Seminars in nephrology
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Magnesium is an important constituent of the intracellular space that affects a number of intracellular and whole body functions. Magnesium balance depends on intake and renal excretion, which is regulated mainly in the thick ascending limb of the loop of Henle. The complex hormonal modulation that responds to changes in plasma concentration of other ions such as calcium and potassium is lacking for magnesium. ⋯ The major direct toxicity of hypomagnesemia is cardiovascular. When urgent correction of hypomagnesemia is required, as with myocardial ischemia, post cardiopulmonary bypass, and torsades de pointes, intravenous or intramuscular magnesium sulfate should be used. Oral magnesium preparations are available for chronic use.
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Although an anion gap at less than 20 mEq/L rarely has a defined etiology, significant elevations in the anion gap almost always signify presence of an acidosis that can be easily identified. Anion gap acidoses can be divided into those caused by lactate accumulation, ketoacid production, toxin/drugs, and uremia. Lactic acidoses caused by decreased oxygen delivery or defective oxygen utilization are associated with high mortality. ⋯ Salicylate toxicity usually is associated with a mild metabolic acidosis and a respiratory alkalosis. Uremia is associated with a mild acidosis secondary to decreased ammonia secretion and an anion gap caused by the retention of unmeasured anions. A decrease in anion gap is caused by numerous mechanisms and thus has little clinical utility.
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Seminars in nephrology · Sep 1997
ReviewFibrosis, a common pathway to organ failure: angiotensin II and tissue repair.
For heart, kidneys, lungs and liver alike, fibrosis represents a common pathway to their failure. Understanding pathophysiologic mechanisms involved in organ fibrosis are therefore of considerable interest, particularly given the potential for protective pharmacological strategies. Tissue repair involves inflammatory cells, including members of the monocyte/macrophage lineage, integral to initiating the repair process; and myofibroblasts, phenotypically transformed interstitial fibroblasts, responsible for collagen turnover and fibrous tissue formation. ⋯ In an autocrine/paracrine manner, this peptide regulates expression of TGF-beta 1 via angiotensin (AT1) receptor-ligand binding. It is this cytokine that contributes to phenotypic conversion of fibroblasts to myofibroblasts (myoFb) and regulates myofibroblast turnover of collagen. Angiotensin-converting enzyme (ACE) inhibition or AT1 receptor antagonism each prevent many of these molecular and cellular responses that eventuate in fibrosis and therefore have been found to be protective interventions.
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Seminars in nephrology · Jul 1997
ReviewAcute dialysis and continuous renal replacement: the emergence of new technology involving the nephrologist in the intensive care setting.
The emergence of dialytic support for patients with reversible renal failure was one of the most significant advances in critical care medicine. Supporting a patient with a failed organ till organ recovery has not had the same success with other organ failures. Despite the indispensable nature of the support, dialysis was intermittent at best, and carried its own morbidity. ⋯ Plastic membrane bio-incompatibility, human physiological responses to foreign material exposure, either in the circuit material itself or introduced from therapy methodology, pose practical and theoretical problems. Recent advances in the field of bio-artificial technology have allowed the development of functioning hybrid "blood processors," which function as a renal tubule and may be able to not only "clean" blood, but also allow for other cellular functions not currently possible with dead membrane technology. Combining living cells with a continuous delivery method may be the next significant step toward a fully functional renal replacement therapy.
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Despite the numerous studies that have been spawned by the cloning of more than 240 G-protein-coupled receptors, the molecular basis for receptor discrimination of receptor-ligand interactions remains a central issue in membrane receptor biology. The receptor's criteria for agonists and antagonists allow these types of ligands to compete for the same binding site on the receptor, but only agonists are able to stimulate intracellular signaling. ⋯ Because the V1a and V2 vasopressin receptors are coupled to different intracellular signaling systems, it should be possible to assay the functional components of binding and G-protein coupling in a series of chimeric receptors. With the ever-increasing database on the structural determinants of G-protein-coupled receptor function, at least some of the underlying mechanisms of transmembrane signal transduction should be better understood in the next few years.