How the kidney handles the potassium and sodium of a high potassium foods diet determines many of its effects on health. The diet can lower blood pressure and can lower the chance of cardiovascular disease. But a small minority of people need special precautions, and some should avoid the diet altogether. The study (1) to be discussed today reviewed how the kidney balances sodium and potassium. It presented the dangers of these types of diets when combined with certain medications. The main concerns are with some of the diuretics that lower potassium blood levels, and with potassium supplements that are often prescribed at the same time.
The high potassium foods diet has a high ratio of potassium to sodium and produces alkaline urine. There are multiple popular diets today that are similar to the high potassium foods diet. These diets also have a higher potassium to sodium ratio than the typical American or Western diet. All of these diets have had medical studies showing that they are associated with lower amounts of cardiovascular disease. These include the DASH diet, the Mediterranean diet, the vegan and vegetarian diets, and some versions of the Paleo diet.
However these diets, like the high potassium foods diet, may present problems to a small percentage of people. Usually these people have pre-existing conditions which they may or may not be aware of. An example is the many hypertensives who are not be aware of their hypertension.
Only a small percentage of those who are unaware of their hypertension will have problems with the high potassium foods diet. But those who have been diagnosed with hypertension will often be on a diuretic and potassium supplements.
These medications often work well for those on a typical acidic, high sodium, Western diet. But when on a low sodium, alkaline diet these medications may result in a dangerous elevation of blood potassium. A diet that is good for prevention in a healthy person on no medications may present dangers when used by someone not so healthy who is on medications.
The previous posts discussed the main ways in which the kidney balances sodium and potassium. A highly studied way that the kidney provides balance is through the ENaC and ROMK. However, when the exchange ratio of sodium and potassium is greater than 0.67, the kidney uses other mechanisms. These other mechanisms involve BK channels that can eliminate potassium independently of sodium.
BK Channels
BK channels are found in many cells. They are in smooth muscle cells throughout the body. One place smooth muscle cells are found is in blood vessels, including the blood vessels of the kidneys. BK is also present in other cells in the kidney – the podocytes and mesangial cells of the glomerulus of the nephron. BK channels are also found in the cortical collecting duct (CCD) cells and the connecting tubule (CNT) cells – in the intercalated cells (IC) and the principal cells (PC). The BK channels in these cells are the major source of potassium excretion when on a high potassium foods diet.
BK channels are made of two subunits – BKa and one of four b subtypes- b1, b2, b3, or b4. The BKa/b4 channels are very important when on a high potassium low-sodium alkaline diet. They allow excretion of potassium beyond the 0.67 ratio.
Regulation Of BK Channels In The Kidney
Regulation of BK channels in the kidney is done by 2 kinase systems – SGK and WNK. SGK is Serum and Glucocorticoid Kinase. It is induced by aldosterone and regulates the ENaC for sodium reabsorption. The other kinase system is WNK, which is the With No lysine Kinase system. In addition to affecting BK channels, it regulates Sodium-Potassium-2-Chloride-Cotransporter (NKCC) and Sodium-Chloride Symporter (NCC). These two proteins help balance sodium and potassium by the kidney.
WNK can have a common mutation that leads to increased sodium and chloride reabsorption. There is also potassium retention with this mutation, most probably because the WNK mutation increases the degradation of BK channels. The result is hypertension (familial hyperkalemic hypertension) and excessive potassium in the blood.
Aldosterone Effect On BK Channels
Regulation of BK channels in the kidney is also done by aldosterone. Aldosterone is secreted by the adrenal gland when blood potassium is high, or when sodium is low in a particular part of the kidney. When aldosterone is high because potassium is high and sodium normal, the BK channels increase and potassium is excreted more. When aldosterone is high because potassium is normal and sodium low, WNK increases. This spurs an increase in NCC at the cell surface so that sodium is reabsorbed more.
Aldosterone also increases ENaC and sodium-potassium-ATPase (sodium pump). It increases the total cellular BKa, but not the surface BKa unless the urine is alkaline. In alkaline urine there are increases of b4 which moves BKa to the cell surface and which combines with BKa at the cell surface to form a functioning channel. This results in greater potassium excretion.
