Follow-up
Further Outpatient Care
- Repeat 24-hour urine testing and appropriate blood determinations are needed until the hypercalciuria is controlled and stable. Once this occurs, repeat testing can be performed less often. Testing once per year is considered reasonable for patients whose stone production and level of hypercalciuria are controlled. If hypercalciuria is not well controlled, appropriate adjustments can be suggested and testing should be repeated more frequently.
- As patients modify their diets, they may substitute new foods and beverages for the ones previously restricted. These new dietary items have an unpredictable effect on the various stone risk factors. Therefore, follow-up 24-hour urine tests should include all of the major stone risk factors and not just calcium.
- Routine radiographs, such as an abdominal flat plate (also called KUB for kidneys, ureters, and bladder) or plain renal tomograms, are useful to find any newly formed stones. This is particularly important and helpful in patients whose hypercalciuria is poorly controlled.
- Some patients pass additional stones and assume their treatment plan is not working when, actually, these stones had already formed before testing or treatment began. Establishing the number, size, and location of any existing calculi before testing or treatment begins is important. In this way, patients can be reassured that their treatment plan is successful in controlling their hypercalciuria and they are only passing old, previously formed stones.
Deterrence/Prevention
- Hypercalciuria and bone density
- Hypercalciuric stone formers have been demonstrated to have a lower average bone mineral density than non–stone formers matched for age and gender. Compared with normocalciuric stone formers, hypercalciuric patients have an average bone density that is 5-15% lower. This holds true for both pediatric and adult populations. The decrease of bone density occurs in both the femoral neck (cortical) and lumbar spine (trabecular) areas. Bone loss is worsened if patients are placed on a calcium-restricted diet. Ninety-nine percent of the body's calcium is stored in the bones. Fortunately, significant clinical bone loss is relatively rare. Female hypercalciuric stone formers who become menopausal are at significantly greater risk of osteoporosis than their healthy female counterparts. The higher the urinary calcium excretion, the greater the risk.
- Untreated patients with an obligatory urinary calcium loss relatively unaffected by diet, as in renal leak hypercalciuria, renal phosphate leak, and resorptive hypercalciuria (hyperparathyroidism), develop a negative calcium balance that can result in osteopenia or osteoporosis. Some patients may have a primary altered bone metabolism, as occurs in postmenopausal women with an estrogen deficiency. Thirty percent of hypercalciuric children already show evidence of bone loss, which suggests a metabolic disorder is responsible. Strong evidence exists suggesting that the underlying disorder causing the hypercalciuria is responsible for the bone demineralization, but other factors, such as an overly zealous dietary calcium restriction, undoubtedly play a role.
- Hypercalciuric patients with known osteopenia, osteoporosis, or bone demineralization and those with untreated or unresponsive hypercalciuria should have periodic bone density measurements, especially if they are 50 years or older.
- Patients on prolonged bedrest will lose bone density and develop hypercalciuria. This also occurs in astronauts during space flights of long duration. Studies on astronauts have shown an increase in their risk of kidney stone formation during prolonged weightlessness. These changes included hypercalciuria as well as decreased fluid intake and reduced urinary volumes.
- Thiazide therapy can resolve the hypercalciuria in many of these patients and also can increase their bone density at a rate of 8% (spine) and 3% (hip) per year. Bisphosphonates and estrogen supplements also can be used.
- An intriguing suggestion has been the possible use of osteocalcin levels before and after dietary calcium restriction.31 Osteocalcin is released during periods of bone resorption, which would be expected with renal leak hypercalciuria, hyperparathyroidism, or any dietary calcium resistant hypercalciuria. Patients with elevated osteocalcin levels theoretically would benefit from thiazide and/or bisphosphonate therapy to prevent bone demineralization over time even if their hypercalciuria is well controlled with dietary therapy alone. Estrogen can be added in women. In other words, a high osteocalcin level could be a useful indicator of increased bone resorption, identifying those at the greatest risk of bone calcium loss. Appropriate therapy then could be used to prevent further bone demineralization and osteoporosis.
- Management of hypercalciuria in osteoporosis
- The issue of management of hypercalciuria can be complicated by the presence of osteoporosis or osteopenia. A serum calcium determination is the first step to identify patients with possible hyperparathyroidism. Elevated serum calcium levels should be followed up with a simultaneous PTH level to diagnose hyperparathyroidism.
- Even without a history of calcium kidney stones, a 24-hour urine test to check urinary calcium excretion can be useful in the management of osteoporosis. If the patient has hypercalciuria (and hyperparathyroidism has been eliminated by serum testing), the patient will benefit from thiazide therapy, which increases serum calcium and reduces excessive urinary calcium excretion. As mentioned earlier, thiazides increase bone density in these patients.
- Estrogen should be used, if appropriate, in postmenopausal women. Bisphosphonates, such as alendronate (Fosamax), risedronate (Actonel), or ibandronate (Boniva), should be used in men and in women when estrogen cannot be used.
- Calcium supplementation can be helpful in osteoporosis, but urinary calcium levels need to be monitored carefully in calcium stone–forming patients, especially if they demonstrate overt hypercalciuria.
- Studies have shown that, for most postmenopausal women with osteoporosis but with no previous history of calcium kidney stone disease, the overall risk of calcium nephrolithiasis does not increase significantly after supplemental calcium or combined calcium with calcitriol despite an increase in urinary calcium excretion.8
- Calcium citrate is recommended for calcium stone formers in this situation because its citrate component limits any increase in stone formation rate. Medical therapy, including thiazides, should be started first. Then calcium citrate can be added until the urinary calcium level reaches the normal upper limit (250 mg of calcium per 24 hours or 4 mg of calcium per kilogram of body weight).
