Background: Anemia, in patients with diabetes, is commonly associated with impaired renal function secondary to diabetic nephropathy. Many studies have analyzed this association of anemia in diabetic patients and have attributed anemia to reduced renal function. However, there has been no known systematic analysis done to evaluate for the prevalence and predictors of anemia in patients with diabetes in the absence of overt nephropathy.
Objective: This retrospective study is designed to measure the prevalence of anemia in diabetic patients with normal renal function of estimated glomerular filtration rate (EGFR) greater than 90 ml/min/1.73m2 and to analyze the presence of other independent risk factors.
Methods: We conducted a retrospective analysis of 200 medical charts of diabetic patients (age > 18) visiting the outpatient endocrine clinic in our institution between January 2015 and June 2015 to identify the prevalence of anemia with and without diabetic nephropathy and any other associated factors.
Results: The prevalence of anemia (defined by the World Health Organization is a Hemoglobin level of less than 13 mg/dl in men and less than 12 mg/dl in women) in our 200 diabetic patients was 22% (44 out of the 200). Out of the 44 anemic patients, 41% had anemia with normal renal function (18 out of 44), 4 men and 14 women aged between 38-80 years old. From the 18 patients with normal renal function, 5 had iron deficiency anemia and 1 had autoimmune disease, while the remaining 12 patients (27% of anemic patients) did not have any known cause of anemia such as renal insufficiency, infection, chronic inflammatory disease, vitamin B12 or folate deficiencies, hemolysis, or acute/chronic blood loss.
Conclusion: Many studies have highlighted an association between anemia and nephropathy in diabetic patients. This retrospective analysis suggests there is a high prevalence of anemia with unidentified etiology in diabetic population. The exact mechanism of such anemia is not fully understood. It is hypothesized to be likely secondary to direct glucose toxicity to erythrocyte precursors in the bone marrow or from oxidative stress to mature erythrocytes. However, further studies are needed to evaluate the underlying pathophysiology of anemia in this particular setting.
No relevant conflicts of interest to declare.
Asterisk with author names denotes non-ASH members.