Correction of Iron Deficiency in the Cardiorenal Syndrome

Impaired energy metabolism is a feature of Congestive Heart Failure (CHF). Iron deficiency has been shown to reduce energy production in the cell in animals and humans. Iron deficiency is common in both Chronic Kidney Disease (CKD) and in CHF. Recent studies suggest that iron deficiency is an independent risk factor for mortality in CHF. Studies of correction of the anemia with intravenous (IV) iron in both CKD and CHF have shown an improvement in the anemia and, in some cases, in the renal function as well. Some CHF studies of correction of the iron deficiency have shown an improvement in cardiac function and structure as well as in exercise capacity and quality of life. This occurred independent of whether or not they had anemia, suggesting that the iron deficiency itself may be independently contributing to the worsening of the CHF and CKD. If future long-term studies confirm the safety and efficacy of IV iron in the treatment of iron deficiency in CKD and CHF, this will become a new addition to the therapeutic armamentarium of the cardiorenal syndrome, and parameters of iron deficiency will become part of the routine measurements performed in both CKD and CHF whether or not the patient is anemic

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Abstract Background: Many patients with congestive heart failure (CHF) have chronic kidney insufficiency (CKI) and anemia. Aims: The purpose of this review is to clarify the relationship between these three factors and to study the effect of correction of anemia in CHF and CKI. Findings: Anemia, CHF and CKI are each capable of causing or worsening each other. Thus they form a vicious circle which can result in progressive CHF, CKI and anemia. Aggressive therapy of CHF, CKI and control of the associated anemia with erythropoietin and i.v. iron can prevent the progression of CHF and CKI, reduce hospitalization, and improve quality of life. Conclusion: CHF patients are a major source of end-stage renal failure patients and deserve special attention. If treated well and early, progressive heart failure and renal failure can be prevented. Cooperation between nephrologists, cardiologists, and other internists will improve the care of all three conditions and prevent their progression

an inhibitor of leukocyte adhesion, exacerbates acute ischemic renal failure and stimulates nitric oxide synthesis

Abstract Objectives. To lessen renal ischemic injury caused by fucoidin, a substance capable of reducing tissue infiltration by neutrophils, and to seek a possible interrelationship with the nitric oxide system which may also modulate leukocyte infiltration. Material and methods. Acute ischemic renal failure was induced in rats by uninephrectomy followed by 60 min of clamping of the renal artery. The rats were injected with fucoidin (25 mg/kg) or fucoidin'/nitroprusside (2.5 mg/kg) before reperfusion, and urine was collected for 24 h afterwards. Serum and urine were examined for creatinine sodium and protein; creatinine clearance and fractional excretion of sodium (FENa) were calculated. The renal tissue of the sacrificed animals was examined histologically for tissue damage and histochemically for myeloperoxidase, a marker of neutrophil infiltration. The nitric oxide system was evaluated by measuring urinary nitrates and inducible nitric oxide synthase messenger RNA (iNOs mRNA). Results. Renal failure was more severe in the fucoidin group than the ischemia only group (creatinine clearance 0.119/0.08 ml/min for ischemia'/fucoidin versus 0.269/0.11 ml/min for ischemia only; p B/0.002). Adding nitroprusside to fucoidin lessened the decline in creatinine clearance (0.139/0.13 ml/min; p0/NS). Fucoidin was associated with greater tubular damage, as evidenced by increased FENa (7.2%9/3.4% vs 1.51%9/1.96% for ischemia only; p B/0.001). Nitroprusside weakened this trend. Fucoidin caused an increase in the fractional excretion of nitrates, a response accompanied by increased iNOS mRNA. Conclusions. Fucoidin failed to protect the kidney from ischemic damage and was even nephrotoxic. It also stimulated the formation of iNOS RNA

Severe defect in clearing postprandial chylomicron remnants in dialysis patients

Severe defect in clearing postprandial chylomicron remnants in dialysis patients. Lipid abnormalities have been suggested as a major cause of the accelerated atherosclerosis and the high incidence of coronary heart disease in chronic renal failure patients. In the present work the postprandial lipoprotein metabolism was studied in chronic dialysis patients with or without fasting hypertriglyceridemia using the vitamin A loading test. This method investigates specifically postprandial lipoprotein metabolism. The determination of vitamin A ester level retinyl palmitate (RP) differentiates the circulating plasma chylomicron and chylomicron remnant fractions from the endogenous VLDL and IDL. Subjects with normal renal function with or without fasting hypertriglyceridemia served as control groups. Dialysis patients have significantly higher level of chylomicron remnants for a more prolonged period of time than controls, irrespective of their fasting triglyceride levels. The area below retinyl palmitate chylomicron remnants curve was 26308 ± 12422 µg/liter · hr in the normolipidemic dialysis patients, significantly higher than (6393 ± 2098 µg/liter · hr; P < 0.0001) in the normolipidemic controls. The retinyl palmitate chylomicron remnants curve of the hypertriglyceridemic dialysis patients was 21021 ± 4560 µg/liter · hr, which was higher than 12969 ±2215 µg/liter · hr (P < 0.0001) in the hypertriglyceridemic controls. Moreover, the hypertriglyceridemic dialysis patients had an additional defect in the lipolysis metabolic step, that is, accumulation of chylomicrons in circulation. These findings show a severe defect in postprandial lipoprotein metabolism in chronic renal failure patients. The prolonged exposure of the vascular wall to high chylomicron remnant concentrations might be an important pathogenetic factor in the accelerated atherosclerosis seen in chronic dialysis patients