Describe the role of the kidneys in the maintenance of acid/base balance
Acids produced by the body can be:
- Volatile (CO2)
- Body produces and eliminates ~13-20mol.day-1
- Removed by the lungs
- Fixed (everything else)
- Include lactate, sulphate, phosphate, and ketones
- Body produces and eliminates 10mmol.kg-1.day-1
- Eliminated by the kidney
Mechanisms for elimination of acid include:
- Reabsorption of HCO3-
This is equivalent to the removal of the same amount of H+.
- As there is usually a net production of acid, under normal circumstances all filtered HCO3- is reabsorbed
- Note that removal of an acid load is associated with greater HCO3- generation and reabsorption, not increased H+ secretion
- Bound to filtered buffers
- As ammonium
- Reabsorption of HCO3-
- The rate and extent of these reactions is dependent on ECF pH and ion concentrations, which gives the kidney control over ion concentrations
- Urinary pH can fall as low as ~4.4, before the active transport of H+ is inhibited
Bicarbonate and the Kidney
Buffer systems minimise changes in pH until the kidney can eliminate excess hydrogen.
Bicarbonate is the predominant ECF buffer system (see Acid-Base physiology for more on buffers). By adjusting the level of HCO3- the kidney is able to adjust pH, as per the Henderson-Hasselbalch equation:
- = 6.1, the pKa of HCO3-
- = 24, the normal [HCO3-] in mmol.L-1
- = 1.2, the normal [CO2] in mmol.L-1
- Freely filtered
4320 mmol.day-1 of HCO3- is filtered (24mmol.L-1 x 180 L.day-1, normal range is 4-5mol.day-1)
- Reabsorbed in the PCT (90%), thick ascending limb, DCT, and CT
Adjusting rate of absorption allows correction of an acidosis or alkalosis. All HCO3- reabsorption is equivalent to a loss of H+.
Reabsorption of Bicarbonate
Reabsorption of bicarbonate involves several steps:
- H+ is secreted into the lumen in one of three ways:
- Secreted H+ combines with filtered HCO3- to form CO2 and H2O
- CO2 and H2O diffuse into the tubular cell
- CO2 and H2O are converted back into HCO3- and H+ in the tubular cell
- HCO3- is reabsorbed into the capillary via the HCO3--Cl- antiporter, and the H+ ion is available to be secreted into the tubule (in exchange for K+ in the collecting ducts and Na+ in the proximal tubule)
This complicated process allows HCO3- to be moved from the tubule to the tubular cell and then to the capillary. There is no elimination of H+ by this method - the purpose of H+ secretion is to facilitate the reabsorption of HCO3- into the tubular cell.
Glutamine provides a mechanism for elimination of a large number of H+ ions:
- This is important in:
- Elimination of excess metabolic acid
- Renal compensation for acidosis
- This occurs via:
- Filtered glutamine is absorbed into proximal tubular cells and metabolised to NH4+ (ammonium) and HCO3-
- HCO3- diffuses into blood, and the NH4+ is secreted into the tubule via the NH4+-Na+ antiporter and eliminated in urine
- The reaction has a pKa of 9.2 meaning:
- Ammonia cannot act as an effective urinary buffer
- Ammonia is not a titratable acid, as it will not release H+ ions as urinary pH increases
This means filtered ammonia does not contribute to the lower limit of urinary pH (4.4), which is why it is so important in the renal correction of severe metabolic acidosis.
Bound to Filtered Buffers
Secreted H+ may also combine with a filtered buffer (e.g. PO43-). These H+ ions are not reabsorbed. About 36mmol of H+ is eliminated with filtered PO43- each day, with each PO43- binding two H+ ions.
- CICM Sep/Nov 2014
- ANZCA Feb/April 2012
- Kam P, Power I. Principles of Physiology for the Anaesthetist. 3rd Ed. Hodder Education. 2012.
- Acid-Base Online Tutorial, University of Conneticut
- Brandis, K. Renal Regulation of Acid-Base Balance, in 'Acid-base pHysiology'.