In haemodialysis patients, FGF-23 and ACI were significantly increased, and FGF-23 was independently associated with aortic calcification.

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BackgroundFasting during the month of Ramadan is a religious obligation for Muslims who represent 20% of the world population. This study explores the safety of fasting for a whole month among patients with chronic kidney disease (CKD) with the possible risk of dehydration and hyperviscosity leading to deterioration of kidney functions and vascular thrombosis.MethodsWe followed CKD patients with stable kidney function who chose to fast during the month of Ramadan. A group of nonfasting CKD patients served as controls. Serum creatinine was recorded at the beginning of the month, after 1 week of fasting, at the end of the month and 3 months later. Patients were followed for major adverse cardiovascular events (MACE).ResultsA total of 131 CKD patients were recruited and included in two groups: fasting and nonfasting (mean baseline estimated glomerular filtration rate 27.7, SD 13 and 21.5, SD 11.8 mL/min/1.73 m2, respectively). A rise of serum creatinine was noted during fasting in 60.4% of patients by Day 7 and was associated with intake of renin angiotensin aldosterone system antagonists [relative risk (RR) 2, P = 0.002]. Adverse cardiovascular events were observed in six patients in the fasting cohort and were associated with a rise of serum creatinine after 1 week of fasting (P = 0.009) and the presence of pre-existing cardiovascular disease (RR 15, P = 0.001); the latter association was confirmed by logistic regression analysis. Only one event was recorded in the nonfasting group, P = 0.036.ConclusionsMACE occurred more frequently among fasting CKD patients with pre-existing cardiovascular disease and were predicted by an early rise of serum creatinine.

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Background: Fibroblast growth factor-23 (FGF-23) has been linked to vascular calcification, ventricular hypertrophy and mortality in chronic kidney disease (CKD), although these links may not be direct and independent. Similar grave outcomes are associated with inflammation and oxidative stress in CKD. Recently, accumulating evidence has linked components of phosphate homeostasis to inflammation and oxidative stress. The interaction between the triad of inflammation, FGF-23 and cardiovascular outcomes is underinvestigated. Methods: We studied 65 patients with stage 5 CKD on hemodialysis. Serum levels of FGF-23, high-sensitivity C-reactive protein (hsCRP), endogenous soluble receptor of advanced glycation end products (esRAGE), advanced oxidation protein products (AOPP), parathormone, lipids, calcium and phosphorous were measured. The aortic calcification index (ACI) was determined using non-contrast CT scans of the abdominal aorta. Results: FGF-23 was elevated (mean: 4,681 pg/ml, SD: 3,906) and correlated with hsCRP, esRAGE, AOPP, dialysis vintage and phosphorus in univariate analysis. In multiple regression analysis, hsCRP, AOPP and phosphorus but not esRAGE were all significantly correlated to FGF-23 (R² = 0.7, p < 0.001). In univariate analysis, ACI correlated with hsCRP, esRAGE, FGF-23, dialysis vintage, systolic blood pressure (BP) and serum cholesterol. In multiple regression analysis not including inflammation markers, ACI was associated with FGF-23. However, inclusion of inflammation markers in another multiple regression analyses showed that ACI correlated with hsCRP, BP, dialysis vintage and esRAGE but not with FGF-23 (R² = 0.65, p < 0.001). Conclusion: FGF-23 is strongly correlated to various markers of inflammation and oxidative stress in hemodialysis patients. The association between FGF-23 and vascular calcification was mitigated when corrected for inflammation markers.