When a person has a blood pH of less than 7.35 (acidosis), the urine pH almost always falls below 5.5. The nephron, however, cannot produce a urine pH that is significantly less than 4.5. In order for more H+ to be excreted, the acid must be buffered. (Actually, even in normal urine, most of the H+ excreted is in a buffered form.) Bicarbonate cannot serve this buffering function because it is normally completely reabsorbed. Instead, the buffering action of phosphates (mainly HPO42-) and ammonia (NH3) provide the means for excreting most of the H+ in the urine. Phosphate enters the urine by filtration. Ammonia (whose presence is strongly evident in a diaper pail or kitty litter box) is produced in the tubule cells by deamination of amino acids. These molecules buffer H+ as described in these equations:
Test Yourself Before You Continue
1. Describe the effects of aldosterone on the renal nephrons and explain how aldosterone secretion is regulated.
4. Explain how the kidneys reabsorb filtered bicarbonate and how this process is affected by acidosis and alkalosis.
5. Suppose a person with diabetes mellitus had an arterial pH of 7.30, an abnormally low arterial PCOj, and an abnormally low bicarbonate concentration. What type of acid-base disturbance would this be? What might have caused the imbalances?
Was this article helpful?