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The link between low serotonin levels and headaches is the basis of many prescription drugs for the treatment and prevention of migraine headaches order 5mg bisoprolol with amex arteriosclerosis obliterans. For example order 10 mg bisoprolol otc blood pressure chart meaning, the serotonin agonist drug sumatriptan (Imitrex) is now among the most popular migraine prescriptions cheap bisoprolol 10 mg without prescription heart attack vegas. In addition to sumatriptan discount bisoprolol 10 mg amex pulse pressure 60 mmhg, monoamine oxidase inhibitors (which increase serotonin levels) have also been shown to prevent headaches. The bottom line is there is considerable evidence that increasing serotonin levels leads to relief from chronic migraine headaches. Many substances produce their effects on cells by ﬁrst binding to receptor sites on the cell membrane. Some serotonin receptors are involved in triggering migraines and others prevent them. This situation is quite clear when we look at the different effects that various drugs exert in binding to these different serotonin receptors. Unified Hypothesis The mechanism of migraine can be described as a three-stage process: initiation, prodrome (time between initiation and appearance of headache), and headache. Although a particular stressor may be associated with the onset of a speciﬁc attack, it appears that initiation is dependent on the accumulation of several stressors over time. Once a critical point of susceptibility (or threshold) is reached, a “cascade event” or domino-like effect is set into motion, ultimately producing a headache. This susceptibility is probably a combination of decreased tissue serotonin levels, changes in the platelets, increased sensitivity to compounds such as substance P, and the buildup of histamine and other mediators of inflammation. The ﬁrst step in treating migraine headache is to identify the precipitating factor or factors. Although food intolerance/allergy is the most important, many other factors must be considered as either primary causes or contributors to the migraine process. Particularly important is to assess the role that headache medications may be playing, especially in chronic headaches. Drug Reaction and Rebound Headaches In the early 1980s it became apparent that headache medications could actually increase the tendency to experience chronic headache. Early reports identiﬁed increased frequency and intensity of headaches in heavy analgesic users. In one study migraine sufferers who took more than 30 analgesic tablets per month had twice as many headache days per month as those who took fewer than 30 tablets. In another study 70 patients with daily headaches who were consuming 14 or more analgesic tablets weekly were advised to discontinue their use. Analgesic-rebound headaches should be suspected in anyone with chronic, predictable migraines who is taking large quantities of analgesics. The critical dosage that can lead to analgesic-rebound migraines is estimated to be 1,000 mg of either acetaminophen or aspirin. Analgesic medications used for migraines typically contain substances in addition to the analgesic such as caffeine or a sedative (e. These substances further contribute to the problem and may lead to withdrawal headache and related symptoms such as nausea, abdominal cramps, diarrhea, restlessness, sleeplessness, and anxiety. Withdrawal symptoms typically start 24 to 48 hours after the last dosage and in most cases subside in five or so days. Food Allergies/Intolerance There is little doubt that food allergies and intolerances play a role in many cases of migraine headache. Clinical studies have demonstrated that the detection and removal of allergenic or intolerable foods can eliminate or greatly reduce migraine symptoms in the majority of patients. Success rates range from 30 to 93%, with the majority of studies showing a remarkably high degree of success. These compounds can also inhibit the enzyme phenolsulfotransferase, which normally breaks down serotonin and other vasoactive amines in platelets. Many migraine sufferers have been found to have signiﬁcantly lower levels of this enzyme. Because red wine contains substances that are potent inhibitors of this enzyme, it often triggers migraines in these individuals, especially if consumed along with foods high in vasoactive amines such as cheese or chocolate. A standard treatment for histamine-induced headaches is a histamine- free diet, along with vitamin B supplementation. Individuals sensitive to dietary histamine have lower levels (about 50%) of this enzyme in their tissues compared with control subjects. Not surprisingly, compounds that antagonize vitamin B6 also inhibit diamine oxidase. Vitamin B6 supplementation (usually 1 mg/kg) has been shown to improve histamine tolerance, presumably by increasing diamine oxidase activity. Interestingly, the level of diamine oxidase in a woman increases by more than 500 times during pregnancy. Miscellaneous Diet-Related Triggers Hypoglycemia can be a trigger for migraine headaches. Making such a dietary change can reduce platelet aggregation and the formation of inﬂammatory mediators and may play a role in