Absorptive Hypercalciuria Type Research Articles

Defining hypercalciuria in nephrolithiasis

The classic definition of hypercalciuria, an upper normal limit of 200 mg/day, is based on a constant diet restricted in calcium, sodium, and animal protein; however, random diet data challenge this. Here our retrospective study determined the validity of the classic definition of hypercalciuria by comparing data from 39 publications analyzing urinary calcium excretion on a constant restricted diet and testing whether hypercalciuria could be defined when extraneous dietary influences were controlled. These papers encompassed 300 non-stone-forming patients, 208 patients with absorptive hypercalciuria type I (presumed due to high intestinal calcium absorption), and 234 stone formers without absorptive hypercalciuria; all evaluated on a constant restricted diet. In non-stone formers, the mean urinary calcium was well below 200 mg/day, and the mean for all patients was 127±46 mg/day with an upper limit of 219 mg/day. In absorptive hypercalciuria type I, the mean urinary calcium significantly exceeded 200 mg/day in all studies with a combined mean of 259±55 mg/day. Receiver operating characteristic curve analysis showed the optimal cutoff point for urinary calcium excretion was 172 mg/day on a restricted diet, a value that approximates the traditional limit of 200 mg/day. Thus, on a restricted diet, a clear demarcation was seen between urinary calcium excretion of kidney stone formers with absorptive hypercalciuria type I and normal individuals. When dietary variables are controlled, the classic definition of hypercalciuria of nephrolithiasis appears valid.

Detection of Absorptive Hypercalciuria Type I Without the Oral Calcium Load Test

We retrospectively analyzed the validity of a simple method of detecting absorptive hypercalciuria type I, a common stone forming condition with hypercalciuria that is believed to be due to high intestinal calcium absorption. The method is based on urinary calcium derived from 24-hour urine collections while on random and restricted diets rather than on a calciuric response to an oral calcium load. A group of 916 well characterized patients with idiopathic calcium oxalate urolithiasis comprised the study group. We also analyzed a subgroup of 695 patients, excluding 221 with dietary abuse, defined as urinary sodium greater than 150 mEq daily and/or sulfate greater than 35 mmol daily, to eliminate potential confounding dietary factors affecting the diagnosis. In each group absorptive hypercalciuria type I was detected by the old criteria, requiring an exaggerated calciuric response to an oral calcium load test, and by the new criteria, based on 24-hour urinary calcium 200 mg or greater daily while on random and restricted diets. Using the old criteria as the gold standard the positive and negative predictive values, sensitivity and specificity of the new criteria were 80.1%, 95.9%, 90.8% and 90.5%, respectively. When excluding patients with dietary abuse the values were 85.9%, 97.2%, 92.4% and 94.5%, respectively. Absorptive hypercalciuria type I may be reliably detected by a simple method based on high 24-hour urinary calcium while on random and restricted diets, especially when excluding patients with evidence of dietary abuse during the restricted diet.

Evidence for metabolic origin of absorptive hypercalciuria Type II

The objective of this retrospective data analysis was to test the hypothesis that absorptive hypercalciuria Type II (AH-II) is a less severe variant of absorptive hypercalciuria Type I (AH-I), a common cause of calcareous stones. 24-h urinary calcium obtained on constant metabolic diets was retrieved from several data sources, including those of the authors and another group. On a low calcium diet (10 mmol calcium), 35 patients with AH-II were compared with 70 non-stone formers (NSF) and 76 patients with AH-I. On a high calcium diet (25 mmol calcium/day), 10 patients with AH-II were compared with 35 NSF and 32 with AH-I. On a low calcium diet for all participants, 24-h urinary calcium in AH-II (4.13 ± 0.63 mmol/day) was significantly higher than in NSF (3.06 ± 1.17 mmol/day), but significantly lower than in AH-I (6.11 ± 1.14 mmol/day) (p < 0.001). In a smaller subset, fractional intestinal calcium absorption in AH-II (65.0 ± 11.1%) was intermediate between NSF (50.0 ± 6.4%) and AH-I (71.0 ± 6.7%) (p < 0.001 between AH-II and other groups). On a high calcium diet, the rise in urinary calcium in AH-II was significantly higher than in NSF, but not as marked as in AH-I. Estimated calcium balance in AH-II was similar to NSF, but significantly more positive than AH-I. In conclusion, AH-II shares with AH-I the same metabolic disturbance(s) stimulating intestinal absorption and renal excretion of calcium but to a lesser degree. Bone might be spared in AH-II.

