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Hypercalciuria: Differential Diagnoses & Workup

Author: Stephen W Leslie, MD, FACS, Founder and Medical Director, Lorain Kidney Stone Research Center; Clinical Assistant Professor, Department of Urology, The University of Toledo College of Medicine
Contributor Information and Disclosures

Updated: Oct 21, 2009

Differential Diagnoses

Hypercalcemia
Nephrocalcinosis
Hyperoxaluria
Nephrolithiasis
Hyperparathyroidism
Nephrolithiasis: Acute Renal Colic
Hypophosphatemia
Osteoporosis

Other Problems to Be Considered

Hypervitaminosis D
Nephrolithiasis—prevention of kidney stones
Hypercalcemic nephropathy

Workup

Laboratory Studies

  • Twenty-four hour urinary calcium determination
    • The obvious initial laboratory evaluation for hypercalciuria is the 24-hour urinary calcium determination, which generally is recommended while patients are feeling well and on their usual diet. A 24-hour urine test is of little value while patients are hospitalized with acute stone attacks or other medical problems; their diet and activity levels are different from the home conditions under which they formed the stones.
    • The 24-hour urine sample should be collected in a standardized fashion. Other 24-hour urine chemistries that are usually performed in stone formers (in addition to calcium) include the following: oxalate, pH, volume, creatinine, specific gravity, phosphorus or phosphate, citrate, sodium, uric acid, magnesium, and either urea nitrogen or sulfate (which are increased in cases of high protein ingestion). If possible, these chemistries should all be performed together.
    • Ensure that the laboratory performing the studies has a reliable methodology for urinary chemistry testing. In the United States, this usually requires sending most 24-hour urine tests to an outside reference laboratory. Because usually only a small portion of the total sample is actually sent, some potential errors are introduced if the urine sample is not handled properly or if the total volume is not measured and recorded accurately.
    • Instructions for proper 24-hour urine collection procedures must be reviewed carefully with every patient. (Patients who are more intelligent often are the ones who rush through the instructions and misunderstand, delivering grossly inaccurate specimens.) One easy way to determine the urine collection accuracy is to compare the total urinary creatinine collected with the expected levels. A properly performed 24-hour urine collection should show a mean urinary creatinine of 22.1 mg/kg in men and 17.2 mg/kg in women. Any values that are significantly different from those predicted probably represent improper or inaccurate collections.
  • Serum laboratory studies
    • Ideally, serum laboratory studies should be drawn at the same time the 24-hour urine sample is being collected. In this way, the action of the kidneys can be viewed in the context of serum levels of these same parameters.
    • Minimum blood tests currently recommended for stone formers include serum calcium, phosphorus, electrolytes, uric acid, and creatinine. High serum calcium levels should be repeated, along with PTH levels to check for hyperparathyroidism. Serum intact PTH and ionized calcium are the most reliable in borderline cases. (Vitamin D and vitamin D-3 are available in some laboratories and, while useful in select cases, still are considered investigational.)
  • Laboratory approaches to hypercalciuria
    • Two distinct approaches to the laboratory evaluation of hypercalciuric patients exist. With both, initial blood testing, such as serum calcium, creatinine, and phosphate, should be performed to identify patients at risk for hyperparathyroidism, renal failure, and renal phosphate leak.
    • Once hyperparathyroidism has been excluded, the two approaches differ. In the traditional approach, a calcium-loading test is performed. This is based on the principle that, during a defined period of fasting, patients with absorptive hypercalciuria show a significant decrease in urinary calcium excretion. Patients with renal leak hypercalciuria, in which the kidney has an obligatory calcium-losing defect, are expected to show relatively little effect from dietary measures alone, including fasting. Patients are then administered a large oral calcium meal, and urine samples are obtained periodically afterwards. Patients with absorptive hypercalciuria tend to greatly increase their urinary calcium excretion after a large calcium meal, while patients with renal leak hypercalciuria do not demonstrate as large an increase.
