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A mixture of both RTA types I and II (distal and proximal).Medication-induced (valproic acid, aminoglycosides) Rarely, the failed re-uptake of bicarbonate occurs in isolation RTA Type II and Fanconi syndrome are not synonymousįanconi syndrome (secondary to cystinosis, galactosemia, or tyrosinemia)Īcquired (vitamin D deficiency, Sjogren’s) This pathology is seen in Fanconi syndrome. Often secondary to a failure of the renal tubule cells to maintain a low concentration of intracellular Na +.Ĭoncentration gradient is required to drive the reuptake of multiple compounds from the renal tubule A decreased secretion of hydrogen ions by the distal tubule in response to increased acidification of the serum.Ĭongenital: deleterious genetic variants in ion transport proteinsĪcquired: immunologic destruction of alpha-intercalated cells or medicationsĪ reduced reabsorption of bicarbonate in the proximal tubule.Note: there is no luminal carbonic anhydrase to drive the re-uptake of CO 2, unlike in the proximal tubule Ammonia and phosphate buffer the secreted hydrogen ions.The resulting hydrogen ion is transported into the lumen by the vacuolar H +-ATPase and the H +-K +-ATPase, with the vacuolar H +-ATPase playing the dominant role. Bicarbonate ion is transported into the blood by the by the chloride-bicarbonate anti-porter AE1.The alpha-intercalated cells play the largest direct role in the acidification of urine, which occurs via the following mechanisms:Ĭarbonic anhydrase ( CA-II) creates carbonic acid which ionizes to form bicarbonate and a hydrogen ion, in a mechanism similar to that which occurs in the proximal tubule. Secreted phosphate provides a buffer as well. The secretion of ammonia in the proximal tubule plays a particularly important role in renal acid-base homeostasisĪmmonia represents the primary buffer for the excreted hydrogen ions. The secretion of hydrogen ions by the alpha-intercalated cells in the cortical collecting duct, which in turn is sensitive circulating levels of aldosterone (see below for details) The continued reabsorption of bicarbonate within the loop of Henle The secretion of ammonia in the proximal tubule The acidification of urine by the distal tubule depends on: Renal Tubular Acidosis: The Clinical Entity.
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RTA TYPE PLUS
Intracellular carbonic anhydrase ( CA-II) creates carbonic acid from water and carbon dioxide, which in turn ionizes to form a hydrogen ion plus bicarbonate.The reabsorption of filtered bicarbonate in the proximal tubule depends on the activity of carbonic anhydrase and several transporters: Proximal Reabsorption of Bicarbonate Soriano JR. Proximal reabsorption of filtered bicarbonate.Normal Acid-Base Homeostasis within the Renal TubulesĪcid-base handling in the renal tubule can be broken down into two stages: The precise pathophysiological mechanism underlying the disorder varies across RTA sub-types (I-IV), which are described in detail below.The abnormal acid-base transport within the tubules cannot be solely explained by decreased a glomerular filtration rate (GFR) secondary to chronic kidney disease, obstructive uropathy, or some other non-specific nephropathic mechanism Renal tubular acidosis (RTA) refers to a normal anion gap metabolic acidosis (also known as a hyperchloremic acidosis) caused by:ĭecreased excretion of hydrogen ions and/orĭecreased reabsorption of sodium bicarbonate in the renal tubules.