Reduced bone formation and relatively increased bone resorption in absorptive hypercalciuria

Absorptive hypercalciuria (AH), a common stone-forming condition characterized biochemically by intestinal hyperabsorption of calcium and hypercalciuria may be associated with bone loss. In AH type I (AH-1), hypercalciuria persists despite restriction in dietary calcium intake. We therefore hypothesized that the skeleton may contribute to the hypercalciuria in this subgroup of patients. Histomorphometric analysis of iliac crest biopsies were performed on nine stone-formers with AH-1 and on nine matched normal subjects. After stabilization on a stone-prevention diet, calcium homeostasis in the stone formers was then evaluated on inpatient constant metabolic diet before and after short-term blockade of bone resorption by alendronate (10 mg daily, 17 days total). Compared with controls, the stone-formers had lower indices of bone formation (osteoblast surface/bone surface 1.8+/-2.1 vs 3.0+/-1.5%, P=0.04; wall thickness 35.8+/-6.9 vs 47.2+/-7.6%, P=0.001) and relatively higher bone resorption (osteoclast surface/bone surface 0.4+/-0.2 vs 0.2+/-0.2%, P=0.05). In the stone-formers, a short-term course of alendronate treatment corrected fasting urinary calcium (0.14+/-0.06 to 0.06+/-0.04 mg Ca/mg Cr, P=0.001) and marginally reduced 24-h urinary calcium by 48 mg/day (P=0.06). Increased intestinal calcium absorption and hypercalciuria persisted, but estimated calcium balance improved (P=0.007). Our results suggest that the hypercalciuria of AH-1 originates primarily from intestinal hyperabsorption of calcium, but bone resorption in excess of bone formation may contribute.

Effect of dietary modification on urinary stone risk factors

AbstractEffect of dietary modification on urinary stone risk factors. BackgroundThis study was undertaken to ascertain the effect of dietary modification on urinary stone risks, and to determine whether the response depends on the prevailing urinary calcium. MethodsA retrospective data analysis was conducted from our stone registry involving 951 patients with calcareous stones undergoing ambulatory evaluation, whereby 24-hour urine samples were collected during random diet and after dietary modification composed of restriction of calcium, oxalate, sodium, and meat products. Samples were analyzed for stone risk factors. Urinary calcium was also obtained after overnight fast and following a 1 g-calcium load. Changes produced by dietary modification from the random diet were evaluated in 356 patients with moderate-severe hypercalciuria (>6.88 mmol/day, group I), 243 patients with mild hypercalciuria (5.00-6.88 mmol/day, group II), and 352 with normocalciuria (<5.00 mmol/day, group III). ResultsUrinary calcium postcalcium load and the percentage of patients with absorptive hypercalciuria type I were highest in group I, intermediate in group II, and lowest in group III. During dietary modification, urinary calcium declined by 29% in group I, 19% in group II, and 10% in group III. Urinary oxalate did not change. Urinary saturation of calcium oxalate declined by only 12% in group I, 6% in group II, and nonsignificantly in group III, owing to various physicochemical changes in urinary biochemistry, which attenuated the effect of the decline in urinary calcium. Urinary saturation of brushite declined in all 3 groups due to the fall in urinary calcium, phosphorus, and pH. This reduction was more marked in the hypercalciuric groups than in the normocalciuric group. Urinary saturation of monosodium urate also decreased from a decline in urinary sodium and uric acid. ConclusionSecondary rise in urinary oxalate occurring from calcium restriction can be avoided by concurrent dietary oxalate restriction. Dietary modification (restriction of dietary calcium, oxalate, sodium, and meat products) is more useful in reducing urinary saturation of calcium oxalate among patients with hypercalciuria than among those with normocalciuria.

