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

Cover Page

Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access


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.

Full Text

Restricted Access

About the authors

Svetlana V. Berstneva

Ryazan State Medical University

Author for correspondence.
Email: berst.ru@mail.ru
ORCID iD: 0000-0002-3141-4199
SPIN-code: 6722-3203

MD, Cand. Sci. (Med.), PhD, Associate Professor, Associate Professor of the Department of Faculty Therapy with a Therapy FAPE Course

Russian Federation, Ryazan

Oleg M. Uryas’yev

Ryazan State Medical University

Email: uryasev08@yandex.ru
ORCID iD: 0000-0001-8693-4696
SPIN-code: 7903-4609
ResearcherId: S-6270-2016

MD, Dr. Sci. (Med.), PhD, Professor, Head of the Department of Faculty Therapy with a Therapy FAPE Course

Russian Federation, Ryazan

Inessa I. Dubinina

Ryazan State Medical University

Email: inessa.dubinina@mail.ru
ORCID iD: 0000-0001-6726-1756

MD, Dr. Sci. (Med.), PhD, Professor, Professor of the Department of Faculty Therapy with a Therapy FAPE Course

Russian Federation, Ryazan

Aleksandr A. Nikiforov

Ryazan State Medical University

Email: a.nikiforov@rzgmu.ru
ORCID iD: 0000-0002-7364-7687
SPIN-code: 8366-5282

MD, Cand. Sci. (Med.), Associate Professor

Russian Federation, Ryazan


  1. Shamkhalova MSh, Yarek-Martynova IR, Trubitcyna NP, et al. Glucose-lowering therapies in patients with diabetes mellitus and chronic kidney disease. Diabetes Mellitus. 2013;(3):97–102. (In Russ). doi: 10.14341/2072-0351-823
  2. Dedov II, M.V. Shestakova MV, editors. Oslozhneniya sakharnogo diabeta: lecheniye i profilaktika. Moscow: MIA; 2017. (In Russ).
  3. Klimontov VV, Korbut AI. Normoalbuminuric chronic kidney disease in diabetes. Therapeutic Archive. 2018;90(10):94–8. (In Russ). doi: 10.26442/terarkh201890104-98
  4. Afkarian M, Zelnick L, Hall Y, et al. Clinical Manifestations of Kidney Disease Among US Adults With Diabetes, 1988–2014. JAMA. 2016;316(6):602–10. doi: 10.1001/jama.2016.10924
  5. Porrini E, Ruggenenti P, Mogensen C, et al. Non-proteinuric pathways in loss of renal function in patients with type 2 diabetes. The Lancet. Diabetes & Endocrinology. 2015;3(5):382–91. doi: 10.1016/S2213-8587(15)00094-7
  6. Marshall S.M. Natural history and clinical characteristics of CKD in type 1 and type 2 diabetes mellitus. Advances in Chronic Kidney Disease. 2014;21(3):267–72. doi: 10.1053/j.ackd.2014.03.007
  7. Orlova MM, Rodionova TI. Sostoyaniye funktsii pochek u patsiyentov s gipotireozom (obzor). Meditsinskiy Al’manakh. 2010;(3):112–4. (In Russ).
  8. Connor А, Taylor JE. Renal impairment resulting from hypothyroidism. NDT Plus. 2008;1(6):440–1. doi: 10.1093/ndtplus/sfn158
  9. Gilles R, der Hejier M, Ross AH, et. al. Thyroid function in patient with proteinuria. The Netherlands Journal of Medicine. 2008;66(11):483–5.
  10. Furukawa S, Yamamoto S, Todo Y, et al. Association between subclinical hypothyroidism and diabetic nephropathy in patients with type 2 diabetes mellitus. Endocrine Journal. 2014;61(10):1011–8. doi: 10.1507/endocrj.ej14-0206
  11. Dubinina II, Uryasev OM, Berstneva SV, et al. Hypertension and endothelial dysfunction in comorbid pathology: diabetes mellitus and primary hypothyroidism. I.P. Pavlov Russian Medical Biological Herald. 2016;24(4):42–55. (In Russ). doi: 10.23888/PAVLOVJ2016442-55
  12. Berstneva SV. Epidemiological aspects of comorbid pathology — diabetes mellitus and hypothyroidism. Science of the young (Eruditio Juvenium). 2020;8(2):154–63. (In Russ). doi: 10.23888/HMJ202082154-163
