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Specific criteria considered in applicability assessments are listed in Appendix B safe zofran 4mg. We used these data to evaluate the applicability to clinical practice buy zofran 4 mg with mastercard, paying special attention to study eligibility criteria zofran 4 mg line, demographic features of the enrolled population in comparison to the target population, characteristics of the intervention used in comparison with care models currently in use, the possibility of surgical learning curves, and clinical relevance and timing of the outcome measures. We summarized issues of applicability qualitatively. Peer Review and Public Commentary Nominations for peer reviewers were solicited from several sources, including the TEP and interested Federal agencies. Experts in general cardiology, heart failure, electrophysiology, ablation, cardioversion, cardiac resynchronization therapy (CRT), cardiothoracic surgery, pharmacological treatments for AF, geriatrics, health services research, and primary care, along with individuals representing stakeholder and user communities, were invited to provide external peer review of the draft report. AHRQ, an associate editor, and members of the TEP also provided comments. A list of peer reviewers submitting comments on the draft report is provided in the front matter of this report. We then provide a brief description of the included studies. The remainder of the chapter is organized by Key Question (KQ). Under each of the six KQs, we begin by listing the key points of the findings, followed by a brief description of included studies and a detailed synthesis of the evidence. The detailed syntheses are organized first by treatment comparison and then by outcome. We conducted quantitative syntheses where possible, as described in the Methods chapter. A list of abbreviations and acronyms used in this chapter is provided at the end of the report. Results of Literature Searches Figure 3 depicts the flow of articles through the literature search and screening process. Manual searching of grey literature databases, bibliographies of key articles, and information received through requests for scientific information packets identified 224 additional citations, for a total of 8,327 citations. After applying inclusion/exclusion criteria at the title-and-abstract level, 505 full-text articles were retrieved and screened. Of these, 323 were excluded at the full-text screening stage, leaving 182 articles for data abstraction. The relationship of studies to the review questions is as follows: 14 studies relevant to KQ 1, 3 studies relevant to KQ 2, 6 studies relevant to KQ 3, 42 studies relevant to KQ 4, 83 studies relevant to KQ 5, and 14 studies relevant to KQ 6 (some studies were relevant to more than one KQ). Appendix C provides a detailed listing of included articles. Appendix D provides a complete list of articles excluded at the full-text screening stage, with reasons for exclusion. Appendix E provides a “study key” table listing the primary and companion publications for the 148 included studies. Literature flow diagram aSome studies were relevant to more than one KQ. Abbreviations: CRT=cardiac resynchronization therapy; KQ=Key Question; RCT=randomized controlled trial Description of Included Studies Overall, we included 148 studies represented by 182 publications: 14 studies were relevant to KQ 1, 3 studies to KQ 2, 6 studies to KQ 3, 42 studies to KQ 4, 83 studies to KQ 5, and 14 studies to KQ 6. Studies were conducted wholly or partly in continental Europe (57%), the United States or Canada (22%), the UK (10%), Asia (9%), South America (5%), Australia or New Zealand (3%), and other locations (7%). Further details on the studies included for each KQ are provided in the relevant results sections, below, and in Appendix F. We acknowledge that this is not an exhaustive strategy, as several other registries 16 also exist with differing geographical focus and varying degrees of overlap in their trial listings; however, in the opinion of the investigators, the widely used, U. Our search yielded 610 trial records; a single reviewer identified 77 of these records as potentially relevant to the review. Of these 77 records, 34 had expected completion dates 1 year or more prior to our search. From that group of 34 