Biochemical and Physicochemical Presentations of Patients With Brushite Stones

We determined whether the biochemical and physicochemical backgrounds of patients with brushite stones differ from those with hydroxyapatite and calcium oxalate stones. From a computer data base of patients completing ambulatory evaluation 19 with brushite stones, 24 with hydroxyapatite stones and 762 with calcium oxalate stones were identified with the specified composition in greater than 70% of stones. Absorptive hypercalciuria type I was present in 63% of patients with brushite, 17% with hydroxyapatite and 30% with calcium oxalate stones. Distal renal tubular acidosis was noted in 32% of patients with brushite, 42% with hydroxyapatite and 3% with calcium oxalate stones. Mean urinary calcium in the brushite group was significantly higher than in the hydroxyapatite and calcium oxalate groups (265 +/- 125 vs 186 +/- 103 and 187 +/- 95 mg daily, respectively). Urinary pH in the brushite group was slightly but significantly higher than in the calcium oxalate group (6.15 +/- 0.30 vs 5.91 +/- 0.42). The brushite relative saturation ratio in the brushite group was marginally higher than in the hydroxyapatite group and significantly higher than in the calcium oxalate group (3.25 +/- 2.03 vs 2.34 +/- 1.51 and 1.83 +/- 1.66, respectively). Patients with predominantly brushite stones could be distinguished from those with predominantly hydroxyapatite and calcium oxalate stones by higher urinary saturation with respect to brushite due mainly to hypercalciuria from absorptive hypercalciuria.

Osteocalcin response to calcium-restricted diet: a helpful tool for the workup of hypercalciuria.

The treatment of hypercalciuria is controversial. This study investigated whether the osteocalcin response (OCR) to a calcium-restricted diet is a potential tool for the differential therapy of hypercalciuria. 56 patients with calcium urolithiasis were investigated. Osteocalcin (OC) was measured on a free diet (OC 1) and after a calcium-restricted diet (400 mg/24 h for 1 week, OC 2). The OCR was expressed as 100 x (OC 2 - OC 1)/OC 1. A calcium load test and vertebral mineral density measurements (L2-L4) were performed additionally. 27 patients showed diet-dependent hypercalciuria, 15 of them being classified as absorptive hypercalciuria type II (AH II). 12 were normocalciuric (NC). 29 patients had diet-independent hypercalciuria, 22 being classified as renal hypercalciuria (RH), 7 as absorptive hypercalciuria type I (AH I). 22 patients (42%) showed a positive OCR, indicating an increased bone turnover. Vertebral mineral density was lower in patients with positive than with negative OCR. Generally patients with RH or NC showed a positive OCR, patients with AH a negative or no OCR. 2 patients with AH, however, showed highly positive OCR, indicating negative calcium balance. Long-term follow-up on a low calcium diet showed a steady decrease in bone mineral density. This demonstrates that the OCR is more reliable to determine the appropriate management of hypercalciuria than calcium load tests. For practical purposes, we suggest treating hypercalciuric patients with positive OCR with thiazides; diet-dependent hypercalciuria with negative OCR should be treated with a low calcium diet.

