title: Critical care nephrology: management of acid-base disorders with CRRT.
abstract: Normal acid-base homeostasis is severely challenged in the intensive care setting. In this review, we address acid-base disturbances, with a special focus on the use of continuous (rather than intermittent) extracorporeal technologies in critical ill patients with acute kidney injury. We consider hypercapnic acidosis and lactic acidosis as examples in which continuous modalities may have different roles and indications than the traditional intermittent approaches to renal replacement therapy. Hypercapnic acidosis develops as a consequence of alveolar hypoventilation. In this condition, correction of pH above 7.2 is not currently recommended, and may even abrogate the beneficial effects of hypercapnic acidosis on overall outcomes. Extracorporeal technologies support lung protection while maintaining overall patient homeostasis. Similarly, in lactic acidosis, current evidence does not support bicarbonate infusions to correct acidosis. The management of lactic acidosis should correct the underlying causative disturbances. Most often, lactic acidosis is a biomarker denoting unfavorable outcomes, rather than an intrinsic pathogenetic mechanism. Extracorporeal procedures may assist in the removal of pathogenic drugs or toxins, as well as partially correcting acidemia. Whether or not these approaches will permit normalization of systemic pH, and the impact of these approaches on patient outcomes, needs to be addressed with prospective controlled trials.
authors.affiliation: Division of Nephrology, Department of Medicine, Albany Medical College, Albany, New York 12209, USA. cerdaj@mail.amc.edu
authors.forename: Jorge
authors.initials: J
authors.lastname: Cerdá
authors.forename: Ashita J
authors.initials: AJ
authors.lastname: Tolwani
authors.forename: David G
authors.initials: DG
authors.lastname: Warnock
mesh_terms: D000136:Acid-Base Equilibrium; D000137:Acid-Base Imbalance / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D000140:Acidosis, Lactic / Q000209:etiology / Q000628:therapy; D000142:Acidosis, Respiratory / Q000209:etiology / Q000628:therapy; D058186:Acute Kidney Injury / Q000150:complications / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D000925:Anticoagulants / Q000627:therapeutic use; D002951:Citrates / Q000627:therapeutic use; D003422:Critical Care; D006706:Homeostasis; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006935:Hypercapnia / Q000209:etiology / Q000628:therapy; D009398:Nephrology / Q000379:methods*; D011379:Prognosis; D017582:Renal Replacement Therapy
chemical_list: D000925:Anticoagulants; D002951:Citrates