Patient's question:
Should people with kidney stones pay attention to dietary restrictions? What is the best diet for daily life?Doctor's answer:
You can refer to the following materials for reference.As the saying goes, "disease enters through the mouth," which clearly illustrates the close relationship between diet and disease, and urinary tract stones are no exception. Some factors in stone formation, such as stone composition, promoters, and inhibitors of stone formation, are not only related to certain metabolic diseases but can also be produced by food metabolism. In recent years, there have been reports that adjusting the diet has effectively reduced the recurrence rate of urinary tract stones. Diet can affect urine composition and pH, thereby influencing stone nucleation and growth. However, arbitrarily changing the diet may seem beneficial but is actually harmful. This means that dietary therapy must be based on objectively confirmed metabolic disorders and targeted strategies for better results. To more accurately understand the impact of dietary components on urine composition and stone formation, the relevant factors affecting stone formation will be discussed separately below.
### 1. Calcium
In 70% of urinary stones, calcium oxalate is the sole or primary component, often combined with other calcium salts. Daudo et al. conducted infrared spectroscopic analysis on 10,617 urinary stones and found that 86% contained calcium oxalate and 80% contained calcium phosphate. They observed a linear relationship between calcium intake and urinary calcium, suggesting that increased calcium intake increases the risk of kidney stone formation. However, it has now been confirmed that the commonly recommended practice of restricting dietary calcium not only fails to reduce but may even increase the occurrence of kidney stones. A low-calcium diet can promote the absorption of oxalates in the intestines and lead to hyperoxaluria, thereby promoting stone formation. Conversely, high-calcium beverages (380 mg/L) may increase urinary calcium excretion but significantly reduce oxalate excretion, with a marked decrease in the oxalate/calcium ratio. Since the maximum crystals form when the calcium/oxalate ratio is 1:1, the effect of increased oxalate on crystal formation is much greater than that of calcium. Ettiger et al. reported that a low-calcium diet for patients with urinary stones was often more harmful than a normal calcium diet. Moreover, Burtis et al. reported that many patients with stones had higher urinary calcium levels on a normal diet, but their urinary calcium levels returned to normal when they consumed a high-calcium, low-sodium diet. This is mainly due to the inverse relationship between urinary oxalate excretion and calcium intake.
Restricting calcium intake can also stimulate the secretion of vitamin D3, promote bone resorption, increase urinary calcium excretion, and thus increase the risk of stone formation. High urinary calcium is classified into three types: Type I is non-diet-dependent; Type II is diet-dependent; and Type III is secondary to renal phosphate leak. Dietary calcium restriction can reduce urinary calcium only in Type I and Type II absorptive hypercalciuria, and only Type II can reach normal levels. Therefore, a low-calcium diet only reduces urinary calcium in Type II absorptive hypercalciuria and must be accompanied by a low-oxalate diet to avoid secondary hyperoxaluria. Dietary calcium restriction is not suitable for other types of hypercalciuria.
The role of calcium supplementation in postmenopausal women remains controversial. For premenopausal women, calcium supplementation may increase urinary calcium in the first few days, followed by a decrease in intestinal calcium absorption due to the inhibition of parathyroid hormone and 1,25-dihydroxyvitamin D3 synthesis, thereby reducing the effect of oral calcium. Postmenopausal women have osteoporosis and metabolic disorders of vitamin D and parathyroid hormone, and the ability of the elderly to absorb calcium from the intestine is reduced. Therefore, calcium supplementation for postmenopausal women does not increase the risk of stone formation, and if there is any risk, it would only occur in the first few months of supplementation. For caution, increasing fluid intake during this period is recommended. Postmenopausal women with Type II absorptive hypercalciuria should, like other patients with Type II, follow a low-calcium, low-oxalate diet.
### 2. Oxalates
Since most urinary stones contain oxalates, reducing urinary oxalate will reduce the incidence of stone disease. 60% of urinary oxalate is derived from endogenous metabolism of glycine, hydroxyacetic acid, and hydroxyproline, 25–30% is the final product of dietary vitamin C metabolism, and only 10–15% comes from dietary oxalates. Another report indicated that 45% of urinary oxalate in healthy individuals comes from food. Currently, there is no way to reduce the endogenous production of oxalate. Although various drugs, including antisense oligonucleotides to block the transcription of mitochondrial aldehyde dehydrogenase, have been used to treat Type I primary hyperoxaluria (lacking peroxidase, alanine, and glyoxylate transaminase activity) and Type II primary hyperoxaluria (lacking glycolate dehydrogenase activity), no significant effects have been achieved. Reducing exogenous oxalate intake can decrease urinary oxalate excretion. Previous reports indicated that 45% of hyperoxaluria patients responded to dietary oxalate restriction. Many stone formers indeed have hyperoxaluria, and their oxalate primarily comes from the diet.