trials, we identified publications for 23. Of the remaining 11 trials for which we did not identify publications, 1 was considered potentially relevant to KQ 1, and 10 were potentially relevant to KQ 5. The one unpublished study potentially relevant to KQ 1 was designed to compare the effects of metoprolol, verapamil, diltiazem, and carvedilol on ventricular rate, working capacity, and quality of life in 80 patients. In comparison, the 14 studies relevant to KQ 1 included in this review provide data for 1,017 patients. Of the 10 unpublished studies potentially relevant to KQ 5, 8 addressed procedural interventions and 2 compared procedural interventions with medical management. One of the completed studies represents the pilot portion of the Catheter Ablation versus Antiarrhythmic Drug Therapy for Atrial Fibrillation (CABANA) trial, which has now moved forward to begin the full-scale trial phase of 3,000 patients comparing ablation to pharmacological therapies for rate and/or rhythm control. In total, data from these 10 unpublished trials could potentially provide additional evidence on the comparative safety and effectiveness of rhythm-control procedures for up to 1,374 patients. By contrast, 83 studies included for KQ 5 involved 11,014 patients. In summary, because of the relatively low proportion of unpublished studies identified through our ClinicalTrials. What are the comparative safety and effectiveness of pharmacological agents used for ventricular rate control in patients with atrial fibrillation? Do the comparative safety and effectiveness of these therapies differ among specific patient subgroups of interest? Key Points • Based on 3 studies (2 good, 1 fair quality) involving 271 patients, evidence suggests that amiodarone is comparable to the calcium channel blocker diltiazem for rate control (low strength of evidence). These include improvement of AF symptoms in patients receiving combined treatment with carvedilol plus digoxin compared with digoxin alone, rate control in patients using 17 metoprolol versus diltiazem or sotalol, and the safety of any one pharmacological agent used for ventricular rate control in patients with AF. Description of Included Studies A total of 14 RCTs involving 1,017 patients were identified that assessed the use of pharmacological agents for ventricular rate control in patients with AF (Appendix Table F-1). Thirteen studies were published between 2000 and 2006, and one was published 145,147,148,150 138-144,146,149,151 in 2009. Four studies were multicenter and 10 were single-center. Only 151 138-140,142,144-147 one study included a site in the United States; eight included sites in Europe, 143,150 148 141 two included sites in Asia, and one each included sites in Canada, the UK, and 149 Australia/New Zealand. The study population consisted entirely of patients with persistent AF 141,144,145,147 143 in four studies, and entirely of patients with paroxysmal AF in one study. Funding 138-140,142-144,146-148,151 was unclear or not reported in 10 studies. A total of three studies included 141,145,150 funding from industry, two received funding from nongovernment/nonindustry 145,149 sources, and no studies were government-only funded. In eight studies the setting was 139,143,148,149,151 inpatient: five of these were in emergency rooms, and the other three did not 138,140,144 include emergency room patients. In the remaining studies, five were classified as 141,142,146,147,150 145 outpatient, and in one the setting was unclear. Most of the studies included patients with no history of heart failure, and the mean ejection fraction varied from 23. Only a few studies included patients with coronary artery disease. Figure 4 represents the treatment comparisons evaluated for this KQ. Overview of treatment comparisons evaluated for KQ 1 aLines running from one oval back to the same oval (e. Abbreviation: KQ=Key Question 141,146 Two studies compared beta blockers with digoxin, one compared beta blockers with 139 calcium channel blockers, and one compared beta blockers with calcium channel blockers in 150 patients using digoxin. One study compared two beta blockers (sotalol and metoprolol) in 142 patients receiving digoxin. Amiodarone was compared with calcium channel blockers in three 138,143,144 140,143,149 studies, and with digoxin in three. One study evaluated the benefits of adding 151 calcium channel blockers to digoxin compared with digoxin alone, and four studies compared 143,145,147,148 calcium channel blockers with digoxin.

