In healthy individuals, glucose is filtered at the glomerulus, with most reabsorbed by sodium-glucose cotransporters (SGLT2 and SGLT1) in the proximal tubule. Kidney disease can impair this process, reducing the ability to filter and reabsorb glucose, potentially causing hyperglycemia or hypoglycemia. Additionally, the kidneys consume glucose for metabolic functions and gluconeogenesis, creating a complex relationship between glucose metabolism and medication clearance, which can lead to variable glycemic outcomes in patients with kidney disease.

Indirect glycemic markers, like hemoglobin A1C, fructosamine, glycated albumin, and 1,5-anhydroglucitol (1,5-AG), are used to assess long-term glucose control. While A1C has been the gold standard, its accuracy is reduced in patients with chronic kidney disease (CKD) due to factors like anemia and medications. Alternative markers such as glycated proteins and 1,5-AG are less affected by these issues but still have limitations in CKD. Continuous glucose monitoring (CGM) offers real-time data, helping to identify glycemic excursions, especially in advanced CKD. However, more studies are needed to validate CGM’s efficacy in managing glycemia in patients with CKD.

Reference: Hassanein M, Shafi T. Assessment of glycemia in chronic kidney disease. BMC Med. 2022;20(1):117. doi: 10.1186/s12916-022-02316-1.