Under normal conditions, only 8–12% of oxalate in the diet is absorbed. The absorption of oxalate in the intestine is passive and depends on the concentration of calcium in the intestinal lumen. Additionally, intestinal bacteria can reduce oxalate absorption, so when there is a deficiency of intestinal bacteria, oxalate absorption will increase. Unbound calcium in the intestine can chelate with oxalate, inhibiting its absorption and thus reducing oxalate excretion from the diet. For the same reason, individuals with poor fat absorption, where calcium combines with fat to form calcium fatty acid, increase the absorption of unbound oxalate, exacerbating hyperoxaluria. For such patients, reducing dietary oxalate content or taking oral calcium supplements to reduce the absorption of unbound oxalate can be therapeutic. However, given that most ordinary diets contain low oxalate and have a low absorption rate, the effect of restricting oxalate intake on hyperoxaluria stone patients without intestinal disease is unpredictable. 25–30% of urinary oxalate is the metabolite of dietary vitamin C, indicating the importance of dietary vitamin C in urinary oxalate and stone formation. Although the recommended dose of vitamin C is 60 mg/day, some populations consume large amounts of vitamin C due to various factors. There is still debate about whether high vitamin C intake significantly increases urinary oxalate excretion, leading to the formation of calcium oxalate stones. Over the past 40 years, extensive research has been conducted on the effect of vitamin C on urinary oxalate excretion, with doses ranging from 1 g to 10 g and durations from 2 days to 6 months, yielding results from no effect to a significant increase in urinary oxalate. The differences mainly lie in the methods used to measure urinary oxalate. Wzilak et al. confirmed that normal individuals consuming 1–10 g/day of vitamin C for 5 days did not increase urinary oxalate excretion. However, Chalmers and Cowley et al. reported that high-dose vitamin C supplementation in patients with stones caused poor vitamin C absorption and increased urinary oxalate levels. This is mainly because unabsorbed vitamin C decomposes into oxalate in the alkaline environment of the small intestine through non-enzymatic pathways, which is then absorbed by the intestine and excreted in the urine. Therefore, caution is advised when using high doses of vitamin C in patients with stones, and avoiding concentrated tea, excessive chocolate, and spinach is recommended.
### 3. Water
It is well known that chronic dehydration and/or insufficient fluid intake are closely related to stone formation. Lifeguards and marathon runners have high incidences of nephrolithiasis, which demonstrates that increasing fluid intake can reduce the incidence of stone disease. This is because chronic dehydration increases urine specific gravity, the saturation of stone-forming substances and uric acid, and decreases urine pH. Under dehydration conditions, uric acid crystals in the urine can serve as templates for the orientation attachment of calcium-containing stones. Increasing fluid intake can reduce the risk of stone formation through multiple mechanisms, such as accelerating crystal passage through the renal tubules and reducing contact time with surfaces with strong adsorption. Of course, increasing fluid intake can dilute some inhibitors of stone formation in the urine, such as citrate and magnesium, but it can also significantly increase the minimum saturation required for the spontaneous nucleation of calcium oxalate, possibly due to the dilution of stone-forming promoters. When urine output is <1 L/day, there is a significant increase in the nucleation of calcium salts, and the excretion of citrate is reduced, as well as the inhibitory activity of Tamm-Horsfall protein on stone formation.
The recommended reasonable fluid intake is not less than 2 L/day with a urine specific gravity of <1.010. It is also important to pay attention to drinking fluids not only during the day but also at night, as drinking a certain amount of water at night is crucial. For this reason, it is recommended to drink 250 ml of non-dairy liquid between meals, during meals, and when urinating at night. Nighttime urination indicates sufficient fluid intake. It is also important to supplement an adequate amount of liquid during nighttime sleep, as this is when urine is most concentrated under normal conditions. To maintain accurate urine dilution, it is necessary to measure urine specific gravity at home, as simply relying on recommended fluid intake may not achieve the desired level of urine dilution. Hoskig et al. reported that drinking 2,500 ml of liquid daily could prevent the formation of new stones in hypercalciuria patients. Generally, it is recommended to drink 250 ml every 4 hours, plus 250 ml with each meal.
