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Kidney stones, medically known as nephrolithiasis, are hard deposits in the kidneys. They are made up of various substances, such as calcium, oxalate, uric acid, and cystine. Kidney stones can vary, ranging from tiny particles to larger, more solid formations.
The formation of kidney stones typically occurs when there is an imbalance in the concentration of substances in the urine. When the urine contains higher levels of these substances, they can crystallise and clump together, forming stones. Several factors contribute to the development of kidney stones, including genetics, diet, dehydration, certain medical conditions, and certain medications.
Kidney stones can cause various symptoms depending on their size and location within the urinary system. Small stones may pass through the urinary tract without causing noticeable symptoms. However, larger stones can become lodged in the ureters (the tubes connecting the kidneys to the bladder), causing intense pain and discomfort. Common symptoms of kidney stones include:
If you suspect you have kidney stones, it is crucial to seek medical attention. A healthcare professional can perform diagnostic tests, such as urine analysis, blood tests, and imaging studies like CT scans or ultrasound, to confirm the presence of stones and determine their size and location.
Crohn’s disease is an inflammatory bowel disease (IBD) affecting any part of the gastrointestinal tract, from the mouth to the anus. The most commonly affected areas are the end of the small intestine (the ileum) and the colon. This inflammation can lead to various complications, including kidney stones.
Kidney stones in individuals with Crohn’s disease typically occur due to problems with absorption in the intestines. Here’s how it happens:
Malabsorption of fat: Inflammation and damage to the intestines in Crohn’s disease can lead to poor absorption of dietary fat. This fat then binds to calcium in the intestines to form a compound that can’t be absorbed.
Increase in oxalate: When calcium is bound up with fat, it’s unavailable to bind to oxalate, another substance commonly found in food. This leaves more oxalate free to be absorbed into the bloodstream. Oxalate is normally excreted in the urine, but if there’s too much, it can combine with calcium in the urine to form calcium oxalate stones, the most common type of kidney stone.
Dehydration: Crohn’s disease can cause diarrhea, leading to dehydration. Dehydration, in turn, can concentrate the urine, making it easier for stones to form. Also, a decrease in urine volume can cause substances like oxalate and calcium to become concentrated, increasing the risk of stone formation.
Medications: Some medications used to treat Crohn’s disease can also increase the risk of kidney stones. For example, corticosteroids can increase calcium levels in the urine, making stone formation more likely.
So, in short, people with Crohn’s disease are more likely to get kidney stones due to a combination of malabsorption leading to an increase in urinary oxalate, possible dehydration from frequent diarrhea, and the use of certain medications.
Diuretics, also known as “water pills,” help the kidneys remove excess water and sodium from the body, which is released through urine. There are several types of diuretics, including thiazide diuretics, loop diuretics, and potassium-sparing diuretics, each with its mechanism of action and potential side effects.
Thiazide diuretics are often used in the management of hypertension and edema. Interestingly, they are generally associated with a decreased risk of kidney stones. They function by decreasing the amount of calcium excreted in the urine, reducing the likelihood of calcium stone formation. This protective effect makes thiazide diuretics a standard treatment for recurrent calcium kidney stones.
However, loop diuretics, such as furosemide (Lasix), could potentially increase the risk of kidney stones. They work in a part of the kidney called the Loop of Henle, increasing the amount of calcium, sodium, and potassium excreted in the urine. The increased urinary calcium can raise the risk of calcium kidney stone formation. Additionally, by increasing urine production, any diuretic can lead to dehydration if fluid intake is not adequately increased. Dehydration can concentrate minerals in the urine, increasing the risk of stone formation.
Potassium-sparing diuretics can increase urine pH, making the urine more alkaline. This change in pH can increase the risk of developing certain types of kidney stones, such as calcium phosphate stones.
It’s important to note that the risk of kidney stone formation due to diuretics is generally lower than the risk associated with other factors like diet, hydration, and genetic predisposition.
Fizzy drinks, also known as carbonated beverages or sodas, can contribute to the formation of kidney stones in a few ways:
High Sugar Content: Many carbonated beverages, particularly non-diet sodas, are high in sugar. High sugar intake can increase the kidney’s excretion of calcium and uric acid, two primary components of some kidney stones. High sugar intake can also lead to obesity and diabetes, both risk factors for kidney stones.