BK Lack And Hypertension
Lack of BKa/b1 leads to hypertension and cardiac hypertrophy if a high potassium diet is taken for 7 to 10 days. BKa associates with b1 in all smooth muscle. This increases the sensitivity of BKa to calcium to provide a feedback regulation of muscle contraction. Without b1, the smooth muscle cells have more resting tone, resulting in higher blood pressure.
On a high potassium diet, with this b1 lack, there is fluid accumulation and an increase in aldosterone from less excretion of potassium. This leads to a buildup of potassium in the blood. But even when the fluid accumulation is eliminated, there is hypertension because of an increased vascular tone. The effect on smooth muscle remains and the blood vessels stay in a less relaxed condition.
There is a similar effect from a high potassium diet when BKa/b4 is absent. But the hypertension is milder than it is with a lack of BKa/b1.
All of these BK channel deficiencies result in very mild elevations of blood pressure. The authors of the article feel that the hypertension that results from this deficiency would only become obvious in people on a high potassium diet. On a low potassium diet the less efficient exchange of sodium for potassium by ENaC can partially compensate for the lack of these BK channels.
Potassium Excretion With Diuretics
On the normal Western diet, ENaC reabsorbs sodium in exchange for potassium via ROMK in principal cells (PC). If on a high potassium foods diet with low-sodium, high potassium and alkaline food intake, the intercalated cells (IC) recycle sodium and chloride to excrete bicarbonate and potassium. This results in a higher urine flow than the urine flow from a normal Western diet.
This natural diuretic effect of the high potassium foods diet is mimicked by some of the blood pressure lowering diuretics, such as furosemide (Lasix) and hydrochlorothiazide (HCTZ). For those on a Western diet there is not the extra excretion of potassium from the diet that occurs on the high potassium foods diet, and thus they need supplementation of potassium. However those on the high potassium foods diet will be getting the extra potassium in their diet, and would be more likely to develop a high blood potassium level if put on a potassium supplement.
Two Genetic Disorders That Mimic Diuretics
There are two genetic disorders that result in low blood pressure and salt (sodium) wasting because of a lack of sodium reabsorption by the kidney – Bartter Syndrome and Gitelman Syndrome. Additionally, in these disorders potassium is excreted excessively to a variable degree.
Each syndrome has a defect at the site of action of a diuretic. Bartter Syndrome's defect is located at the site that furosemide (Lasix) acts. Gitelman Syndrome's defect is at the site that hydrochlorothiazide (HCTZ) acts. Thus they mimic these two diuretics.
So it can be seen that if there is malfunction in the balance of potassium and sodium from any of these mechanisms in the kidney, the result will affect blood pressure. For some, a diet that is normally highly preventive for hypertension can lead to problems. Someone with a disorder leading to excessive potassium in the blood, or someone who has been put on a diuretic and potassium supplement may develop serious problems with the low sodium high potassium alkaline diet.
The article (1) focused on disorders of the BK channels that could be made worse by a low sodium, high potassium, alkaline diet. These are relatively rare. Many of these unusual disorders are evident at an early age. But a few may not affect someone until they are on a particular type of diet.
Although unusual, these disorders include some that will only become evident when a person goes on a low sodium, high potassium, alkaline diet and is also on a diuretic with potassium supplement. Anyone who is on a diuretic and potassium supplement needs careful monitoring on such a diet. But for the large majority of people, a low sodium, high potassium, alkaline diet will improve blood pressure and improve health.
For a population of people to switch from a typical Western diet to a low sodium high potassium alkaline diet, the result will be that a large percentage improve their blood pressure and health. But a few will develop problems on the diet, and will have to have careful monitoring of their diet and medications.
The kidneys are very sensitive to the potassium and sodium intake in the diet. And through the mechanisms discussed, they seek to balance potassium and sodium so that cells throughout the body will have the correct electrochemical gradient to function properly. If any of these mechanisms are disturbed, special care may be needed to manage blood potassium levels.
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1. Interacting influence of diuretics and diet on BK channel-regulated K homeostasis. Wen D, Cornelius RJ, Sansom SC. Curr Opin Pharmacol. 2014 Apr;15:28-32. doi: 10.1016/j.coph.2013.11.001. Epub 2013 Dec 11.
