Dialysis deficiency

Although EPO deficiency is the primary cause of CKD anemia, iron deficiency is often present, and it is essential to assess and monitor the CKD patient s iron status (NKF-K/DOQI guidelines). Iron stores in patients with CKD should be maintained so that transferrin saturation (TSAT) is greater than 20% and serum ferritin is greater than 100 ng/mL (100 mcg/L or 225 pmol/L). If iron stores are not maintained appropriately, epoetin or darbepoetin will not be effective, and most CKD patients will require iron supplementation. Oral iron therapy can be used, but it is often ineffective, particularly in CKD patients on dialysis. Therefore, intravenous iron therapy is used extensively in these patients. Details of the pharmacology, pharmacokinetics, adverse effects, interactions, dose, and administration of erythropoietin and iron products have been discussed previously. 

Hepatic steatosis usually is a result of excessive administration of carbohydrates and/or lipids, but deficiencies of carnitine, choline, and essential fatty acids also may contribute. Hepatic steatosis can be minimized or reversed by avoiding overfeeding, especially from dextrose and lipids.35,38 Carnitine is an important amine that transports long-chain triglycerides into the mitochondria for oxidation, but carnitine deficiency in adults is extremely rare and is mostly a problem in premature infants and patients receiving chronic dialysis. Choline is an essential amine required for synthesis of cell membrane components such as phospholipids. Although a true choline deficiency is rare, preliminary studies of choline supplementation to adult patients PN caused reversal of steatosis. 

Other workers have determined zinc in serum by direct dilution 87> 88). McPherson and George 89) determined total copper and zinc of red cells and the free copper and zinc of plasma and dialysis fluids of patients undergoing regular hemodialysis, using atomic absorption spectroscopy. Spry and Piper 90) determined zinc in whole blood and plasma in blood cells of iron deficient rats. The zinc concentrations were raised in the iron deficient rats. 

Pharmacology Erythropoietin is a glycoprotein that stimulates red blood cell production. It is produced in the kidney and stimulates the division and differentiation of erythroid progenitors in bone marrow. Hypoxia and anemia generally increase the production of erythropoietin, which in turn stimulates erythropoiesis. In patients with CRF, erythropoietin production is impaired this deficiency is the primary cause of their anemia. Epoetin alfa stimulates erythropoiesis in anemic patients on dialysis and those who do not require regular dialysis. 

WARNING Anaphylactic Rxns w/ use use only if oral Fe not possible administer where resuscitation techniques available Uses Fe deficiency when cannot supl PO Action Fe supl Dose Adul. Iron defic anemia Estimate Fe deficiency, give 25-100 mg IM/IV /d until total dose total dose (mL) = [-.0442 x (desired Hgb - observed Hgb) x LBW] + (0.26 x LBW) Iron replacement, blood loss Total dose (mg) = blood loss (mL) x Hct (as decimal fraction) max 100 mg/d Peds >4 mo. As for adults max 0.5 mL (wt <5 kg), 1 mL (5-10 kg), 2 mL (>10 kg) p dose IM or direct IV Caution [C, M] Contra Anemia w/o Fe deficiency. Disp Inj SE Anaphylaxis, flushing, dizziness, inj site inf Rxns, metallic taste Interactions X Effects W/ chloramphenicol, X absorption of oral Fe EMS Anaphylactic Rxns common taking oral Fe t risk of tox and SEs OD May cause N/V, HA, muscle/joint pain and fev symptomatic and supportive Iron Sucrose (Venofer) [Iron Supplement] Uses Fe deficiency anemia w/ chronic HD in those receiving erythropoietin Actions Fe r lacement. Dose 5 mL (100 mg) IV on dialysis, 1 mL (20 mg)/min max Caution [C, M] Contra Anemia w/o Fe deficiency Disp Inj SE Anaphylaxis, -1- BP, cramps, N/V/D, HA Interactions i Absorption OF oral Fe supls EMS See Iron Dextran OD See Iron Dextran... 

The answer is D. The most likely diagnosis in this case is CPT-II deficiency, although this is apparently a fairly mild case. The patient s muscle weakness and brown urine (myoglobinuria) are characteristic of this disorder. CPT-I deficiency would most likely manifest as liver dysfunction. A secondary form of carnitine deficiency due to exogenous factors such as malnutrition, infection, or dialysis, is unlikely. MCAD ordinarily manifests within the first 3-5 years of life. The patient s normal stature is inconsistent with Marfan syndrome, which is characterized by tall stature and very long bones in the extremities. 

Iron deficiency anemia IV Dosage is expressed in terms of milligrams of elemental iron. 5 ml iron sucrose, or 100 mg elemental iron, delivered during dialysis administer 1-3 times a wk to total dose of 1,000 mg in 10 doses. Give no more than 3 times a wk. 

Dialysis causes a deficiency in MEGA surfactant which has patched hydrophobic portion of dialkyl amphiphilic molecular assembly. 

Folic acid deficiency, unlike vitamin B12 deficiency, is often caused by inadequate dietary intake of folates. Patients with alcohol dependence and patients with liver disease can develop folic acid deficiency because of poor diet and diminished hepatic storage of folates. Pregnant women and patients with hemolytic anemia have increased folate requirements and may become folic acid-deficient, especially if their diets are marginal. Evidence implicates maternal folic acid deficiency in the occurrence of fetal neural tube defects, eg, spina bifida. (See Folic Acid Supplementation A Public Health Dilemma.) Patients with malabsorption syndromes also frequently develop folic acid deficiency. Patients who require renal dialysis develop folic acid deficiency because folates are removed from the plasma during the dialysis procedure. 

