الفهرس 
Chronic Kidney Disease and Estimation of Kidney FunctionsOnly 14 pages are availabe for public view
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Abstract
Chronic kidney disease is a public health epidemic that affects millions of people worldwide. Presence of CKD predisposes individuals to high risks of ESRD, cardiovascular disease, and premature death.
Disordered phosphate homeostasis with elevated circulating levels of fibroblast growth factor 23 is an early and pervasive complication of CKD. CKD is likely the most common cause of chronically elevated FGF23 levels, and the clinical condition in which levels are most markedly elevated.
Hypophosphatemia complicating administration of parenteral iron was first reported in 1982 in the Japanese literature.
Our study included (59) adult Chronic Kidney disease patients selected from Nephrology department in Theodor Belhars Research Institute TBRI.
Patients were classified in two groups:
Group A: 47 patients ESRD on hemodialysis with mean age (50).
Group B: 12 patients stage 3 and 4 CKD patients on conservative treatment with mean age (45).
On comparing both groups the following were concluded:
Age didn’t show any significant correlation to each of serum FGF23, Hb and serum ferritin in both Group A & B.
The idea of presence of high turn-over bone disease in Group A and secondary hyperparathyroidism in Group B was reinforced by finding serum alkaline phosphatase levels above normal in the two groups.
Serum FGF23 levels were higher than normal level in the two groups of our study. Multiple Regression Analysis for all parameters included in the study showed that serum creatinine was the only dependent factor affecting FGF23 serum level in HD patients of Group A.
In our study FGF23 was above normal and also PTH was very much higher than recommended range in K/DOQI guidelines, in the two groups of the study.
We found a borderline significant positive correlation between PTH and Hb within HD patients of Group A. This relationship didn’t exist in CKD patient of Group B.
PTH had a highly significant positive correlation with serum ferritin level in HD patients of Group A. Such a significant positive correlation also existed in CKD patients of Group B. In Multiple Regression Analysis, PTH was the most influencing factor affecting ferritin level.
In CKD patients of Group B, serum Iron showed an inverse significant correlation to serum FGF23. This relationship didn’t exist in HD patients of Group A, although there was a non-significant inverse relationship between FGF23 and serum Iron. This may be due to the more preserved renal function in CKD patients, although serum FGF23 level and serum Iron were nearly at the same level in the two groups.
Hb had an inverse significant correlation to FGF23 in CKD of Group B, and this relationship didn’t exist in HD patients of Group A, may be due to the same reasons as for serum Iron. Hb level in both HD patients of Group A and CKD patients of Group B, was around the recommended range by K/DOQI guidelines.
TSAT had also an inverse significant correlation to FGF23 in CKD of Group B. This relation didn’t also exist in HD patients of Group A of our study.
None of the three parameters: serum Iron, Hb and TSAT, have shown to affect FGF23 serum level as dependent factors in Multiple Regression Analysis.
Lack of IV Iron infusion was accompanied by elevation of FGF23 in our CKD patients of Group B, and phosphorus level was around the recommended range by K/DOQI guidelines and it didn’t show any significant relationship to FGF23 serum level in our study, while IV infusion in HD patients of Group A could explain elevation of FGF23 serum level in this group.
Hb had a significant positive correlation to serum ferritin in CKD patients of Group B. This relationship didn’t exist in HD patients of Group A.
Serum ferritin had a significant positive correlation to serum creatinine in CKD patients of Group B, but this relationship didn’t exist in HD patients of Group A may be due to the more complex situation of HD dialysis affected by many factors related to ESRD, HD vintage, oxidative stress factors and drug intake, rather than the more simple situation of chronic inflammatory state and partially preserved renal function of CKD patients.
Serum ferritin didn’t have any significant relationship with FGF23 serum level in both HD patients of Group A and CKD patients of Group B as ferritin was below recommended range by K/DOQI guidelines, although it is a well-known acute phase reactant.
Serum ferritin was positively correlated to serum Iron and TSAT in HD patients of Group A. But these relationships didn’t exist in CKD patients of Group B, may be due to presence of IV Iron and EPO supplementation in HD patients.
We couldn`t perform a Multiple Regression Analysis for all studied parameters affecting FGF23, Hb and ferritin in CKD patients of Group B due to the small number of patients (Only 12).
ALL our drugs supplemented to HD patients of Group A and CKD patients of Group B, didn’t affect FGF23, Hb and ferritin in our study except for calcium dose affecting Hb level.