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PubMed1979

Dietary treatment of idiopathic hypercalciuria.

Eighty-eight urinary tract stone formers (74 men) with idiopathic hypercalciuria were treated by dietary calcium restriction alone. Short-term control of hypercalciuria was achieved in only 27 patients and all but 12 eventually escaped control. Failure of control was twice as likely in patients with severe hypercalciuria. Almost all patients lived in a hard water area. In such areas at least, attempts to control hypercalciuria by diet alone are likely to fail and early introduction of additional treatment is advisable. In most severe hypercalciurics, such treatment should be introduced from the start.

Calcium↗
PubMed1987

Idiopathic hypercalciuria in children. Classification, clinical manifestations and outcome.

Between 1981 and 1983, 49 children aged 2 to 15 years were diagnosed as having idiopathic hypercalciuria (IH). They were divided into 3 groups based on their response to dietary manipulation: group I (32/49) had absorptive hypercalciuria; group II (8/49) had renal hypercalciuria and group III (6/49) had sodium-dependent hypercalciuria. Response to diet was more reliable than Pak's test in differentiating between the three groups. A control group (CG) of 45 healthy, age matched children determined baseline levels for all metabolic parameters. At the time of presentation IH children did not differ from the CG in height or weight. Fifty percent of IH children had first degree relatives with urolithiasis. Yet, only 16% of the IH children had urolithiasis, the majority presenting with gross hematuria and urinary tract infections (UTI). With few exceptions the clinical symptoms resolved when urine calcium excretion was controlled. Severe calcium restriction in a few patients produced osteoporosis and delayed bone age although growth velocity was unaffected. Thiazide therapy in a few patients produced some metabolic derangements. The authors conclude that IH in childhood is a benign disease which may present with UTI or hematuria. They further propose a new classification method based on response to dietary manipulation.

Adolescent↗
PubMed1978

Mechanism of lithium-induced hypercalciuria in rats.

Chronic administration of lithium salts is associated with hypercalciuria in the rat. To study the renal and extrarenal mechanisms of this phenomenon, we utilized balance and clearance techniques in rats pair-fed diets with or without Li2CO3 (0.5 meq/day per rat). Lithium induced hypercalcemia (mean +/- SE: 5.40 +/- 0.09 VS. 5.06 +/- 0.05 meq/liter) and hypercalciuria (Ca/creatinine = 0.28 +/- 0.04 vs. 0.13 +/- 0.03) only during feeding. When CaCO2 supplement to a calcium-deficient diet was abruptly withdrawn, hypercalciuria was abolished. However, polyuria and polydipsia persisted. No significant changes in serum phosphate, urine phosphate, sodium, pH, or citrate were observed. Chronic parathyroidectomy (PTX) also abolished this effect. During clearance studies, fasting excretion of calcium was similar between treated and control animals. Superimposed acute PTX resulted in comparable changes, hence arguing against primary changes in renal calcium reabsorption or changes in parathyroid hormone effects on the renal tubule. Thus, lithium produces absorptive hypercalciuria by a mechanism dependent on intact parathyroid glands and adequate diet calcium, but independent of urine sodium, phosphate, or pH. The active component of gut calcium transport may be involved, possibly via alterations of vitamin D metabolism.

Animals↗
PubMed1984

Evidence for an intestinal mechanism in hypercalciuria of spontaneously hypertensive rats.

To define the mechanism for the hypercalciuria in spontaneously hypertensive rats (SHR), Ca clearance was evaluated in fasted 23-wk-old SHR and normotensive Wistar Kyoto (WKy) controls. There was no exaggerated calciuria before or after parathyroidectomy. Ca balance was therefore measured in the nonfasted animals, which revealed hyperabsorption in SHR of both sexes with increments 10-fold that of Ca excretion, supporting the primacy of intestinal hyperabsorption. In situ duodenal Ca uptake was also increased in the SHR. Parathyroidectomy did not affect the hyperabsorption. Hypercalcemia (total and ionized) and hypercalciuria in SHR associated with reduced adenosine 3',5'-cyclic monophosphate excretion, were abolished by fasting. Correction of hypertension for 6 mo failed to abolish the hypercalciuria. Bone Ca deposits were increased in 1-yr-old SHR. Ten-week-old SHR, in contrast, displayed mild malabsorption. Our data do not support the "renal leak" hypothesis. Instead, the adult SHR is characterized by increased Ca retention due to primary hyperabsorption, absorptive hypercalciuria, and increased bone Ca deposition. These phenomena are independent of sex, parathyroid hormone, and treatment of the established hypertension.

