States
  • Shirazi, Mina, Northwestern University, Chicago, Illinois, United States
  • Ye, Minghao, Northwestern University, Chicago, Illinois, United States
  • Wysocki, Jan, Northwestern University, Chicago, Illinois, United States
  • Vallés, Patricia G., Notti Pediatric Hospital School of Medicine, Mendoza, Argentina
  • Sequeira Lopez, Maria Luisa S., University of Virginia, Charlottesville, Virginia, United States
  • Gomez, Roberto Ariel, University of Virginia, Charlottesville, Virginia, United States
  • Batlle, Daniel, Northwestern University Feinberg Medical School, Chicago, Illinois, United States

Urinary renin is increased in patients with diabetes and models of diabetic kidney disease but its source is not clear. The intensity of renin staining in the collecting tubule is increased in the STZ model of diabetes and in Angiotensin (Ang) II-induced hypertension which could lead to RAS activation locally at this site. We examined the distribution of renin expressing cells using a renin reporter mouse made diabetic by STZ to trace the localization of renin lineage cells (RLC).


The Ren1d-Cre; mT/mG, a double transgenic reporter mouse model, expresses both Cre-recombinase from the endogenous renin locus (Ren1D) and the mT/mG cassette from the Rosa26 locus (mRenCre-mT/mG). The membrane-directed tomato protein (mT) is expressed ubiquitously and fluorescents in red, while the membrane-targeted green fluorescent protein (mG) is found only in those cells undergoing Cre-recombination. In RLC the mT/mG construct switches from red fluorescent to green fluorescent (mG), while all non-RLC remain mT positive. Ren1d-Cre;mT/mG were made diabetic using STZ. Animals were studied 11-12 weeks after STZ injection.


In WT mice made diabetic by STZ, renin staining by immunohistochemistry was increased in the collecting tubule and by immunofluorescence aquaporin 2 (AQP2), a marker of principal cells, co-localized with renin protein. In the renin reporter mice AQP2 co-localized with green fluorescent protein (GFP+) reflecting that renin producing cells are or had been present at this site. A quantitative comparison of this GFP+ cells between kidney sections of STZ treated and untreated reporter mice, however, revealed no significant differences. Within the glomerulus, RLC were strongly present in parietal areas and within the glomerulus but no significant differences were found between diabetic and non-diabetic renin reporter mice.


In collecting tubules from diabetic mice there is an increased expression of renin which cannot be attributed to increased number of renin producing cells at that site. Alternative explanations such as increased uptake of filtered renin and impaired reabsorption mainly in the proximal tubule need to be considered as the source of collecting tubule renin.


  • NIDDK Support