    • In practice, performing the calcium-loading test is difficult, tedious, and usually reserved for selected cases in a tertiary care center or for research purposes. The simplified clinical approach is becoming increasingly popular. It involves an attempt to use dietary measures alone to control urinary calcium excretion (after first screening the patient with blood tests for kidney failure, hyperuricemia, hypophosphatemia, and hypercalcemia.) If successful, no further treatment is necessary other than routine monitoring. If unsuccessful, the patient requires medical therapy.
    • Not only is the simplified clinical approach much easier to perform and follow, but it also corresponds to what many experts actually carry out in their own clinical practices. The precise diagnosis may not always be clear, but the patient receives essentially the same treatment without the need for an inconvenient expensive test that is hard to interpret.
  •  [#calciumloading]Traditional approach to hypercalciuria: The calcium-loading test
    • The theoretical advantage of a formal calcium-loading test is a more precise diagnosis, which leads more quickly to definitive therapy.
    • This is particularly useful in differentiating absorptive hypercalciuria type I and type II from renal leak hypercalciuria.
    • Performing the calcium-loading test
      • Usually, 2 separate 24-hour urine collections are collected and analyzed for calcium while the patient is on a regular diet. This is undertaken to confirm the diagnosis, establish the baseline urinary calcium level, and to determine if the degree of hypercalciuria is consistent and reproducible.
      • The patient is placed on a strict low calcium diet of 400 mg of calcium and 100 mEq of sodium per day for 1 week. At the end of the week, an additional 24-hour urine sample is taken and tested for calcium and creatinine.
      • The fasting phase begins at 9 pm and continues until 7 am the following morning. The patient voids at 7 am, and the specimen is discarded. He or she is provided an additional 400-600 cc of water to drink. For the next 2 hours, the patient continues fasting but does not urinate again until 9 am, when he or she is asked to void. The urine is collected and analyzed for calcium and creatinine. This specimen is called the fasting sample.
      • The patient next is administered a 1-g oral calcium load, which usually consists of an appropriate amount of calcium gluconate. All urine that is passed from this point until 1 pm, 4 hours later, is collected and analyzed for calcium and creatinine. This specimen is called the post–calcium load sample.
      • The calcium/creatinine ratio is measured in the urine specimen taken on the 400-mg calcium-restricted diet and both the fasting and post–calcium load samples. In healthy people, the calcium/creatinine ratio is no more than 0.11 for the fasting sample and no more than 0.20 for the post–calcium load sample.
      • Note that, in this testing series, hypercalciuria is defined as the excretion of more than 200 mg of urinary calcium per 24 hours on the 400-mg calcium-restricted diet.
    • Interpreting the calcium-loading test
      • Patients with absorptive hypercalciuria normalize their urinary calcium excretion while on a fasting diet but greatly increase their urinary calcium excretion after the calcium load. Therefore, their fasting calcium/creatinine ratio is equal to or less than 0.11, but their post–calcium load samples are greater than 0.20, demonstrating an exaggerated calcium absorption and subsequent excretion.
      • Patients with type I absorptive hypercalciuria typically do not normalize their urinary calciums to less than 200 mg per 24 hours on the 400-mg calcium restricted diet, while patients with type 2 hypercalciuria do demonstrate less than 200 mg of urinary calcium per day while on that same diet.
      • Patients with renal leak hypercalciuria and hyperparathyroid (resorptive) hypercalciuria are hypercalciuric regardless of oral calcium intake, so they show more than 200 mg of urinary calcium excretion per 24 hours on the calcium-restricted diet and high calcium/creatinine ratios in both phases of the calcium-loading test. Serum calcium level differentiates between these 2 diagnoses because renal leak hypercalciuria has low serum calcium levels while hyperparathyroid patients are hypercalcemic.
    Table 3. Calcium-Loading Test Interpretation Guide