- Other possible urinary stone risk factors, such as uric acid, citrate, volume, phosphate, sodium, magnesium, and oxalate, should be optimized.
Patient Education
- Patient education is extremely important in the treatment of hypercalciuria. Only a very motivated patient with an understanding of the need for continuing treatment can be expected to maintain any long-term preventive program, which typically lasts years. Additionally, no immediate penalty exists for cheating, such as occurs in a patient with diabetes who forgets to take his morning insulin. In a hypercalciuric patient who fails to follow the treatment regimen, the penalty (the next kidney stone) may not become apparent for many months or even years. This means that only a truly motivated and informed patient can be expected to follow any therapeutic program for hypercalciuria on a truly long-term basis.
- Two excellent sources of general patient information on kidney stones and hypercalciuria include " Medical Management of Kidney Stones," by Paul Pietrow and Michael Karellas, which is available free online from American Family Physician, and the Institute of Diabetes and Digestive and Kidney Diseases at (301-654-4415).
- For patients who desire more complete information, the National Institutes of Health (NIH) recommends The Kidney Stones Handbook by Savtiz, G and Leslie, S published by Four Geez Press.
- It can be ordered by phone (530-889-1727) or by writing directly to the publisher at the following address: Grant Gibbs
Four Geez Press
600 Auburn Ravine Road, #313
Auburn, CA 95603 - This book includes a clearly written chapter on hypercalciuria as well as many other aspects of kidney stone disease that would be of great interest to patients with nephrolithiasis and their families.
- It can be ordered by phone (530-889-1727) or by writing directly to the publisher at the following address: Grant Gibbs
Miscellaneous
Medicolegal Pitfalls
- Every patient with at least one kidney stone should be offered the opportunity for stone prevention testing and prophylactic therapy. This is most critical in children and in patients with renal failure or a single functioning kidney. For most adult patients, this is optional, but testing and preventive treatment needs to be offered and the consequences of additional preventable stones reviewed.
- An excellent patient education book on nephrolithiasis is now available. Written by a urologist, the book is entitled The Kidney Stones Handbook and is recommended by the National Institutes of Health. There are separate chapters on hypercalciuria and kidney stone preventive testing and treatment. For more information on this book, contact the publisher, Grant Gibbs, at 530-889-1727 or send an email to gsavitz@earthlink.net.
- Even if patients refuse preventive testing and prophylactic therapy, they should be advised of the potential risks of recurrent stones and provided general dietary advice regarding moderation of calcium, animal protein, sodium, purines, and oxalate ingestion. All patients with history of kidney stones need to increase their fluid intake. Hypercalciuric patients must be cautioned about the risks of an overly severe reduction in oral calcium intake, which actually can increase their risk of new stone formation.
- Do not fail to offer preventive testing and therapy to patients. Virtually all hypercalciuria patients can be helped if they are willing and able to follow a long term treatment program.
Special Concerns
- Future research
- As noted above, a distinct possibility exists that something as basic as the definition of hypercalciuria may be flawed due to improper control groups used in establishing the original reference range for 24-hour urinary calcium excretion. If this proves to be correct, these values will need to be revised and their validity established. The addition of calcium/creatinine ratio and urinary calcium concentration to the standard 24-hour total urinary calcium excretion should be helpful in identifying hypercalciuric patients.
- Molecular genetics and other research has indicated potential lines of future investigation into the nature of hypercalciuria. Avenues, such as mutations in the CLCN5 chloride channel gene or in the calcium-sensing receptor, appear promising. Other promising lines of research involve overexpression of vitamin D receptors and deficiencies in various renal tubular enzymes.
- PTH or its amino-terminal fragment has been shown to increase bone formation without causing hypercalcemia. PTH stimulates both bone formation and resorption. Once daily injections of PTH tends to maximize the osteoblastic activity while minimizing bone resorption for a net gain in bone mass.
- This treatment was tested in a large, multicenter trial of 9347 postmenopausal women with osteoporosis. All of the patients received vitamin D and calcium supplementation. The group that received the PTH injections had reductions in fracture rates of 65-86%. Urinary calcium excretion was increased only slightly (roughly by 30 mg of calcium per day in the treated group), but the overall incidence of hypercalciuria was no different between the PTH-treated group and placebo. This most likely was due to the single daily dosing of the PTH, which minimized the hypercalcemic and hypercalciuric responses.
- In short, this is a promising avenue of research for osteoporosis and osteopenia that appears to have no significant effect on hypercalciuria or calcium stone formation. Further research on this and other osteoblast-enhancing therapies hold promise in treating both osteoporosis and, possibly, select cases of hypercalciuria.
- The ultimate goal is to develop therapies that eliminate the risk of calcium stone disease and osteoporosis from hypercalciuric individuals.
More on Hypercalciuria |
| Overview: Hypercalciuria |
| Differential Diagnoses & Workup: Hypercalciuria |
| Treatment & Medication: Hypercalciuria |
 Follow-up: Hypercalciuria |
| Multimedia: Hypercalciuria |
| References |
| Further Reading |
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Keywords
absorptive hypercalciuria, calcium-loading test, calcium stone disease, calcium stones, Dent disease, elevated urinary calcium, high urinary calcium, hyperparathyroidism, geriatric hypercalciuria, idiopathic hypercalciuria, ketogenic diet, medullary sponge kidney, MSK, nephrolithiasis, osteoporosis, pediatric hypercalciuria, renal calculi, renal leak hypercalciuria, renal phosphate leak, resorptive hypercalciuria, sarcoid, urolithiasis
