Education
"I am at grips with the worst of all maladies, the most sudden, the most painful, the most mortal and the most irremediable."
-Michel de Montaigne; Donald M. Frame (1958). The Complete Essays of Montaigne
"Being gut-stabbed with a dirty spoon in a prison cafeteria is less painful."
-Kevin Murphy (2002). A Year at the Movies: One Man's Filmgoing Odyssey
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Kidney Stones
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Our approach
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Diet
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Medications
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My friend mentioned that I should try this
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Other diseases
What are Kidney Stones?
Kidney stones are made up of minerals in the urine that eventually aggregate into a stone. These minerals typically contain calcium with oxalate, calcium with phosphate, or uric acid. Rarely, there are other minerals that form stones that are related to genetic disease or chronic urinary tract infection.
Kidney stones form at the junction between the kidney and ureter. The ureter is the tube that connects the kidney to the bladder. Kidney stones generally do not cause problems until they break off and get stuck in the ureter. A stone typically gets stuck in the middle part of the ureter or in the last part as it enters the bladder. When a stone blocks urine flow, the ureter contracts, which causes severe pain. We call this pain “renal colic."
Our approach to kidney stones - a two-part process
Take out the stone
Surgery with the urologist is sometimes needed for the following indications:
- stone is stuck and does not pass after observation of a few days to weeks
- stone is so large that it is unlikely to pass on its own
- stone with fever
- stone with heavy bleeding in the urine
Urologists are the surgeons who perform stone removal surgery. There are three types of surgery:
- ureteroscopy with laser lithotripsy
- extracorporeal shock wave lithotripsy (ESWL)
- percutaneous nephrolithotomy (PCNL)
The decision about whether to extract the stone by surgery, when to do surgery, and what type of surgery should be done is best discussed with a urologist.
For information on Urology at Stanford, please see this link: Stanford Urology
Prevent the next stone
Removal of the stone is only one part of kidney stone care. The other part is to determine why the stone formed in the first place. This information can provide concrete steps for patients to modify their diet (and possibly start a new medication) so that the next stone can be prevented.
Stone prevention is guided by three pieces of information:
- stone analysis
- review of the diet
- 24-hour urine testing
Since kidney stones are made up of minerals in the urine, the logical approach for stone prevention is to consider the following relationships:
- mineral composition of the stone and excretion of minerals in a 24-hour urine sample
- mineral composition of a 24-hour urine sample and dietary habit
One of the functions of the kidney is to excrete minerals so that the level of minerals in the body are in steady state balance. We look at the chemical composition of the kidney stone and link this information with the concentration and amount of minerals in a 24-hour urine sample from a patient. We then ask the patient what he or she ate that day of the 24-hour urine collection. By correlating the dietary log with a 24-hour urine sample, we can advise patients on how to modify their diet to improve the urine profile and reduce stone risk. Since there is variation in diet and collection of a 24-hour urine sample, we usually ask our patients to consume their typical diet and collect two baseline 24-hour urine collections.
Do I need genetic testing?
There is indeed a heritable component to a kidney stone disease: patients with a family history of kidney stones are almost three times more likely to develop a stone compared with those without a family history. Metabolic predisposition to stone disease, which can be uncovered by blood or 24-hour urine testing, is also heritable.
However, the fact that kidney stone disease can be heritable does not necessarily mean that all patients should undergo genetic testing. Most patients with a family history of kidney stone disease still likely have numerous genes with small effects that conrtibute to stone risk. We acknowledge that in select cases, particularly when stone disease is severe or accompanied by kidney disease, it will be valuable to test for a genetic cause for stone disease.
Diet - what should I eat?
At the Stanford Stone Clinic, we first pursue dietary strategies for prevention of recurrent stone disease before considering medications. A healthy diet should be the cornerstone of prevention of human disease including kidney stone disease. We provide nutritional support to help patients modify their diets so that they can translate 24-hour urine findings to dietary action. We often partner with nutritionists at Stanford to help patients reach their dietary goals: Stanford Clinical Nutritional Services
Below we present general and specific recommendations for dietary prevention of stone disease.
General Recommendations
General recommendations for stone prevention include high fluid intake, low dietary sodium, and moderation of protein intake. We recommend these dietary approaches for all patients regardless of their stone type or 24-hour urine abnormality.
Water
High fluid intake is a key strategy for preventing stone recurrence because it increases urine volume. High urine volume will reduce the likelihood that minerals will form crystals in the urine that contribute to stone growth. We recommend that patients drink enough fluids so that their daily urine volume is above 2.5 liters (85 oz). This is not easy. Patients need to re-wire their habits so that they learn to drink fluids regularly even when they are not thirsty. Every little bit helps. Even increasing daily urine volume by 0.32 liters (11 oz) can reduce stone risk.
Calcium & Sodium
Many patients with calcium stones are surprised to learn that they should NOT reduce their daily calcium intake. This may seem counter-intuitive but we can refer to a landmark clinical trial demonstrating that a combination diet of normal calcium (1200 mg daily), low sodium (50 mEq daily), and moderate protein (1.2 grams/kg body weight/day) is better than a low calcium diet (400 mg daily) for lowering stone risk.