Physicochemical effects of a new slow-release potassium phosphate preparation (UroPhos-K) in absorptive hypercalciuria

A new slow-release, neutral potassium phosphate salt (UroPhos-K) has been formulated in order to minimize gastrointestinal side effects and avoid sodium-induced calciuria. It was tested in a prospective randomized, double-blind trial in a group of 21 kidney stone patients with absorptive hypercalciuria type I (AH). Twelve patients allocated to the UroPhos-K group received four tablets twice daily with breakfast and an evening snack providing 1240 mg of phosphorus and 63.5 mEq of potassium daily. Nine patients assigned to the placebo group received placebo tablets of the same appearance containing excipient only. Subjects were studied during a 3-day period in the hospital while consuming a constant metabolic diet containing 400 mg Ca, 100 mEq Na, and 800 mg P per day before and after 3 months of treatment. Treatment with UroPhos-K did not cause any significant gastrointestinal side effects; nor did it raise fasting serum K or phosphorus, or reduce hemoglobin or creatinine clearance. It was associated with a rise in urinary K from 46 +/- 7 to 98 +/- 9 mEq per day and phosphorus from 744 +/- 185 to 1535 +/- 112 mg per day (p < 0.001 each). UroPhos-K treatment reduced urinary Ca from 288 +/- 63 to 171 +/- 49 mg/day (p < 0.001), without altering oxalate excretion. It reduced the urinary saturation of calcium oxalate without altering that of brushite. Moreover, by increasing urinary excretion of inhibitors (citrate and pyrophosphate), it reduced the propensity for spontaneous nucleation of brushite (increased formation product of brushite) and inhibited crystal agglomeration of calcium oxalate.(ABSTRACT TRUNCATED AT 250 WORDS)

Ambulatory evaluation of nephrolithiasis: An update of a 1980 protocol

Evaluations of 1,270 patients with recurrent nephrolithiasis in an outpatient setting were analyzed for the purpose of updating the classification of nephrolithiasis. All but 4% had abnormal urinary biochemistry that placed them into one or more of 20 etiologic categories. A single diagnosis was documented in 41.3% of patients. The remaining 58.7% had more than one diagnosis. Hypercalciuric calcium (Ca) nephrolithiasis, encountered in 60.9% of patients, comprised six variants--absorptive hypercalciuria Type I and II, renal hypercalciuria, primary hyperparathyroidism, and unclassified hypercalciuria (renal phosphate leak and fasting hypercalciuria). Hyperuricosuria Ca nephrolithiasis (HUCN) and gouty diathesis (GD) accounted for 35.8% and 10.0% of patients, respectively. Distinguishing features were hyperuricosuria and normal urinary pH in HUCN, and normal urinary uric acid and low urinary pH (< 5.5) in GD. Hyperoxaluric Ca nephrolithiasis, occurring in 8.1% of patients, was subdivided into enteric, primary, and dietary variants. Hypocitraturic Ca nephrolithiasis affected 28% of patients in its idiopathic variant. Many of these patients' problems were probably dietary in origin, while some could have had incomplete renal tubular acidosis. Hypocitraturia due to renal tubular acidosis or chronic diarrheal syndrome affected only 3.3% of patients. Hypomagnesiuric Ca nephrolithiasis, infection stones, and cystinuria were uncommon, accounting for 6.8%, 5.9%, and 0.9% of patients, respectively. The acquired problem of low urine volume (< 1 L/d) was found in 15.3% of patients. The remaining 3.5% of patients were difficult to classify despite the presence of abnormal urinary biochemistry.

Calcium metabolism in normal and in hypercalciuric patients on Farnolith, a dietary fibre preparation.

In the present study Farnolith (a granular powder consisting of different dietary fibres) was given to normals (n = 6), patients suffering from absorptive hypercalciuria type I (n = 6) and to one patient suffering from renal hypercalciuria. Farnolith binds calcium and reduces the calcium absorption from the intestine. In normals the urine- and serum parameters of calcium metabolism (total- and ionised calcium, parathyroid hormone and vitamin-D-metabolites) remained unchanged. In patients suffering from absorptive hypercalciuria type I a significant reduction of hypercalciuria was found; oxalic acid excretion had decreased as well. Lowered parathyroid hormone values returned to normal, vitamin-D-metabolites remained unaffected. In one patient suffering from renal hypercalciuria parathyroid hormone and 1,25-dihydroxy-vitamin D values increased, calcium excretion had not decreased, though. Our investigation shows that Farnolith is suitable for the treatment of absorptive hypercalciuria. Calcium homoeostasis is returned to normal by Farnolith, at the same time it does not produce secondary hyperoxaluria (as e.g. sodium cellulose phosphate). Patients with primary renal calcium loss should not be treated by Farnolith.

