Is there Correlation between Subclinical Hypothyroidism and Diabetic Nephropathy?

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Diabetes mellitus (DM) is the most common chronic metabolic disease which its incidence is increasing rapidly. The prevalence of DM in urban Iranian population aged ≥20 years was 8.1% in 2008. Diabetic nephropathy (DN) is one of the main chronic complications in type 1 and 2 diabetes and is currently the most common cause for end stage renal disease (ESRD). It is reported that diabetes contributes to approximately 40 percent of newly developed ESRD patients each year. Diabetic nephropathy is likely multi-factorial. Although genetic and environmental factors can involved in diabetic nephropathy, resulted hemodynamic and metabolic changes can not clearly justify the diabetic nephropathy progression.

The prevalence of thyroid disorders is higher in diabetic patients and subclinical hypothyroidism (SCH) being the most disorder. SCH has been associated with endothelial dysfunction and probably atherosclerotic risk factors. Hypothyroidism causes remarkable changes in glomerular filtration rate (GFR), tubular function, water and electrolyte balances but association of SCH and diabetic nephropathy (DN) has not been evaluated so far. The aim of this study was to correlate SCH with DN in Iranian patients with type 2 diabetes.

In a cross- sectional study, we recruited 150 patients with type 2 diabetes. Patients with: past history of thyroid disease, taking drugs with effects on thyroid tests and albuminuria and any sever intercurrent illness were excluded. Furthermore, patients with type 1 diabetes, pregnancy, lactation, malignancy and liver failure were also excluded. Patients were informed completely about the study’s aims and if they fulfilled the written informed consent, they were entered in the study. We recorded the demographic characteristics including: age, height, weight, blood pressure and body mass index (BMI). BMI was calculated according to this formula: Weight (kg)/height (m2). Blood pressure of the right arm was taken in a sitting position after resting for ten minutes. After 8 hours overnight fasting, blood samples were obtained from the brachial vein. Fasting plasma glucose was measured by the glucose oxidase method (Human, Germany). Total cholesterol, triglyceride (TG), and high density lipoprotein (HDL) were measured by enzymatic method (Parsazmon Karaj, Iran). Low density lipoprotein (LDL) was calculated according to Friedwall formula {LDL= total cholesterol-(HDL+TG/5)}. Glycated hemoglobin A1C (HbA1C) was assessed by Column chromatography (Biosource kit, Barcelona, Spain).Urinary albumin was measured as the albumin to creatinine ratio (ACR) in a morning sample. Urine albumin in spot urine was measured by Immunoturbidometry assay (Parsazmon, Karaj, Iran). Urine creatinine was measured by enzymatic colorimetric assay. Urinary microalbumin ≥30 and < 300 mg per gram of creatinine in urine was considered as microalbuminuria and level ≥300 was considered as macroalbumiuria. Estimated GFR (e GFR) (ml/min/1.73 m2) was calculated according to equation of the Modification of Diet in Renal Disease. DN was defined as an increased ACR of ≥ 30 mg/gr in the absence of other renal abnormalities or e GFR less than 60 ml/min/1.73 m2according to KDOQI recommendation. Serum thyroid stimulating hormone (TSH) was measured by immunoradiometric assay, and free T4 was determined using radioimmunoassay.