Serum iFGF-23, sKlotho, and 1,25 (OH)&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt; D&amp;lt;sub&amp;gt;3&amp;lt;/sub&amp;gt; Vitamin Levels in Kidney Transplant

Ayse Senelmis,Ozant Helvaci,Hatice Pasaoglu,Ozge Tugce Pasaoglu,Ulver Derici

doi:10.11648/j.bmb.20200502.11

Abstract

Aim of the study: Chronic kidney disease is characterized by elevated iFGF-23 level, which is known to regulate phosphate, little is known about the relationship between iFGF-23 and phosphate homeostasis in posttransplant patients, however. We will look at the iFGF-23 level and correlate it with sKlotho, and 1,25 (OH)2 D3 Vitamin in posttransplant patients. Material and methods: This study was conducted using 60 kidney transplant patients. 34 healthy subjects enrolled as a control group. Blood samples were withdrawn for measuring the levels of serum iFGF-23, sKlotho, 1,25 (OH)2 D3 Vitamin, Calcium, Phosphorus, iPTH, 25 (OH) D vitamin. CKD-EPI is used to calculate GFR. Results: iFGF-23 levels were elevated in the posttransplant period compared with healthy subjects. iFGF-23 levels were measured as 263.64±153.08 pg/ml in transplant patients and 155.05±73.40 pg/ml within the control group. sKlotho levels were measured as 2.82±1.76 ng/ml and 3.72±3.59 ng/ml in transplant patients and control groups respectively. 1,25 (OH)2 D3 Vitamin levels were measured as 49.56±13.73 pg/ml and 48.42±12.13 pg/ml in transplant patients and control group respectively. The results of this study revealed a significant correlation between iFGF-23 and sKlotho both in transplant patients and in the control group. Conclusions: Significantly elevated iFGF-23 and iPTH level accompanied by decreased GFR activity suggests a progressive deficiency in phosphate homeostasis.

Highlights

Calcium homeostasis has been extensively studied over the past several decades
This study revealed a significant increase in iFGF-23 and iPTH in transplant patients compared with the control group (p
It was seen that 1,25 (OH)2 D3 Vitamin increased in transplant patients compared to the control group, but it is not significant

Summary

Introduction

Calcium homeostasis has been extensively studied over the past several decades. We know relatively little about the regulation of phosphate homeostasis [1]. Fibroblast growth factor-23 (FGF-23) is known to regulate calcium and phosphate homeostasis. Increased serum phosphate concentration increases FGF-23 expression by osteocytes and osteoblasts in bone. Reduction in renal function increases serum phosphate level contributing to the secretion of FGF23 further enhancing the excretion of phosphate per nephron. Decreased 1,25 (OH) D3 level induces PTH secretion by the parathyroid gland [2, 3]. Klotho is produced mostly in the kidney and the parathyroid gland. It is known that it is expressed from cleavage of the intracellular domain of the full-length protein by secretases. Both ways result in soluble Klotho [4]. It is suggested that sKlotho deficiency causes FGF-23 resistance to further causes CKD [6, 7]

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Discussion

Conclusion