Epidemiological and Metabolic Aspects and Risk Factors of Chronic Kidney Disease in Comorbid Pathology of Type 2 Diabetes Mellitus and Primary Hypothyroidism

INTRODUCTION: The increasing number of patients with diabetes mellitus (DM) and chronic kidney disease (CKD) is one of the most pressing problems of modern medicine. In comorbid pathology — a combination of type 2 DM and thyroid hypofunction — the negative effect of hypothyroidism on carbohydrate metabolism, lipid metabolism, endothelial function, and glomerular filtration rate (GFR) is a risk factor for the formation and progression of diabetic nephropathy and CKD and requires further study. AIM: To identify risk factors and epidemiological peculiarities of CKD in type 2 DM in combination with thyroid hypofunction and to determine the possibility of using cystatin C levels for the evaluation of the kidney function in this pathology. MATERIALS AND METHODS: The prospective study involved 203 patients with type 2 DM undergoing inpatient treatment in the endocrinology department of the Ryazan Regional Clinical Hospital: group 1 (n = 76), type 2 DM combined with the primary hypothyroidism, and group 2 (n = 127), type 2 DM without thyroid pathology. Carbohydrate, lipid metabolism, albuminuria (AU), thyroid hormone spectrum, adipokines (leptin, plasminogen activator inhibitor-1, interleukin-6, and tumor necrosis factor-α) were analyzed. The GFR was calculated using the CKD-EPI formula based on the levels of creatinine and cystatin C. Arterial pressure daily monitoring (APDM) was conducted, and intra-abdominal fat thickness was evaluated by ultrasonography. RESULTS: The incidence of kidney pathology in patients with type 2 DM was 52.22%. In group 1, there was a significant increase in the prevalence of CKD (64.47%, p = 0.006) and of normoalbuminuric CKD (NAU-CKD, 32.89%; p = 0.010). The risk of CKD development in patients with concomitant PH was more than twice that in patients without thyroid pathology with an odds ratio of 2.229 (95% confidence interval (CI) 1.241–4.003) and that for NAU-CKD was 2.474 (95% CI 1.267–4.833). Significant impairment of several metabolic parameters and individual APDM parameters was revealed in group 1 in comparison with group 2. The dependence of AU and GFR on the body mass index and of AU on the intra-abdominal fat thickness was noted. A negative relationship between GFR and leptin was revealed; in group 1, a correlation of interleukin-6 and thyrotropic hormone was found (r = 0.809, p = 0.001). With concomitant PH, cystatin C values were lower, and the GFR (CKD-EPI-cys) was reliably higher. CONCLUSION: Hypothyroidism is a risk factor for CKD development including NAU-CKD in type 2 DM. Obesity and hormonal activities of the intra-abdominal fatty tissue facilitate AU progression and GFR reduction. The use of cystatin C as a marker of the filtration function of the kidney in patients with hypothyroidism may lead to the underestimation of kidney function; thus, further investigation is required.