Treatment of a Patient with End-Stage Renal Disease, Severe Iron Overload and Ascites by Weekly Phlebotomy Combined with Recombinant Human Erythropoietin

Abstract

A 41-year-old hemodialyzed woman developed ascites and was found to have secondary iron overload. The dose ofadministered iron was approximately 11–12 g, and her serum ferritin level was 15,000 ng/ml (15,000 μg/l). There were no signs of congestive heart failure, fluid overload, or liver cirrhosis. A program of weekly phlebotomy combined with recombinant human erythropoietin (rhEPO) therapy was tried to eliminate the iron congestion. After 9 months of this therapy, about 5 g of iron had been removed. The ascites completely disappeared, and her serum ferritin level fell to 5,800 ng/ml (5,800 μg/l). This suggests that such combined therapy would be useful when iron overload must be corrected rapidly. Before therapy, the sterile ascitic fluid showed exudative characteristics with 3.7 g/dl (37 g/l) of total protein. The serum-ascites albumin difference was 0.6 g/dl (6 g/l), and the fluid contained 1,400 inflammatory cells/mm³ (1.4 × 10⁹/l). Notably, the serum-ascites albumin difference increased in parallel with iron elimination. These findings suggested that iron deposition may have played a role in changing the permeability of the peritoneum, or in impairing lymphatic drainage, both of which are presumed to be pathogenetic factors of nephrogenic ascites.

Iron Storage Indices: Novel Predictors of Bacteremia in Hemodialysis Patients Initiating Intravenous Iron Therapy

“…Furthermore, the long-term safety of repetitive administration of intravenous iron therapy has recently been questioned, with mounting evidence suggesting that iron overload may increase the risk of infection, hospitalization, and mortality in HD patients [10,11]. However, to date, no published studies have evaluated the DOQI guidelines on iron storage levels and risk of bacterial infection.…”

A Real Neglected Problem With a Grave Prognosis: Nephrogenic Ascites

“…The underlying pathophysiologic factors that contribute to nephrogenic ascites formation include: 1) Hepatic vein hydrostatic pressure secondary to liver disease could lead to accumulation of protein-rich fluid in the peritoneal cavity, and the absence of varices on endoscopy and SAAG of less than 1.1 g/dL reinforce the absence of clinically significant degree of postal hypertension [4]; 2) Changes in peritoneal membrane permeability caused by an inflammatory effect of uremic toxins, circulating immune complexes, and prior exposure to dialysis solutions, hemosiderosis, renin-angiotensin-aldosterone system (RAAS) activation [1,5,6]; 3) Obstruction of lymphatic channels caused by inflammatory infiltrate resulting in an alteration in the peritoneal fluid absorption and ascetic fluid accumulation [6][7][8]; and 4) Other predisposing factors could be hypoalbuminemia, hyperparathyroidism, congestive heart failure, constrictive pericarditis, pancreatitis, and cirrhosis with portal hypertension [9].…”

Management of Hemosiderosis Complicated by Coexistent Anemia with Recombinant Human Erythropoietin and Phlebotomy

“…Erythropoietin has also been com bined successfully with phlebotomy to deplete excess body iron in patients with porphyria cutanea tarda and in ironoverloaded patients with renal failure undergoing hemo dialysis [7][8][9], At our institution, the cost of administration of r-Hu-EPO is less than half the cost of desferrioxamine mesylate and the rent and maintenance expenses of its equipment. Therefore, not only is the combination of r-Hu-EPO and phlebotomy less cumbersome and perhaps more efficient in clearing the body of excess iron, it may also prove to be more cost-effective.…”