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Both unc- of the second messenger 3′ buy zofran 4mg low price,5′-cyclic adenosine monophos- 1 and unc-8 are expressed in neurons zofran 8 mg mastercard, and both genes can phate (cAMP) buy 4 mg zofran. Conversely, long-term ethanol exposure ap- be mutated to confer either resistance or hypersensitivity to pears to decrease intracellular cAMP levels. Allele-specific genetic interactions between and chronic effects of ethanol have also been linked to unc-1, unc-8, and the yet uncloned unc-79 and unc-80 genes changes in dopaminergic neurotransmission (46). In partic- suggest that their products may physically interact in a mul- ular, ethanol has been shown to promote release of dopa- timeric channel complex specifically involved in anesthetic mine in the mesolimbic pathways of the brain, in particular responses. Since stomatin has been shown to function as the so-called reward pathway synapses between the ventral a negative regulator of cation channels in erythrocytes, a tegmental area (VTA) and the nucleus accumbens (NAc). Homologues of both stomatins remains to be determined. Moreover, although sensitivity and ENaC channels have been identified in mammals, and to both the acute and chronic effects of ethanol are clearly are known to be expressed in the central nervous system; affected by genetic factors, the nature of the genes affecting thus, in principle stomatin-regulated ENaC channels could human ethanol sensitivity are not known. Recent work in Drosophila has provided support for both In summary, there are two distinct sets of genes that the dopamine and cAMP hypotheses of ethanol action. At present, it is not clear which of and ultimately immobilization. Using an instrument called the two (or whether both) might encode homologues of an inebriometer (47), lines of mutant flies have been identi- biologically relevant human anesthetic targets. Although the fied that exhibit abnormal sensitivity to volatilized ethanol. Conversely, although the stomatin/de- lian pituitary adenylyl cyclase activating peptide (PACAP) generin genes affect a paralytic response that closely resem- (48,49). Consistent with the implications of this homology, bles anesthesia, the response also has a relatively long time the effects of amnesiac on ethanol response appeared to delay and occurs at concentrations well above those clini- involve the adenylyl cyclase pathway, since the adenylyl cy- cally relevant in humans. Given the effective drug concen- clase activator foskolin blocks the ethanol sensitivity associ- trations for these two behavioral responses, it is possible that the synaptic genes might encode targets relevant to ated with amnesiac loss-of-function mutations. Moreover, anesthesia, while the stomatin/degenerin genes might en- several other loss-of-function mutations affecting cAMP code targets relevant for side effects of anesthetics. Alterna- pathway components, including the adenylyl cyclase gene tively, it is possible that genes affecting high-concentration rutabaga and the cAMP-dependent protein kinase gene anesthetic responses do define molecules involved in anes- DCO, also conferred ethanol sensitivity. Although one thesia, especially since the nematode cuticle is relatively im- might suppose based on these results that the response to permeant and presents a significant barrier for the entry of ethanol is simply a function of the level of cAMP signaling many drugs. Since well-defined mammalian homologues in the relevant neuronal targets (with increased ethanol re- exist for both classes of anesthetic response genes, it should sponse corresponding to low cAMP signaling), a variety of be possible in the future to examine these issues directly in data are inconsistent with this simple model. Nonetheless, these ge- Drugs of Abuse netic data provide the first conclusive link between the activ- ity of the cAMP pathway and the behavioral effects of Ethanol ethanol in an intact organism; the precise nature of that Unlike many neuroactive substances, ethanol is not believed link remains to be determined, but should be accessible to to have a single molecular target in