Parenteral administration of folic acid is rarely necessary, since oral folic acid is well absorbed even in patients with malabsorption syndromes. A dose of 1 mg folic acid orally daily is sufficient to reverse megaloblastic anemia, restore normal serum folate levels, and replenish body stores of folates in almost all patients. Therapy should be continued until the underlying cause of the deficiency is removed or corrected. Therapy may be required indefinitely for patients with malabsorption or dietary inadequacy. Folic acid supplementation to prevent folic acid deficiency should be considered in high-risk patients, including pregnant women, patients with alcohol dependence, hemolytic anemia, liver disease, or certain skin diseases, and patients on renal dialysis. 

Suppose the K+ salt of an RNA is added to a dialysis chamber that has been equilibrated with a mixture of MgCl2 and KC1 (Fig. 21.3A). As in the monovalent salt example (Fig. 21.1 A), KC1 ion pairs will tend to diffuse into the right chamber, leaving an excess of K+ and creating a deficiency of CD in the left chamber. However, there will also be a tendency for the RNA to accumulate Mg2 in preference to K+ the resulting net diffusion of Mg2 1 ions into the left chamber must be accompanied by enough Cl- ions to... 

Acylcamitines or amino acids may also be important in disease monitoring and treatment or as markers for new therapies, toxicities, etc. In one application using dried plasma spots, carnitine and acylcamitines may be useful in detecting possible carnitine deficiency as a result of kidney dialysis for patients with end-stage renal disease (36,37). A deficiency should result in carnitine supplementation in those patients that cannot replenish their levels fast enough. In fact, this is one of the first pharmaceutical-related applications of screening. The measurement of certain amino acids such as Phe and Tyr and their ratio is also routinely performed to monitor the effectiveness of dietary intervention in patients with PKU. 

Erythropoietin [ery throw PO eetin] is a glycoprotein, normally made by the kidney, that regulates red cell proliferation and differentiation in bone marrow. Human erythropoietin, produced by recombinant DNA technology, is effective in the treatment of anemia caused by end-stage renal disease, anemia associated with HIV-infected patients, and anemia in some cancer patients. Supplementation with iron may be required to assure an adequate response. The protein is usually administered intravenously in renal dialysis patients, but in others the subcutaneous route is preferred. Side effects such as iron deficiency and an elevation in blood pressure occur. [Note The latter may be due to increases in peripheral vascular resistance and/or blood viscosity.]... 

Among dialysis patients, a microcytic anemia most commonly arises due to iron deficiency but Al toxicity should be suspected in all cases where iron deficiency is unlikely. Probably most patients with acute and chronic Al intoxication develop microcytic anemia [93, 95-98, 105]. 

Second, modified microorganisms could correct errors of metabolism resulting from either gastric or intestinal enzyme deficiencies (e.g., lipase or lactase) [11] or organ failure (by removing urea in the case of kidney failure or ammonia in the case of liver failure) [12,13]. This could constitute an alternative to current therapy such as renal dialysis, which is time consuming and uncomfortable for the patient. 

There is a great deal of evidence that deficiency of serotonin (5-hydroxytryptamine) is a factor in depressive illness, and many antidepressant drugs act to decrease its catabolism or enhance its interaction with receptors. A key enzyme involved in the synthesis of serotonin (and the catecholamines) is aromatic amino acid decarboxylase, which is pyridoxal phosphate-dependent. Therefore, it has been suggested that vitamin Be deficiency may result in reduced formation of the neurotransmitters and thus be a factor in the etiology of depression. Conversely, it has been suggested that supplements of vitamin Be may increase aromatic amino acid decarboxylase activity, and increase amine synthesis and have a mood-elevating or antidepressant effect. There is little evidence that vitamin Be deficiency affects the activity of aromatic amino acid decarboxylase. In patients with kidney failure, undergoing renal dialysis, the brain concentration of pyridoxal phosphate falls to about 50% of normal, with no effect on serotonin, catecholamines, or their metabolites (Perry etal., 1985). 

The initial dose in cobalamin deficiency anaemias, including uncomplicated pernicious anaemia, is hydroxocobalamin 1 mg i.m. every 2-3 days for 5 doses to induce remission and to replenish stores. Maintenance may be 1 mg every 3 months higher doses will not find binding sites and will be eliminated in the urine. Higher doses are justified during renal or peritoneal dialysis where hydroxy-cobalamin clearance is increased, and resultant raised plasma methylmalonic acid and homocysteine represent an independent risk factor for vascular events in these patients (see later). 

The immune response is mainly influenced by age, gender and immune status. Women usually show a better immune response than men. In almost every case, children form adequately high antibody titres (100% responders). Older people, starting at the age of about 50, show a slowly decreasing immune response. (152) Smokers, patients suffering from coeliac disease and overweight persons are more frequently non-responders, as are certain HLA typ>es or those with IL-2 deficiency (e.g. dialysis patients). Dialysis patients or immunosuppressed persons are only capable of an immune response in about 50% of cases (or even less). In 5-10% of cases, no antibodies are formed (non-responders). (199, 235)... 

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