preventing migraine headaches. However, the adolescents responded equally well to olive oil supplements, the placebo chosen for this study. Although a number of drugs have been shown to be useful in the prevention of migraine headache, all of the currently used drugs carry with them a risk of signiﬁcant adverse effects. Although some studies have employed a dosage of 600 mg per day, equally impressive results have been achieved at a dosage as low as 200 mg per day. In fact, ﬁve patients in the methysergide group had to withdraw during the trial because of side effects. Riboflavin (Vitamin B2) Migraine headaches may be the result of a deﬁcit in the production of energy by the mitochondria, the energy-producing compartments of the cell. A double-blind study demonstrated that a dose of 400 mg riboﬂavin per day was superior to a placebo in preventing migraine attacks. Magnesium The high frequency of magnesium deﬁciency seen in migraine sufferers is well established in research. Magnesium levels are depleted by a multitude of common factors, including stress, excessive alcohol intake, high estrogen levels, low progesterone, certain drugs, hyperthyroidism, and hyperparathyroidism. Substantial documentation linking low magnesium levels to both migraine and tension headaches exists in the medical literature. Low brain and tissue magnesium concentrations have been found in patients with migraines, indicating a need for supplementation. Positive results with magnesium supplementation have been shown in preventing migraines, speciﬁcally in people with low levels of magnesium. Because most of the body’s magnesium is intracellular, serum levels are unreliable indicators. More sensitive tests of magnesium status include red blood cell magnesium levels and ionized magnesium, the most physiologically active form. The hypothesis that patients with an acute migraine episode and low serum levels (less than 0. Pain reduction of 50% or more, as measured on a headache intensity verbal scale of 1 to 10, occurred within 15 minutes of infusion in 35 patients. In 21 patients, at least this degree of improvement or complete relief persisted for 24 hours or more.
Primary audience: Pathologists buy bisoprolol 5mg cheap hypertension yoga poses, neurologists 5mg bisoprolol heart attack from stress, neurophysiology fellows order bisoprolol on line amex blood pressure chart cholesterol, pathology and neurology residents buy generic bisoprolol pills pulse pressure 2012. Primary audience: Pathologists, neurologists, neurosurgeons, pathology, neurology, and neurosurgery residents, medical students. Purpose: Review of classic or unusual cases from current surgical specimens, including consultation cases. Primary audience: Neurosurgeons, neurologists, neuroradiologists, neuropathologists, neurosurgery and neurology residents. Scholarly Activities and Research During Rotation Research within the Division of Neuropathology is an option that residents may choose for research elective activities. Incorporation of residents into experimental neuropathological work ongoing in the Division or selection of projects in clinically related research, e. Residents will be evaluated on their demonstrated ability to provide useful consultation to the clinical service teams, medical knowledge, application of this knowledge to efficient/quality patient care, and gross and microscopic diagnostic, technical and observational skills. Residents are also evaluated on their interpersonal skills, professional attitudes, reliability, and ethics with members of the teaching faculty, peers, laboratory staff, and clinicians. They are further evaluated on their initiative in fostering quality patient care and use of the medical literature, as it relates to their assigned cases. Their timely completion of assigned interpretive reports is another component of the evaluation. Chapters 27-28, Robbins and Cotran Pathologic Basis of th Disease, 7 Edition, Elsevier Saunders, Philadelphia, 2005. Surgical Pathology of the Nervous System and its Coverings, th 4 ed, Churchill Livingstone, New York, 2002. Diagnostic Pathology of Nervous System Tumours, Churchill Livingstone, London, 2002. Tumors of the Peripheral Nervous System, Armed Forces Institute of Pathology, Washington, D. Tumors of the Pituitary Gland, Armed Forces Institute of Pathology, Washington, D. Practice Guidelines for Autopsy Pathology: Autopsy Procedures for Brain, Spinal Cord, and Neuromuscular System, Arch Pathol Lab Med 119:777–783, 1995. Residents must obtain permission from the appropriate faculty member prior to scheduling the elective. Residents must obtain permission from the appropriate faculty member prior to signing up for the elective. A one month rotation can be designed to teach research skills and allow a resident time to begin a clinically related research project that will be carried forward during the rest of the training program. A goal of the rotation is to encourage pathology residents to participate in a research project that will result in formal presentation at national meetings and publication in peer-reviewed journals. Research rotations must have a focused research project and must follow the below described process for formalizing the