Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The immature kidney may be adversely affected by a variety of vasoactive or diuretic drugs, either administered to the mother during pregnancy, or to the neonate. Inhibitors of the angiotensin-converting enzyme administered to the hypertensive pregnant woman can severely and sometimes definitely impair renal function in the fetus, leading to postnatal anuria. Pathogenesis involves interference with the renin-angiotensin system and the prostaglandins. Beta-adrenergic agents administered during labor depress glomerular filtration rate transiently. Tolazoline, an alpha-adrenergic blocking agent useful in the treatment of persistent pulmonary hypertension of the neonate induces intense renal vasoconstriction with consequent hypoperfusion. Indomethacin, a prostaglandin synthetase inhibitor used for the pharmacological closure of a patent ductus arteriosus, also increases renal vascular resistance, and decreases urine output. Furosemide, the drug most often used in oliguric neonates, may also adversely affect the newborn infant. Its use has been associated with an increase in the incidence of patent ductus arteriosus, hypercalciuria, nephrocalcinosis and secondary hyperparathyroidism. These observations demonstrate that the proper use of drugs requires that the therapeutic endpoint be clearly defined and the predictable side effects be anticipated.
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PMID:Adverse effects of drugs on the immature kidney. 290 Dec 76

Hyperparathyroidism was described initially in the mid 1920s in patients suffering from a rare and severe form of bone disease, osteitis fibrosa cystica. In the 1940s and 1950s renal stone disease was recognized as a far more frequent complication of primary hyperparathyroidism than bone disease, and approximately half of the patients with primary hyperparathyroidism in clinical series published through the 1970s presented with renal stones. The introduction of routine determination of serum calcium concentration in the mid 1970s has had a dramatic impact on the frequency with which primary hyperparathyroidism is diagnosed in the population, particularly in older individuals with predominantly nonspecific symptoms of the disease. Stone complications appear to occur in less than 10 per cent of such patients. Underlying primary hyperparathyroidism is diagnosed in approximately 1 to 5 per cent of the patients with calcium stone disease. The predominant risk factor for stone formation in primary hyperparathyroidism is hypercalciuria, and patients typically present with moderate to marked hypercalciuria but with only mild hypercalcemia, in the range of 11 mg. per dl. or less. Hypercalciuria in these patients is principally the result of 1,25-dihydroxyvitamin D-mediated hyperabsorption of calcium from the intestine. The pattern of hypercalciuria disproportionate to the degree of hypercalcemia that typifies patients with primary hyperparathyroidism and stone disease reaches an extreme degree in patients with so-called subtle or normocalcemic primary hyperparathyroidism, in whom diagnosis by routine techniques may be difficult. Parathyroid exploration remains the treatment of choice in patients with primary hyperparathyroidism and stone complications.
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PMID:Primary hyperparathyroidism. 291 15

Phosphorus intake was evaluated in 27 appropriate weight for gestational age, critically ill neonates who required total parenteral nutrition for 2 weeks. All received approximately 30 mg/kg/d elemental calcium. The low P intake group (1.01 mmol/kg/d, 30 mg/kg/d) showed signs of phosphate depletion: hypercalciuria, hypophosphatemia, and absence of phosphaturia. The high P intake group (1.67 mmol/kg/d, 50 mg/kg/d) did not have signs of P depletion; however, they had high urinary cyclic adenosine monophosphate excretion and marked phosphaturia, suggesting secondary hyperparathyroidism. The moderate P intake group (1.34 mmol/kg/d, 40 mg/kg/d) had evidence of neither phosphate depletion nor secondary hyperparathyroidism. This phosphorus dose appears to be appropriate for the very sick, poorly growing infant receiving total parenteral nutrition.
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PMID:Effect of phosphorus intake in total parenteral nutrition infusates in premature neonates. 303 Dec 60

