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Insulin Metabolism in Chronic Uremia and in the Anephric State: Effect of the Dialytic Treatment1
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1975
Year
Insulin SignalingMetabolic SyndromeChronic UremiaRenal FunctionBody CompositionDialysis ProgramInsulin DeliveryChronic Kidney DiseaseInsulin MetabolismHealth SciencesHemodialysisDialytic Treatment1Kidney FailureInsulin ManagementImpaired Insulin CatabolismUrologyDiabetesPhysiologyDiabetic Kidney DiseaseDialysis TreatmentHyperglycemiaDiabetes MellitusMetabolismMedicineNephrology
The mechanism of impaired insulin catabolism in chronic uremia was investigated in 8 patients with chronic renal failure, before and after admission to the dialysis program, in 4 regularly dialyzed anephric patients and in a group of 10 normal control subjects. Plasma disappearance curve of insulin after a single injection was determined by immunoprecipitation. Results were analyzed to obtain the insulin metabolic clearance rate (MCR), delivery rate (IDR), the total insulin body mass (TIM) and its fractional catabolic rate (FCR), the mass of insulin affected by renewal during the experimental interval (RIM)and its fractional catabolic rate (RFCR). Both MCR and IDR were strongly reduced predialysis in uremic patients (203 ml/min/m2 and 296 mU/hr/m2, respectively) as compared to the normal values (432 ml/min/m2 and 502 mU/hr/m2, respectively) (p < 0.01 and p < 0.05, respectively); after dialysis treatment both MCR (424 ml/min/m2) and IDR (579 mU/hr/m2) increased to the normal range. TIM was found increased in predialysis uremic patients (363 mU/m2), with respect to normals (136 mU/m2, p < 0.01), and essentially unaffected by dialysis treatment both in non nephrectomized (418 mU/m2) and in nephrectomized patients (492 mU/m2). As a consequence, FCR, very low in uremicpatients predialysis (1.35 min−1, p < 0.01) as compared to normals, increased after dialysis (2.36% min−1, p < 0.05 as compared to predialysis) remaining largely below the normal values (8.6% min−1, p < 0.01). These findings suggest that reduced insulin catabolism in uremia is mainly due to the lack of functioning renal tissue accompanied by toxic depression of both insulin secretion and degradation, removed by dialysis. The slight improvement of FCR (from 1.4 to 2.4% min−1, p < 0.05) and RFCR (from 3.6 to 4.5% min−1, p < 0.01) observed in dialyzed nonnephrectomized uremic patients as compared to the behavior of dialyzed anephric patients (1.7 and 3.7% min−1, respectively) was interpreted as a consequence of the removal of a toxic inhibition on theresidual renal parenchyma by dialysis treatment. In conclusion, lack of renal tissue and toxic factors inhibiting both secretion and utilization combine to determine the insulin metabolic pattern inuremia.