Plasma Osteocalcin Levels in Stone Disease. A Potential Aid in the Differential Diagnosis of Calcium Nephrolithiasis

Plasma osteocalcin levels were measured by radioimmunoassay in 70 consecutive patients with recurrent calcium (sterile) nephrolithiasis during diagnostic evaluation for the cause of the disease. Nephrogenous cyclic adenosine 3,5′-monophosphate levels also were measured in most of the subjects. Included in the sampling, as determined by standard diagnostic criteria, were 12 patients with absorptive hypercalciuria type I, 15 with absorptive hypercalciuria type II, 22 with renal leak hypercalciuria, 11 with normocalciuria, 6 with primary hyperparathyroidism, 3 with renal tubular acidosis and 1 with Paget’s disease, as well as 12 control subjects. The observed plasma osteocalcin levels (ng. per ml. mean ± standard error) were absorptive hypercalciuria I 2.6 ± 0.20, absorptive hypercalciuria II 3.1 ± 0.21, renal hypercalciuria 8.7 ± 0.45, normocalciuric nephrolithiasis 3.3 ± 0.25, primary hyperparathyroidism 13.2 ± 0.91, renal tubular acidosis (range) 5.2 to 10.6, Paget’s disease 18.0 and control 3.1 ± 0.20. There were significant differences between the plasma osteocalcin levels of renal hypercalciuria versus primary hyperparathyroidism and renal hypercalciuria/primary hyperparathyroidism versus any other group. There was good correlation between plasma osteocalcin and cyclic adenosine 3,5′-monophosphate data (correlation coefficient 0.72, p less than 0.005). Plasma osteocalcin levels are a potential differential diagnostic tool for patients with stone disease. The diagnostic value compares favorably with that of cyclic adenosine 3,5′-monophosphate, with the advantage that the determination of plasma osteocalcin requires only a single test.

Dietary Protein Levels Affect the Excretion of Oxalate and Calcium in Patients with Absorptive Hypercalciuria Type II

A total of 12 patients with absorptive hypercalciuria type II and 11 normal controls participated in a study to evaluate the effects of dietary protein levels on urinary calcium and oxalate excretion before and after a 1 gm. dose of oxalate. Two test periods were used during which calcium (less than 400mg. per day) and oxalate were restricted. The first test was done under conditions of low dietary protein (12 per cent total caloric intake, 60 gm.) and the second test was done at a high protein level (25 per cent, 125 gm. protein). Twelve-hour urine specimens were obtained after dinner on day 3 of each diet (low and high protein) and again on day 4 when 1 gm. oxalate (spinach) was added to the dinner meal. The specimens were analyzed for calcium, oxalate and relative calcium oxalate saturation (concentration product ratio). There were no significant differences between the controls and subjects with absorptive hypercalciuria type II in oxalate excretion before the oxalate load on the low protein (controls 31.4 ± 4.2 standard error, expressed as mmol, oxalate per mol. creatinine, and absorptive hypercalciuria type II 23.1 ± 3.1) and high protein (controls 30.4 ± 4.2 and absorptive hypercalciuria type II 28.8 ± 5.9) diets. After the oxalate bolus the positive changes in oxalate excretion were 11.8 ± 4.8 (low protein) and 17.8 ± 4.7 (high protein) for controls, and 11.4 ± 4.4 (low protein) and 31.8 ± 5.2 (high protein) for patients with absorptive hypercalciuria type II. Thus, the increases in post-load urinary oxalate levels observed for controls and patients were greater on the high protein than on the low protein diets. After the oxalate load the increases in urinary oxalate and calcium oxalate supersaturation were significantly greater for patients with absorptive hypercalciuria type II than for control subjects for the high protein but not the low protein diets (p less than 0.05).

