![]() When the plasma bicarbonate exceeds the tubular maximum, the urine pH will be alkaline and urine sodium and potassium will be increased whereas urine chloride is low. Proximal (type 2) RTA is the result of impaired bicarbonate reclamation in the proximal tubule due to a decrease in the tubular maximum for reabsorption. Impairment in activity of the H +-K +-ATPase can also contribute to kidney K + wasting. The urine pH is always alkaline (pH 6–7) and urine potassium is increased due to coupling of increased distal sodium delivery with increased aldosterone resulting from acidosis-induced decreased sodium reabsorption in the proximal tubule (36). Distal (type 1) RTA results from defects in hydrogen ion secretion in the distal nephron interfering with bicarbonate regeneration. (C) Distal (type 1) and proximal (type 2) renal tubular acidosis (RTA) are characterized by hypokalemic hyperchloremic normal anion gap metabolic acidosis. The urine osmolal gap is increased due to the large amount of ammonium in the urine indicating the acidosis is of extrakidney origin. Although some ammonium is excreted as NH 4Cl, a large amount of ammonium is excreted coupled to the anion salts of the acids. ![]() Urine sodium and potassium concentration will be greater than the urine chloride concentration because chloride is retained in response to volume contraction. The excretion of the sodium or potassium salts of these acids (NaA) into the urine represent the indirect loss of bicarbonate from the body and cause the urine anion gap to remain positive despite large amounts of ammonium excretion. (B) Shown are various examples of overproduction aciduria. The urine pH (U pH) is not maximally acidic despite robust distal hydrogen ion secretion because the free hydrogen ion concentration is reduced due to the buffering effect of urinary ammonium. Ammonium is excreted coupled to chloride, accounting for the development of a negative urinary anion gap and increased osmolal gap. ![]() Acidemia and hypokalemia stimulate kidney ammoniagenesis allowing for increased amounts of distal hydrogen ion secretion to occur. (A) In diarrhea, stool loss of potential bicarbonate, sodium chloride, and potassium lead to a normal gap hyperchloremic metabolic acidosis, hypokalemia, and extracellular fluid volume contraction. Urine chemistry profile in metabolic acidosis of kidney and nonkidney origin. Increased distal delivery of sodium is due to inhibition of proximal reabsorption brought about by effective volume expansion. (D) A primary increase in mineralocorticoid levels (Conn syndrome) or effect (Liddle syndrome) leads to a chloride resistant form of metabolic alkalosis accompanied by kidney potassium wasting and hypertension. Bicarbonate acts as a nonreabsorbable anion, causing increased distal sodium delivery and development of potassium wasting (29). (C) Active vomiting or nasogastric suction generates a chloride-sensitive form of metabolic alkalosis. The urine pH (U pH) in this setting is acidic because of augmented hydrogen ion secretion. (B) Antibiotics such as carbenicillin, ticarcillin, and piperacillin given in the setting of decreased effective volume act as nonreabsorbable anions, causing increased delivery of sodium to the distal nephron, resulting in development of hypokalemia and a chloride-responsive from of metabolic alkalosis. Metabolic alkalosis due to remote use of diuretics is sensitive to chloride-containing solutions but resistant in genetic disorders. The fractional excretion (FE) of urea is reduced to <35% because proximal reabsorption of urea is stimulated and unaffected by the downstream impairment in sodium chloride transport. Increased distal delivery of sodium coupled with increased mineralocorticoid levels causes increased potassium secretion and an increased rate of hydrogen ion secretion in the distal nephron, leading to the development of hypokalemic metabolic alkalosis (27). ![]() (A) Loop and thiazide diuretics and their genetic equivalent (Bartter and Gitelman syndrome, respectively) cause contraction of effective circulatory volume and activation of the renin-angiotensin-aldosterone axis. Urine chemistry profile in metabolic alkalosis. ![]()
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