“…Several mechanisms may be responsi ble for the potassium-conserving response including a decrease in aldosterone secretion, diminished delivery of sodium and fluid to distal nephron sites, an increase in renal ammonia production and excretion, and a fall in the Proximal RTA is characterized by an abnormality in bicarbonate reabsorption by the proximal nephron, while H+ transport by the distal nephron is normal. Serum potassium levels may be normal or slightly reduced in untreated cases [7], However, marked renal potassium wasting commonly occurs during treatment with NaHCOi [8]. Alkali therapy increases plasma bicarbon ate concentration and thereby results in an increased fil tered load of bicarbonate.…”