Ammoniagenesis, renal

Mg < 1 mEq/L) depletion (renal ammoniagenesis, renal H+ losses, and stimulate renal bicarbonate reabsorption)... 

Diuretic pharmacotherapy (renal H+/chloride losses/2° hyperaldosteronism, renal ammoniagenesis)... 

Excretion of metabolic fixed acids and generation of new HCO3 is achieved through renal ammoniagenesis and distal tubular hydrogen ion secretion. Ammoniagenesis plays a critical role in acid-base homeostasis, with ammonium (NH4+) excretion comprising approxi-... 

Henle (e.g., furosemide, bumetanide, and torsemide) and distal convoluted tubule (thiazides), have most commonly been associated with the generation of metabolic alkalosis. These agents promote the excretion of sodium and potassium almost exclusively in association with chloride, without a proportionate increase in bicarbonate excretion. Collecting duct hydrogen ion secretion is stimulated directly by the increased luminal flow rate and sodium delivery, and indirectly by intravascular volume contraction, which results in secondary hyperaldosteronism. Renal ammoniagenesis may also be stimulated by concomitant hypokalemia, further augmenting net acid excretion. 

Mineralocorticoid excess also plays a significant role in the maintenance of metabolic alkalosis. In patients with volume-responsive metabolic alkalosis, intravascular volume depletion stimulates aldosterone secretion. As discussed earlier, excess mineralocorticoid activity may also underlie the generation of metabolic alkalosis. In either situation, the increased mineralocorticoid effect stimulates collecting duct H+ secretion. Metabolic alkalosis may also be maintained by persistent hypokalemia. Hypokalemia has a multitude of effects on renal acid-base homeostasis, enhancing proximal tubular bicarbonate reabsorption, stimulating ammoniagenesis and increasing distal tubular H secretion. ... 

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