neurons; rather, a num- further genetic analysis. During the first 7 to 10 minutes of Genetic analysis in C. When flies are depleted of dopamine through traction of body wall muscles, stimulation of egg laying, ingestion of a tyrosine hydroxylase inhibitor, they become and increased pharyngeal pumping. The effects of nicotine significantly less susceptible to this stimulation of motor on the body and egg-laying muscles are mediated through activity by ethanol. However, these dopamine-depleted flies a nicotinic receptor known as the levamisole receptor (57, exhibited no abnormalities in their sensitivities to ethanol- 58). The antihelminthic drug [and ganglionic nAChR ago- induced uncoordination or immobilization. Thus, the stim- nist (59)] levamisole is a potent agonist of this receptor; like ulation of motor activity by ethanol may involve ethanol- nicotine, levamisole causes body muscle hypercontraction induced enhancement of dopaminergic transmission in and (at high doses) spastic paralysis. Although the levamisole brain areas controlling locomotion, whereas the other be- receptor is found on nematode muscle, its pharmacologic havioral effects of ethanol are likely to involve other neuro- profile generally resembles that of ganglionic nicotinic re- transmitter systems. By screening for levamisole-resistant The genetic analysis of ethanol response mechanisms in mutants, it has been possible to identify genes affecting the Drosophila is still in its early stages. However, it is already function of the levamisole receptor (60). Mutations confer- clear that mutants with altered responses to ethanol can be ring strong resistance to levamisole have been identified in identified in straightforward genetic screens, and at least in six genes. Three of these genes, unc-38, unc-29, and lev-1, some cases analyzed in the context of well-defined neuronal encode nicotinic receptor subunits (61,62). Perhaps the greatest promise for future protein is most similar to the insect -like subunits ALS and studies is the possibility that novel ethanol response genes, SAD (49% amino acid identity); among vertebrate receptor possibly including the direct molecular targets of ethanol, subunits, the closest similarity is to neuronal subunits can be identified in ethanol-resistant or ethanol-hypersensi- (61). UNC-29 and LEV-1 are closely related proteins whose tive screens. Three addi- tional genes conferring strong levamisole resistance, unc-50, Nicotine unc-74, and unc-63, have not been cloned, but have been Tobacco has been implicated in more deaths than any other shown to be required for assembly of a functional levamisole addictive substance (51), yet the biochemical basis for com- receptor as assayed in vitro (63). In addition to conferring pulsive tobacco use remains poorly understood. The sub- resistance to levamisole (and other nicotinic agonists), mu- stance most responsible for the addictive properties of to- tations in these genes cause defects in the coordination of bacco is nicotine, a potent stimulant and cholinergic body movement (60). Long-term exposure to nicotine is known to cause (lev-8, lev-9, and lev-10) confer weaker resistance to levami- adaptive changes in the activity and number of nicotinic sole, do not cause defects in locomotion, and have no detect- receptors in the brain, which are thought to be important able effect on the biochemical properties of the receptor as for nicotine addiction (52). For example, nicotinic receptors assayed in vitro (60,63). Thus, the proteins encoded by these exist in multiple functional states, some of which are rela- genes have been hypothesized to regulate the activity of the tively refractory to channel opening though they retain af- receptor indirectly. Chronic exposure to nicotine or other Long treatments with nicotine and other nicotinic recep- agonists results in an increased fraction of receptors adopt- tor agonists lead to adaptation (57). Animals treated with ing the lower activity states, leading to an attenuation of exogenous nicotine initially hypercontract to the point of the overall nicotine response (53). Long-term nicotine treat- spastic paralysis; however, after several hours in the presence ment also causes a long-lasting functional inactivation of of nicotine, they recover their ability to move and regain some nicotinic receptors (54), which