Age Factors↗
PubMed1984

Pathophysiology of hypercalciuria.

The mechanisms responsible for hypercalciuria may involve intestinal calcium transport, renal tubule calcium reabsorption, and the regulation of bone mineral content. Both parathyroid hormone and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) may alter urine calcium. For these reasons, understanding the pathogenesis of hypercalciuria in patients has proven to be difficult. We present here an analysis of pathways that regulate systemic calcium homeostasis and of the various mechanisms that have been proposed to explain normocalcemic hypercalciuria in humans. Available evidence seems to implicate disordered regulation of 1,25(OH)2D3 as a basis for at least one common form of hypercalciuria.

Benzothiadiazines↗
PubMed1985

Magnesium excretion in idiopathic hypercalciuria.

Given the parallelism in calcium and magnesium metabolisms, we have studied urinary magnesium in normal subjects and in patients with idiopathic hypercalciuria under conditions of basal and restricted diet, fasting, and after oral calcium overload. Serum magnesium values showed no differences between groups. Urinary magnesium levels are increased in absorptive hypercalciuria under free and restricted diet and calcium overload, returning to normal during fasting. Renal hypercalciuria patients maintain a high magnesium excretion under all conditions. This suggests that in idiopathic hypercalciuria there is an impairment of renal magnesium management, dependent on that of calcium because it normalizes when urinary calcium is normal.

Adult↗
PubMed1992

Idiopathic hypercalciuria causing osteoporosis and hypocalcemia.

Idiopathic hypercalciuria, though a common cause of nephrolithiasis, has not been recognized to cause hypocalcemia and severe bone disease. We describe an adolescent with idiopathic hypercalciuria who presented initially with severe hypocalcemia and osteoporosis and this was later complicated by recurrent renal calculi formation after calcium and vitamin D supplement. After treatment with thiazide, hypercalciuria was controlled and serum biochemistry normalized. While idiopathic renal hypercalciuria may cause a negative calcium balance in adults, a variant of this syndrome with severe renal calcium leak occurring in a growing subject could lead to severe hypocalcemia and osteoporosis.

Adolescent↗
PubMed1981

Incidence of normocalcemic hyperparathyroidism in idiopathic hypercalciuria: evaluation by dietary calcium deprivation test.

Calcium metabolism was studied in 37 patients with "idiopathic hypercalciuria" on a home diet and after 10 days of low calcium dietary intake (less than 400 mg/24h). After low calcium intake, urinary calcium excretion returned to within normal limits in 70% of the cases. In the group of patients which failed to respond to calcium restriction, TmPO4/GFR values were reduced and, furthermore, in 20% of them plasma iPTH and urinary cAMP levels were increased. These data seem to indicate that: the incidence of absorptive hypercalciuria is higher than hypercalciuria of renal origin; normocalcemic hyperparathyroidism due to primary calcium leak is present only in a limited number of cases, consequently, hypercalciuria secondary to renal phosphate leak is a rather frequent occurrence.

Calcium↗
PubMed1985

Pathophysiology of spontaneous hypercalciuria in laboratory rats. Role of deranged vitamin D metabolism.