  13. Maratou E, Hadjidakis DJ, Kollias A, et al. Studies of insulin resistance in patients with clinical and subclinical hypothyroidism. European Journal of Endocrinology. 2009;160(5):785–90. doi: 10.1530/EJE-08-0797
  14. Zambon A, Bertocco S, Vitturi N, et al. Relevance of hepatic lipase to the metabolism of triacylglycerol rich lipoproteins. Biochemical Society Transactions. 2003;31(Pt 5):1070–4. doi: 10.1042/bst0311070
  15. Deicher R, Hörl WH. Anaemia as a risk factor for the progression of chronic kidney disease. Current Opinion in Nephrology and Hypertension. 2003;12(2):139–43. doi: 10.1097/00041552-200303000-00003
  16. Klimontov VV, Eremenko NV, Myakina NE, et al. Cystatin C and collagen type IV in diagnostics of chronic kidney disease in type 2 diabetic patients. Diabetes Mellitus. 2015;18(1):87–93. (In Russ). doi: 10.14341/DM2015187-93
  17. Udovcic M, Pena RH, Patham B, et al. Hypothyroidism and the Heart. Methodist DeBakey Cardiovascular Journal. 2017;13(2):55–9. doi: 10.14797/mdcj-13-2-55
  18. Vyalkova AA, Lebedeva EN, Krasikov SI, et al. Clinical and paphogenical aspects of kidney damage in obesity (review). Nephrology. 2014;18(3):24–33. (In Russ).
  19. Zakharova SM, Savelieva LV, Fadeeva MI. Obesity and hypothyroidism. Obesity and Metabolism. 2013;(2):24–33. (In Russ).
  20. Sazonova YeG, Mokhort TV. Thyroid functioning in diabetes mellitus complicated with chronic renal disease. Mezhdunarodnyy Endokrinologicheskiy Zhurnal. 2013;(2):62–7. (In Russ).
  21. Roos JF, Doust J, Tett SE, et al. Diagnostic accuracy of cystatin C compared to serum creatinine for the estimation of renal dysfunction in adults and children-a meta-analysis. Clinical Biochemistry. 2007;40(5–6):383–91. doi: 10.1016/j.clinbiochem.2006.10.026
  22. Čabarkapa V, Mijović R, Stošić Z, et al. Estimation of glomerular filtration rate from serum cystatin С and creatinine in patients with thyroid dysfunction. Journal of Medical Biochemistry. 2012;31(2):88–93. doi: 10.2478/v10011-011-0044-0
  23. Wiesli P, Schwegler B, Spinas GA, et al. Serum cystatin C is sensitive to small changes in thyroid function. Clinica Chimica Acta. 2003;338(1–2):87–90. doi: 10.1016/j.cccn.2003.07.022
  24. Naour N, Fellahi S, Renucci J–F, et al. Potential contribution of adipose tissue to elevated serum cystatin C in human obesity. Obesity. 2009;17(12):2121–6. doi: 10.1038/oby.2009.96

Supplementary files

Supplementary Files
1. Fig. 1. Incidence of renal pathology in patients with type 2 diabetes mellitus with and without primary hypothyroidism.

Download (90KB)
2. Fig. 2. Incidence of anemia in patients with type 2 diabetes mellitus with and without primary hypothyroidism and chronic kidney disease. Note: * р < 0.05, comparison with the group of type 2 diabetes mellitus and group with type 2 diabetes mellitus in combination with primary hypothyroidism.

Download (59KB)
3. Fig. 3. Hemoglobin level in patients with diabetes mellitus and chronic kidney disease (stages C1–C3b).

Download (61KB)
4. Fig. 4. Parameters of cystatin C in the groups of patients with type 2 diabetes mellitus, primary hypothyroidism, combination of type 2 diabetes mellitus and primary hypothyroidism, and control group. Note: * p < 0.05, comparison with the control group; # p < 0.05, comparison with the type 2 diabetes mellitus group.

Download (32KB)

Copyright (c) 2022 ООО "Эко-Вектор"

Свидетельство о регистрации СМИ ПИ № ФС77-76803 от 24 сентября 2019 года выдано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies