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Dialysis supplements

Peritoneal dialysis Supplemental doses of valacyclovir should not be required following chronic ambulatory peritoneal dialysis (CARD) or continuous arteriovenous hemofiltration/hemodialysis (CAVHD). [Pg.1764]

When replacing iron stores in patients receiving ESA therapy, the general approach to treatment is to give a total of 1 g of IV iron, administered in smaller, sequential doses. Because iron stores deplete quickly in patients who do not receive iron supplementation, maintenance doses are often used, particularly in patients receiving hemodialysis. Maintenance doses consist of smaller doses of iron administered weekly or with each dialysis session (e.g., iron dextran or iron sucrose 20 to 100 mg per week sodium ferric gluconate 62.5 to 125 mg per week). [Pg.386]

Hypotension may be related to alterations in levocarnitine levels during dialysis. Patients who have low levels of levocarnitine may benefit from supplementation. Levocarnitine is administered as doses of 20 mg/kg intravenously at the end of each dialysis session. However, levocarnitine should not be used as a first-line agent for the treatment of hypotension because of the significant cost associated with the treatment. Patients receiving levocarnitine should be evaluated every 3 months for response to therapy.47 Other preventive measures that have not been well studied include caffeine, sertraline, or fludrocortisone. [Pg.396]

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. [Pg.985]

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. [Pg.1506]

Vitamins A and E are elevated in ESRD whereas water-soluble vitamins should be supplemented to replace dialysis-induced loss. [Pg.887]

Renal Impairment-Adjust dosage according to degree of renal impairment and carefully monitor patients. Because only a minimal amount of clonidine is removed during hemodialysis, there is no need to give supplemental clonidine following dialysis. [Pg.554]

Renal function impairment Take caution in dosing patients with moderate and severe renal impairment and patients undergoing hemodialysis. Reduce dosage in patients with impaired renal function receiving levetiracetam, and give supplemental doses to patients after dialysis (see Actions and Administration and Dosage). [Pg.1233]

Hemodialysis Topiramate is cleared by hemodialysis 4 to 6 times greater than in a healthy individual a prolonged period of dialysis may cause topiramate levels to fall below that required to maintain an antiseizure effect. To avoid rapid drops in topiramate plasma concentration during hemodialysis, a supplemental dose of topiramate may be required. The actual adjustment should take into account 1) the duration of the dialysis period, 2) the clearance rate of the dialysis system being used, and 3) the effective renal clearance of topiramate in the patient being dialyzed. [Pg.1266]

Hemodialysis - For patients that require hemodialysis, adjust dosing schedule so that a dose is administered after each dialysis. No supplemental dose is necessary after peritoneal dialysis. [Pg.1755]

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... [Pg.195]

End-stage renal disease using dialysis 500-1,000 mg ql2h after dialysis, a 250- to 500-mg supplemental dose is recommended. [Pg.684]

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. [Pg.741]

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. [Pg.741]

Peritoneal Dialyis There is no information specific to administration of VALTREX in patients receiving peritoneal dialysis. The effect of chronic ambulatory peritoneal dialysis (CARD) and continuous arteriovenous hemofiltration/dialysis (CAVHD) on acyclovir pharmacokinetics has been studied. The removal of acyclovir after CARD and CAVHD is less pronounced than with hemodialysis, and the pharmacokinetic parameters closely resemble those observed in patients with ESRD not receiving hemodialysis. Therefore, supplemental doses of VALTREX should not be required following CARD or CAVHD. [Pg.32]

Thin-film dialysis can thus be considered as a way to estimate Stokes radius with a precision approximating 3% (24) when suitable models of known dimensions are available for comparison. In addition to this it offers an excellent approach to the study of molecular interactions, selfassociation, and binding (29, 30). It therefore is excellent for supplementing the type of information which can be derived from high-resolu-tion NMR study which in many cases together with model building and the restrictions of steric hindrance can reveal the precise positions certain atoms in a molecule occupy in space relative to each other. Many times however with NMR, a single unique position cannot be extracted from the data but instead only several possibilities. Here supplementary knowl-... [Pg.296]

In this short review it is not possible to cover more than a bare outline of the possibilities presented by only two approaches to the study of. conformation. These were chosen because of our own current interest and because they supplement each other well. From the practical standpoint high-resolution NMR is a very expensive and intricate approach while thin-film dialysis is very simple and inexpensive. [Pg.300]

Nutrient medium is supplemented with 5% fetal bovine serum. Low molecular weight serum proteins diffuse across the dialysis membrane between the nutrient and production modules. A reservoir of low molecular proteins is required in the nutrient module to maintain the equilibrium for hybridoma growth and survival. Accumulation of foam in the nutrient module can be a problem. To counteract foaming, do not exceed a concentration of 5% FBS in the nutrient module and add AntiFOAMa antifoaming agent. Do not fill the nutrient module with more than 400 mL of nutrient medium. An air space is required within the module to ensure successful hybridoma growth. [Pg.203]

Arnadottir M et al. The effect of high-dose pyridoxine and folic acid supplementation on serum lipid and plasma homocysteine concentrations in dialysis patients. Clin Nephrol 1993 40(4) 236-240. [Pg.182]

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. [Pg.330]

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.]... [Pg.217]

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). [Pg.264]

Patients on dialysis may require doses between 500 mg and 1000 mg once a day, with a supplemental dose of 250-500 mg following dialysis... [Pg.245]

Routine low dose supplements of hydroxyco-balamin, folate and pyridoxine fail to control h q)erhomocysteinaemia in 75% of dialysis patients but supraphysiological doses are effective hyd-roxycobalamin 1 mg/d, folic acid 15 mg/d and pyridoxine 100 mg/d. [Pg.595]


See other pages where Dialysis supplements is mentioned: [Pg.2640]    [Pg.2640]    [Pg.248]    [Pg.330]    [Pg.1485]    [Pg.101]    [Pg.381]    [Pg.226]    [Pg.397]    [Pg.1232]    [Pg.612]    [Pg.968]    [Pg.122]    [Pg.250]    [Pg.1025]    [Pg.202]    [Pg.198]    [Pg.608]    [Pg.24]    [Pg.368]    [Pg.142]    [Pg.68]    [Pg.2]    [Pg.574]   
See also in sourсe #XX -- [ Pg.378 , Pg.511 ]




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