Recent data suggest a causal role of deranged 1,25(OH)2D metabolism in the syndrome of idiopathic hypercalciuria. To test this hypothesis, we evaluated if vitamin D availability and/or increased serum 1,25(OH)2D were critical for the expression of hypercalciuria in laboratory rats. Ca balance, serum 25OHD3, and 1,25(OH)2D3 were studied in D-deprived (-D) and D-repleted (+D) male progeny (p) born to normocalciuric (NC) and spontaneously hypercalciuric (SH) rats. 7 of the 14 pSH and 2 of 21 pNC had SH, which was defined as urinary Ca greater than two standard deviations above the mean of values for control animals on days 5 and 6 of a low Ca +D diet (1.19 vs. 0.58 mg/d, P less than 0.001). Fasting serum Ca and 25OHD3 were similar to control. Serum 1,25(OH)2D3 was elevated in these nine SH rats (232 vs. 145 pg/ml, P less than 0.005). However, during vitamin D deprivation, their Ca excretion was also increased (1.53 vs. 0.45 mg/d, P less than 0.001), despite comparably reduced serum 1,25(OH)2D3 (102 vs. 106 pg/ml) and undetectable serum 25OHD3. Net intestinal Ca absorption on a low Ca diet was comparable during D repletion (-0.75 vs. -0.82 mg/d) or D deprivation (-0.80 vs. -2.15 mg/d), excluding primary hyperabsorption as the mediator of the hypercalciuria. Mild hypophosphatemia was present in SH on +D (5.8 vs. 6.9 mg/dl, P less than 0.005) and -D diets (6.2 vs. 7.9 mg/dl, P less than 0.005), and was associated with higher rates of cyclic adenosine monophosphate excretion (32.8 vs. 26.9 and 48.5 vs. 41.0 nmol/mg of creatinine, respectively). Spontaneous hypercalciuria is therefore dissociable from increased Ca absorption, serum levels of 25OHD3, or 1,25(OH)2D3. The data are most compatible with the hypothesis of a renal Ca leak which stimulates parathyroid hormone activity and increases serum 1,25(OH)2D3, if provided adequate 25OHD3 as substrate.

Animals↗
PubMed1988

Mechanism of hypercalciuria in genetic hypercalciuric rats. Inherited defect in intestinal calcium transport.

Excessive urine calcium excretion in patients with idiopathic hypercalciuria may involve a primary increase in intestinal calcium absorption, overproduction of 1,25-dihydroxyvitamin D3 or a defect in renal tubular calcium reabsorption. To determine the mechanism of hypercalciuria in an animal model, hypercalciuria was selected for in rats and the most hypercalciuric animals inbred. Animals from the fourth generation were utilized to study mineral balance and intestinal transport in relation to levels of serum 1,25(OH)2D3. Both urine calcium excretion and net intestinal calcium absorption were greater in hypercalciuric males (HM) than in normocalciuric males (NM) and in hypercalciuric females (HF) than in normocalciuric females (NF). However, serum 1,25(OH)2D3 was lower in HM than in NM and not different in HF than in NF. Net calcium balance was more positive in HM than in NM and in HF than in NF. In vitro duodenal calcium net flux was correlated with serum 1,25(OH)2D3 in HM and HF and in NM and NF. However, with increasing serum 1,25(OH)2D3 there was greater calcium net flux in hypercalciuric rats than in normocalciuric controls. Hypercalciuria in this colony of hypercalciuric rats is due to a primary intestinal overabsorption of dietary calcium and not an overproduction of 1,25(OH)2D3 or a defect in the renal tubular reabsorption of calcium.

Animals↗
PubMed2004

Hypercalciuria in familial hyperkalemia and hypertension accompanies hyperkalemia and precedes hypertension: description of a large family with the Q565E WNK4 mutation.

