Approach to the Patient: Hyperchloremic Metabolic Acidoses In diarrhea, stools contain a higher [HCO3–] and decomposed HCO3– than plasma so that metabolic acidosis develops along with volume depletion. Instead of an acid urine pH (as anticipated with systemic acidosis), urine pH is usually around 6 because metabolic acidosis and hypokalemia increase renal synthesis and excretion of NH4+, thus providing a urinary buffer that increases urine pH. Metabolic acidosis due to gastrointestinal losses with a high urine pH can be differentiated from RTA (Chap. 278) because urinary NH 4+ excretion is typically low in RTA and high with diarrhea. Urinary. | Chapter 048. Acidosis and Alkalosis Part 9 Approach to the Patient Hyperchloremic Metabolic Acidoses In diarrhea stools contain a higher HCO3 and decomposed HCO3 than plasma so that metabolic acidosis develops along with volume depletion. Instead of an acid urine pH as anticipated with systemic acidosis urine pH is usually around 6 because metabolic acidosis and hypokalemia increase renal synthesis and excretion of NH4 thus providing a urinary buffer that increases urine pH. Metabolic acidosis due to gastrointestinal losses with a high urine pH can be differentiated from RTA Chap. 278 because urinary NH4 excretion is typically low in RTA and high with diarrhea. Urinary NH4 levels can be estimated by calculating the urine anion gap UAG UAG Na K u - Cl u. When Cl u Na K the urine gap is negative by definition. This indicates that the urine ammonium level is appropriately increased suggesting an extrarenal cause of the acidosis. Conversely when the urine anion gap is positive the urine ammonium level is low suggesting a renal cause of the acidosis. Loss of functioning renal parenchyma by progressive renal disease leads to hyperchloremic acidosis when the glomerular filtration rate GFR is between 20 and 50 mL min and to uremic acidosis with a high AG when the GFR falls to 20 mL min. Such a progression occurs commonly with tubulointerstitial forms of renal disease but hyperchloremic metabolic acidosis can persist with advanced glomerular disease. In advanced renal failure ammoniagenesis is reduced in proportion to the loss of functional renal mass and ammonium accumulation and trapping in the outer medullary collecting tubule may also be impaired. Because of adaptive increases in K secretion by the collecting duct and colon the acidosis of chronic renal insufficiency is typically normokalemic. Proximal RTA type 2 RTA Chap. 278 is most often due to generalized proximal tubular dysfunction manifested by glycosuria generalized aminoaciduria and phosphaturia Fanconi .