rotation. A longer period of research training is available as elective time for those who wish to pursue an academic career. Procedure: Listed below are the required procedures for the Research Rotation • The academic year prior to scheduling a research rotation, the resident should identify a faculty sponsor, have the faculty member sign the attached form stating that they will agree to be the mentor and agree to be responsible for the research activity during the scheduled month. The faculty sponsor must submit the progress report along with the standard evaluation of the resident to the resident education committee. He continued to improve his fund of knowledge and diagnostic skills and received positive comments on performance evaluations. Overall, his performance during the last six months of his residency was very good. He interacted very well with faculty, fellow residents and staff, and was an active mentor to junior residents. His excellent background in research allowed him to continue to be actively involved in scholarly activity including publication of five manuscripts and presentation of abstracts at five national or local meetings. Was physician subject to any disciplinary action, such as imposition of consultation requirements, suspension, or termination or probation? This Committee should consist of representative Teaching Faculty and chaired by the Program Director. From this review, an Annual Program Improvement Action Plan (last section of this form) is to be developed to improve deficit areas. All these items should be reviewed and the corresponding box checked next to the item. As a way of documenting this annually, please have all institutional site directors sign this report as well. I have discussed this report as it pertains to each Participating Institution with each Participating Institutional Site Director. Today Internet resources may not readily provide information on who is responsible for the content, and where that person or organization may be. For example, a site may provide an organization name, but have no indication of where that organization is geographically. Authors can spend hours searching for this information to include it in brackets, or choose the allowable [publisher unknown], [place unknown], etc. Perhaps it is time to rethink the necessary information to identify a cited work today, and to better standardize citations across diferent media and publication types. Authorship, titles, and dates (content created or published, revised, and cited if on the Internet) are still crucial – but what else is essential? In addition, is it possible to apply the same order xvi Citing Medicine and punctuation to all references? Print materials are still used and need consideration; however, electronic resources prevail and citing these materials needs to be simplifed. Backus / Joyce Backus Associate Director for Library Operations National Library of Medicine xvii Foreword Te Internet has fundamentally changed the publishing model that authors, editors and publishers have followed for centuries. Information that took months or years to publish, edit and distribute in print is now produced and available to the public worldwide on an accelerated schedule. Despite changes brought by technology, the need to accurately cite the source of information for scholarly publication remains. And, while the need to cite remains, the challenges of collecting and reporting accurate, lasting citation information have increased tremendously. Electronic publishing creates new issues of impermanence that paper did not present. With this publication, Citing Medicine, the National Library of Medicine strives to provide those charged with capturing an accurate scholarly citation with a guide to do so in this new era of electronic information, both permanent and ephemeral. Tese same rules and examples can be used for magazines and other types of periodicals. Journal Articles • Sample Citation and Introduction • Citation Rules with Examples • Examples B. Parts of Journal Articles • Sample Citation and Introduction • Citation Rules with Examples • Examples C. Sample Citation and Introduction to Citing Journal Articles Te general format for a reference to a journal article, including punctuation: Examples of Citations to Journal Articles 4 Citing Medicine By tradition, the rules for formatting references to journal articles permit greater abbreviation compared to books: • Journal references omit information on place of publication and publisher, whereas book references carry these details.
