ECE2011 Poster Presentations Diabetes complications (23 abstracts)
Nephrology, Tzaneio General Hospital, Pireas, Greece.
Introduction and aims: Diabetic neuropathy may trigger the development of anemia in patients even before the onset of advanced renal failure. Autonomic neuropathy with subsequent renal denervation, combined with damaged erythropoetin producing fibroblasts in renal cortex, may have contributed to the early development of anemia in the patients with diabetes. Proliferative retonopathy, autonomic neuropathy, microalbuminuria, and moderate renal failure, suggesting that, factors other than CKD can contributed to anemia development.
Methods: We studied 35 diabetic patients with type II diabetes, ages 4778, with anemia, but without overt renal failure. We measured erythropoetin levels, heamoglobulin (Hb) levels, serum creatinin (Cr), microaluminuria, glomerular filtration rate (GFR), low density lipoproteins (LDL), glycosylation of Hb (HbA1c), glycose levels. We also examined the patients for the insidence of cardiovascular disease (CVD), diabetic retinopathy and macular edema. We used questionnaires scoring the quality of life in these patients. Obesity and lifestyle had taken in thought. We treated the whole anemic group with darbepoetin and we measured the new results.
Results: Twenty from 35 patients were found aneamic, (mean Hb of 10.6 g/dl), with decreased production of erythropoetin, which means blunted erythropoetin response to aneamia, mild retinopathy (OR, 5.3, 95% CI, 2.312.6) Cr levels <1.87 mg/dl. Mild microaluminuria was found to 18 of the 20 anemic patients. GFR was between 110 and 88 ml/h per 1.73, glucose levels between 92 and 213 mg/dl, HbA1c levels >5.5% to all patients, LDL levels >200 mg/dl for 18 patients, 6 patients had mild heart failure (ER<60%), 3 had a stroke in their medical history. Low scores measuring quality of life were obtained from all the anemic patients. Thirteen patients were obese and had sedentary lifestyles. After treating the whole anemic group of diabetic patients with darbepoetin in order to keep Hb>12 g, diabetic retinopathy and macular edema have been shown to respond to therapy. Most of the patients achieved a more active life and improved quality of life scores. Creatinine levels remained unchanged also proteinuria. The EF increased in 8 patients, sympathetic neuropathy improved in 50% of the patients, LDL levels were measured <180 mg/dl to 45% after the darbepoetin treatment.
Conclusions: The cause of early aneamia in patients with diabetes, is not only the renal nephropathy. As diabetes progresses, the basement membrane of glomeruli thickens as a result of glycosylation, leading to increased intrarenal pressure. Factors other than CKD contributed to anemia development. Autonomic neuropathy maybe showing the need of erythropoetin treatment, as hyperglycemia affects the function of nerves and muscles acutely and possibly all other tissues aswell. Therefore, erythropoetin responses to anemia in diabetes may also be disturbed. Determining the causes of early anemia in evidence of the need for early anemia screening and treatment in patients with diabetic and early stages of renal failure.