title: Clinical approach to renal tubular acidosis in adult patients.
abstract: Renal tubular acidosis (RTA) is a group of disorders observed in patients with normal anion gap metabolic acidosis. There are three major forms of RTA: A proximal (type II) RTA and two types of distal RTAs (type I and type IV). Proximal (type II) RTA originates from the inability to reabsorb bicarbonate normally in the proximal tubule. Type I RTA is associated with inability to excrete the daily acid load and may present with hyperkalaemia or hypokalaemia. The most prominent abnormality in type IV RTA is hyperkalaemia caused by hypoaldosteronism. This article extensively reviews the mechanism of hydrogen ion generation from metabolism of normal diet and various forms of RTA leading to disruptions of normal acid-base handling by the kidneys.
authors.affiliation: Department of Medicine, University of Florida College of Medicine, Jacksonville, FL 32209, USA. pramod.reddy@jax.ufl.edu
authors.forename: P
authors.initials: P
authors.lastname: Reddy
mesh_terms: D000136:Acid-Base Equilibrium / Q000502:physiology; D000141:Acidosis, Renal Tubular / Q000175:diagnosis / Q000378:metabolism / Q000628:therapy*; D000143:Acids / Q000378:metabolism; D000328:Adult; D002245:Carbon Dioxide / Q000097:blood / Q000652:urine; D002255:Carbonic Acid / Q000378:metabolism; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006947:Hyperkalemia / Q000209:etiology; D007008:Hypokalemia / Q000209:etiology; D007684:Kidney Tubules / Q000502:physiology; D008901:Mineralocorticoids / Q000627:therapeutic use; D011522:Protons; D049994:Sodium Potassium Chloride Symporter Inhibitors / Q000627:therapeutic use
chemical_list: D000143:Acids; D008901:Mineralocorticoids; D011522:Protons; D049994:Sodium Potassium Chloride Symporter Inhibitors; D002245:Carbon Dioxide; D002255:Carbonic Acid