Given that STZ treatment resulted in increased urine nephrin excretion (Figure 2E), this suggests that the remaining glomerular podocytes were hypertrophic.39 It bears noting that TRPC5 channels have also been implicated in the pathogenesis of chronic kidney disease.1, 40, 41 Here, we note that there was no change in renal cortical TRPC5 abundance as a result of TRPC6 inactivation, STZ treatment, or both (Figure 4C). This evidence concerns the gene NPHS1 and chronic kidney disease.