Phosphoric Acid: Some sodas, especially colas, contain phosphoric acid. This can increase the acidity of the urine, which can promote the formation of kidney stones, especially uric acid stones.
Dehydration: Carbonated beverages, particularly those containing caffeine, can act as diuretics, increasing urine production. If not accompanied by increased water intake, this could lead to dehydration. Dehydration concentrates the substances in urine that can form stones, increasing the risk of stone formation.
Sodium: Some fizzy drinks can be high in sodium. A high sodium intake can increase calcium excretion in the urine, increasing the risk of calcium stones.
Gout is a type of inflammatory arthritis that develops in people with high uric acid levels in the blood. The acid can form needle-like crystals in a joint and cause sudden, severe episodes of pain, tenderness, redness, warmth, and swelling.
Interestingly, uric acid is also a common component of kidney stones, which is why having gout can increase the risk of kidney stones. Here’s how this happens:
Hyperuricemia: This condition is characterised by high levels of uric acid in the blood, a common feature in people with gout. Excess uric acid can form crystal deposits in the joints, causing gout attacks. This same uric acid can also be excreted in the urine, which can crystallise to form uric acid kidney stones.
Urine pH: Uric acid stones are more likely to form in acidic urine. People with gout often have more acidic urine, partly due to the body’s attempts to excrete the excess uric acid. This can create an environment more conducive to the formation of uric acid stones.
Dehydration: Gout attacks can often cause a person to drink less fluid, leading to dehydration. Dehydration can concentrate the urine, allowing stones to form more easily.
Medications: Some medications used to treat gout, such as probenecid, can increase uric acid in the urine and potentially increase the risk of uric acid stones.
High Oxalate Intake: Oxalate is found in many foods, including fruits and vegetables, nuts and seeds, grains, legumes, chocolate, and tea. Some examples of high-oxalate foods include spinach, rhubarb, nuts, and wheat bran. When you eat foods high in oxalate, the extra oxalate can combine with calcium in the urine to form calcium oxalate stones, the most common type of kidney stone.
High Purine Intake: Purines are natural substances found in some foods, including organ meats like liver, certain types of fish like sardines and anchovies, and some game meats. When purines are broken down in the body, they produce uric acid. A high-purine diet, therefore, leads to increased production and excretion of uric acid, which can lead to the formation of uric acid stones.
High meat diet
A diet high in animal proteins, such as red meat, poultry, eggs, and seafood, can increase the risk of kidney stones in several ways:
Increased Uric Acid: Metabolism of animal proteins produces uric acid. Therefore, a high intake of such proteins leads to increased production and excretion of uric acid, which could lead to the formation of uric acid stones.
Increased Calcium Excretion: Animal proteins contain sulphur amino acids that can cause increased acidity in the urine. The body may use calcium from the bones to counterbalance this acidity, resulting in higher calcium levels in the urine. Higher urinary calcium can increase the risk of calcium oxalate or calcium phosphate stones.
Reduced Citrate Excretion: Citrate in the urine can help prevent the formation of kidney stones by binding to calcium and preventing the growth of crystals. However, the increased acid load from a high meat diet can lower citrate excretion, reducing this protective effect and potentially increasing stone risk.
Increased Oxalate Absorption: Diets high in animal protein can also lead to changes in the gut that facilitate the absorption of oxalate, a compound found in many foods and a primary component of the most common type of kidney stone (calcium oxalate stones).
For these reasons, a diet high in animal protein can increase the risk of kidney stones, particularly uric acid and calcium oxalate stones. However, this does not mean that all meats should be avoided. Instead, maintaining a balanced diet with a variety of proteins (including plant-based proteins), staying well-hydrated, and limiting sodium intake can help reduce the risk of kidney stones.
Hyperparathyroidism is a condition characterised by the overactivity of the parathyroid glands, which are four tiny glands located in the neck around the thyroid. These glands produce parathyroid hormone (PTH), which plays a crucial role in regulating calcium levels in the body.
In hyperparathyroidism, excessive amounts of PTH are produced, leading to higher calcium levels in the blood, a condition known as hypercalcemia. Here’s how this can contribute to kidney stone formation:
Increased Calcium in Urine: The kidneys maintain the body’s calcium balance. When blood calcium levels are high, the kidneys respond by excreting more calcium in the urine. Higher calcium levels in the urine can increase the risk of calcium stone formation, particularly calcium oxalate or calcium phosphate stones.
