Bicarbonate regulation is intimately linked to net acid secretion throughout the kidney tubule. In the proximal tubule, where 85 to 90 per cent of filtered HCO 3- is resorbed, reclamation of HCO3- is mediated by secretion of H+ (Fig 1); reabsorption of HCO3- is enhanced by increased CO2 tension, volume contraction, and hypokalemia (Emmettefa/ 1992). H+ secretion in the distal tubule and collecting ducts is associated with HCO 3- generation intracellularly and its subsequent transport into the blood (Emmettefa/ 1992).
Fig. 1 Renal acid-base homeostasis. Filtered bicarbonate (HCO3-) is reclaimed and titrated bicarbonate is regenerated. The diagrams from left to right represent the renal microcirculation, then renal tubular cells, and finally the tubular lumen. Relative ion concentrations are indicated by the width of the line under each heading. Secretion of hydrogen ion (H+) in the proximal tubule is largely responsible for reclamation (RCL) of equimolar amounts of HCO 3-. Further H+ secretion is used to titrate ammonia (and inorganic phosphate), particularly in the distal nephron. This regenerates (RG) HCO 3-. (CA, carbonic anhydrase; A-, anions.) (Reproduced with permission from Schmidt,,, (1992).)
Urinary ammonium excretion is an important mechanism of net acid excretion. Ammonia (NH3) is produced in the proximal renal tubular cells, enters the lumen, and is then reabsorbed in the loop of Henle. In the distal nephron, NH 3 diffuses back into the lumen where it is trapped by acidification to produce ammonium (NH 4+). The net result of this process is secretion of acid as NH4+ and generation of an equimolar quantity of HCO3- (Em.m.ett.etal 1992). Renal ammonia synthesis and thus handling of net acid load is augmented by acidosis (positive feedback) and hypokalemia, and is inhibited by low glomerular filtration rate, low levels of glutamine (due to malnutrition), high levels of alternative renal fuel sources (e.g. fat in parenteral nutrition), and hyperkalemia ( Emme.tLet.al, 1992; Schmidt 1992).
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