Journal
INTERNATIONAL UROLOGY AND NEPHROLOGY
Volume 51, Issue 10, Pages 1831-1840Publisher
SPRINGER
DOI: 10.1007/s11255-019-02190-6
Keywords
Platelet growth factors; IGF-1; PDGF-B; TGF-beta; Chronic kidney disease
Categories
Funding
- NCN [2011/01/B/NZ5/04235]
- Pomeranian Medical University [MB-134-141/15]
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Introduction Chronic kidney disease (CKD) is a systemic disease affecting many organs. Progression of renal failure aggravates ongoing inflammation and increases oxidative stress. In the final stage of CKD, it is necessary to use renal replacement therapy. A side effect of dialysis therapy is the synthesis of proinflammatory factors and increased oxidative stress, which activates platelets and immune cells. Aim of the study To determine the regenerative potential of platelets in patients with CKD based on the analysis of the relationships between substances with potential regenerative action, as well as analysis of the influence of the type of renal replacement therapy used on regeneration of platelets. Materials and methods The study group consisted of 117 patients. Based on the type of therapy used, patients were divided into four groups: hemodialysis, peritoneal dialysis, kidney transplant patients, and conservative treatment (30, 30, 27, and 30 patients). The control group consisted of 30 healthy volunteers. The concentrations of IGF-1, TGF-beta, and PDGF-B in the blood serum were measured by ELISA methods. Results It was shown that renal replacement therapy significantly influences the concentration of platelet growth factors (IGF-1: p = 0.025 and PDGF-B: p = 0.012). There was a relationship between the type of renal replacement therapy and the duration of dialysis, and the concentration of IGF-1, PDGF-B (p < 0.00001, p < 0.001). Conclusions The type of renal replacement therapy has a different effect on the concentration of platelet-derived growth factors IGF-1 and PDGF-B. PD patients had the highest concentrations of all growth factors, and this may be due to the presence of inflammation induced by dialysis-related advanced end-products of glycosylation (AGE).
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