This can be accomplished by helping them set goals best buy bisoprolol blood pressure over 60, use positive self-talk and afﬁrmations cheap 5mg bisoprolol with mastercard prehypertension how to treat, identify self-empowering questions discount generic bisoprolol canada blood pressure normal low high, and ﬁnd ways to inject humor and laughter into their lives purchase discount bisoprolol on line blood pressure below normal. It is very important to eat a low-glycemic Mediterranean-style diet, increase consumption of ﬁber-rich plant foods (fruits, vegetables, grains, legumes, and raw nuts and seeds), and avoid caffeine and alcohol. Lifestyle and Attitude • Exercise at least 30 minutes at least three times a week, but preferably every day. Diabetes can occur when the pancreas does not secrete enough insulin or if the cells of the body become resistant to insulin. Hence, the blood sugar cannot get into the cells, and this condition then leads to serious complications. Adults with diabetes have death rates from cardiovascular disease about two to four times higher than adults without diabetes. Diabetes is the leading reason for dialysis treatment, accounting for 43% of new cases. About 60 to 70% of people with diabetes have mild to severe forms of nervous system damage. Severe forms of diabetic nerve disease are a major contributing cause of lower- extremity amputations. More than 60% of lower-limb amputations in the United States occur among people with diabetes. Many diabetics fall victim to chronic pain due to conditions such as arthritis, neuropathy, circulatory insufficiency, or muscle pain (fibromyalgia). Thyroid disease, inﬂammatory arthritis, and other diseases of the immune system commonly add to the suffering of diabetes. Type 1 is associated with complete destruction of the beta cells of the pancreas, which manufacture the hormone insulin. Type 1 results from injury to the insulin-producing beta cells, coupled with some defect in tissue regeneration capacity. Antibodies for beta cells are present in 75% of all individuals with type 1 diabetes, compared with 0. It is probable that the antibodies to the beta cells develop in response to cell damage due to other mechanisms (chemical, free radical, viral, food allergy, etc. It appears that normal individuals either do not develop as severe an antibody reaction or are better able to repair the damage once it occurs. Initially, insulin levels are typically elevated in type 2, indicating a loss of sensitivity to insulin by the cells of the body. Achieving ideal body weight in these patients is associated with restoration of normal blood glucose levels in many cases. Even if type 2 has progressed to the point where insulin deﬁciency is present, weight loss nearly always results in signiﬁcant improvements in blood glucose control and dramatic reductions in other health risks such as cardiovascular disease. Type 2 is a disease characterized by progressive worsening of blood sugar control. It starts with mild alterations in after-meal (postprandial) glucose elevations, followed by an increase in fasting plasma glucose and often ultimately a lack of production of insulin and the need for insulin therapy. Gestational diabetes occurs more frequently among African-Americans, Hispanic/Latino-Americans, and American Indians. It is also more common among obese women and women with a family history of diabetes. After pregnancy, 5 to 10% of women with gestational diabetes develop type 2; that increases to a 20 to 50% chance of developing diabetes in the 5 to 10 years after pregnancy. Prediabetes and Metabolic Syndrome Prediabetes (also called impaired glucose tolerance) is categorized by a fasting glucose of 100–125 mg/dl and/or postprandial glucose of 140–199 mg/dl. It is the ﬁrst step in insulin resistance and is estimated to affect 57 million Americans. Many people with prediabetes will go on to develop full- blown type 2 despite the fact that prediabetes is usually reversible and, in most cases, diabetes can be completely avoided through dietary and lifestyle changes. Factors implicated in prediabetes, insulin resistance, and the progression to type 2 include a diet high in reﬁned carbohydrates, particularly high-fructose corn syrup; elevated saturated fat intake; overeating due to increased portion sizes of food; increase in inﬂammatory markers; lack of exercise; industrial pollution; abdominal weight gain; hormonal imbalances; inadequate sleep; and nutrient deficiencies. For that reason and others, many people with type 2 do not even know they have the disease. Excess abdominal weight, fatigue, blurred vision, poor wound healing, periodontal disease, and frequent infections are often presenting symptoms of type 2. Blood Glucose Levels The standard method for diagnosing diabetes involves the measurement of blood glucose levels. The initial measurement is generally a fasting blood glucose level taken after avoiding food for at least 10 hours but not more than 16. If a person has a fasting blood glucose measurement greater than 126 mg/dl (7 mmol/L) on two separate occasions, the diagnosis is diabetes. As mentioned above, a fasting glucose greater than 100 but less than 126 mg/dl is classified as prediabetes. A postprandial measurement is usually made one to two hours after a meal, while a random measurement is one that is made anytime during the day without regard for the time of the last meal. Any reading greater than 200 mg/dl (11 mmol/l) is considered indicative of diabetes. Glycosylation of Red Blood Cells Glycosylated Hemoglobin A valuable laboratory test for evaluating long-term blood glucose levels is measuring glycosylated HbA1C. Proteins that have glucose molecules attached to them (glycosylated peptides) are elevated severalfold in diabetics. A1C measurements are particularly helpful in patients with unclear results from fasting blood sugar levels. They can be coupled