Glucose-Induced Insulin Secretion in Uremia: Role of Anemia

Dr. Vincenzo Allegra, Servizio Emodialisi, Ospedale Civile, I-33057 Palmanova (Italy) Dear Sir, Impaired glucose metabolism in uremic patients has long been recognized [1]. However, until recently, little has been known about the pathogenetic mechanisms responsible for the disturbance in glucose metabolism [1]. Recently Kokot et al. [2] have found that erythro-poietin treatment improves insulin response and glucose tolerance after a test meal in maintenance hemodialysis (MH) patients, and concluded that anemia plays a major role in the derangement of glucose metabolism in uremia. Vasile et al. [3], using the intravenous glucose tolerance test (IVGTT), have not confirmed this report. Also studies in animals [4] have demonstrated that red blood cells actively participate in glucose homeostasis by regulating glucose transport to peripheric tissues. To clear the role of anemia in the pathogenesis of insulin response and glucose tolerance abnormalities in uremia, we studied glucose metabolism, by IVGTT, in nondialyzed and dialyzed uremic patients with different hemoglobin (Hb) levels. 54 patients with endstage chronic renal failure (ESRF) and 119 patients on MH were studied. Their body weights varied between 90 and 110% of ideal body weight; none showed severe hyperkale-mia. Abnormalities of acid-base balance in ESRF patients, if present, were corrected by oral bicarbonate therapy before the test. For MH patients dialysis schedule was as follows: 3.5-4.5 h × 3/week, plate or hollow fiber dia-lyzer with cuprophan membrane of 1-1.5 m2 surface and 8 μm thickness, blood flow 250-350 ml/min, dialysate flow 500 ml/min. IVGTT was performed 2-6 months after start of MH in the morning after the second weekly hemodialysis treatment, 39 patients were examined both in the phase of ESRF and after start of MH. Both ESRF and MH patients were divided into groups according to their Hb levels (A Hb≤6 g/dl, B6 < Hb≤8 g/dl, C8 < Hb≤10 g/dl, D Hb > lO g/dl). Four MH patients of group A were examined even after blood transfusions. For each test we measured plasma levels of glucose (G), immunoreactive insulin (IRI) and C-peptide (C-p) at -30,0,2, 5,15,30,45,60 min and we calculated glucose constant decay (K), IRI and C-p areas of response (IRI area, C-p area), insulinogenic index (IGI) and insulin resistance index (RI). The technique was described in detail in a previous investigation [5]. Results are summarized in table 1. No differences were found in the various glucose metabolism parameters among the groups both in ESRF and MH patients. The 39 patients examined before