When is base administration associated with persistent metabolic alkalosis?
Base administration may be a generation phase of metabolic alkalosis when kidney function is reduced and the kidneys do not excrete the bicarbonate as rapidly as usual. Occasionally patients with kidney failure may take NaHCO 3 as an antacid and with very low GFR develop metabolic alkalosis. They may have correction of the high [HCO 3 ] at the time of their next dialysis treatment, at which time they should undergo hemodialysis with a lower dialysate [HCO 3 ]. Eventually, normal metabolism and diet will lead to production of protons that will also reduce the [HCO 3 ].
Another cause is the milk-alkali syndrome. Administration of calcium-containing antacids, mostly calcium carbonate, cause reduced GFR, hypercalcemia, and hypercalciuria. Deposition of calcium phosphate in the kidney parenchyma is a cause of nephrocalcinosis and chronic kidney disease, which also reduces GFR. The carbonate is potential base, titrating protons, and vomiting is sometimes present as well. Metabolic alkalosis contributes to perpetuating the hypercalcemia as it stimulates distal tubular reabsorption of calcium. Hypercalcemia worsens GFR by causing renal vasoconstriction and stimulating the Ca-SR, leading to natriuresis and diuresis and volume depletion. Suppression of PTH leads to reduced bone turnover, which suppressed the ability of bone to take up calcium.
