Hyperglycemia can impair tubulo-glomerular balance and cause kidney disease by opening pre-glomerular resistances. Susceptibility to kidney disease is heterogeneous among diabetic patients, and renal capacities to reabsorb glucose may contribute to it. We studied if renal capacities to reabsorb glucose relate to kidney disease in diabetic patients. The diabetic patients attending over 6 months our tertiary referral center in Paris, France (where SGLT2 inhibitors are not available), were studied consecutively for their fractional glucose reabsorption (1-[urinary glucose x plasma creatinine]/[urinary creatinine x plasma glucose]) according to their glycemia (<6, 6-11, >11mM), and kidney disease (normo-, micro-, macroalbuminuria, and estimated Glomerular Filtration Rate (eGFR, CKP-EPI equation) >90, 90-60, 59-30, and <30-16 ml/min/1.73m2; patients with eGFR ≤15ml/min/1.73m2 were excluded). Of 637 participants, 106 displayed glycemia <6mM, 288 6-11mM, and 243 >11mM. Fractional glucose reabsorption was similar in participants with glycemia <6mM and 6-11mM: median 99.90 (interquartiles 99.60-99.94)%. It was lower in those with glycemia >11mM, proportional to kidney disease: normoalbuminuria (n=135) 93.50 (81.60-99.34)%, microalbuminuria (n=77) 96.56 (93.77-99.71)%, macroalbuminuria (n=31) 99.12 (94.20-99.64)% (p<0.001); eGFR >90ml/min/1.73m2 (n=111) 94.13 (82.34-98.58)%, 90-60ml/min/1.73m2 (n=72) 96.35 (87.81-99.75)%, 59-30ml/min/1.73m2 (n=46) 98.88 (92.19-99.78)%, <30-16 ml/min/1.73m2 (n=14), 99.11 (97.57-99.77)% (p<0.01). On multivariate analyses, fractional glucose reabsorption in participants with glycemia >11mM contributed independently to their urinary albumin excretions and eGFR values. Renal capacities to reabsorb glucose were linked to kidney disease in diabetic patients with glycemia >11mM. Inter-individual capacities to reabsorb glucose may contribute to kidney disease of diabetic patients.


O. Matar: None. L. Potier: Advisory Panel; Self; Merck Sharp & Dohme Corp. Consultant; Self; Sanofi. Y. Abouleka: None. F. Fumeron: None. K. Mohammedi: None. S. Hadjadj: Consultant; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, Merck & Co., Inc., Novo Nordisk A/S, Sanofi, Servier. Research Support; Self; Bayer AG, Janssen Research & Development. Speaker's Bureau; Self; Abbott, Valbiotis. R. Roussel: Advisory Panel; Self; Merck Sharp & Dohme Corp., Sanofi. Consultant; Self; Abbott, AstraZeneca, Eli Lilly and Company, Medtronic, Novo Nordisk A/S, Physiogenex. Research Support; Self; Janssen Pharmaceuticals, Inc. G. Velho: None. M. Marre: Advisory Panel; Self; Servier. Board Member; Self; Merck Sharp & Dohme Corp., Novo Nordisk A/S.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at http://www.diabetesjournals.org/content/license.