    Open table in new window

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    Table
    CriteriaAbsorptive Type IVitamin D–Dependent, Classic TypeAbsorptive Type IVitamin D–Dependent, Variant TypeAbsorptive Type IIDietary Calcium ResponsiveAbsorptive Type III(Renal Phosphate Leak)Renal Calcium LeakResorptive*
    Urinary calcium on regular diet† HighHighHighHighHighHigh
    Urinary calcium on low calcium diet‡ HighHighNLHighHighHigh
    Urinary calcium fasting§ NLHighNLHighHighHigh
    Urinary calcium after 1-g calcium loadII HighHighNLHighHighHigh
    Serum PO4 fastingNLNLNLLowNL or highLow
    Serum calcium fastingNLNL or highNLNL or highNL or lowHigh
    Serum PTHNL or lowNL or lowNLLowHighHigh
    Serum PTH after 1-g calcium loadNL or lowNL or lowNLLowHighHigh
    Serum vitamin D-3 (calcitriol)NLHighNLHighHighHigh
    Fasting normocalciuria while on ketoconazoleNoYesNoYesNoNo
    Bone calcium densityNLNL or lowNLNL or lowLowLow
    CriteriaAbsorptive Type IVitamin D–Dependent, Classic TypeAbsorptive Type IVitamin D–Dependent, Variant TypeAbsorptive Type IIDietary Calcium ResponsiveAbsorptive Type III(Renal Phosphate Leak)Renal Calcium LeakResorptive*
    Urinary calcium on regular diet† HighHighHighHighHighHigh
    Urinary calcium on low calcium diet‡ HighHighNLHighHighHigh
    Urinary calcium fasting§ NLHighNLHighHighHigh
    Urinary calcium after 1-g calcium loadII HighHighNLHighHighHigh
    Serum PO4 fastingNLNLNLLowNL or highLow
    Serum calcium fastingNLNL or highNLNL or highNL or lowHigh
    Serum PTHNL or lowNL or lowNLLowHighHigh
    Serum PTH after 1-g calcium loadNL or lowNL or lowNLLowHighHigh
    Serum vitamin D-3 (calcitriol)NLHighNLHighHighHigh
    Fasting normocalciuria while on ketoconazoleNoYesNoYesNoNo
    Bone calcium densityNLNL or lowNLNL or lowLowLow
    *Resorptive means hyperparathyroidism.† Regular diet is unrestricted calcium and sodium intake. Normal upper limit calciuria is <4 mg/kg body weight per day.‡ Low-calcium diet is 400 mg calcium and 100 mEq of sodium per day. Normal upper limit calciuria is <200 mg/day.§ Fasting is a 12-hour fast. Normal upper limit is <0.11 mg calcium/mg creatinine.II After 1-g calcium load, normal upper limit is <0.20 mg calcium/mg creatinine.

Simplified clinical approach to hypercalciuria

Virtually all patients can be treated quite successfully using a simplified approach to hypercalciuria without the need for a formal calcium-loading test.

After initial history and laboratory testing, including serum and 24-hour urinary chemistries as outlined previously, hypercalciuric patients undergo a short-term trial of dietary modification. Patients with hypercalcemia and elevated PTH levels probably have hyperparathyroidism and should be treated appropriately. The test diet includes a moderate dietary calcium intake of about 600-800 mg/day. This corresponds to roughly one good calcium meal per day and possibly one additional dairy snack (eg, one glass of milk with a second small dairy serving). Restricting dietary salt, which can increase hypercalciuria, is important. Animal protein should be ingested in moderation (<1.7 g/kg of body weight daily), and dietary fiber should be increased. Limiting dietary oxalate also is advantageous to avoid an increase in oxaluria due to the loss of intestinal oxalate-binding sites from the diminished dietary calcium.

The 24-hour urinary chemistries are repeated while the patient is on this modified diet. The author tests all of the urinary chemistries and not just calcium because of the possibility of finding new chemical risk factors caused by the dietary changes. If patients have normalized their urinary calcium solely with dietary modifications, then they can be treated successfully with this method. If they still have significant hypercalciuria, patients need medical therapy such as thiazides, orthophosphates, sodium cellulose phosphate, or bisphosphonates. The cause of the failure to control urinary calcium with dietary therapy is not particularly important at this point in therapy, although it most likely is a lack of effectiveness of the prescribed diet or a lack of patient compliance.

