Men's Osteoporosis Support Group

Kidney stones and osteoporosis

Curr Opin Urol. 2005 Mar;15(2):119-26, Developments in stone prevention, Straub M, Hautmann R. PMID: 15725936. Kidney stones (nephrolithiasis) develop through complex biological processes, and may relate to osteoporosis or osteopenia. Stones are becoming an increasing problem, with a 37% increase in the U.S. over the last 20 years. Thus I'm going to summarize this Straub and Hautmann review of kidney stones hoping to educate those individuals dealing with kidney stones and those who also concomitantly have osteoporosis as a result of the physiological/pathological processes involved in stone formation.

Diagnostic and treatment updates. One reason for the increase in stones may be that there are now better diagnostic tools, especially ultrasound, to detect asymptomatic stones. Therapy improvements are important too, and include: extracorporeal shock-wave lithotripsy (ESWL), ureterorenoscopy (URS), and percutaneous nephrolitholapaxy (PCNL), renal pelvis puncture via the flank approach. After positioning a nephroscopy shaft and nephroscope, renal stones can be removed. These are all modern treatment methods that make stone management relatively comfortable and which have reduced the need for open stone surgery to less than 1% of the time. And the authors fear that stone prevention takes a back seat to therapy, which they dislike.

Prevention. Although the authors stress prevention's importance, they note that more than 50% of all recurrent stone formers have just one lifetime recurrence. Thus, in these patients, general drinking and nutritional advice suffices. Particularly, in the group of about 10% of stone formers who have more than three recurrences, specific measures and pharmacological therapy are justified.

Stone disease general risk factors. 1) not drinking enough water, and not drinking it frequently enough. 2) eating food too rich in calories and too much table salt. 3) having a diet deficient in fiber and alkali. 4) inadequate exercise. These lead to: 1) supersaturated urine. 2) urine deficient in inhibitory substances. 3) A multitude of overweight or obese individuals. The authors state: "A first but essential step towards stone prevention is the normalization of the BMI." The body mass index should be between 18 and 25 kg/m2. A correlation also exists between cardiovascular risk factors and stone disease. One study of police officers with nephrolithiasis showed 89% were overweight, 43.5% had hypercholesterolemia, 31.5% had concurrent hypertension (high blood pressure), 14% were physically inactive, and 3.5% had diabetes. A high sodium chloride (salt) intake directly relates to a significant increase in renal calcium excretion. Modern diets have up to 10/g salt per day, whereas about 3 g/day, or less, is suggested. The authors note: "And finally, salt restriction has beneficial effects in--or even cures--both diseases." Both diseases being nephrolithiasis and hypertension. Polyunsaturated fatty acids have proven to be a stone formation preventive, and should be included in the diet. Stone formation appears to be a part of the 'metabolic syndrome' which correlates with disorders like diabetes mellitus type II, gout, hyperlipidemia, hypertension and kidney stone formation. Particularly insulin resistance is the common pathological cause for patients with recurrent uric acid stones. Insulin resistance, usually a problem in obese individuals, stems from decreased insulin receptor density. The authors present this anti-stone-forming advice:

Fluid intake, 'drinking advice'

Balanced diet, 'nutrition advice'

Normalized general risk factors, 'lifestyle advice'

