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REVIEW ARTICLE

JOURNAL OF RENAL NUTRITION AND METABOLISM (2015) 1: 22-23


Urolithiasis:Nutritional Management

#MS Ansari, Sohrab Arora

•Additional Professor, Department of Urology and Renal Transplant Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow.



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ood is derived from different kind of plants, different soils, depends on different eating habits, and a single food item contains hundreds of biologically active compounds. Intake of different nutrients does not take place in isolation. People of different cultures derive the same nutrients from different foods and preparation methods. People also vary in their eating habits over time and place. Ingredients in food interact in synergistic and antagonistic manner in the way they get digested and the way they get absorbed. Evidence based data on the subject of diet in prevention of stone disease is shockingly low. Most evidence studies the effects of diet on stone risk factors such as super saturation rather than

stone formation in vivo.

We must assess the individual patient on his eating habits and metabolic profile before advising dietary modification rather than general advice on food which might make the compliance difficult. There are time constraints to this approach in the OPD so the services of a dietician must be sought. This has the advantage of avoiding unnecessary recommendations and doesn't conflict with the information patient might get from other physicians. Individualized approach is also practical and allows for alternative food choices that the patient can include in his lifestyle. The dietician may then use methods like 24 hour diet recall, multiple day diet records and then prescribe the amounts specific for the age and gender.

It is also necessary to be aware of various mechanisms for the same metabolic abnormality. Like, for example oxaluria may be due to high oxalate intake which might necessitate reduction of oxalate in diet, but it may also be due to low calcium intake not timed with meals. It is important to distinguish between the two because the dietary modification required for both of them is different. We must also be aware of coexisting medical conditions like chronic acidosis which causes hypercalciuria, malabsorption leading to hyperoxaluria, chronic and frequent use of antibiotics leading to reduction in oxalobacter fermigenes which causes oxaluria, obesity, metabolic syndrome, etc.


One cannot over-emphasize the importance of making a nutritional diagnosis. For example, saying "increased nutritional lithogenic risk related to suboptimal calcium intake not timed with meals, contributing to low oxalate binding potential in gastrointestinal tract and resulting in hyperoxaluria'' is a much better way of stating the diagnosis rather than "hyperoxaluria':

Apart from various individual constituents of diet, it is also important to be aware of dietary patterns as a whole prescribed for the patient elsewhere. For example, a popular diet for weight loss known as the Atkins diet is known to cause stone disease by various mechanisms. Ketogenic diet prescribed for seizure disorders is also known to cause increase in stone risk. On the contrary, a diet rich in vegetables despite being high in oxalate, reduces risk of stones by reducing hypocitrauria and reducing uric acid in urine. A low salt, adequate calcium, moderate protein, high fluid intake diet (not very different from DASH diet prescribed for hypertension) -reduces risk of stone disease

In practice, factors affecting hypercalciuria include

  1. High sodium intake which must be reduced.

  2. Acid load from diet (from flesh, cheese, eggs, etc) which causes bone resorption to buffer this acid load. Itis not necessary to exclude these food from diet. Assessment of potential renal acid load (PRAL) of diet can help in tailoring a diet which includes negative PRAL food (vegetables) along with high PRAL food items.

  3. GI and renal calcium handling - Dietary fiber in a recommended level of 25-30 mg/day should be increased and refined carbohydrate reduced.

  4. Omega 3 fatty acids - have been shown to reduce hypercalciuria but the dosages are not clear.

Factors affecting hyperoxaluria include

  1. High oxalate diet -it is a matter of controversy as foods that are rich in oxalates (vegetables) reduce the risk

    JOURNAL OF RENAL NUTRITION AND METABOLISM (2015) 1: 22-23


    of stone disease by other mechanisms which include fiber, potassium and antioxidants. In addition, oxalate restriction can lead to higher absorption of calcium. Total avoidance of oxalate is not possible and results in decreased compliance.

  2. Calcium intake - 300 mg calcium with every meal binds oxalate. Diet alone can take care of this. No need to supplement. But indian diet is severely deficient in calcium so tailored approach is best.

  3. Malabsorption leads to binding of calcium to fatty acids leaving oxalate free to get absorbed

  4. Magnesium can be incorporated in diet as it binds oxalate in gut.

  5. Role of over the counter supplements like cinnamon, turmeric and cranberry which might increase hyperoxluria is not dear.