Testing should be repeated at periodic intervals to ascertain continued patient compliance and effectiveness. Once a stable, satisfactory urinary calcium level is established, periodic 24-hour urinary testing is not necessary more often than perhaps once a year for monitoring. Difficult or unresponsive cases can be referred to an appropriate expert or tertiary care center for further evaluation and treatment.

The advantage of the simplified approach is obvious. Only a short term trial of dietary therapy is needed to determine if dietary modification is potentially adequate as a treatment. Medical treatment, usually beginning with thiazides, is used if dietary therapy alone is unsuccessful for any reason. Serum testing for PTH excess, hypercalcemia, and hypophosphatemia helps to identify those entities (hyperparathyroidism, renal leak hypercalciuria, renal phosphate leak) that should not be treated with dietary therapy alone. The vast majority of hypercalciuric patients can be treated with this simplified plan. Ensuring that patients are retested while on the modified diet is important, otherwise judging the effectiveness of the therapy or patient compliance is impossible.

Summary of the simplified approach to hypercalciuria

  • Complete medical history with initial blood and 24-hour urine testing.
  • Identify hypercalciuric patients.
  • Check hypercalcemic patients for hyperparathyroidism with PTH levels. Consider thiazide challenge test if PTH alone is inconclusive.
  • Check hypophosphatemic patients for hyperphosphaturia and possible absorptive type III hypercalciuria. Verify diagnosis with a vitamin D-3 level or a clinical trial of orthophosphate therapy.
  • Start a therapeutic trial of dietary modification treatment.
  • Repeat blood and 24-hour urine testing.
  • If the hypercalciuria is controlled successfully with dietary modification, continue therapy and repeat testing periodically. If unsuccessful, consider a trial of thiazide therapy.
  • Orthophosphates, bisphosphonates, or sodium cellulose phosphate can be used if thiazides are not tolerated well or fail to control urinary calcium levels adequately. Patients who fail all of these therapies require further evaluation.

Imaging Studies

  • Medullary sponge kidney is a congenital condition that can be diagnosed only by intravenous pyelogram (IVP). It appears as a whitish blush in the renal papilla, which is caused by the cystic dilation of the distal collecting ducts before they empty into the renal pelvis. Patients with medullary sponge kidney are quite likely to produce kidney stones, with about 60% developing nephrolithiasis at some point. About 12% of all stone formers are thought to have medullary sponge kidney. (Although the exact number is not known for certain, it ranges from 2.6-21% in various studies.) No specific treatment exists, but renal leak hypercalciuria is more frequently found in patients with medullary sponge kidney than in other hypercalciuric calcium stone formers.

Histologic Findings

Histopathologic and ultrastructural examinations using light and electron microscopy have shown significant changes in the lower urinary tracts and kidneys in chronic hypercalciuria specimens.

Transitional epithelial cells of the ureters and bladder demonstrate increased cell proliferation and apical cytoplasmic vacuole formation. These effects were more prominent in the proximal urinary tract epithelial cells. Deeper structures showed increased mitotic activity, edema, vasodilatation, and separation of collagen fibers.

In the kidney, findings include interstitial edema, vasodilatation, tubular degeneration, and vacuolization of both the proximal and distal convoluted tubules.

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

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Contributor Information and Disclosures

Author

Stephen W Leslie, MD, FACS, Founder and Medical Director, Lorain Kidney Stone Research Center; Clinical Assistant Professor, Department of Urology, The University of Toledo College of Medicine
Stephen W Leslie, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, National Kidney Foundation, and Ohio State Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Martha K Terris, MD, FACS, Professor, Department of Surgery, Medical College of Georgia
Martha K Terris, MD, FACS is a member of the following medical societies: American Cancer Society, American College of Surgeons, American Institute of Ultrasound in Medicine, American Urological Association, New York Academy of Sciences, and Society of University Urologists
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

CME Editor

J Stuart Wolf Jr, MD, FACS, David A Bloom Professor of Urology, Director of Division of Minimally Invasive Urology, Department of Urology, University of Michigan
J Stuart Wolf Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, Society of University Urologists, and Society of Urologic Oncology
Disclosure: Terumo Corporation Consulting fee Consulting; Gyrus-ACMI Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

 
 
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