Renal regulation of Potassium
ECF K+ conc. is about 4.2 mEq/L and is very tightly regulated.
In a normal 70 kg adult, this ECF value is about 59 mEq in total.
Most of K+ is found in the ICF, which therefore acts as a reservoir for K+ when level are low in the ECF
(hypokalemia) or as a recipient if K+ are high in the ECF (hyperkalemia).
The following factors control movement of K+ between ICF and ECF, resulting in either hyper- or
hypokalemia when in excess:
1) Insulin causes K+ ions to move into the cells. Therefore, in a person with diabetes, low insulin
leads to hyperkalemia.
2) Aldosterone increases Na+ uptake while decreasing K+ uptake. Therefore, hyperkalemia results
in Addison’s disease (low aldosterone production) and Cushing’s syndrome (high aldosterone
production) results in hypokalemia.
3) B-adrenergic receptors like epinephrine also cause K+ to move into the ICF. Therefore, when
patients of hypertension are given beta blockers, the receptors don’t work, and they’re at risk
for hyperkalemia.
4) H+ reduce the activity of Na+/K+ ATPase pumps, which in turn reduces the movement of K+
from ECF to ICF. Therefore, acidosis results in hyperkalemia while alkalosis results in
hypokalemia.
5) Cell lysis results in hyperkalemia.
6) Strenuous exercise results in hyperkalemia.
7) An increase in osmolarity of the ECF results in water moving into the ECF. This causes the ICF K+
concentration to rise, causing it to diffuse out of the cells into the ECF, leading to hyperkalemia.
Renal excretion of potassium depends on 3 things; filtration rate, reabsorption rate, and secretion rate
of K+ in the kidneys.
750 mEq or 180 L of K+ is filtered everyday. 65% of this is reabsorbed in the proximal tubules, while 25-
30% is reabsorbed in the thick ascending portion of the loop of Henle. About 92 mEq (12%) is excreted
everyday.
Since the above values don’t vary too much on a daily basis, renal K+ excretion is mainly controlled by
the level of secretion of K+ by the late distal and collecting tubules. If K+ in the body is in excess,
secretion increases, and the opposite happens when ECF K+ levels are low.
This secretion occurs as follows. K+ in the renal interstitial fluid moves into the principal cells via the
Na+/K+ ATPase pump. The K+ concentration increases in the principal cells, which then allow it to diffuse
into the renal tubules via the luminal membrane with the help of special potassium channels called
ROMK and BK channels.
Type A intercalated cells increase K+ reabsorption while type B intercalated cells increase K+ secretion.
ECF K+ conc. is about 4.2 mEq/L and is very tightly regulated.
In a normal 70 kg adult, this ECF value is about 59 mEq in total.
Most of K+ is found in the ICF, which therefore acts as a reservoir for K+ when level are low in the ECF
(hypokalemia) or as a recipient if K+ are high in the ECF (hyperkalemia).
The following factors control movement of K+ between ICF and ECF, resulting in either hyper- or
hypokalemia when in excess:
1) Insulin causes K+ ions to move into the cells. Therefore, in a person with diabetes, low insulin
leads to hyperkalemia.
2) Aldosterone increases Na+ uptake while decreasing K+ uptake. Therefore, hyperkalemia results
in Addison’s disease (low aldosterone production) and Cushing’s syndrome (high aldosterone
production) results in hypokalemia.
3) B-adrenergic receptors like epinephrine also cause K+ to move into the ICF. Therefore, when
patients of hypertension are given beta blockers, the receptors don’t work, and they’re at risk
for hyperkalemia.
4) H+ reduce the activity of Na+/K+ ATPase pumps, which in turn reduces the movement of K+
from ECF to ICF. Therefore, acidosis results in hyperkalemia while alkalosis results in
hypokalemia.
5) Cell lysis results in hyperkalemia.
6) Strenuous exercise results in hyperkalemia.
7) An increase in osmolarity of the ECF results in water moving into the ECF. This causes the ICF K+
concentration to rise, causing it to diffuse out of the cells into the ECF, leading to hyperkalemia.
Renal excretion of potassium depends on 3 things; filtration rate, reabsorption rate, and secretion rate
of K+ in the kidneys.
750 mEq or 180 L of K+ is filtered everyday. 65% of this is reabsorbed in the proximal tubules, while 25-
30% is reabsorbed in the thick ascending portion of the loop of Henle. About 92 mEq (12%) is excreted
everyday.
Since the above values don’t vary too much on a daily basis, renal K+ excretion is mainly controlled by
the level of secretion of K+ by the late distal and collecting tubules. If K+ in the body is in excess,
secretion increases, and the opposite happens when ECF K+ levels are low.
This secretion occurs as follows. K+ in the renal interstitial fluid moves into the principal cells via the
Na+/K+ ATPase pump. The K+ concentration increases in the principal cells, which then allow it to diffuse
into the renal tubules via the luminal membrane with the help of special potassium channels called
ROMK and BK channels.
Type A intercalated cells increase K+ reabsorption while type B intercalated cells increase K+ secretion.