has a slower time much of their body length. Moreover, when nico- treatment can also either increase or decrease the number tine-adapted animals are removed from nicotine, their loco- of nicotinic receptors on the cell surface, effects that appear motive behavior becomes uncoordinated and resembles that to be mediated at the level of protein turnover (55,56). The of mutants with strong defects in the levamisole receptor cellular pathways that promote these changes are not well (i. Thus, long treat- understood; for example, little is known about the cellular ments with nicotine cause nicotine dependence in addition 270 Neuropsychopharmacology: The Fifth Generation of Progress to nicotine tolerance in the C. However, dopamine is probably not the only neuro- term nicotine treatment also down-regulates levamisole re- transmitter involved in cocaine addiction, since mice lack- ceptors in the egg-laying muscles. Overnight treatment with ing the vesicular dopamine transporter will still self-admin- nicotine leads to an almost complete attenuation of levami- ister cocaine after repeated administration of the drug (66, sole sensitivity with respect to egg laying, and this attenua- 67). Although dopaminergic transmission in the limbic re- tion of levamisole response persists for up to 24 hours after ward pathways has been implicated in the reinforcing prop- removal from nicotine. This loss of levamisole responsive- erties of a wide range of addictive substances in addition to ness is accompanied by a corresponding decrease in the cocaine, the molecular and cellular mechanisms that lead abundance of UNC-29–containing receptors in the vulval to addiction in these neurons are not well understood. Interestingly, the nicotine-dependent de- of cocaine action may be accessible to genetic analysis. For example, at low doses treated flies possibility that direct phosphorylation of nicotinic receptors become hyperactive and exhibit compulsive, continuous might represent a signal for increased turnover. At intermediate doses animals move ture, it should be possible to test this hypothesis, as well more slowly and display stereotyped locomotive behaviors as identify other genes required for long-term responses to such as circling. Finally, at high doses animals undergo nicotine in C. Repeated treat- Another set of genes, the weak levamisole-resistance ment of flies with low doses of cocaine results in an increased genes lev-8 and lev-9, appear to represent positive regulators behavioral response, a phenomenon known as sensitization; of nicotinic receptor activity. Mutations in these genes con- cocaine sensitization also occurs in mammals and is thought fer partial resistance to levamisole and nicotine with respect to underlie some aspects of addiction in humans. Interest- to body muscle contraction and strong resistance with re- ingly, male flies are more sensitive to cocaine than females, spect to egg laying (65). However, lev-8 and lev-9 mutations a sexual dimorphism that also holds true in mammals (69). In fact, recent evidence or essential accessory proteins. Insects contain co- mechanism for functional inactivation of nicotinic recep- caine sensitive reuptake transporters for dopamine, seroto- tors.

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Risperidone vs haloperidol for pre- cacy of risperidone vs olanzapine in the treatment of patients vention of relapse in schizophrenia and schizoaffective disorders: with schizophrenia or schizoaffective disorder trusted 8mg zofran. The 10th Biennial Win- chopharmacol 2000;3(Suppl 1):S151(P purchase 4mg zofran visa. Effects of risperidone in tardive dyskinesia: an controlled dose-finding study of ziprasidone in hospitalized pa- analysis of the Canadian multicenter risperidone study zofran 8 mg generic. JClin tients with schizophrenia or schizoaffective disorder. Ziprasidone: efficacy Risperidone vs olanzapine in the treatment of patients with in the prevention of relapse and in the long-term treatment schizophrenia or schizoaffective disorder: safety comparisons. Clinical and biologic trolled, long-term study of the comparative incidence of treat- response to clozapine in patients with schizophrenia. Crossover ment-emergent tardive dyskinesia with olanzapine or haloperi- comparison with fluphenazine. A high- and low-dose double-blind compar- psychotic