Renal functional reserve in patients with type 2 diabetes mellitus
Vol 79 No 2–3 (2018), Therapy
Vol 79 No 2–3 (2018)

Renal functional reserve in patients with type 2 diabetes mellitus

Therapy
Published July 10, 2020
I. I. Topchii
National Institute of Therapy named after L.T. Small Academy of Medical Sciences of Ukraine
P. S. Semenovykh
National Institute of Therapy named after L.T. Small Academy of Medical Sciences of Ukraine
V.Yu. Galchinskaya
National Institute of Therapy named after L.T. Small Academy of Medical Sciences of Ukraine
T.D. Shcherban
National Institute of Therapy named after L.T. Small Academy of Medical Sciences of Ukraine
Yu. S. Yakimenko
National Institute of Therapy named after L.T. Small Academy of Medical Sciences of Ukraine
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Keywords

diabetes mellitus
renal functional reserve
inflammation
fibrosis

How to Cite

Topchii, I. I., Semenovykh, P. S., Galchinskaya, V., Shcherban, T., & Yakimenko, Y. S. (2020). Renal functional reserve in patients with type 2 diabetes mellitus. Experimental and Clinical Medicine, 79(2–3), 88-93. Retrieved from https://ecm.knmu.edu.ua/article/view/414
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Abstract

The state of renal functional reserve (RFR) is a very important diagnostic and prognostic criterion of the functional state of kidneys in various forms of nephropathy. The aim of the study was to investigate RFR in patients with type 2 diabetes mellitus (DM) taking into account the main clinical and laboratory indicators and the levels of inflammatory and fibrotic markers. We established lack of RFR in 46.8% of patients with type 2 DM without clinical signs of nephropathy under amino acid stimulation. At the same time, lack of RFR is associated with a high basal level of glomerular filtration rate and a longer course of the disease compared with patients with preserved RFR. Lack of RFR is accompanied by increase of inflammatory and fibrotic mediators, in particular monocyte chemoattractant protein type 1 and inhibitor of plasminogen activator type 1, in the blood plasma of patients, which indicates the undoubtful participation of these agents in the mechanisms diabetic kidney damage.
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