In our recent publications, concerned with various phases of neutrality regulation, certain alternative concepts have been proposed. In the present abbreviated review, we are submitting a few new thoughts and some additional data from the literature which we feel tend to support our alternative viewpoint. Figs. 1 and 2, which are included, should facilitate visualization of the mechanisms involved. Fig. 1 envisions the intracellular disposal of strong metabolic acid transfer to HCO 3 −. The HCO 3 −, so protons by buffer binding followed by formed, decomposes into CO 2+H 2O− thus the metabolic protons are retained in the body water. Acidification in the proximal tubule (Fig. 2) is a consequence of reabsorption from the glomerular filtrate of Na +, K +, Cl − and HCO 3 −; H 2CO 3 is not reabsorbed—it contributes to the acidification in this segment. Synthesis of H 2CO 3 within the cell serves to buffer the reabsorbed bicarbonate. In the distal segment (Fig. 2) acidification is accomplished by reabsorption of Na + accompanied by OH − from the water equilibrium k H 2O ↔ H + × OH −; H + from the same equilibrium balances the rejected A −; diffusion of NH 3 partially neutralizes the HA so formed. Intracellular neutrality again, is preserved by the synthesis of H 2CO 3. Potassium, reabsorbed in the proximal segment is secreted in the distal segment as potassium alkali and neutralizes a fraction of the liberated acid. Uremic patients and normal controls on an ordinary acid-ash diet give similar values for net proton excretion. With acid-loading, kalinuria is increased in uremia; partial neutralization of liberated acid and a reduction in the excretion of net proton is observed. The acidosis is due to fixed anion retention; replacement of plasma HCO 3 by SO 4 −+H 2PO 4 −. In renal tubular acidosis, low values for urinary acidity may be a consequence of excessive kalinuria. The acidosis is due to abnormal proximal tubular preference for reabsorption of Cl −. Diabetic acidosis and also lactate acidosis are other examples of fixed anion acidosis.