drugs in treatment-refractory schizophrenia. Quetiapine: are we overreacting in our con- of clozapine in chronic schizophrenia: response to treatment and cern about cataracts (the beagle effect)? Curr Opin CPNS Invest Drugs 2000;2: dose clozapine for treatment-resistant schizophrenia. An open comparison ity among state hospital patients. Schizophr Bull 1996;22: of clozapine and risperidone in treatment-resistant schizophre- 15–25. Clozapine and risperidone and haloperidol in hospitalized patients with refractory schizo- in chronic schizophrenia: effects on symptoms, parkinsonian phrenia. Department of Veterans Affairs Cooperative Study side effects, and neuroendocrine response. Am JPsychiatry 1999; Group on Clozapine in Refractory Schizophrenia. Reduction of hospital days in chronic schizophrenic patients treated with risperidone: risperidone, and haloperidol in treatment-resistant patients with a retrospective study. Efficacy of olanzapine: haloperidol for patients with treatment-resistant schizophrenia. JClin Psychiatry 1997; Biol Psychiatry 1999;45:403–411. Oral olanzapine pared with chlorpromazine in treatment-resistant schizophrenia. Past and future—National Institute of Mental Health Division 98. Cost-effectiveness of atypical antipsychotics in chronic of Services and Intervention Research Workshop, July 14, 1998. Treatment of schizophrenia and spectrum disor- antipsychotic therapy for schizophrenia. JClin Psychiatry 1997; ders: pharmacotherapy, psychosocial treatments, and neuro- 58(Suppl 10):50–54. Non-motor side effects of nomic outcomes of olanzapine compared with haloperidol for novel antipsychotics. A cost-effectiveness ics: comparison of weight gain liabilities. JClin Psychiatry 1999; clinical decision analysis model for schizophrenia. Time course and biologic chotics and new onset diabetes. Biol Psychiatry 1998;44: correlates of treatment response in first-episode schizophrenia. Neuropsychology Chapter 56: Therapeutics of Schizophrenia 799 of first-episode schizophrenia: initial characterization and clini- ization during maintenance treatment of schizophrenia. Study of Recent Onset Psychosis: one-year follow-up of first- 125. Arch Gen Psychia- fectiveness for patients in state hospitals: results from a random- try 1991;48:739–745. A study of the pharmaco- clinical symptoms in first-episode schizophrenia: response to logic treatment of medication-compliant schizophrenics who low-dose risperidone. Olanzapine versus of patients recently discharged on a regimen of risperidone or haloperidol treatment in first-episode psychosis. Psychosocial treatments in results of a 52 week randomized double blind trial. Multiple-family groups haloperidol in the treatment of first-episode psychosis. Research update on the psychosocial chosis and outcome in first-episode schizophrenia. Is there an association Conceptual model, treatment program, and clinical evaluation. Compliance with medication regi- schizoaffective disorder. Medication compliance and substance Schizophr Bull 1996;22:305–326. Why do schizophrenic patients refuse to take Bull 1996;22:283–303. A self-report scale predictive tive-behavioural interventions in early psychosis. Br JPsychiatry of drug compliance in schizophrenics: reliability and discrimina- (Suppl) 1998;172:101–106. Predicting medication compliance in a expressed emotion and relapse in recent onset schizophrenic psychotic population. Depot neuroleptics: the relevance of psychosocial 143. Subjective utility ratings factors—a United States perspective. JClin Psychiatry 1984;45: of neuroleptics in treating schizophrenia. Subjective experience of treatment, side- netics of long-acting injectable neuroleptic drugs: clinical impli- effects, mental state and quality of life in chronic schizophrenic cations. Compliance therapy: an inter- lized treatment option. Clozapine: pattern of efficacy in treatment-resis- outpatients. Addition of lithium to haloperidol in non-affec- drugs. Patient re- blind, placebo controlled, parallel design clinical trial. Psycho- sponse and resource management: another view of clozapine pharmacology 1993;111:359–366. Am JPsychiatry choosing among alternative somatic treatments for schizophre- 1995;152:821–825. Carbamazepine in violent non-epileptic schizo- 1374–1379. Carbamazepine as adjunctive treatment in nonepi- parative study of risperidone and conventional neuroleptics for leptic chronic inpatients with EEG temporal lobe abnormalities. The Quebec Schizophrenia JClin Psychiatry 1983;44:326–331. 