After addressing the quantity issue, the next step is to determine what type of liquid to drink. It is generally agreed that non-dairy, low-oxalate liquids are preferable. As for whether to drink hard water (non-filtered water containing calcium and magnesium salts) or soft water, opinions are divided. To date, there is no evidence that hard water is more likely to cause stones than soft water, and some epidemiological studies have shown a negative correlation between water hardness and kidney stones. In Thailand and the southeastern United States, the incidence of kidney stones is high, but the water consumed there is soft. The situation in China is similar, with higher stone incidence in the southeastern regions that drink soft water compared to the northwestern regions that drink hard water. Therefore, the hardness of drinking water is not as important as the quantity, and it is essential to consider both day and night.
### 4. Protein
Worldwide and in China, the development of nephrolithiasis and epidemiological studies have confirmed that the occurrence of stones is related to a higher standard of living, i.e., a high-protein diet. Trichieri et al. pointed out that a high-protein diet increases the incidence of kidney stones. This is also reflected in China. In the early days after the founding of the People's Republic of China, bladder stones were common among children in impoverished rural areas, but with economic development and increased wealth, the prevalence of upper urinary tract stones has shifted to urban populations. Conversely, a vegetable diet without animal protein, although containing higher oxalates, has a lower risk of stone formation.
The factors contributing to the promotion of stone formation by a high-protein diet are multifaceted, including: ① the production of transient endogenous acidic metabolites excreted in the urine, leading to temporary metabolic acidosis, increasing bone calcium absorption and glomerular calcium filtration while inhibiting calcium reabsorption in the distal tubular cells, resulting in hypercalciuria; ② the high-oxalate effect of proteins rich in methionine or other sulfur-containing amino acids is more pronounced, as urinary sulfate and calcium form complexes that affect their absorption in the renal tubules, leading to hypercalciuria; ③ combined with hyperoxaluria from high-protein intake, it promotes the recurrence of calcium oxalate stones; ④ the uricosuria accompanying a high-protein diet increases the risk of calcium oxalate formation. Uric acid crystals can adsorb glutamate and other organic substances, promoting the oriented attachment and growth of calcium oxalate crystals; ⑤ increasing the reabsorption of citrate in the renal tubules, thereby reducing urinary citrate levels and increasing the risk of calcium crystal formation. Therefore, restricting dietary protein, especially animal protein, is beneficial for all stone patients.
### 5. Sodium
Most agents that promote sodium excretion can stimulate urinary calcium excretion, as the handling of sodium and calcium in the renal tubules is similar. High sodium intake increases urinary calcium excretion, whereas a low-sodium diet reduces it. Adding sodium to a low-calcium diet for hypercalciuria patients can exacerbate hypercalciuria. Therefore, it is emphasized that a low-sodium diet should be maintained before and during the collection of urine samples for 24-hour urinary calcium measurement.
Generally, there is no significant difference in sodium intake between stone formers and controls, but some stone patients do have higher urinary sodium excretion. In the United States, 25% of stone patients have daily urinary sodium excretion exceeding 200 mmol. Theoretically, high-sodium diet-induced hypernatremia can inhibit calcium reabsorption in the renal tubules, leading to hypercalciuria and increasing the saturation of calcium salts that form stones, as well as increasing the saturation of urinary urate-sodium, leading to urate-induced calcium oxalate crystals. Additionally, high sodium intake can reduce the renal excretion of citrate. Sakhaee et al. studied 14 normal individuals and found that a high-sodium diet (basic diet plus 250 mmol of sodium chloride daily) significantly increased urinary sodium, urinary calcium, and urinary pH while significantly reducing citrate excretion. Therefore, they concluded that a high-sodium diet increases the tendency for calcium salt crystallization in the urine. The recommended daily salt intake is <10 g.
### 6. Citrate
Citrate is a natural inhibitor of stone formation. It can chelate with calcium to form highly soluble calcium citrate, thereby reducing urinary calcium concentration and the saturation of calcium oxalate and calcium phosphate in the urine. The renal excretion of citrate depends on serum pH. Acidosis, renal tubular acidosis, chronic diarrhea, intense exercise, hypokalemia, hypernatremia, and high-protein diets can all reduce urinary citrate excretion, whereas alkalosis can increase it. 19–63% of calcium salt stone patients have hypocitraturia. However, some scholars have reported no difference in urinary citrate concentration between stone formers and normal individuals.
