Metabolic acidosis is a common complication of CKD stages 4-5 resulting from impaired renal acid excretion (reduced ammonium generation by damaged tubules) and decreased bicarbonate regeneration. Normal serum bicarbonate is 22-28 mEq/L; CKD-related metabolic acidosis typically manifests as a non-anion gap metabolic acidosis with bicarbonate 16-22 mEq/L. Chronic metabolic acidosis has significant clinical consequences: accelerated CKD progression (acidosis promotes tubulointerstitial inflammation and fibrosis), muscle catabolism (acidosis stimulates branched-chain amino acid oxidation and ubiquitin-proteasome proteolysis), bone demineralization (chronic buffering of acid by bone calcium carbonate and phosphate stores), worsened insulin resistance, and increased cardiovascular mortality. Oral bicarbonate supplementation (sodium bicarbonate 650 mg tablets = 7.7 mEq/tablet; or sodium citrate/citric acid solution) is indicated when serum bicarbonate falls below 22 mEq/L. The UBI trial and meta-analyses demonstrate that maintaining bicarbonate ≥22 mEq/L slows CKD progression by 50-60%. Dosing typically starts at 650 mg (1 tablet) TID and is titrated to maintain serum bicarbonate 22-28 mEq/L. The NP must also consider the sodium load from bicarbonate supplementation (each 650 mg tablet contains 7.7 mEq sodium) in patients with hypertension, heart failure, or fluid...