Bone Resorption: PTH promotes the release of calcium from the bones into the bloodstream, a process known as bone resorption. In hyperparathyroidism, excessive PTH levels can increase bone resorption, further contributing to hypercalcemia and potentially leading to osteoporosis.
Decreased Citrate in Urine: PTH can also decrease the kidneys’ citrate reabsorption. This substance typically helps to inhibit stone formation by binding to calcium in the urine and preventing the growth of crystals.
Dehydration can significantly increase the risk of kidney stones. This occurs through a few mechanisms:
Increased Urine Concentration: When dehydrated, your body needs to conserve water. It does this by decreasing urine production, leading to more concentrated urine. This concentrated urine has higher levels of substances that can form stones, such as calcium and oxalate, increasing the chance that they’ll form crystals.
Reduced Urine Volume: With dehydration, the total urine volume is decreased. This means there’s less fluid available to dissolve substances that can form stones. As a result, these substances are more likely to crystallise and form stones.
Acidic Urine: Dehydration can also make the urine more acidic, increasing the likelihood of certain types of stones forming, such as uric acid stones.
Sedentary lifestyle
A sedentary lifestyle, characterised by prolonged periods of inactivity or sitting, can contribute to the formation of kidney stones in several ways:
Obesity: Lack of physical activity can lead to weight gain and obesity, known risk factors for kidney stones. Obesity may alter the environment in the kidneys in a way that promotes stone formation.
Calcium Metabolism: Regular exercise helps the body regulate calcium balance. Inactivity may disrupt this balance, increasing calcium excretion in the urine, which could increase the risk of calcium kidney stones.
Chronic Dehydration: Sedentary individuals may not feel the need to hydrate as frequently as those who are more active. Chronic mild dehydration can lead to more concentrated urine, which increases the likelihood of stone formation.
Bone Health: Weight-bearing exercise helps maintain bone health. Inactivity can lead to decreased bone density, and the body may compensate by increasing calcium resorption from the bones, potentially leading to increased urinary calcium and an increased risk of calcium stones.
Digestive Health: Physical activity helps maintain a healthy digestive system. Inactivity can lead to constipation, altering the gut environment and potentially affecting the balance of stone-promoting and stone-inhibiting substances in the urine.
Diuretics: Certain types of diuretics, such as loop diuretics, can increase calcium in the urine, which can lead to calcium stones.
Protease Inhibitors: These are a type of medication used to treat HIV. They can increase the risk of kidney stones.
Topiramate (Topamax) and Zonisamide (Zonegran): These medications, used for treating epilepsy and migraine, can increase the risk of kidney stones by altering the properties of urine.
Allopurinol: Although this medication is often used to treat gout and kidney stones, it can paradoxically cause kidney stones in rare cases.
Indinavir: This is an antiretroviral medication used to treat HIV. It can cause kidney stones in some cases.
Triamterene: This medication is a diuretic (water pill) that can cause a specific type of kidney stone called triamterene stones.
Certain Antibiotics: Some antibiotics, such as ciprofloxacin and sulfa antibiotics, have been associated with an increased risk of certain types of kidney stones.
Chronic urinary tract infections (UTIs) can contribute to forming a specific type of kidney stone known as struvite stones, also called infection stones or magnesium ammonium phosphate stones. Here’s how:
Bacterial Action: Some bacteria, particularly Proteus species, but also others like Klebsiella and Pseudomonas, can produce an enzyme called urease. Urease breaks down the urea found in urine into ammonia and carbon dioxide. This process increases the pH of the urine, making it more alkaline.
Struvite Stone Formation: In alkaline urine, magnesium, ammonia, and phosphate (all components of urine) can combine to form the crystal structures of struvite stones. These stones can grow large, sometimes filling the entire renal collecting system, known as staghorn calculi.
Recurrent Infections: Struvite stones can also lead to recurring UTIs. The stones provide a place for bacteria to hide, making the infection difficult to clear entirely, even with antibiotics.
Research into the human microbiome, the collective genome of the trillions of microorganisms that live on and within us, has begun to shed light on the role of these microbial communities in a wide range of health conditions, including kidney stones.
