Anemia mortality

Anemia decreases oxygen delivery to the renal tubules, promoting the release of inflammatory and vasoactive cytokines, which contribute to the progression of CKD. Treatment of anemia in patients with CKD reduces the cardiovascular effects of anemia and has been demonstrated to decrease morbidity and mortality by as much as 20%.25 Studies have demonstrated that treatment of anemia may slow the progression of CKD.26 The management of anemia will be discussed later. 

The progenitor cells of the kidney produce 90% of the hormone erythropoietin (EPO), which stimulates red blood cell (RBC) production. Reduction in nephron mass decreases renal production of EPO, which is the primary cause of anemia in patients with CKD. The development of anemia of CKD results in decreased oxygen delivery and utilization, leading to increased cardiac output and left ventricular hypertrophy (LVH), which increase the cardiovascular risk and mortality in patients with CKD. 

Studies have demonstrated that initiation of treatment for anemia before stage 5 CKD decreases mortality in patients with ESRD receiving dialysis, particularly in the elderly.33 The treatment of anemia can decrease morbidity, increase exercise capacity and tolerance, and slow the progression of CKD if target Hgb levels are achieved.34... 

AIDS is associated with aberrant lymphocyte production and it has been proposed that Li+ may have a potential role in reversing this. Additionally, 3 -azido-3"deoxythymidine (AZT, zidovudine), an effective inhibitor of viral reverse transcriptase that reduces mortality in AIDS patients, induces hematopoietic suppression in patients resulting in anemia, neutropenia, and overall bone-marrow failure [220]. In murine AIDS, the coadministration of Li+ effectively moderates this toxicity of AZT in vivo [221,222]. There are several case reports where Li+ has been administered to help reduce the hematopoietic suppression in HIV-infected patients taking AZT (for example, see ref. 223). To date, the use of Li+ has been limited to a few weeks of treatment, and varying degrees of success have been achieved nevertheless the outlook in this field is quite hopeful. 

Fed diets containing 700 mg/kg ration for several months High mortality survivors had anemia, gastric ulcers, liver pathology, and 100-170 mg/kg FW in liver 15... 

Biood dyscrasias Agranulocytosis, bone marrow depression, neutropenia, hypoplastic anemia and thrombocytopenia in patients receiving procainamide have been reported at a rate of approximately 0.5%. Fatalities have occurred (with approximately 20% to 25% mortality in reported cases of agranulocytosis). Perform complete blood counts including white cell, differential, and platelet counts at weekly intervals for the first 3 months of therapy, and periodically thereafter. Perform complete blood counts promptly if the patient develops any signs of infection (eg. 

Blood dyscrasias An irreversible type of marrow depression leading to aplastic anemia with a high rate of mortality is characterized by appearance of bone marrow aplasia or hypoplasia weeks or months after therapy. Peripherally, pancytopenia is most often observed, but only 1 or 2 of the 3 major cell types may be depressed. 

Epoetin Alfa [Erythropoietin/ EPO] (Epogen/ Procrit) [Recombinant Human Erythropoietin] WARNING Use lowest dose possible may be associated w/1 CV, thromboembolic events /or mortality D/C if Hgb >12 g/dL Uses CRF associated anemia zidovudine Rx in HIV-infected pts, CA chemo -1- transfusions associated w/ surgery Action Induces ery-thropoiesis Dose Adul Peds. 50-150 Units/kg IV/SQ 3x/wk adjust dose q4-6wk PRN Surgery 300 Units/kg/d x 10 d before to 4 d after -I dose if Hct 36% or Hgb, T > 12 g/dL or Hgb t >1 g/dL in 2-wk pmod hold dose if Hgb >12 g/dL Caution [C, +] Contra Uncontrolled HTN Disp Inj SE HTN, HA, fatigue, fever, tach, NA Interactions None noted EMS Monitor ECG for hypokalemia (peaked T waves) t risk of CV thrombotic events OD May cause HA, dizziness, SOB and polycythemia symptomatic and supportive... 

Al-Ahmad A, Rand WM, Manjunath G, et al. Reduced kidney function and anemia as risk factors for mortality in patients with left ventricular dysfunction. J Am Coll Cardiol. Oct 2001 38(4) 955-962. 

Horwich TB, Fonarow GC, Hamilton MA, et al. Anemia is associated with worse symptoms, greater impairment in functional capacity and a significant increase in mortality in patients with advanced heart failure. J Am Coll Cardiol. Jun 5 2002 39(11) 1780-1786. 

Vitamin E may be indicated in some rare forms of anemia such as macrocytic, megaloblastic anemia observed in children with severe malnutrition and the hemolytic anemia seen in premature infants on a diet rich in polyunsaturated fatty acids. Also anemia s in malabsorption syndromes have shown to be responsive to vitamin E treatment. Finally, hemolysis in patients with the acanthocytosis syndrome, a rare genetic disorder where there is a lack of plasma jS-lipoprotein and consequently no circulating alpha tocopherol, responds to vitamin E treatment. In neonates requiring oxygen therapy vitamin E has been used for its antioxidant properties to prevent the development retrolental fibroplasia. It should be noted that high dose vitamin E supplements are associated with an increased risk in allcause mortality. 

Any consideration of major issues relating to the balance of benefit and harm, such as cancer or mortality rates, should be supplemented by a consideration of less prominent ones, for example, a reduction in disorders of the menstrual cycle (such as dysmenorrhea, menorrhagia, and the premenstrual syndrome) and the reduced risks of iron deficiency anemia, functional ovarian cysts, uterine fibroids, benign breast disease, pelvic inflammatory disease, and ectopic pregnancy (10,11). 

Dharmarajan TS, Pais W, Norkus EP Does anemia matter Anemia, morbidity, and mortality in older adults Need for greater recognition. Geriatrics 60 22-27,2005. 

Toxicity. The toxicity of Mn for chicks was recently reviewed (40). Signs of toxicosis have been shown to vary depending on type of diet used, mineral composition of the diet and on source of Mn. Heller and Penquite (41) reported that 4779 ppm Mn from MnC03 reduced chick growth and caused 52% mortality. More recently, similar levels of Mn were fed to chicks with only mild anemia and a slight growth depression observed (18,19,22). 

---