New drug therapy for kidney stones: a review of cellulose sodium phosphate, acetohydroxamic acid, and potassium citrate.

Kidney stones have an overall incidence of two to three percent in western countries. In many patients, the disease process is difficult to control and recurrence rates are high: 20 to 50 percent over the subsequent ten years. The pathogenesis and standard methods of treatment for the five major types of stones (i.e., calcium oxalate, struvite, calcium phosphate, uric acid, and cystine) are reviewed. Three new drugs are reviewed in the context of their roles in the selective treatment of kidney stones. Cellulose sodium phosphate (Calcibind) is a nonabsorbable ion-exchange resin with a limited indication for the treatment of calcium stones associated with absorptive hypercalciuria Type I. Acetohydroxamic acid (Lithostat) is an urease-inhibitor that is indicated as adjunctive therapy in patients with chronic urea-splitting urinary tract infections and struvite stones. Potassium citrate (Urocit) is an investigational agent that has clinical efficacy in patients with calcium oxalate and calcium phosphate stones who are hypocitraturic. In addition, potassium citrate is an alkalinizing agent that can be used in patients with uric acid stones.

Effect of Calcium Restriction on Renal Excretion of Oxalate and the Probability of Stones in the Various Pathophysiological Groups with Calcium Stones

To evaluate the adequacy of simple calcium restriction for patients with idiopathic calcium stones the effect of 5 days of calcium restriction without oxalate restriction on renal excretion of calcium and oxalate, and the corresponding probability of stones were assessed in 50 controls and 48 patients. Renal excretion of calcium decreased and that of oxalate increased significantly in all groups but the importance of the changes was critically dependent upon the underlying pathophysiological condition. The probability of stones decreased only in patients with absorptive hypercalciuria type II owing to the usual excessive calcium intake and increased in those with absorptive hypercalciuria type I and renal hypercalciuria, which are associated with true hyperabsorption of calcium and represent the 2 forms of idiopathic hypercalciuria.We believe that simple calcium restriction is beneficial for patients with idiopathic calculi only when the hypercalciuria is caused by exaggerated intake of calcium, since it increases the probability of stones in patients with idiopathic hypercalciuria. Calcium restriction always is associated with an increase in oxalate excretion, suggesting that simultaneous oxalate restriction should be added in all cases to decrease the probability of stones.

Ambulatory evaluation of nephrolithiasis: Classification, clinical presentation and diagnostic criteria

Using the ambulatory protocol previously described, 241 patients with nephrolithiasis were evaluated. They could be categorized into 10 groups from the results obtained. Absorptive hypercalciuria type I (87 per cent male) comprised 24.5 per cent and was characterized by normocalcemia, normal fasting urinary calcium (< 0.11 mg/100 nil glomerular filtration), an exaggerated urinary calcium following an oral calcium load (>0.20 mg/mg creatinine), normal urinary cyclic adenosine monophosphate (AMP) (< 5.4 nmol/100 ml glomerular filtration) and serum parathyroid hormone (PTH), and hypercalciuria (>200 mg/day during a calcium- and sodium-restricted diet). Absorptive hypercalciuria type II (58 per cent male) accounted for 29.8 per cent; its biochemical features were the same as those for absorptive hypercalciuria type I, except for normocalciuria during a restricted diet and low urine volume (1.42 ± 0.55 SD liter/day). Renal hypercalciuria (56 per cent male), disclosed in 8.3 per cent, was represented by normocalcemia and high values for fasting urinary calcium (0.160 ± 0.054 mg/100 ml glomerular filtration), urinary cyclic AMP (6.80 ± 2.10nmol/100 ml glomerular filtration) and serum PTH. Primary hyperparathyroidism (57 per cent female), accounted for 5.8 per cent, typically included hypercalcemia, hypophosphatemia, hypercalciuria and high urinary cyclic AMP. Hyperuricosuric calcium urolithiasis (100 per cent male) comprised 8.7 per cent, and was characterized by hyperuricosuria (776 ± 164 mg/day) and urinary pH exceeding pK for uric acid (5.91 ± 0.33). In enteric hyperoxaluria (60 per cent female), encountered in 2.1 per cent of cases, urinary oxalate was increased (6.29 ± 13.2 mg/day). Noncalcium-containing stones were found in 2.1 per cent of the patients with uric acid lithiasis (100 per cent male) and in another 2.1 per cent of the patients with infection lithiasis (60 per cent female). These conditions were typified by low urinary pH (5.29 ± 0.12) and high urinary pH (6.69 ± 1.16), respectively. Renal tubular acidosis was found in one patient (male, 0.4 per cent). In 10.8 per cent of the patients (81 per cent male), no metabolic abnormality could be found, although urine volume was low (1.41 ± 0.51 liter/day). Hypercalciuria could not be differentiated between absorptive hypercalciuria and renal hypercalciuria in 5.4 per cent of the patients. Thus, this ambulatory protocol disclosed a physiologic disturbance in nearly 90 per cent of the cases and provided a definitive diagnosis in 95 per cent of the patients.