with a fasting blood glucose level and a two-hour postprandial glucose level for a more accurate diagnosis. An A1C of 5% indicates that the median blood glucose level for the last three months has been around 100 mg/dl; each point of elevation in the percentage means roughly a 35 mg/dl higher average blood sugar level. Thus, an A1C of 7% means that on average over the last three months the patient’s blood glucose was 170 mg/dl. The A1C test is extremely valuable in providing a simple, useful method for assessing treatment effectiveness and should be checked every three to six months. Type 1 Diabetes Causes We know that in type 1 diabetes ultimately the insulin-producing cells of the pancreas are destroyed, in most cases by the body’s own immune system, but what triggers this destruction can vary from one person to another. Genetic factors may predispose the insulin-producing cells to damage through either impaired defense mechanisms, immune system oversensitivity, or some defect in tissue regeneration capacity. The entire set of genetic factors linked to type 1 has been termed “susceptibility genes,” as they modify the risk of diabetes but are neither necessary nor sufﬁcient for disease to develop. These results and others indicate that environmental and dietary factors are more important than a true genetic predisposition in most cases. Such a rise simply cannot be explained by an increased number of people genetically predisposed to type 1. Changes to the human genetic code across large populations take much more than one generation to occur. Environmental and Dietary Risk Factors Accumulating data indicate that abnormalities of the gut’s immune system may play a fundamental role in the immune attack on beta cells and the subsequent development of type 1. What appears to happen in the development of some cases of type 1 is the development by the gastrointestinal immune system of antibodies that ultimately attack the beta cells.
Interestingly generic bisoprolol 10mg on-line blood pressure medication rash, injection cheap 5 mg bisoprolol visa blood pressure stroke, but cannot be filtered out into the collecting recent data discusses the superiority of sodium bicar- system due to the acute renal failure that has ensued purchase bisoprolol with a mastercard arteria aorta definicion. These Asymptomatic (nonoliguric) transient rise in cre- authors contend that the bicarbonate ion is inhibitory atinine mentioned earlier is a common early clinical toward free radical formation due to its increasing pH presentation suggestive of a benign course cheap 10 mg bisoprolol otc blood pressure 200100. The antioxidant drug N-acetylcysteine (adult dose of 600mg administered twice the day before and 20. These benefits have are several simple principles for the clinician to con- been particularly noted in high-risk patients with renal sider and some obvious questions to ponder: insufficiency [47, 52]. Nevertheless, the results of clini- › Is the study that utilizes contrast material really cal studies have shown significant variation as recently needed for the child’s care? Patients conflicting evidence (some experimental trials show- at risk could be observed more closely and timely ing efficacy while others show no statistical advan- intervention be initiated, potentially ameliorating the tage), none of the aforementioned agents can clearly disease course; also, avoidance of additional renal insults be recommended. Without a doubt, more experimental data are required before these agents can be definitively added 20. Certainly continued ing contrast agent could limit renal exposure to its toxic hydration and optimization of the extracellular volume effects. Identify and discontinue any nephrotoxic drugs at a few days regardless of treatment regimen, particu- least 48–72 h prior to contrast administration. Asif A, Epstein M (2004) Prevention of radiocontrast sidered safe with virtually no recognizable or repro- induced nephropathy. N Engl J Med 332:647–655 stage renal disease), the administration of gadolinium 7. A possible mech- Using a dopamine type 1A receptor agonist in high risk anism to explain the etiology is the dissociation of the patients to ameliorate contrast associated nephropathy. Fishbane S (2008) N-Acetylcysteine in the prevention of children recover with no long-term renal sequelae. Grobner T (2006) Gadolinium—a specific trigger for the - High-dose of contrast material (exceeding 5 mL kg−1) development of nephrogenic systemic fibrosis? Pediatr Nephrol 22:2089–2095 - Administration of N-acetylcysteine twice a day admin- 21. Am J Kidney Dis Nephrogenic systemic fibrosis: a review of 6 cases related 24:713–727 to gadolinium injection. Tommaso C (1994) Contrast induced nephrotoxicity in patients systemic fibrosis: suspected etiological role of gadolin- undergoing cardiac catheterization. Margulies K, Schirger J, Burnett J Jr (1992) Radiocontrast Pract 93:29–34 induced nephropathy: current status and future prospects. Rev Cardiovasc Med 4:3–9 nephropathy after coronary angioplasty in chronic renal 39. Kidney Int 41:1408–1415 rial induced renal failure in patients with diabetes, renal 61. They elect to monitor the child closely with neurologic monitoring and