Search

Peritonitis is the “Achilles heel” of patients on peritoneal dialysis. Fungal peritonitis though not that common is associated with increased morbidity and mortality. We report the first case in the literature of a patient who developed peritonitis caused by Curvularia geniculata. We discuss the reported cases of Curvularia lunata peritonitis in literature and emphasize the early removal of catheter and treatment with intravenous amphotericin B. [ABSTRACT FROM AUTHOR]

Disorders of sodium and water metabolism are frequently encountered in hospitalized patients. Hyponatremia in critically ill patients can cause significant morbidity and mortality. Inappropriate treatment of hyponatremia can add to the problem. The diagnosis and management of salt and water abnormalities in critically ill patients is often challenging. The increasing knowledge about aquaporins and the role of vasopressin in water metabolism has enhanced our understanding of these disorders. The authors have outlined the general approach to the diagnosis and management of hyponatremia. A systematic approach by clinicians, using a detailed history, physical examination, and relevant diagnostic tests, will assist in efficient management of salt and water problems. [ABSTRACT FROM PUBLISHER]

Although the full mechanisms are not yet elucidated, research into the mechanism of toxicity of aluminum (Al) on bone formation and remodeling and on hematopoietic tissue is ongoing. In contrast, little information exists on the interactive effects of systemic Al and the kidney. In bone, both clinically and experimentally, high doses of Al inhibit remodeling, slowing both osteoblast and osteoclast activities and producing osteomalacia and adynamic bone disease. In contrast, while very low levels of Al are mitogenic in bones of experimental animals, the effect of low levels of Al in humans is unknown. Aluminum has been shown to have its mitogenic action at the osteoblast, but whether the effect on resorption is via osteoblast-directed changes in osteoclast activity has not yet been determined. Parathyroid hormone (PTH) levels are disrupted by Al in humans and animals. Whether altered PTH levels play a major or even a minor role in Al-dependent osteotoxicity requires clarification. In hematopoietic tissue, Al causes a microcytic anemia, not reversible by iron. Friend leukemia cells treated with Al have been reported to accumulate excess iron, without incorporating it into ferritin or heme. It is not yet known which steps in iron metabolism are disrupted by Al, if they involve a single mechanism of action, or even if this disruption in iron metabolism accounts for the anemia seen in Al toxicosis. In kidney, research is needed to evaluate Al nephrotoxicity; there are almost no studies in this area. Furthermore, research is needed to evaluate mechanisms of renal Al excretion, presently shown by one study to occur at the distal tubule. Such studies might well throw light on whether Al plays a role in aggravating renal insufficiency, or whether the role of the kidney in Al toxicosis is limited to the causative effect of renal compromise on Al accumulation. In summary, while a number of mechanisms have been proposed for the toxic action of Al, no single mechanism emerges to explain these diverse effects of systemic Al. Recommendations for future research are presented and summarized in Table 1. [ABSTRACT FROM AUTHOR]