Familial hyperkalemia and hypertension (FHH; pseudohypoaldosteronism type II) is an autosomal dominant disorder characterized by hyperkalemia, hypertension, and low renin. WNK1 kinase overexpression and WNK4 kinase inactivating missense mutations cause FHH. When expressed in frog oocyte, WNK4 inhibits Na-Cl cotransporter surface expression, and WNK1 relieves this inhibition. We have reported hypercalciuria in subjects with the WNK4 Q565E mutation. In contrast, in subjects with WNK1 overexpression, normocalciuria was found. Here we report a major extension of our previously described kindred that contains 34 subjects, 18 of them affected by the mutation. Hypertension was diagnosed in 13 affected subjects at the age of 31 +/- 12 yr. Five of the affected or obligatory affected subjects had stroke, in four at the age of 50-62 yr. Seven subjects with FHH were diagnosed 27 yr previously. All four subjects who were normotensive at diagnosis became hypertensive during follow-up. The mean time between detection of hyperkalemia and appearance of hypertension was 13 yr. In the extended kindred, compared with the unaffected subjects, affected subjects had hyperkalemia, low transtubular potassium gradient, hyperchloremia, low bicarbonate, higher aldosterone, and marked suppression of renin. Urinary calcium levels in affected and unaffected subjects were 0.85 +/- 0.27 and 0.28 +/- 0.12 mmol/mmol creatinine, respectively (P < 0.0001). Hypercalciuria was accompanied by lower serum calcium levels [9.44 +/- 0.15 vs. 9.81 +/- 0.31 mg/dl (2.36 +/- 0.04 vs. 2.45 +/- 0.08 mmol/liter); P = 0.01], supporting a mechanism of renal calcium leak. The six affected, currently normotensive subjects had the same degree of hyperkalemia, hypercalciuria, and low renin as the affected hypertensive subjects. We conclude that in FHH with WNK4 mutations, with time all affected subjects will apparently develop hypertension. Hypercalciuria accompanies hyperkalemia, and both precede hypertension. Based on the recent findings that WNK4 regulates the renal outer medullary potassium channel as well as epithelial Cl(-)/base exchanger and the Na(+)-K(+)-2Cl(-) cotransporter, we suggest that WNK4 interacts with a calcium channel or transporter.

Adult↗
PubMed1985

Elevated production rate of 1,25-dihydroxyvitamin D in patients with absorptive hypercalciuria.

Previous studies of 1,25-dihydroxyvitamin D [1,25-(OH)2D] kinetics in normal subjects using the pulse injection technique have led to conflicting results, and only limited data are available concerning 1,25-(OH)2D kinetics in hypercalciuric patients. We developed an infusion equilibrium technique that measures the metabolic clearance and production rates of 1,25-(OH)2D and applied this technique in 13 normal subjects and 9 well characterized patients with absorptive hypercalciuria; all subjects were studied after 10 days on a 400-mg calcium intake. All subjects received a constant infusion of [3H]1,25-(OH)2D3 (20,000 dpm/min). Purified plasma radioactivity reached steady state levels after 15 h, and between 15 and 19 h, serial measurements of purified plasma radioactivity and endogenous 1,25-(OH)2D were made for calculation of metabolic clearance and production rates. In the 13 normal subjects, the MCR values were within a narrow range, with a mean +/- SD value of 37 +/- 6 ml/min, which, when combined with the mean steady state concentration of endogenous 1,25-(OH)2D (42 +/- 6 pg/ml), yielded a mean production rate of 2.2 +/- 0.5 micrograms/day. In the 9 patients with absorptive hypercalciuria, MCR values also were tightly clustered, with a mean of 35 +/- 4 ml/min. However, the mean endogenous steady state 1,25-(OH)2D level was significantly elevated in these patients, such that the calculated mean 1,25-(OH)2D production rate was significantly elevated at 3.4 +/- 0.5 micrograms/day. In 7 of the 9 patients with absorptive hypercalciuria, production rates exceeded the highest values found in the normal subjects. These data demonstrate disordered 1,25-(OH)2D production as opposed to metabolic clearance in the syndrome of absorptive hypercalciuria.

Adult↗
PubMed1997

The relationship between urinary calcium, sodium, and potassium excretion and the role of potassium in treating idiopathic hypercalciuria.

