Oral Iron Absorption of Ferric Citrate Hydrate and Hepcidin-25 in Hemodialysis Patients: A Prospective, Multicenter, Observational Riona-Oral Iron Absorption Trial.

Oral ferric citrate hydrate (FCH) is effective for iron deficiencies in hemodialysis patients; however, how iron balance in the body affects iron absorption in the intestinal tract remains unclear. This prospective observational study (Riona-Oral Iron Absorption Trial, R-OIAT, UMIN 000031406) was conducted at 42 hemodialysis centers in Japan, wherein 268 hemodialysis patients without inflammation were enrolled and treated with a fixed amount of FCH for 6 months. We assessed the predictive value of hepcidin-25 for iron absorption and iron shift between ferritin (FTN) and red blood cells (RBCs) following FCH therapy. Serum iron changes at 2 h (ΔFe2h) after FCH ingestion were evaluated as iron absorption. The primary outcome was the quantitative delineation of iron variables with respect to ΔFe2h, and the secondary outcome was the description of the predictors of the body's iron balance. Generalized estimating equations (GEEs) were used to identify the determinants of iron absorption during each phase of FCH treatment. ΔFe2h increased when hepcidin-25 and TSAT decreased (-0.459, -0.643 to -0.276, p = 0.000; -0.648, -1.099 to -0.197, p = 0.005, respectively) in GEEs. FTN increased when RBCs decreased (-1.392, -1.749 to -1.035, p = 0.000) and hepcidin-25 increased (0.297, 0.239 to 0.355, p = 0.000). Limiting erythropoiesis to maintain hemoglobin levels induces RBC reduction in hemodialysis patients, resulting in increased hepcidin-25 and FTN levels. Hepcidin-25 production may prompt an iron shift from RBC iron to FTN iron, inhibiting iron absorption even with continued FCH intake.

Subclavian steal syndrome in a hemodialysis patient after percutaneous transluminal angioplasty of arteriovenous access.

INTRODUCTION: We describe a hemodialysis patient who developed subclavian steal syndrome via an arteriovenous fistula after percutaneous transluminal angioplasty. CASE DESCRIPTION: A 55-year-old female with end-stage renal failure due to polycystic kidney disease had been treated with hemodialysis for 10 years. Because of an autologous arteriovenous fistula stenosis, percutaneous transluminal angioplasty was performed. After successful treatment with percutaneous transluminal angioplasty, the patient developed dizziness. Magnetic resonance imaging with angiography of the brain and neck revealed normal bilateral subclavian and carotid arteries. However, flow in the left vertebral artery was not detected in time-of-flight magnetic resonance angiography. The left vertebral artery showed completely reversed blood flow as detected by color duplex ultrasound. We also confirmed anterograde flow in the left vertebral artery by color duplex ultrasound with arteriovenous fistula compression. Arteriovenous flows before the arteriovenous fistula stenosis and post-percutaneous transluminal angioplasty were 1146 and 2239 mL/min, respectively. These findings suggested high-flow arteriovenous fistula led to the subclavian steal syndrome. The patient was subsequently treated by a flow reduction in the high-flow arteriovenous access using a modified graft inclusion technique. We decreased the arteriovenous fistula flow to 851 mL/min, which remained under 850 mL/min, 1 year later. The brain natriuretic peptide level and right-ventricular pressure also decreased after treatment. A modified graft inclusion technique was successful in decreasing the high flow of the arteriovenous fistula, and improved subclavian steal syndrome symptom and cardiac overload. CONCLUSION: This case shows that percutaneous transluminal angioplasty for an arteriovenous fistula may induce subclavian steal syndrome, and a modified graft inclusion technique was useful in improving the high flow of an arteriovenous fistula.