Daily supplementation with 20.0–36.7 mmol of potassium citrate can significantly increase urinary citrate and urinary pH, reducing the recurrence rate of urinary stones. For calcium oxalate stone formers, urinary concentration is highest from late night to early morning, increasing the saturation of calcium oxalate and reducing pH. Therefore, a single dose of 3.5–5.0 mg of potassium citrate sodium at night is more effective. Compared to the pre-treatment period, the stone formation rate was reduced by 76–91% during treatment, with no recurrence in 67–92% of cases, and the single-stone formation rate was reduced by 95–100%. Professor Mei Hua of China also obtained similar results.
The above are the results of drug treatment. Consuming large amounts of citrus fruits and vegetables rich in citrate can lead to hyperoxaluria, counteracting the benefits of increasing dietary citrate. The main goal of treating hypocitraturic calcium salt kidney stones is to ensure that the 24-hour urinary citrate excretion exceeds 320 mg. From this standard, Waher et al. treated 8 normal individuals and 3 cases of hypocitraturia with citrus juice, increasing daily urinary citrate from 571 mg to 952 mg in 11 cases during the citrus juice consumption period, achieving the desired effect. The following fruits are rich in citrate: oranges, grapefruits, raspberries, pineapples, and boysenberries. Oranges are commonly used as an adjunctive treatment for low-citrate, calcium-containing kidney stones.
### 7. Fat
Stone-forming patients with calcium-containing stones excrete higher levels of lipids in their urine compared to normal individuals, but this is unrelated to diet. Hypercalciuria patients excrete higher levels of dihydroxyprostaglandin in their urine compared to normal individuals. Non-steroidal anti-inflammatory drugs can reduce urinary calcium excretion by inhibiting prostaglandin synthesis but do not reduce urinary calcium excretion in normal individuals with recurrent kidney stones. The diuretic effect of thiazide diuretics on reducing urinary calcium is also due to the reduction in renal prostaglandin synthesis.
In Greenland, the incidence of coronary artery disease and kidney stones in Inuit people is low, which is related to their high intake of polyunsaturated fatty acids, especially eicosapentaenoic acid. Eicosapentaenoic acid is synthesized in the human body in small amounts and is supplemented from the diet to protect the heart, which has been proven in Western countries. Once ingested, it is quickly absorbed into cell membranes, stored, and enters the bloodstream, where it inhibits the conversion of dietary octadecadienoic acid to octadecatetraenoic acid and competes with octadecatetraenoic acid for storage in cell membranes. Eicosapentaenoic acid competes with octadecatetraenoic acid as a substrate for cyclooxygenase and a precursor of triene prostaglandin, each having a different range of activity. Fish oil can reduce the synthesis of dihydroxyprostaglandin, thereby reducing urinary calcium excretion in idiopathic hypercalciuria patients, but without the toxicity of non-steroidal anti-inflammatory drugs. Additionally, fish oil can increase fibrinolytic activity in the bloodstream. Charlfo believes that urinary fibrinolytic activity, dependent on fibrinolytic activity in the bloodstream, is an important protective factor against stones. Buck et al. pointed out that fish oil can correct the biochemical abnormalities of idiopathic stone disease. Patients taking 10 mg of fish oil daily for 8 weeks significantly reduced 24-hour urinary calcium and oxalate excretion but had no effect on phosphate excretion. However, Rothwell et al. gave 18 recurrent stone patients with hypercalciuria fish oil and found that while it significantly reduced urinary calcium excretion, it also reduced the excretion of citrate and magnesium, limiting its effect on recurrent stones. If citrate is taken concurrently with fish oil, it may provide greater benefits for the treatment of recurrent hypercalciuria stones.
### 8. Alcohol
Alcohol can alter some factors in stone formation. Alcoholic beverages often contain calcium, oxalate, and guanine nucleoside. Elevated acute alcohol concentrations in the blood are often associated with hypercalciuria, hypermagnesuria, and increased cortisol, accelerating bone resorption. Long-term alcohol consumption leads to more pronounced hypercalciuria and hyperphosphaturia, but blood calcium and inorganic phosphorus remain unchanged. There is a linear correlation between alcohol consumption, hyperuricemia, and hyperuricosuria. Conversely, the diuretic effect of alcohol can reduce the concentration of urinary components. In summary, moderate alcohol consumption does not increase the risk of stone formation.