Protein
We recommend that patients with kidney stones should not exceed protein intake of one gram per kilogram of body weight per day. This means that a 70 kg person should eat up to 70 grams of protein each day. Excess protein consumption can increase risk of calcium and uric acid stones, and the source of protein may matter. Eating animal meat particularly increases stone risk. In this context, animal meat is defined as flesh meat, including beef, pork, chicken, or fish, eggs, and milk products. Eating white meat (poultry or fish) or eggs does NOT confer advantage over red meat in reducing risk factors associated with stone risk. In contrast, eating vegetable protein (soybean or pea) may protect against stone formation or recurrence.
Specific Recommendations
The value of 24-hour urine testing for stone prevention is that it can pinpoint specific urine abnormalities that raise stone risk. In this sense, 24-hour urine testing is a form of personalized or precision medicine promoted by Stanford Health.
While all kidney stone formers will benefit from general diet recommendations, only 24-hour urine testing can reveal the potential benefit of additional, more specific treatments. Moreover, 24-hour urine testing can provide a benchmark to determine how close patients are to their goal of normalizing stone risk.
Some common examples that 24-hours urine testing can specifically reveal:
- patients with uric acid stones and acidic urine need to increase their alkali intake
- patients with calcium oxalate stones and low urine citrate need to increase their alkali intake
- patients with calcium oxalate stones and high urine oxalate need to lower their oxalate intake
- patients with calcuium oxalate stones and high urine calcium need to maintain a low sodium diet or even start thiazide medications
Oxalate
High urine oxalate excretion or hyperoxaluria is defined as urine oxalate excretion > 25 mg per day, a cut off for when the risk increases for calcium oxalate stones. The most common cause of hyperoxaluria is high dietary intake of oxalate rich foods, such as spinach and nuts (all of them!). The problem is that many foods contain oxalate, so it can be difficult to control hyperoxaluria on a long-term basis. Twenty-four urine testing for urine oxalate can be very instructive to help patients see if their diet is low enough to keep their urine oxalate in the normal range. We also use the 24-hour urine test to calibrate a lower oxalate diet that is specific and realistic for patients.
Citrate
Citrate is a key inhibitor of calcium stones because it keeps calcium dissolvable in the urine so that less calcium oxalate or calcium phosphate stones form. Low urine citrate excretion, called hypocitraturia, is generally defined as <320 mg per day, a cut off for when the risk increases for calcium stones. Eating less animal meat and increasing more fruits and vegetables can help raise urine citrate. More acidogenic foods (like animal meat) will reduce urine citrate whereas more alkaline foods (like fruits and vegetables) will raise urine citrate. However, many patients will ultimately need alkali supplementation to raise urine citrate on a long-term basis.
Medications - what should I take?
If dietary strategies fall short of reducing stone recurrence, three classes of medications can be prescribed: 1) thiazide and thiazide-type diuretics, 2) alkali supplements, and 3) allopurinol. At the Stanford Stone Center, we consider medications if stones recur or if we are unable to control 24-hour urine abnormalities with diet alone.
Thiazide and thiazide-type diuretics
- Reduce urine calcium excretion
- Helpful for treating high urine calcium, also known as hypercalciuria, generally defined as > 200mg per day
- Reduce stone recurrence but need to be prescribed at doeses that are higher than those prescribed for treatment of hypertension
Alkali (or base)
- Used to treat patients with calcium oxalate stones and hypocitraturia or patients with uric acid stones and acidic urine
- Typically prescribed in the form of potassium citrate or sodium bicarbonate
- The required dose of alkali depends on several factors, including the level of kidney function, how well alkali is absorbed from food, and overall acid-base status of the patient. This can be challenging for some patients to tolerate oral alkali because of gastrointestinal side effects, which include nausea, vomiting, constipation, diarrhea, stomach discomfort, or bloating
- We try to find the best formulation for patients, which may include switching from alkali precriptions to over-the-counter alkali supplements that can deliver a similar base load
Allopurinol
- Can be described for prevention of calcium oxalate stones
- Should be prescribed at 300mg daily in patients with calcium stones and high uric acid excretion, defined as > 800 mg/day
- The mechaism of action is not clear, but allopurinol is typically embraced as a second- or third-line treatment option or a convenient option for those patients with concomitant gout
My friend mentioned that I should try this for kidney stones - should I try it?
Different diet regimens
Many diet regimens aim to help patents lose weight. While these diets restrict consumption of specific nutrients, they typically counterbalance this restriction with an increase in other nutrients or food groups, some of which may increase stone risk. For example, the Atkins diet imposes severe restriction on carbohydrate intake, which is replaced by an increase in protein or fat consumption. In the short term, consumption of an Atkins diet can increase urine calcium excretion and decrease urine pH and urine citrate excretion. This can increase risk for either calcium oxalate or uric acid stones.
A similar mechanism operates for patients who ingest a ketogenic “keto” diet, which typically consists of 5% carbohydrate, 15% protein, and 80% fat. Patients who consume a ketogenic diet often develop acidic urine, hypocitraturia, and hypercalciuria. Ketogenic diets have been linked to recurrence of uric acid stones, calcium stones, or a mixture of both patients uric acid and calcium stones.
