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Blunted erythropoietin response to anemia in patients with Type 1 diabetes
Author(s) -
Cotroneo Patrizia,
Maria Ricerca Bianca,
Todaro Lucia,
Pitocco Dario,
Manto Andrea,
Ruotolo Valeria,
Storti Sergio,
Damiani Patrizia,
Caputo Salvatore,
Ghirlanda Giovanni
Publication year - 2000
Publication title -
diabetes/metabolism research and reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.307
H-Index - 110
eISSN - 1520-7560
pISSN - 1520-7552
DOI - 10.1002/1520-7560(200005/06)16:3<172::aid-dmrr117>3.0.co;2-d
Subject(s) - medicine , anemia , erythropoietin , nephropathy , endocrinology , renal function , diabetes mellitus , diabetic nephropathy , type 2 diabetes , pathogenesis , gastroenterology , hematocrit
Background It is known that patients with renal failure have normochromic normocytic anemia due to impaired endogenous erythropoietin (EPO) synthesis. The aim of this work was to determine whether low serum erythropoietin (s‐EPO) levels play a role in the pathogenesis of anemia in patients with Type 1 diabetes without overt nephropathy. Methods We included in the study 13 patients with Type 1 diabetes whose Hb levels were <11 g/dl. Blood cell count, s‐EPO, urinary albumin excretion rate (AER), HbA 1c , glomerular filtration rate, serum iron, serum ferritin, the presence of neuropathy, retinopathy and nephropathy were determined. Results Ten out of 13 patients with anemia (77%) had a blunted EPO response to anemia. All ten patients with low EPO levels had autonomic neuropathy; five had clinical nephropathy but with serum creatinine<1.6 mg/dl. Three patients were treated with rHuEPO and showed an improvement in their anemia after treatment. Conclusion The majority of patients with Type 1 diabetes who had anemia also had low EPO levels. The pathogenesis of this phenomenon is probably multifactorial. Autonomic neuropathy appears to play a role, but it is not sufficient, per se , to be the only cause. Dysautonomia might enhance the effect of renal damage. Copyright © 2000 John Wiley & Sons, Ltd.