Factors affecting hyperuricosuria include mainly the urine volume, purine intake, fructose and acid load of diet. Not every purine is the same. Organ meats like brain, liver and kidney are the richest sources of purines and increase the risk while purines from dairy products lower the risk and purines from plants have been shown not to increase the risk. Alcohol has been anecdotally known to prevent stone disease by causing diuresis. On the contrary, alcohol increases xanthine oxidase expression and causes uric acid stones.

Factors affecting hypocitrauria include mainly the dietary citrate and the acid load of diet. High acid load of diet leads to high citrate reabsorption causing hypocitrauria. Increasing citrus fruit intake leads to decreased hypocitrauria. Commercially available bottled lemonade contains minimal lemon juice and high carbohydrate thus leading to increased risk, therefore home made preparations are better.

Consumption of eicosapentaenoic acid (EPA) is associated with reduction of liothogenic factors in urine. EPA is an inhibitor of arachidonic acid metabolism which causes decreased synthesis of prostaglandin E2, a substance that is known to potentiate urinary calcium excretion. Buck eal 1 found that on treating hypercalciuric recurrent stone formers with an 8-week course of fish oil significantly reduced oxalate and calcium excretion. Results of Yasui et al's, prospective study on recurrent stone formers in three phases; phase-I before initiation of EPA (mean 47.8 months), phase-II of EPA supplementation (1800mg/d; mean 36.4 months) and phase-III after stopping EPA (mean 50.6 months) showed a statistically significant reduction in stone episodes during supplementation phase than before or after (0.22, 0.07 and 0.17 times/year, respectively; RR 3.29 before and RR 2.51 after EPA).

Fluid Intake : Increased fluid intake for a urine-output of 2 liters/day is one of the most important and the least expensive form of conservative measure to reduce stone­ recurrence. Its effect is through mechanical diuresis and decreased solute-supersaturation and formation-product ratio. Large epidemiological studies on >45,000 men (health

Nutritional Management 23


professional follow-up study; HPFS) and 91,000 women (Nurses' health study; NHS-I and NHS-II) found a 30-40% risk-reduction associated with doubling of fluid intake to

2.5 liters/day or more. There have been pervasive concerns regarding lithogenic potential of hard water (by virtue of being richer in calcium); however, consensus is lacking. In a large cohort of 3270 stone-patients, Schwartz et al, found higher calcium and citrate excretion in patients living in areas with hard water supply versus soft water supply (P<0.0001). However, the life-time incidence of stone episodes was remarkably similar across populations. Curham et al, found that with every 8-oz/d of coffee, tea, beer and wine stone­ risk decreased by 10%, 14%, 21% and 39%, respectively (inhibitory action on vasopressin probably decreases stone risk); whereas, with the same amount of apple juice and grapefruit juice, it increased by 35% and 37%, respectively. Similarly, Krieger et al, reported a significant protective effect of beer (OR 0.41), in a case-control study enrolling

240 cases and 392 controls. This effect is not entirely explainable, because apart from causing diuresis, it leads to hypocitraturia, uricosuria and lowering of pH.

To summarize, there is a need to move away from generic dietary charts and old misconceptions about stone disease and understand the metabolism and therefore be able to individualize the dietary patterns of your patient with the help of a dietician so that your patient has a palatable diet which has better compliance and results for prevention of stones. Regulation of fluid and dietary intake habits is essential in comprehensive preventive management of urolithiasis.


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References:

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  3. Curhan GC, Willett WC, Rimm EB, Stampfer MJ. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med. 1993;328:833-8.

  4. Curhan GC, Willett WC, Knight EL, Stampfer MJ. Dietary factors and the risk of incident kidney stones in younger women nurses' health study II. Arch Intern med. 2004;164:885--91.

  5. Schwartz BF,Schenkman NS, Bruce JE, Leslie SW,Stoller ML. Calcium nephrolithiasis: Effect of water hardness on urinary electrolytes. Urology.2002;60:23-7. Shuster J, Jenkins A, Logan C, Barnett T, Riehle R, Zackson D, et al. Soft drink consumption and urinary stone recurrence: A randomized prevention trial. J Clin Epidemiol. 1992;45:911-6.

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  3. Yasui T, Suzuki S, Itoh Y, Tozawa K, Tokudome S, Kohri K. Eicosapentaenoic acid has a preventive effect on the recurrence of nephrolithiasis. Urol Int. 2008;81:135-8.