ABSTRACT
Maintenance of metabolic alkalosis generated by chloride depletion is often attributed to volume contraction. In balance and clearance studies in rats and humans, we showed that chloride repletion in the face of persisting alkali loading, volume contraction, and potassium and sodium depletion completely corrects alkalosis by a renal mechanism. Nephron segment studies strongly suggest the corrective response is orchestrated in the collecting duct, which has several transporters integral to acid-base regulation, the most important of which is pendrin, a luminal Cl/HCO(3)(-) exchanger. Chloride depletion alkalosis should replace the notion of contraction alkalosis.
Subject(s)
Alkalosis/etiology , Chlorides/metabolism , Aldosterone/physiology , Alkalosis/therapy , Animals , Bicarbonates/metabolism , Extracellular Fluid/metabolism , Humans , Hydrogen-Ion Concentration , Kidney/metabolism , RatsABSTRACT
Effective management of acid-base disorders depends on accurate diagnosis. Three distinct approaches are currently used in assessing acid-base disorders: the physiological approach, the base-excess approach, and the physicochemical approach. There are considerable differences among the three approaches. In this review, we first describe the conceptual framework of each approach, and comment on its attributes and drawbacks. We then highlight the application of each approach to patient care. We conclude with a brief synthesis and our recommendations for choosing an approach.
