Determination Of Plasma Levels Of Fibroblast Growth Factor 23 In Ghanaian Individuals With Hypertension And Chronic Kidney Disease

Abstract

Background: Fibroblast growth factor 23 (FGF23) is a newly found hormone that promotes renal phosphate excretion. It is secreted by osteocytes. In progressive chronic kidney disease (CKD), FGF23 levels increase in parallel with the deterioration of renal function, thus serves as a novel risk marker for progression of chronic kidney disease. The physiologic stimulus for FGF23 secretion is linked to hyperphosphatemia caused by phosphate load. Elevated FGF23 levels have spurious effects such as vascular calcification, left ventricular hypertrophy, end stage renal disease and death especially in renal impaired patients and patients at risk of developing renal impairment such as hypertensive patients. Aim: The aim of the study was to measure the levels of FGF23 in non-hypertensive, hypertensive and chronic kidney disease patients. Specific objectives: The study determined and compared the level of FGF23 among normotensive, hypertensive, and CKD individuals as well as identified risk factors associated with increase in FGF23 plasma level in individuals with hypertension. Materials and methods: The study was a hospital based case control study in which purposive sampling was used to select the study subjects. It was conducted at the Holy Family Hospital, Techiman. In all, 146 respondents took part in the study. A structured questionnaire was used to gather their anthropometric and demographic characteristics. Blood and urine samples were taken for biochemical analysis for urea, creatinine, sodium, calcium, phosphate, and albumin whiles FGF23 was analyzed from citrated plasma. Results: There were 86 study subjects with hypertension and 60 without hypertension. Out of the 86 subjects with hypertension, 24 (27.9%) had CKD, ranging from stages 2 to 4. There was significant difference in the plasma levels of FGF23 among the subjects with hypertension, CKD and those without hypertension (P <0.05). Again, there was significant difference in FGF23 levels in all the stages of CKD. A significant inverse correlation was found between FGF23 levels and estimated GFR (r = -0.505, P= 0.000), calcium (r=-0.568, P=0.000) in both hypertensive and CKD subjects. A significant direct correlation between FGF23 levels and urea (r=0.700, P=0.000), creatinine (r=0.715, P=0.000) and phosphate (r= 0.679, P=0.000) was reported. Systolic and diastolic blood pressure also correlated significantly and directly with FGF23 levels in subjects with hypertension (P=0.000) but not statistically significant in those with CKD (P>0.05). Hypertensive individuals on angiotensin converting enzyme inhibitors (OR=9.1X107, 95% CI: 1.1X106 – 6.9 X107, P<0.0001) were at risk of increasing their FGF23 plasma levels. Systolic and diastolic blood pressure, urea, creatinine and phosphate were all significant risk factors for increasing plasma FGF23 levels (OR >1, P<0.05). Conclusion: There is significant difference in the plasma levels of FGF23 between individuals with hypertension and CKD. Angiotensin converting enzyme inhibitors, phosphate load, urea, and creatinine concentrations were risk factors for increasing the plasma levels of FGF23 in hypertensive patients.