Dialysis Disequilibrium Syndrome (DDS) is characterized by neurological symptoms caused by rapid removal of urea during hemodialysis. It develops primarily from an osmotic gradient that develops between the brain and the plasma as a result of rapid hemodialysis. This results in brain edema that manifests as neurological symptoms such as headache, nausea, vomiting, muscle cramps, tremors, disturbed consciousness, and convulsions. In severe cases, patients can die from advanced cerebral edema. Recent advancements in cell biology implicate the role of urea disequilibrium (with a smaller contribution from organic osmolytes) as the pathophysiological mechanism responsible for this syndrome. In this review, we discuss the pathogenesis, clinical features and prevention of DDS.
Nephrogenic systemic fibrosis (NSF) is a rare and a debilitating disease noted uncommonly in patients with impaired renal function when exposed to low-stability gadolinium-based contrast agents (Gd-CAs). According to experimental studies, cytokines released by the stimulation of effector cells such as skin macrophages and peripheral blood monocytes activate circulating fibroblasts which play a major role in the development of NSF lesions. The presence of permissive factors, presumably, provides an environment conducive to facilitate the process of fibrosis. Multiple treatment modalities have been tried with variable success rates. More research is necessary to elucidate the underlying pathophysiological mechanisms which could potentially target the initial steps of fibrosis in these patients. This paper attempts to collate the inferences from the in vivo and in vitro experiments to the clinical observations to understand the pathogenesis of NSF. Schematic representations of receptor-mediated molecular pathways of activation of macrophages and fibroblasts by gadolinium and the final pathway to fibrosis are incorporated in the discussion.
Nephrogenic systemic fibrosis (NSF) has been observed with increased frequency in recent years. Progressive hardening of the skin advancing to severe woody induration and the development of thickened hyperpigmented plaques on the extremities and the trunk are the main clinical features. Further progression of the disease results in flexion contractures of the upper and lower extremities, resulting in immobilization and severe morbidity. In this study, we reviewed our experience with seven end-stage renal disease patients who were referred to our center between January 2004 and June 2005 for kidney transplant evaluation or for diagnosis and treatment of their deteriorating condition. Diagnosis in all patients was confirmed by skin and muscle biopsy. Three of these patients underwent renal transplantations, and softening of the skin and improved mobility of the joints was noted after kidney transplantation. Three of the four patients who remained on dialysis showed further deterioration of their NSF despite a trial of immunosuppressive therapy. Improvement after transplantation could be secondary to immunosuppression, increased renal clearance and/or more effective fluid management.
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