Several mechanisms have been proposed to explain how the gut microbiome might influence kidney stone formation:
Oxalate Metabolism: Some gut bacteria, most notably Oxalobacter formigenes, are known to metabolise dietary oxalate, a compound that contributes to the formation of the most common type of kidney stone (calcium oxalate stones). By breaking down oxalate, these bacteria can potentially reduce the amount of oxalate absorbed from the gut into the bloodstream and excreted in the urine, thereby reducing the risk of stone formation.
Uric Acid Metabolism: The gut microbiome is also involved in the metabolism of purines, compounds broken down into uric acid in the body. Dysregulation of purine metabolism by the gut microbiome could lead to increased uric acid excretion in the urine, which can increase the risk of uric acid stones.
Urine pH: The gut microbiome regulates systemic pH and may also influence urine pH, a critical factor in forming certain kidney stones. For example, an overly alkaline urine pH can contribute to the formation of struvite and calcium phosphate stones. In contrast, an overly acidic urine pH can contribute to the formation of uric acid stones.
Immune Regulation: The gut microbiome plays a critical role in training and regulating the immune system. Disruption of the gut microbiome (dysbiosis) can lead to inappropriate immune responses that might contribute to kidney inflammation and increase the risk of stone formation.
Phosphorus is a mineral that plays a key role in the formation of DNA, the maintenance of the body’s energy stores, and the strengthening of bones. It is found in many foods, particularly dairy products, meat, and beans. However, a high phosphorus intake could contribute to kidney stone formation, particularly calcium phosphate stones.
The mechanism by which a high intake of phosphorus could lead to stone formation is complex and not completely understood, but here are a few possible ways it could happen:
Increased Calcium Excretion: High dietary phosphorus can increase calcium excretion in the urine (hypercalciuria), a risk factor for calcium-containing kidney stones.
Changes in Urine pH: A high phosphorus intake may also raise the urine pH, making it more alkaline. Calcium phosphate stones are more likely to form in alkaline urine.
Formation of Calcium Phosphate Crystals: If the concentration of calcium and phosphate is high enough in the urine, these minerals can combine to form calcium phosphate crystals, which can then grow into stones.
Impaired Kidney Function: Over time, consistently high phosphorus levels can harm the kidneys and impair their ability to filter out waste products, potentially increasing the risk of stone formation.
However, it’s worth noting that the relationship between phosphorus intake and kidney stones is more complex and well-established than the relationship between other dietary factors (like sodium, protein, and oxalate intake) and kidney stones.
Genetics can indeed play a role in the formation of kidney stones. Several genetic factors have been linked to an increased risk of developing kidney stones, though the relationship is complex and not fully understood.
Monogenic Disorders: Certain rare, single-gene (monogenic) disorders can directly lead to kidney stone formation. For example, primary hyperoxaluria is a condition caused by mutations in specific genes that lead to the overproduction of oxalate. This compound can form crystals in the urine and lead to kidney stones. Similarly, Dent disease and cystinuria are genetic disorders that cause abnormalities in the way the kidneys reabsorb certain substances, leading to high levels of these substances in the urine and increasing the risk of stone formation.
Polymorphisms and Polygenic Factors: Many common genetic variants, known as polymorphisms, have been associated with kidney stones in genome-wide association studies. These studies suggest that a combination of many different genes likely influences the risk of kidney stones, each contributing a small amount to the overall risk. This type of genetic influence is known as polygenic.
Family History: A family history of kidney stones is a known risk factor for developing stones. This suggests that genetic factors are at play, but it can be difficult to disentangle the effects of shared genes from the effects of shared environmental factors (like diet and lifestyle) in these cases.
Genetic Influence on Metabolic Factors: Genetics can also influence various metabolic factors known to increase the risk of kidney stones, such as the tendency to excrete high levels of calcium, oxalate, or uric acid in the urine.
https://www.healthhub.sg/a-z/diseases-and-conditions/629/kidney-stones
Kidney stones, or renal calculi, are solid masses made of crystals. They commonly originate in your kidneys, but they can develop anywhere along your urinary tract, which includes your kidneys, ureters, bladder, and urethra. The different types of kidney stones include:
These are the most common type of kidney stones. They occur in two major forms: calcium oxalate and calcium phosphate.
Calcium oxalate stones are the most common. They can form when your body has high oxalate levels, a substance found in many foods. Certain fruits, vegetables, nuts, and chocolate have high oxalate levels. Your liver also produces oxalate. Dietary factors, metabolic disorders, and intestinal bypass surgery can increase the concentration of calcium or oxalate in urine.
