The formation of kidney stones is complex, with influence from multiple factors including genetic and environment. Stones can be costly. Not only can they be painful, if left unaddressed, more serious conditions can arise such as obstruction and permanent damage to the kidneys. In this blog we focus on electrolyte imbalances and kidney stone formation.
As discussed in a previous blog, there are five major types of kidney stones: calcium oxalate, calcium phosphate, uric acid, struvite (magnesium ammonium phosphate), and cystine. Calcium oxalate is by far the most common, comprising approximately 75% of kidney stones. Therefore, the first step in evaluating a kidney stone patient is identifying the type of kidney stone they are forming. This can be done by stone analysis and by obtaining a 24-hour urine analysis for various metabolites and electrolytes.
In this series, we’re focusing on the integrative approach to preventing kidney stone formation.
Conventional approaches to kidney stones typically focus on medications, surgical removal, and using ultrasonic waves to break up a stone. It rarely addresses the root cause including risk factors to prevent stone formation.
We covered dietary approach and microbiome and gut health in previous blogs. In this blog, we will discuss the impact of electrolyte imbalances on kidney stone formation and prevention.
Calcium imbalances
Since most kidney stones are composed of calcium oxalate, oftentimes patients ask if restriction of dietary calcium is necessary. Dietary calcium intake has many benefits including maintaining adequate bone health and decreasing oxalate absorption from the gut. In fact, evidence suggests that restricting calcium intake leads to increased oxalate absorption, in turn increasing the risk for kidney stone formation. Furthermore, there is a significant link between kidney stones and metabolic bone diseases such as osteoporosis, although it is not yet clear if this link is related to calcium imbalances or other causes.
It’s the concentration of calcium in the urine that is important to track. The higher the urinary concentration of calcium, the higher the risk of oxalate binding to calcium (or other minerals) and forming kidney stones.
There are several factors that lead to increased calcium concentrations in the urine, including increased calcium excretion by the kidneys and decreased water intake. Factors increasing urinary calcium excretion include high sodium (salt) intake, genetic factors, certain medications, and certain medical conditions such as disorders of the parathyroid gland.
This explains why restricting sodium intake and increasing water intake are useful for decreasing the risk of stone formation. It is generally recommended that kidney stone formers drink at least 2 liters of filtered free water every day (some require more, especially if they are overweight/obese or losing fluid from physical activity or sweating). In general, we recommend that patients maintain a balanced diet providing 1000 mg per day of calcium. When taken with meals, calcium supplements bind oxalate in the food and prevent it from getting absorbed; however, calcium supplementation is controversial and should be monitored closely by a provider.
Oxalate imbalances
In a previous blog, we mentioned that oxalates play a role in the formation of kidney stones with 75% of kidney stones a result of calcium oxalate formation. As we discussed above, there is a significant connection between calcium consumption and the level of absorbed oxalate. Low oxalate diets have been proposed as a way to minimize stone formation. However, these are incredibly challenging to maintain. Oxalate restriction is challenging because oxalates are present in a large number of healthy foods, risking nutrient deficiencies. Furthermore, the gut microbiome plays an important role in the absorption of oxalate.
Additionally, there are a few genetic variations in the oxalate gatekeepers in the gut and red blood cell transporters that impact/increase oxalates in the urine. Problems with fat digestion and absorption as seen in small bowel disease, gastric bypass, or pancreatic insufficiency can lead to increased oxalate absorption in the colon. That is why it is important to address gut integrity with a comprehensive gut restoration protocol in patients with kidney stones.
Citrate imbalances
Urinary citrate may be the most significant factor in formation of calcium oxalate stones. Citrate helps increase urinary pH (making it more alkaline or basic), preventing the binding of calcium and oxalate. It also binds calcium in the urine, further preventing kidney stone formation. The concentration of citrate in the urine is dependent on blood acidity, the higher the dietary acid load, the higher the risk of developing kidney stones. This phenomenon may explain why diets high in animal protein have been associated with the development of kidney stones (more about that in another blog here).
In addition, potassium depletion is often associated with pH changes that lead to decreased urinary citrate levels. Potassium depletion can also increase calcium excretion in the urine. Therefore, it is important to correct any potassium depletion in patients with kidney stones. This is why most citrate supplements that are used for kidney stone prevention are usually in the form of potassium citrate.
Magnesium imbalances
Magnesium plays an important role in the prevention of kidney stones. Although the way magnesium decreases the risk of kidney stones is not completely clear, evidence suggests that magnesium lowers oxalate absorption in the gut. Magnesium also increases the level of citrate in the urine which, as we saw above, decreases the risk of kidney stones.
Finally, magnesium can bind oxalate in the urine making it less available for binding with calcium and forming kidney stones. Magnesium oxalate compounds are 100 times more soluble than calcium oxalate. In fact, supplementing magnesium was found to be effective in preventing kidney stones even with patients with normal magnesium.
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Uric acid imbalances
Uric acid stones are common in patients with metabolic syndrome and type 2 Diabetes. Elevated uric acid levels in the urine can lead not only to uric acid stones but also to calcium oxalate stone formation. In many instances, calcium oxalate stones have a center (nidus) composed of uric acid. Uric acid is the end product of the breakdown of purine, a product of digestion of nucleic acid in food (meat, poultry and fish) or tissue breakdown. Therefore, limiting the intake of animal protein may be a useful therapeutic approach for prevention of kidney stone formation.
Uric acid forms crystals in highly acidic urine. This is another contributing factor linking a high (animal) protein diet to increased acid load and increased uric crystal stone formation, compounding the impact of uric acid release
The Bottom Line
Many factors impact kidney stone formation, including electrolyte imbalances. Stone formation is usually not caused by a single electrolyte but rather it is likely a combination of factors impacting electrolyte balance, including nutrient depletion and dehydration. Diets low in plant-based foods and high animal protein tend to increase risk of stone formation due to an interplay of factors. Risk of kidney stone formation should be evaluated by weighing the impact of poor dietary choices combined with environmental factors, genetics, gut integrity and microbiome balance.
This is the foundation of our integrative approach to managing and prevention of kidney stones. Practitioners working with individuals to prevent kidney stone formation should formulate a personalized approach that modifies all relevant components in their comprehensive approach for best outcomes.
