WCN25-405 eGFR Trajectories in Iraqi Cancer Patients at First Presentation

Introduction: Diabetes is closely associated with K+ disturbances during disease progression and treatment.However, it remains unclear whether K+ imbalance occurs in diabetes with normal kidney function.In this study, we examined the effects of dietary K+ intake on systemic K+ balance and renal K+ handling in streptozotocin (STZ)-induced diabetic mice.Methods: The control and STZ mice were fed low or high K+ diet for 7 days to investigate the role of dietary K+ intake in renal K+ excretion and K+ homeostasis, and to explore the underlying mechanism by evaluating K+ secretion-related transport proteins in distal nephrons.Results: K+-deficient diet caused excessive urinary K+ loss, decreased daily K+ balance, and led to severe hypokalemia in STZ mice compared to control mice.In contrast, STZ mice showed an increased daily K+ balance and elevated plasma K+ level under K+-loading conditions.Dysregulation of the NaCl cotransporter (NCC), epithelia Na+ channel (ENaC), and renal outer medullary K+ channel (ROMK) was observed in diabetic mice fed either low or high K+ diet.Moreover, amiloride treatment reduced urinary K+ excretion and corrected hypokalemia in K+-restricted STZ mice.On the other hand, inhibition of SGLT2 by dapagliflozin promoted urinary K+ excretion and normalized plasma K+ level in K+-supplemented STZ mice, at least partly by increasing ENaC activity.Conclusions: We conclude that STZ mice exhibited abnormal K+ balance and impaired renal K+ handling under either low or high K+ diet, which could be primarily attributed to the dysfunction of ENaC-dependent renal K+ excretion pathway, despite the possible role of NCC.I have no potential conflict of interest to disclose.I did not use generative AI and AI-assisted technologies in the writing process.