Calcitonin Load in Absorptive Hypercalciuria Type I

The persistence of hypercalciuria (HCU), despite long-lasting calcium restriction in the diet in patients with absorptive HCU type I gives evidence of an additional endogenous source of calcium contributing to the pathogenesis of this disorder. The role of calcium mobilization from the bone is documented by the effective suppression of enhanced calcium mobilization from the bone, by means of calcitonin load in 5 patients with absorptive HCU type I and comparison with 7 normal controls.

Evaluation of calcium urolithiasis in ambulatory patients: Comparison of results with those of inpatient evaluation

A protocol for ambulatory patients (ambulatory protocol or evaluation) was developed for the diagnosis of different causes of calcium urolithiasis; it consisted of a collection of two 24-hour urine samples with the subjects ingesting a random diet and another with the subjects adhering to an instructed diet restricted in calcium and sodium, followed by the test of “fast” and “oral calcium load.” The results of ambulatory evaluation were compared with those of inpatient evaluation in 24 patients with various causes of calcium stones. The “match” in defining abnormalities between outpatient and inpatient evaluations was found to be virtually complete with respect to urinary calcium during fasting and following an oral calcium load, urinary oxalate and cyclic adenosine monophosphate (AMP), and serum calcium and immunoreactive parathyroid hormone (iPTH). However, six patients with normocalciuria during the inpatient setting (adhering to a low calcium diet) had hypercalciuria while adhering to the restricted diet used during outpatient evaluation. Serum phosphate and renal threshold phosphate concentrations were generally lower during the outpatient setting. The urinary uric acid level was significantly higher in outpatients, a finding probably reflecting the low purine content of the inpatient diet. The two evaluations yielded the same diagnoses in 18 patients: seven with absorptive hypercalciuria type I (hypercalciuria during both low and high calcium intakes), 2 with absorptive hypercalciuria type II (hypercalciuria only during a high calcium intake), one with hypophosphatemic absorptive hypercalciuria, three with renal hypercalciuria, one with primary hyperparathyroidism, two with hyperuricosuric calcium oxalate nephrolithiasis and two with enteric hyperoxaluria. Moreover, the ambulatory evaluation may be superior to the inpatient evaluation in disclosing hyperuricosuria. One patient in whom no obvious abnormalities were found during inpatient study, was found to have hyperuricosuric calcium oxalate nephrolithiasis during outpatient study. Hyperuricosuria was shown to coexist with other causes of calcium stones in 14 patients during outpatient evaluation, whereas it was present in three patients during inpatient study. However, utilizing the ambulatory evaluation, absorptive hypercalciuria type II was “confused” with the type I presentation in four patients, and hypophosphatemic absorptive hypercalciuria was “erroneously” diagnosed in one patient.