Potassium is the principal intracellular cation, and maintenance of the distribution of potassium between the intracellular and the extracellular compartments relies on several homeostatic mechanisms. When these mechanisms are perturbed, hypokalemia or hyperkalemia may occur. This review covers hyperkalemia, that is, a serum potassium concentration exceeding 5 mmol/L. The review includes a discussion of potassium homeostasis and the etiologies of hyperkalemia and focuses on the prompt recognition and treatment of hyperkalemia. This disorder should be of major concern to clinicians because of its propensity to cause fatal arrhythmias. Hyperkalemia is easily diagnosed, and rapid and effective treatments are readily available. Unfortunately, treatment of this life-threatening condition is often delayed or insufficiently attentive or aggressive.
Congestive heart failure (CHF) and hyperkalemia are the two leading reasons for emergency dialysis among individuals with end-stage renal disease (ESRD). While hemodialysis provides definitive treatment of both hyperkalemia and volume overload among ESRD patients, for those who present outside of "regular dialysis hours," institution of dialysis may be delayed. Nondialytic management can be instituted immediately and should be
TCR signaling plays a critical role in regulatory T cell (Treg) development. However, the mechanism for tissue specific induction of Tregs in the periphery remains unclear. Surfactant protein A (SP-A) is a major immune defense protein in the lung. To determine if SP-A contributes to the normal non-inflammatory status mediated by Tregs in the lung, T cells were activated with various stimuli. Compared to WT mice, on ex vivo culture, T cells from lungs of SP-A deficient mice have impaired expression of Foxp3 and fewer CD25+Foxp3+ Treg phenotype cells. These phenotypic effects could be rescued by the addition of exogenous SP-A. Even as cell cycle progression is blocked, both IL-2 levels as well as active TGFβ levels increase on extended culture. In addition, kinetic suppression assays demonstrate that SP-A enhances the frequency of functional Foxp3+Tregs in responder T cell populations in a TGFβ dependent manner. To induce Tregs in the lung in vivo, we modified the extended LPS model described by d’Alessio et al (1). While the proportion of Tregs increased ≈160% in WT mice ~8d post-exposure, SP-A-/- mice showed a much more modest 50% increase over their near identical baselines. We also observed a strong correlation between FR4 and Foxp3 expression in functional Tregs induced by SP-A. Together, these findings suggest that SP-A exerts long-term effects on T cell immune function by the induction of Tregs during activation. (1) D’Alessio et al J Clin Invest. (2009) 119: 2898
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