Clin Nephrol
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Much progress has been made in recent years in the management of anemia associated with chronic and renal failure with recombinant human erythropoietin (r-Hu EPO). However, there remains much debate surrounding the diagnosis and treatment of iron deficiency. To ensure that full benefit from erythropoietin therapy is received, most patients require iron supplement during treatment. ⋯ Thus, intravenous iron supplementation should be administered only in patients who do not tolerate available intravenous iron preparations or who are on continuous ambulatory peritoneal dialysis with no evidence of functional iron deficiency. This article provides guidelines for the diagnosis of absolute or functional iron deficiency in patients with renal anemia and suggests treatment schedules for intravenous iron supplementation. We hope that all dialysis patients will be able on this basis to achieve a satisfactory iron status and benefit fully from r-Hu EPO therapy.
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Trimethoprim-sulfamethoxazole is a frequently prescribed antibiotic with a wide spectrum of antimicrobial activity. As a result of the increasing number of AIDS patients requiring therapy for Pneumocystis carinii pneumonia, high dose trimethoprim-sulfamethoxazole use had dramatically increased. A previously unreported and potentially lethal adverse reaction associated with high dose trimethoprim-sulfamethoxazole therapy, hyperkalemia, subsequently developed. ⋯ A prospective surveillance study of patients treated with standard dose trimethoprim-sulfamethoxazole as compared to similar controls treated with other antibiotics confirmed the rise in potassium concentration associated with trimethoprim-sulfamethoxazole therapy. Patients with mild renal insufficiency were the only group at significant risk for more severe hyperkalemia. Hence, trimethoprim-sulfamethoxazole therapy can be complicated by hyperkalemia regardless of the dose employed.
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Patients with hyponatremia are exposed to major neurological complications. On the one hand hyponatremia itself produces brain edema, increased intracranial pressure which potentially leads to subsequent neuropathological sequelae or death. On the other hand excessive correction could be followed by development of brain demyelinating lesions (central pontine or extrapontine myelinolysis) with major disability or fatal outcome. ⋯ In hyponatremic patients without symptoms, there is no need for rapid correction and the treatment should be more conservative. Close monitoring of the serum sodium is indicated initially and if necessary, correction must be stopped and diuresis interrupted with dDAVP. Given recent experimental data, in patients overly corrected (delta SNa > 15 mEq/1/24 h), the risk of myelinolysis could be greatly reduced by rapidly decreasing the serum sodium through hypotonic fluids administration and dDAVP.
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The association of severe hyponatremia and the ingestion of large quantities of beer, termed beer potomania, has been known for several years. We report two new cases, and review 20 others from the medical literature. These patients usually have a history of binge beer drinking, poor dietary intake, and then present with severe hyponatremia and various mental status changes or seizures. ⋯ We propose that the pivotal pathophysiologic mechanism in beer potomania syndrome is the minimal intake of solute and the hypoosmolality of the beer ingested. This will lead to the inability to excrete sufficient amounts of free water to keep up with the ingestion of large quantities of the hyposmolar beer. Treatment with isotonic sodium chloride results in the rapid clearance of the accumulated excess free water.
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Continuous renal replacement therapies are extensively utilized for the treatment of acute renal failure in the critically ill patient. The arterio-venous circulation has been partially substituted by the veno-venous pump driven circulation. Diffusion has been added to convection in order to increase the small solutes clearance even though sometimes the pure convection is still advantageously utilized. ⋯ The improved understanding of the multiple organ failure syndrome and the pathophysiology of the septic syndrome, suggest today newer indications for continuous renal replacement therapies. The proposed mechanisms of action of the therapy should be the removal of chemical mediators such as platelet activating factor, interleukin-1 and tumor necrosing factor alfa, not only by a filtration process, but also by the adsorption on the surface and structure of the artificial membrane. These new mechanisms may in part be responsible for the beneficial effects of continuous therapies in the patients affected by acute renal failure and other organ dysfunctions.