Diet: a status report. The authors note, "Studies showed that a diet low in animal protein, sodium, and normal in calcium content, proved to be highly efficient in recurrence prevention." Other studies have these items: more ingested fluid, potassium, and phosphate, as being the main factors in recurrence prevention. The authors show a figure that charts oxalate intestinal absorption on the vertical axis and calcium intake on the horizontal axis. At 200 mg/day calcium intake, oxalate absorption is about 17%. At 1800 mg/day calcium intake, oxalate absorption is about 2%. If less oxalate is present this reduces oxalate stone formation risk. So, for oxalate stone formers, calcium intake is important. Nutritional acid load can be an important issue regarding osteoporosis, more important than calcium intake, since it causes skeletal calcium resorption while being a final step in hypercalciuria. In this case, calcium intake restriction coupled with dietary acid load leads to skeletal bone loss and severe osteoporosis can result. Urol Int. 2004;72 Suppl 1:29-33. Body weight, diet and water intake in preventing stone disease. Meschi T, Schianchi T, Ridolo E and others. PMID: 15133330. This article has a recommended diet for stone formers which I'll summarize: total calories, 2,540 kcal; total proteins (g), 93 from meat or fish, milk products, and bread, pasta, or vegetable protein; total fat (g), 93 (33% of total calories); total carbohydrates (g), 333 (52% of total calories); fiber content (g), 40; sodium chloride, 3,000 mg; potassium, 4,788 mg; calcium, 1,200 mg, phosphorus, 1,508 mg; magnesium, 353 mg; oxalate, 200 mg; water from foods, 1,550 ml; water to drink, 2,000 ml.

Calcium, the pros and cons. Normal calcium intake, 1,2,00-1,500 mg/day, preferably from foods, is now recommended for most stone formers. The only condition where calcium restriction may be warranted is for patients with absorptive hypercalciuria type I. This uncommon condition is defined as an absorptive hypercalciuria variation that doesn't respond to diet changes, even to severe calcium restriction. However, urinary calcium levels are normal during fasting periods. Note that stone formers with type I absorptive hypercalciuria are osteoporosis-prone. This because the skeleton becomes the body's calcium source rather than through normal gut absorption. Additionally resorptive hypercalciuria, which results from excess parathyroid hormone, can also cause osteoporosis. Serum parathyroid hormone would be elevated which would simplify the diagnosis of this osteoporosis-related condition.

Pharmacological prevention or treatment. This article has five complex tables showing the recommended therapeutic or preventive strategy for various stone former types. I am not going to list all these, but will suggest if you have been diagnosed in a listed category, that you acquire the full article PMID: 15725936. Here are the major categories: calcium oxalate stones (whewellite, weddellite), renal tubular acidosis (type I), calcium phosphate stones (carbonate apatite, brushite), uric acid and ammonium urate stones, and infection stones (struvite). The authors note that one recent finding has shown that combining magnesium and citrates is more effective than using citrates alone, with magnesium potassium citrate given over three years being shown to reduce the recurrence risk by 85%.

Conclusions. The authors state, "Normalization of body weight (BMI) and cardiovascular risk factors, sufficient physical activity, balanced nutrition and sufficient circadian fluid intake would be the appropriate measures to avoid new calculus formation in about 85% of all stone formers." They also highlight the importance of low animal protein and sodium chloride intakes, and a high alkaline potassium intake, as being the keys to efficient stone prevention. Additionally, except for absorptive hypercalciuria type I, restricted calcium intake is not recommended.

Editor's comments: This article provides excellent guidelines for stone-forming individuals to follow to prevent recurrences. Not mentioned, but that you might want to include, are: 1) referral to a urologist to find out which, if any, diagnostic tests should be performed to diagnose the cause of your stones and to evaluate what preventive measures you might need in the future. 2) if you are currently trying to pass a stone, trying to catch and save it appears important. The various preventive and treatment strategies generally evolve around the stone's chemical makeup. If you haven't captured one, how would you know which treatment your condition requires? Perhaps peeing through a small fine-mesh strainer or into a clear bottle would allow you to catch or see a stone that passes. Then take it to your physician for chemical analysis. Since 85% of stones will not recur if proper dietary measure are taken, that might make you not want to see a urologist for a diagnostic workup. However, remember that a small percentage of those stone formers have absorptive hypercalciuria type I, placing them at high risk for osteoporosis and skeletal fractures, and resorptive hypercalciuria also increases osteoporosis risk, but elevated serum parathyroid hormone would simplify diagnosis of this problem. That isn't the case with absorptive hypercalciuria type I. So, if you have osteoporosis and aren't responding to therapy, you may have absorptive hypercalciuria type I (without stone formation). So ask your physician for the fasting urine calcium test to rule this out. For an extensive online kidney stone article see: http://www.emedicine.com/med/topic1069.htm.

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