1,25-Dihydroxyvitamin D (1,25-(OH)2D) plays a crucial role in the maintenance of blood calcium and phosphorus levels and in normal skeletal mineralization. The concentration of this metabolite in the blood is, by necessity, tightly regulated. The most important stimuli for renal 1,25-(OH)2D synthesis include parathyroid hormone (PTH), its second messenger cyclic adenosine monophosphate (cAMP) and phosphate deprivation. Hypocalcemia and calcitonin, initially thought to act via stimulation of PTH release, have now been shown to directly stimulate 1-hydroxylation. Estrogens also increase 1,25-(OH)2D production, probably by upregulating renal PTH receptors. Inhibitors of the renal 25-(OH)D 1 alpha-hydroxylase include 1,25-(OH)2D itself, hypercalcemia, and phosphate loading. The PTH-vitamin D axis as modulated by the serum ionized calcium level controls adaptation to alterations in dietary calcium and sodium intake and to changes in skeletal turnover based on the level of physical activity. Although normally the renal production of 1,25-(OH)2D is tightly regulated and changes little in response to vitamin D challenge, there are certain conditions in which 1,25-(OH)2D appears to be substrate-dependent. These include hypoparathyroidism, hyperparathyroidism, vitamin D deficiency, sarcoidosis and the anephric state, conditions in which PTH is not well-modulated by alterations in serum ionized calcium or in which extrarenal synthesis of 1,25-(OH)2D occurs. In several disorders, including absorptive hypercalciuria, pseudohypoparathyroidism, hypophosphatemic rickets, and tumoral calcinosis, the regulation of the renal 1 alpha-hydroxylase appears to be altered.
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PMID:Normal and abnormal regulation of 1,25-(OH)2D synthesis. 306 16

An 8-year-old boy with idiopathic juvenile osteoporosis and multiple fractures had three abnormalities of bone mineral metabolism: calcitonin deficiency, elevated serum calcitriol concentrations, and hypercalciuria. Calcitonin deficiency was documented by two attempts to stimulate calcitonin secretion with intravenous calcium and pentagastrin. Treatment for 11 months with daily subcutaneous injections of human calcitonin and oral administration of calcitriol failed to reduce the excessive bone resorption observed on bone biopsy, and the fracture rate did not decrease. Treatment was discontinued for two months, then resumed with calcitonin injections and oral calcium supplementation. The fracture rate decreased but bone biopsy continued to show excessive resorption. Therapy was discontinued. After the onset of puberty, endogenous calcitonin was detectable. Exogenous calcitonin therapy may have failed to control bone resorption for several reasons: insufficient dose, reduction of bone receptors from long-term calcitonin exposure, secondary hyperparathyroidism, or lack of association between calcitonin deficiency and the bone disease.
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PMID:Effect of calcitonin replacement therapy in idiopathic juvenile osteoporosis. 317 35

A 25-year-old woman with persistent nephrogenic diabetes insipidus (NDI) following parathyroidectomy for primary hyperparathyroidism is described. NDI is a well recognized complication of primary hyperparathyroidism, generally imputed to hypercalcemia, and promptly reversible after correcting it. In our case, the impaired concentrating ability of the renal tubule was irreversible after the removal of the parathyroid adenoma and the correction of the hypercalcemia, presumptively due to the morphological irreversible changes in the kidney. In addition, hypercalciuria persisted and was the cause of a compensatory hyperparathyroidism. Treatment with thiazide diuretic was effective to decrease relative hypercalciuria, thus reversing the compensatory hyperparathyroidism.
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PMID:A case with persistent nephrogenic diabetes insipidus following parathyroidectomy for hyperparathyroidism. 322 2

Out of five children with hypercalciuria, four had nephrocalcinosis and one recurrent bladder calculi. Two out of four patients with nephrocalcinosis (patients 1 and 2) had the "hyperprostaglandin E syndrome" and the other two (patients 3 and 4, siblings) had the Royer syndrome (osteopathy, dwarfism, secondary hyperparathyroidism). Treatment with hydrochlorothiazide is effective in patients without increased urinary excretion of prostaglandin, whereas patients with increased prostaglandin excretion respond better to indomethacin therapy.
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PMID:[Clinical variants of idiopathic hypercalciuria in children]. 332 40