The Paleolithic diet replicates the diet of hunter-gatherer from prehistory, a time in which processed food (cereals and dairy products) was absent and unprocessed food (meat, eggs, nuts, fruits, and vegetables) predominated. The higher intake of fruits and vegetables should increase delivery of alkali to the body, leading to an increase in urine citrate and a decrease in urine calcium. However, it is also possible that higher intake of fruits and vegetables would increase urine oxalate excretion. We thus do not know for certain what is the net effect of the Paleolithic diet on stone prevention. The same is true for the Mediterranean diet: there may be offsetting effects of Mediterranean diet on stone prevention. On the one hand, the Mediterranean diet will lower sodium intake and raise fruit and vegetable intake, which will lower urine calcium and increase urine citrate and pH. On the other hand, the Mediterranean diet contains a rich supply of nuts, which have high oxalate content.
Alkaline water
Alkaline water has been advertised to be healthy because the pH is higher, typically around 9.0. This advertising claim begs the question of whether alkaline water can be used for kidney stone prevention. We believe that the answer depends on what is in the alkaline water. Without knowing the specific contents inside different formulations of alkaline water, we cannot recommend it over regular water for stone prevention.
Why? The reason is that water is a not a buffered solution, so it takes very little acid or alkali to change the pH of water. For example, in distilled water, it takes < 1 mEq of alkali to change the pH from 7 to 9. As a comparison, one-half teaspoon of baking soda contains approximately 25 mEq of alkali. There is not enough alkali in plain water to deliver alkali in a clinically meaningful way. It is possible that alkaline water formulations may contain alkali but the ingredient labels usually do not give quantitative information about the amount of alkali.
Citrus-based drinks
The physiological basis for consuming citrus-based beverages is that they provide a source of alkali, which will increase urine pH and urine citrate. In theory this urine profile can lower risk of uric acid or calcium stones. However, whether a given citrus-based beverage contains alkali depends on the proportion of protons (H+) and citrate. If the proportion is 1:1, the citrus-based beverage contains citric acid, and citric acid will not provide alkali to the body. As a result, there will be no effect on either urine pH or urine citrate.
Over-the-counter beverages can provide an alternative source of alkali that may be more palatable and cost less than prescribed medications. We believe that these beverages should not be used be used as a general recommendation for stone prevention but rather as a specific recommendation-- to be initiated in response to either a low urine pH or hypocitraturia. Moreover, these beverages should be dosed to normalize urine pH or level of urine citrate excretion with the aim to lower stone recurrence. For appropriate dosing of a citrus-based drink, we must know the exact proportion of citric acid (which is not a base equivalent) to citrate (a base equivalent) for that drink.
Knowledge of the proportion of citric acid to citrate for each drink will dictate the volume needed to deliver sufficient alkali to the body; for lemon water or juice, this volume may require ingestion of two quarts a day to raise urine citrate to an effective range. Other citrus drinks, such as orange and grapefruit juice, may represent a good source of citrate but come with high sugar content and may cause heartburn when ingested in high volumes. We have recommended lower calorie options such as Diet 7-Up, Diet Sunkist Orange, or Crystal Light Lemonade. A newer formulation of alkali is Moonstone, which contains 30 mEq per serving, can be served as a dissolved packet, gummy, or capsule.
Are there other diseases I should think about if I have kidney stones?
Renal tubular acidosis and nephrocalcinosis
Renal tubular acidosis is a rare condition in which the kidney cannot retain or regenerate bicarbonate in the body that can neutralize acid that is generated daily. The result is that urine citrate excretion is low and urine calcium excretion is high, leading to formation of calcium phosphate stones and even calcium phosphate deposition in the kidney (called nephrocalcinosis). Treatments for this condition include alkali therapy, but paradoxically, alkali therapy can accelerate stone formation if urine pH becomes too high.
Hyperoxaluria
Some cases of high urine oxalate excretion can be explained by altered gut physiology. Enteric hyperoxaluria is a condition in which the gut absorbs more oxalate than normal and is classically found in conditions such as fat malabsorption, inflammatory bowel disease, or gastric bypass surgery such as Roux-en-Y bypass. Oxalate can also be high in the body because more oxalate is produced by the liver. Primary hyperoxaluria (PH) is a rare example in which a genetic disease in oxalate metabolism leads to oxalate accumulation in the plasma, liver, and kidney. Expression of primary hyperoxaluria is variable; patients with PH1 will develop end-stage kidney disease at an early age, and those with PH2 and PH3 tend manifest with calcium oxalate stone disease.
Bone disease and kidney stone disease
Patients who form kidney stones may be at risk for lower bone mineral density and fracture. This risk is modest compared to the risk posed by factors such as smoking history and menopause. As a result, no guidelines exist on how to screen for bone disease in kidney stone formers. However, there are specific dietary recommendations and medications that both strengthen bone and reduce the risk for stone recurrence that may be beneficial to individual patients with kidney stones.