OBJECTIVES: 1) To evaluate the relationships between urinary sodium (UNa), potassium (UK), and calcium (UCa) excretion in the pediatric population; and 2) to determine the effect of increasing potassium intake in patients with idiopathic hypercalciuria and investigate whether this intervention can be offered as another mode of therapy in this patient population. DESIGN: Prospectively, we determined UNa, UK, UCa, and creatinine (Cr) concentrations in randomly collected urine samples from children on initial evaluation for urinary frequency, dysuria, hematuria, enuresis, or kidney stones to identify children with hypercalciuria. SETTING: The outpatient renal clinic of an academic hospital. PARTICIPANTS: Twenty-three black children (13 girls and 10 boys) and 77 white children (44 girls and 33 boys) 3.92 to 16.67 years of age. INTERVENTIONS: Eleven children with hypercalciuria were given potassium supplementation or placed on a high-potassium diet for at least 2 weeks. OUTCOME MEASURES: UNa to UK, UNa to Cr, UK to Cr, and UCa to Cr ratios were calculated from measured levels of urinary minerals. These were repeated in 11 hypercalciuric patients after 2 weeks of increased potassium intake. RESULTS: A total of 100 urine samples were analyzed. The UCa/Cr ratio in blacks 0.04 +/- 0.06 (mean +/- standard deviation) was significantly lower than in whites 0.16 +/- 0.12. There were 21 hypercalciuric white children versus only 1 black child. Linear regression analysis revealed a positive direct correlation between UNa/Cr and UCa/Cr in all 100 subjects and in whites alone but not in blacks. An inverse relationship existed between UK/Cr and UCa/Cr in all subjects and in whites and showed a strong trend in blacks. A marked direct relationship was found between UNa/K and UCa/Cr in all subjects (r = .43) as well as in whites (r = .59) and blacks (r = .49). One black child and 10 white hypercalciuric children were treated with "extra" K for at least 2 weeks. The UNa/K decreased from 4.73 +/- 2.28 to 1.98 +/- 1.09, and the UCa/Cr decreased from 0. 31 +/- 0.10 to 0.14 +/- 0.07, with resolution or improvement of the patients' symptoms. CONCLUSIONS: In our patient population with urinary symptoms, the UCa/Cr ratio in black children is lower and hypercalciuria less common than in white children. In both white and black populations, the UNa/K ratio had the strongest association with the UCa/Cr ratio, indicating an opposing role of UNa and UK on the UCa/Cr ratio. Increased potassium intake was found to be beneficial for hypercalciuric children by decreasing the UNa/K ratio and, consequently, the UCa/Cr ratio.

Adolescent↗
PubMed1994

Hypercalciuria: lessons from studies of genetic hypercalciuric rats.

Human idiopathic hypercalciuria (IH) is a common cause of hypercalciuria that contributes to calcium oxalate nephrolithiasis. The disorder is characterized by normocalcemia, increased intestinal Ca absorption, and normal or elevated circulating 1,25(OH)2D3. Intestinal Ca hyperabsorption, which is a source of excess urine Ca excretion, may result from either a primary increase in renal 1,25(OH)2D3 production; a primary, vitamin D-independent defect in enterocyte regulation of Ca transport; or a secondary increase in 1,25(OH)2D3 production in response to a defect in renal tubular Ca reabsorption. Breeding male and female Sprague Dawley rats with spontaneous hypercalciuria has resulted in offspring with hypercalciuria, increased intestinal Ca absorption, and normal serum 1,25(OH)2D3. In male IH rats, vitamin D receptor (VDR) content measured by saturation binding and western blotting revealed a twofold increase in VDR number in the duodenum, kidney cortex, and splenic monocytes. The molecular basis for the increase in VDR appears not to be due to increased VDR gene expression, but may result from increased efficiency of translation of the VDR message or prolongation of the half-life of VDR. Comparable migration of normal and IH intestinal VDR on western blots and of intestinal VDR mRNA on northern blots suggests that the abundant VDR in IH rat intestine is not a mutation of the wild-type VDR. These observations strongly suggest that, in IH rats, normal serum 1,25(OH)2D3 and increased VDR results in increased VDR-1,25(OH)2D3 complexes and enhanced biologic actions of 1,25(OH)2D3, including increased intestinal Ca transport. IH in rats may be the first genetic disorder due to a pathologic increase in the VDR.