Studies were conducted in a patient with idiopathic hypophosphatemic osteomalacia to delineate the roles of parathyroid hormone (PTH), vitamin D and renal tubular function. A 43-year-old woman presented with progressive skeletal pains resulting in severe incapacity. Workup revealed: hypophosphatemia with a low tubular maximal phosphate reabsorption per glomerular filtrate (TmP/GFR) of 1.05 mg/dl, normocalcemia, hypocalciuria, elevated alkaline phosphatase and glycinuria. PTH and urinary cyclic AMP (UcAMP) were normal, while calcitriol was low. Renal tubular acidosis or other transport defects were not present and no tumor was found. Biopsy was diagnostic for osteomalacia, and the patient responded to 1-alpha OHD3 and phosphate therapy. Hyperparathyroidism was ruled out by 1) normocalcemia persisting after 1-alpha OHD3 and calcium loading and 2) normal PTH and UcAMP challenged by phosphate supplements. Combined calcium and 1-alpha OHD3 administration resulted in hypercalciuria, decreased UcAMP and increased, but not corrected, TmP/GFR. These findings suggest that the osteomalacia was due to hypophosphatemia caused by a renal leak. PTH is only contributory to the phosphaturia. Low calcitriol level contributes to the osteomalacia directly and indirectly through impaired mineral absorption and, therefore, is also responsible for the hypocalciuria.
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PMID:Metabolic studies in a patient with idiopathic hypophosphatemic osteomalacia. 334 50

According to the dynamics of the urinary calcium excretion mechanism, we have classified the patients with urolithiasis into 4 groups, namely group I (normocalciuria; urinary calcium excretion of 270 mg/day or less for male patients and 210 mg/day or less for female patients), group II (absorptive hypercalciuria; hypercalciuric with urinary calcium excretion of 200 mg/day or less under the low calcium diet), group III (renal hypercalciuria; hypercalciuric with urinary calcium excretion exceeds 200 mg/day even under a low calcium diet), and group IV (hyperparathyroidism; hypercalciuric patients as in group III with high serum calcium). Of the 97 stone formers, 77 were classified into group I, 9 into group II, 8 into group III and 3 into group IV. Both under the restricted diet and under the ambulatory free diet, urinary calcium excretion of groups II, III and IV was significantly higher than that of the group I patients. It was noteworthy, however, that some of the patients in group I excreted much calcium without restriction of their diet. Although no difference in excretion of oxalate, magnesium and phosphate was observed between the 4 groups, the patients in groups II, and III excreted more uric acid into their urine than group I patients. As for stone recurrence rate, no difference was noted between group I and group II, III or IV. Based on these findings, we conclude that hypercalciuria has no significant role in the stone forming mechanism. However, lowering of urinary calcium and other stone forming constituents is mandatory in preventing stone recurrence until the mechanism of stone formation is elucidated more precisely.
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PMID:[Clinical studies on recurrence of urolithiasis. (2) Hypercalciuria and recurrence of urolithiasis]. 344 58

The selective determination of mid-C-regional parathyroid hormone (mid-C-PTH) in combination with other laboratory parameters is a reliable tool for diagnosis and treatment of extra-renal (primary) and renal (secondary) hyperparathyroidism. Early stages, which show either high-to-normal serum calcium and elevated mid-C-PTH or increased serum calcium but normal mid-C-PTH, can be distinguished from overt hyperparathyroidism. Alkaline phosphatase (AP) activity and mid-C-regional PTH provide biochemical confirmation of histologically classified renal osteodystrophy. Since the index AP X PTH signifies osseous changes in dialysis patients at an early stage, therapeutic regimens may be altered without additional invasive procedures. After renal transplantation mid-C-PTH normalizes and serum creatinine decreases. Increased mid-C-PTH in patients with normal renal graft function reflects autonomous PTH secretion, which requires careful monitoring to prevent PTH-induced hypercalciuria.
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PMID:[Mid C regional parathyroid hormone in the clinical workup: diagnostic value in extrarenal (primary) and renal (secondary) hyperparathyroidism]. 352 Jan 30


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