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Nutrition and M etabolism in Acute Renal Failure 18 order 4 mg zofran. FIGURE 18-33 Am ino acid (AA) solutions for parenteral nutrition in acute renal tions or in special proportions designed to counteract the failure (ARF) generic zofran 4mg free shipping. The m ost controversial choice regards the type of m etabolic changes of renal failure (“nephro” solutions) generic zofran 8 mg fast delivery, includ- am ino acid solution to be used: either essential am ino acids (EAAs) ing the am ino acids that m ight becom e conditionally essential exclusively, solutions of EAA plus nonessential am ino acids in ARF. O ne Use of solutions of EAA alone is based on principles established for should be aware of the fact that the am ino acid analogue N -acetyl treating chronic renal failure (CRF) with a low-protein diet and an tyrosine, which previously was used frequently as a tyrosine EAA supplement. This may be inappropriate as the metabolic adapta- source, cannot be converted into tyrosine in hum ans and m ight tions to low-protein diets in response to CRF may not have occurred even stim ulate protein catabolism. Plus, there are fundamental differences in the Despite considerable investigation, there is no persuasive evi- goals of nutritional therapy in the two groups of patients, and conse- dence that am ino acid solutions enriched in branched-chain am ino quently, infusion solutions of EAA may be sub-optimal. System atic Thus, a solution should be chosen that includes both essential studies using glutam ine supplem entation for patients with ARF are and nonessential am ino acids (EAA, N EAA) in standard propor- lacking (see Fig. Because of the well-docu- m ented effects of overfeeding, energy intake of patients with ARF m ust not exceed their actual energy expenditure (ie, in m ost cases 100% to 130% of resting energy expenditure [REE]; see Figs. Glucose should be the principal energy substrate because it can be utilized by all organs, even under hypoxic conditions, and has the potential for nitrogen sparing. Since ARF im pairs glucose tolerance, insulin is frequently necessary to m aintain norm oglycem ia. Any hyperglycem ia m ust be avoided because of the untoward associated side effects— such as aggravation of tissue injury, glycation of pro- teins, activation of protein catabolism , am ong others. W hen intake is increased above 5 g/kg of body weight per day infused glu- cose will not be oxidized but will prom ote lipogenesis with fatty infiltration of the liver and excessive carbon dioxide production and hypercarbia. O ften, energy requirem ents cannot be m et by glucose infusion without adding large am ounts of insulin, so a portion of the energy should be supplied by lipid em ulsions. The m ost suitable m eans of providing the energy substrates for parenteral nutrition for patients with ARF is not glucose or lipids, but glucose and lipids. In experim ental urem ia in rats, TPN with 30% of nonprotein energy as fat prom oted weight gain and am eliorated the urem ic state and survival. Advantages of intravenous lipids include high specific energy content, low osm olality, provision of essential fatty acids and phospholipids to prevent deficiency syndrom es, fewer hepatic side effects (such as steato- sis, hyperbilirubinem ia), and reduced carbon dioxide production, especially relevant for patients with respiratory failure. Changes in lipid m etabolism associated with acute renal failure (ARF) should not pre- vent the use of lipid em ulsions. Usually, 1 g/kg of body weight per day of fat will not increase plasm a triglycerides substantially, so about 20% to 25% of energy requirem ents can be m et. Lipids should not be adm inistered to patients with hyperlipidem ia (ie, plas- m a triglycerides above 350 m g/dL) activated intravascular coagulation, acidosis (pH below 7. Parenteral lipid em ulsions usually contain long-chain triglycerides (LCT), m ost derived from soybean oil. Recently, fat em ulsions containing a m ixture of LCT and m edium -chain triglycerides (M CT) have been introduced for intravenous use. Proposed advantages include faster elim ination from the plasm a owing to