Animals↗
PubMed1994

Idiopathic hypercalciuria: the contribution of Dr. Jacob Lemann, Jr.

The original contributions of Jacob Lemann to mineral metabolism, especially calcium metabolism and idopathic hypercalciuria, are reviewed. One group of studies concern acid base balance and calcium loss, showing that acid loads increase calcium loss in the urine. Another group of studies concern the calciuria of glucose or carbohydrate ingestion, with the observation that stone patients, who as a population are enriched with hypercalciuria, respond with more exaggerated calciuria to glucose loads than do normal people. Yet another body of work shows that normal men, when given noncalcemic loads of calcitriol, exhibit two essential features of idiopathic hypercalciuria--hyperabsorptive hypercalciuria and bone mineral loss on a low-calcium diet. The final group of studies presented worked on the problem of thiazide hypocalciuric action, and where the calcium goes that does not appear in the urine, as well as the effects of potassium bicarbonate and sodium loads on mineral balance and acid base status.

Acid-Base Equilibrium↗
PubMed1991

[Bone mineral densitometry by dual photon absorptiometry in patients with urolithiasis--on the possibility of the differential diagnosis of idiopathic hypercalciuria].

Bone mineral density (BMD) of the 3rd lumbar spine was measured by dual photon absorptiometry (DPA) in 8 patients with primary hyperparathyroidism (PHP) and 39 patients with idiopathic urolithiasis (IU). Of the patients, 15 were classified into idiopathic hypercalciuria (IH) which were further classified into 2 types of IH--renal hypercalciuria (RH) and absorptive hypercalciuria (AH)--by Ca restriction and load test. BMD of the IH patients tended to be lower than patients with normocalciuria, but significantly higher than the PHP patients. BMD of the RH patients was significantly lower than the AH patients. In conclusion, DPA may be a simple method for classifying the types of idiopathic hypercalciuria.

Absorptiometry, Photon↗
PubMed1992

[The pathogenesis of hypercalciuria from the aspect of the response to human parathyroid hormone in Ca containing stone formers].

In order to clarify the pathogenesis of hypercalciuria, the response to extrinsic human parathyroid hormone (h-PTH) was studied the 21 patients with calcium containing urinary stone(s) and 5 normal controls (NO). The stone patients were classified into 3 groups from the result of the oral calcium loading test, i.e. Non-hypercalciura (NH, n = 8) and absorptive hypercalciuria (AH, n = 8) and renal hypercalciuria (RH, n = 5). Only in the AH group, urinary excretion of calcium (u-Ca) was strongly correlated to that of sodium (u-Na) in pre-load of h-PTH, and both increments were also correlated in post-load of h-PTH. As of this fact the increase in Na excretion seems to be responsible for a cause of hypercalciuria in the AH group. There was a significant correlation between the value of %TRP in pre-load of h-PTH and the rate of urinary phosphorus (P) increment between pre-load and post-load of h-PTH in the NO and NH groups. However, this relationship was not found in the AH and RH groups. These findings indicate that there is response disorder of P to h-PTH. In addition, serum P was low, plasma 1,25 (OH)2D was high, N-c-AMP was low in the AH group, whereas both serum P and %TRP were low in the RH group in pre-load of h-PTH. These findings are compatible with the primary renal P leak.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

[Importance of dietary sodium in the hypercalciuria syndrome and nephrolithiasis].

The studies involved 20 children with idiopathic hypercalciuria (IH). An influence of urinary sodium excretion, and reflection of its intake, on urinary calcium excretion has been assessed. Children who were normocalciuric had significancy lower values of urine sodium excretion when compared with those with persisting hypercalciuria. The main factor responsible for hypercalciuria in children seemed to be urine sodium excretion. As urine sodium excretion reflects its intake, reduction dietary salt, rather than calcium intake, may be useful in the management of children with hypercalciuria and nephrolithiasis.

Calcium↗