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Myostatin in protein-energy wasting in patients on hemodialysis

https://doi.org/10.24884/1561-6274-2019-23-3-36-41

Abstract

The aim: to assess the effect of myostatin (MSTN) on the development of clinical and laboratory manifestations of protein metabolism disorders in patients receiving hemodialysis.

Patients and methods: 80 patients with CKD 5D stage (47 males and 33 females) were treated with programmed hemodialysis. All patients underwent a thorough collection of clinical and anamnesis data, laboratory monitoring with the determination of the level of MSTN in the blood by enzyme immunoassay, dynamometric and bioelectrical impedance research. Statistical analysis was performed using “STATISTICA 10.0” (“StatSoft Inc.”, USA) and “Microsoft Office Excel 2010” (“Microsoft Corp.”, USA).

Results: the regression analysis did not reveal a statistically significant association of MSTN levels with clinical indicators of protein-energy insufficiency (PED), albumin, β2-microglobulin, CRP, and blood ferritin. Neither the use of various drugs (with the exception of ketoamino acids), nor the presence of a concomitant pathology in history, did not change the level of MSTN. At the same time, the dependence of the local increase in the thickness of the skin folds with the test marker was revealed, the increase in which is associated with a progressive decrease in muscle strength.

Conclusion: as a result of the study, the relationship between the serum concentration of myostatin and the clinical and laboratory manifestations of PEM was evaluated. The obtained data characterize the contribution of MSTN to the process of muscle protein degradation, which may become a target for targeted therapeutic effects and requires further study.

About the Authors

A. S. Kuzyarova
Rostov State Medical University
Russian Federation

Angelina S. Kuzyarova - MD., Resident, Internal Medicine Department №2.

344022, Rostov-on-Don, 29 Nakhichevansky Ln, Phone: +7 904-508-46-37



M. Z. Gasanov
Rostov State Medical University
Russian Federation

Mitkhat Z. Gasanov - MD, PhD., Associate prof.,Internal Medicine Department №1.

344022, Rostov-on-Don, 29 Nakhichevan-sky Ln, Phone: +7(988) 947-37-50



M. M. Batyushin
Rostov State Medical University
Russian Federation

Mikhail M. Batyushin - MD, PhD, DMedSci, Prof., Internal Medicine Department №2.

344022, Rostov-on-Don, 29 Nakhichevan-sky Ln, Phone: +7 918-501-88-01



O. V. Golubeva
Hemodialysis Center Rostov
Russian Federation

Oksana V. Golubeva - MD, Chief Physician.

344029, Rostov-on-Don, 1st Konnoy Army St., 33, Phone: +7 903-436-48-66



References

1. Tomilina ON, Andrusev AM, Peregudova NG, Shinkarev MB. Renal replacement therapy for ESRD in Russian Rederation, 2010-2015. Report of the Russian Renal Replacement Therapy Registry. Part 1. Nephrology and dialysis 2017; аpp. to T. 19 (4): 1-95 (In Russ.). Doi: 10.28996/1680-4422-2017-4suppl-1-95

2. Agranovich NV, Knyshova SA, Batyushin MM, Baida AP. Chronic kidney disease in outpatient practice. Diagnosis, treatment, prevention, medical and social expertise, Stavropol, StSMU, 2014; 57 (In Russ.)

3. Vetchinnikova ON, Pichugin IS. Protein-energy deficiency in patients with chronic kidney disease on dialysis therapy, MONIKI 1775, Moscow, 2015; 3-5 (In Russ.)

4. Xiaonan HW, William EM. Mechanisms of muscle wasting in chronic kidney disease. Nat Rev Nephrol 2014; 10 (9): 504-516. Doi:10.1038/nrneph.2014.112

5. Smirnov AV, Golubev RV, Korosteleva NY et al. Decline of physical performance in patients receiving renal replacement therapy: focus on sarcopenia. Nephrology Journal 2017; 21(4): 9-29 (In Russ.)

6. Willem MH. Hoogaars, Richard T. Jaspers. Past, Present, and Future Perspective of Targeting Myostatin and Related Signaling Pathways to Counteract Muscle Atrophy. In: Xiao J et al. Muscle Atrophy. Advances in Experimental Medicine and Biology 2018, Springer, Singapore; 153-206

7. Gasanov MZ. Molecular aspects of sarcopenia pathogenesis pathogenesis in patients with chronic kidney disease: integrated role of mTOR. Nephrology Journal 2018; 22(5): 9-16 (In Russ.)

8. Sharma M, McFarlane C, Kambadur R et al. Myostatin: expanding horizons. IUBMB Life 2015; 67(8): 589-600. Doi:10.1002/iub.1392

9. Liping Z, Xiaonan HW, Huiling W et al. Satellite cell dysfunction and impaired IGF-1 signaling cause CKD-induced muscle atrophy. J Am Soc Nephrol 2010; 21(3): 419-427. Doi: 10.1681/ASN.2009060571

10. Jiangling D, Yanjun D, Zihong C et al. The pathway to muscle fibrosis depends on myostatin stimulating the differentiation of fibro/adipogenic progenitor cells in chronic kidney disease. Kidney Int 2017; 91(1): 119-128. Doi: 10.1016/j.kint.2016.07.029

11. Anat J. The origin, molecular regulation and therapeutic potential of myogenic stem cell populations. Journal of anatomy 2009; 215(5): 477-497. Doi: 10.1111/j.1469-7580.2009.01138.x

12. Lee EJ, Jan AT, Baig MH et al. Fibromodulin: a master regulator of myostatin controlling progression of satellite cells through a myogenic program. The FASEB Journal 2016; 30(8): 2708-2719. Doi: 10.1096/fj.201500133R

13. Cheema B, Abas H, Smith B et al. Investigation of skeletal muscle quantity and quality in end-stage renal disease. Nephrology 2010; 15(4): 454-463. Doi: 10.1111/j.1440-1797.2009.01261.x

14. Raj DSC, Sun Y, Tzamaloukas AH. Hypercatabolism in dialysis patients. Current Opinion in Nephrology and Hypertension 2008; 17(6): 589-594. Doi: 10.1097/MNH.0b013e32830d5bfa

15. Bing D, Feng Z, Jianghui W et al. The function of myostatin in the regulation of fat mass in mammals. Nutr Metab 2017; 14(29). Doi: 10.1186/s12986-017-0179-1


Review

For citations:


Kuzyarova A.S., Gasanov M.Z., Batyushin M.M., Golubeva O.V. Myostatin in protein-energy wasting in patients on hemodialysis. Nephrology (Saint-Petersburg). 2019;23(3):36-41. (In Russ.) https://doi.org/10.24884/1561-6274-2019-23-3-36-41

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ISSN 1561-6274 (Print)
ISSN 2541-9439 (Online)