attention to any symptoms of 21. The patient was discharged after an Case Vignette uneventful stay of 48 h following admission. In the emergency room, lithium blood Poisonings, intoxications, and medication overdoses are level returns at 5mmol L−1. The emergency room phy- the leading causes for admission of pediatric patients sician reviews available written references and con- to the intensive care unit. In some circumstances, altering of the acid– Alcohols Slurred speech, base status or augmentation of urine output may reduce desinhibition, ataxia, the morbidity and mortality of a toxin. In even rarer cir- hypothermia, confusion, cumstances, extracorporeal removal of the toxin may be memory loss helpful. To achieve excellent outcomes, close abdominal pain, increased communication between the intensivist and nephrologist respiratory effort, hyperthermia, coma is vital, especially in circumstances when initiation of renal replacement therapies is considered. Close collab- Lithium Vomiting, diarrhea, vertigo, confusion, hyperreflexia, oration with a poison control center as well as vigilant coma monitoring are essential components to the management Anticholinergics Fever, tachycardia, dry skin, of any patient with a significant intoxication. This is defined Cyclic antidepressants Tachycardia, drowsiness, as a constellation of signs and symptoms, a syndrome hypotension, insomnia, typical for a specific kind of poisoning. Key to the agitation, cardiac treatment of any pathology is the identification of the arrhythmia syndrome and the offending agent (Table 21. It is important to differentiate the multitude of potential pharmacologic toxins, which can contrib- The toxin can either be eliminated unchanged (as in ute to or be exclusively responsible for renal injury. It has been estimated that toxins contrib- unintended result of treatment for an underlying con- ute to renal failure in up to 20% of patients. As the It is useful from the start to have an accurate picture majority of those agents (including aminoglycosides, of the toxin’s pharmacokinetics. Many toxins in high nonsteroidal anti-inflammatory drugs, contrast material concentrations deviate from their published half-lives [see previous chapter]) are readily appreciated as a and therefore plotting out the concentration of the drug potential source of iatrogenic renal failure they will with serial levels can be useful. We recom- rapid decreases in toxicity over time as the patient mend close consultation with the laboratory to specify quickly returns to nontoxic concentrations. However, what substances are possible based on the history, physical some drugs such as ethanol exhibit zero-order kinetics, and laboratory analysis available at presentation. The velocity of those reactions is independent of the dose of the toxin and a linear decrease in the 21. Elimination of a toxin is primarily through the metabo- Chronic renal failure involves not only decreasing lism of the substance through the liver and elimination toxin clearance of renal-eliminated toxins but also or clearance of the substance through the kidneys. Major clearance systems, Chapter 21 Intoxications 283 C C o o n n c c e e n n t t r r a a t t i i o o n n Time Time Fig. The majority of drug metabolism order kinetic elimination is ethanol intoxication takes place with first-order kinetics (the velocity of the elimina- tion reaction is dependent on the concentration of the toxin) used approach. Theoretically, urine alkalinization such as the hepatic cytochrome P450 system, are should decrease the toxic effects of a myoglobinuria. The proposed mechanisms are by decreasing the pre- The pediatric nephrologist and the intensivist share cipitation of hemoglobin . Alkalinization may be accomplished by giving 1–2 meq kg−1 of sodium bicarbonate intravenously acid–base disturbances markedly alter patient’s toxic- ity, binding to serum proteins, and availability to the over 30min. This alkalinization may be continued by preparing a solution of D5W with 80meq L−1 of kidneys for clearance. Potential complications from alkali- Perhaps the greatest role for the nephrologist (and nization of the urine include local tissue infiltration the kidney) in the management of the poisoned pedi- with resulting tissue necrosis as well as hypokalemia. This is especially important if there is evidence of Alkalinization may also be useful for the enhanced acute renal injury related to an acute intoxication or elimination of toxin. Alkalinization is likely to be in the presence of documented nephrotoxicity with- most effective if a toxin is eliminated by the kidneys out systemic involvement. Cases of increased pigment essentially unchanged, has a small volume of distribu- load (i. Essentially, a toxin has increased elimina- a of decreased volume status and the formation of tion from the renal tubules if it crosses the renal tubular intratubular casts. Maintenance of intravascular vol- lumen and cannot readily diffuse across the renal epi- ume status is essential to decrease precipitation of the thelium. Volume loading with 20 mL kg−1 of isotonic of poisonings such as phenobarbital, methotrexate, solution and maintenance fluids at 3,000mL m−2 to chlorpropamide, and fluoride.