higher affinity to the lipoprotein lipase enzym e, com plete, rapid, and carnitine-independent m etabolism , and a triglyceride- lowering effect; however, use of M CT does not prom ote lipolysis, and elim ination of triglycerides of both types of fat em ulsions is equally retarded in ARF. Com plications: Technical problem s and infectious com plica- tions originating from the central venous catheter, chem ical Metabolic Status incom patibilities, and m etabolic com plications of parenteral nutrition are sim ilar in ARF patients and in nonurem ic subjects. Variables Unstable Stable H owever, tolerance to volum e load is lim ited, electrolyte derange- Blood glucose 1–6 daily Daily m ents can develop rapidly, exaggerated protein or am ino acid Osmolality Daily 2 weekly intake stim ulates excessive blood urea nitrogen (BUN ) and waste Electrolytes (Na+, K+, Cl+) Daily Daily product accum ulation and glucose intolerance, and decreased fat Calcium, phosphate, magnesium Daily 3 weekly clearance can cause hyperglycem ia and hypertriglyceridem ia. Daily BUN increment Daily Daily Thus, nutritional therapy for ARF patients requires m ore fre- Urea nitrogen appearance rate Daily 2 weekly quent m onitoring than it does for other patient groups, to avoid Triglycerides Daily 2 weekly m etabolic com plications. M onitoring: This table sum m arizes laboratory tests that m oni- Blood gas analysis, pH Daily 1 weekly tor parenteral nutrition and avoid m etabolic com plications. Ammonia 2 weekly 1 weekly The frequency of testing depends on the m etabolic stability of Transaminases bilirubin 2 weekly 1 weekly the patient. In particular, plasm a glucose, potassium , and phos- phate should be m onitored repeatedly after the start of parenter- al nutrition. Drum l W : N utritional support in acute renal failure. Philadelphia: Lippincott- m odel of acute renal failure and sepsis in rats. Drum l W , M itch W E: M etabolism in acute renal failure. Bergström J: Factors causing catabolism in m aintenance hem odialysis 1996, 9:484–490. O m P, H ohenegger M : Energy m etabolism in acute urem ic rats. Soop M , Forsberg E, Thˆrne A, Alvestrand A: Energy expenditure in 18. M itch W E, Chesney RW : Am ino acid m etabolism by the kidney. Laidlaw SA, Kopple JD: N ewer concepts of indispensable am ino 6. Spreiter SC, M yers BD, Swenson RS: Protein-energy requirem ents in acids. N aschitz JE, Barak C, Yeshurun D: Reversible dim inished insulin Am J Clin N utr 1980, 33:1433–1437. M itch W E: Am ino acid release from the hindquarter and urea appear- 21. Salusky IB, Flügel-Link RM , Jones M R, Kopple JD: Effect of acute 1991, 260:E280–E285. Clark AS, M itch W E: M uscle protein turnover and glucose uptake in 23. Stehle P: The potential use of dipeptides in clinical nutrition. M aroni BJ, Karapanos G, M itch W E: System A am ino acid transport 24. H übl W , Drum l W , Roth E, Lochs H : Im portance of liver and kidney in incubated m uscle: Effects of insulin and acute urem ia. Am J Physiol for the utilization of glutam ine-containing dipeptides in m an. Drum l W , Kelly RA, M itch W E, M ay RC: Abnorm al cation transport 25. H asik J, H ryniewiecki L, Baczyk K, Grala T: An attem pt to evaluate in urem ia. Lopez-M artinez J, Caparros T, Perez-Picouto F: N utrition parenteral nesis in isolated perfused rat liver. M ay RC, Kelly RA, M itch W E: M echanism s for defects in m uscle Clin Esp 1980, 157:171–178. Kierdorf H : Continuous versus interm ittent treatm ent: Clinical results m etabolic acidosis. Drum l W : Im pact of continuous renal replacem ent therapies on patients with acute renal failure on continuous arteriovenous hem ofil- m etabolism. Frankenfeld DC, Badellino M M , Reynolds H N , et al. Toback FG: Regeneration after acute tubular necrosis. Ikizler TA, Greene JH , W ingard RL, H akim RM : N itrogen balance in 50. Toback FG, Dodd RC, M aier ER, H avener LJ: Am ino acid adm inis- acute renal failure patients. M ay RC, Clark AS, Goheer M A, M itch W E: Specific defects in sis. N Engl J of glucose, lactate and am ino acids in acutely urem ic dogs. O ken DE, Sprinkel M , Kirschbaum BB, Landwehr DM : Am ino acid 33. Zager RA, Venkatachalam M A: Potentiation of ischem ic renal injury 34. Dobyan DC, Bulger RE, Eknoyan G: The role of phosphate in the M etab 1996, 22:168–177.

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