Calcium phosphate stones are less common. They’re associated with specific metabolic conditions, such as renal tubular acidosis. They can also occur when there’s a high intake of dietary phosphate or a high pH level in urine.
These stones are often horn-shaped and large, and they can occur when an infection, such as a urinary tract infection, alters the chemical balance in the urine. This can cause struvite stones to grow quickly with few or no symptoms until they’re quite large.
Struvite stones are more common in women than men and can be associated with ongoing urinary tract infections.
These stones form when the urine is too acidic, resulting from a high-protein diet, genetic factors, or diseases like diabetes or gout. Uric acid stones are more common in men than women and can also occur in people undergoing chemotherapy.
These are the least common type and tend to run in families. They can form in people with a hereditary disorder that leads to the kidneys excreting massive amounts of specific amino acids (cystinuria).
The type of kidney stone someone has can guide treatment decisions. It’s also important to note that certain medical conditions can increase the risk of certain types of kidney stones, such as hyperparathyroidism for calcium stones and urinary tract infections for struvite stones.
Xanthine stones are a very rare type of kidney stone, making up less than 1% of all kidney stones. These stones form from the compound xanthine, a purine metabolism product.
In most people, xanthine is metabolised to uric acid, then excreted in the urine. However, in individuals with specific genetic disorders like xanthinuria, the enzymes needed to convert xanthine to uric acid are either deficient or completely absent. This results in elevated levels of xanthine, which can accumulate in the urine and form xanthine stones.
Xanthine stones are radiolucent, meaning they don’t appear on regular X-ray examinations, making them difficult to diagnose. They are typically identified through other imaging techniques, such as ultrasound or CT scan, or by analysing the chemical composition of passed or surgically removed stones.
Silica stones are another rare type of kidney stone. Silica, also known as silicon dioxide, is a naturally occurring compound in certain rocks, sand, and quartz. It is also used in various industrial applications and can be ingested or inhaled in certain types of food or food additives.
In the human body, small amounts of ingested silica are usually excreted through the kidneys without causing problems. However, in rare cases, silica can accumulate in the kidneys and form stones.
There is little known about silica stones due to their extreme rarity.
Silicosis is a form of occupational lung disease caused by inhalation of crystalline silica dust, typically found in workplaces that involve cutting, grinding, drilling, or crushing silica-containing materials like concrete, rock, and sand. It’s especially common in construction, mining, and sandblasting industries and, at least here in Australia, is becoming more common.
Silicosis can lead to inflammation and scarring in the lungs, reducing the lungs’ ability to take in oxygen. Symptoms of silicosis may include cough, shortness of breath, chest pain, and fatigue. Chronic silicosis can develop after many years of lower levels of exposure, while acute silicosis can occur after brief exposure to very high levels of silica dust.
Now, as for the relationship between silicosis and silica stones, it’s important to understand that these are separate medical conditions. Silicosis affects the lungs, while silica stones form in the kidneys.
However, they share a common element, which is exposure to silica. While occupational inhalation of silica dust is a well-known cause of silicosis, it’s less clear how often this type of exposure might contribute to the formation of silica stones in the kidneys. It’s thought to be a very rare occurrence.
Individuals with prolonged exposure to silica dust could inadvertently or indirectly ingest some amount of silica dust, which could then be excreted through the kidneys and potentially contribute to stone formation. However, this is mostly speculative, and the risk of silica stone formation in people with silicosis is poorly defined.
Diagnosis of silica stones typically involves imaging studies, such as ultrasound or CT scan, to detect the presence of stones in the kidneys. The stones may also be analysed chemically if passed naturally or surgically removed.
Treatment for silica stones is similar to treatment for other kidney stones. Generally, it involves a combination of dietary modifications, increased fluid intake, and possibly medication to help prevent new stone formation. In some cases, surgical intervention may be necessary to remove the stones.
If occupational exposure to silica is a factor, it may also be necessary to implement workplace interventions to reduce silica exposure.
Knowing which type of kidney stone you have is imperative to know how to treat it best and prevent future stone formation. Ask your healthcare provider exactly which type of kidney stone you have.
In my next article, we will look at natural ways to prevent and treat kidney stones. So stay tuned.
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