Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The highest degree of urinary supersaturation with respect to calcium oxalate monohydrate (COM) and brushite at which secondary nucleation and growth of small amounts of COM and hydroxyapatite (HAP) are inhibited was determined by new and simple methods. There were 39 subjects who produced 24 h-urine collections (11 idiopathic stone formers (ISF), 12 patients suffering from primary hyperparathyroidism (HPT) and 16 healthy controls (HC). These subjects had a moderate calcium and low oxalate intake. The results obtained were compared with the state of urinary saturation and with urine chemistry. The measurements of crystallization conditions with respect to COM were repeated in 26 subjects (11 ISF, 5 HPT, 10 HC) after a dietary oxalate load. In 24 h-urines of HC diluted to 2.4 1/24 h the degree of supersaturation necessary to induce crystallization of COM and HAP was 2-5 times higher than the state of urinary saturation measured under the same test conditions. ISF showed a decreased pyrophosphate concentration and a decreased inhibitory activity to HAP crystallization in their 24 h-urine. The urinary inhibitory activity towards crystallization of HAP showed a positive correlation to urinary pyrophosphate concentration. In the 24 h-urine of HPT hypercalciuria and increased saturation with respect to brushite which reached values to induce HAP crystallization were found. After a dietary oxalate load urinary supersaturation with respect to COM reached values to induce COM crystallization in ISF and HPT but not in HC.
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PMID:Crystallization conditions in urine of patients with idiopathic recurrent calcium nephrolithiasis and with hyperparathyroidism. 404 2

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 (less than 0.11 mg/100 ml glomerular filtration), an exaggerated urinary calcium following an oral calcium load (greater than 0.20 mg/mg creatinine), normal urinary cyclic adenosine monophosphate (AMP) (less than 5.4 nmol/100 ml glomerular filtration) and serum parathyroid hormone (PTH), and hypercalciuria (greater than 200 mg/day during a calcium- and sodium-restricted diet). Absorptive hypercalciuria type II (50 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 +/- 2.10 nmol/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.
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PMID:Ambulatory evaluation of nephrolithiasis. Classification, clinical presentation and diagnostic criteria. 624 14

Phosphate stones are divided in two groups: I. Infection stones = triple phosphate stones (struvite and carbonate apatite). II. Calcium phosphate stones = Hydroxy apatite. Ad I. For the formation of this stone, infection with urease-producing bacteria is essential. It is important to look for factors that cause infection and for metabolic abnormalities. Three possibilities for treatment are discussed: Acidifying the urine: orally with NH4NO3 or NH4Cl; dosage is possible up to 12 g a day (metabolic acidosis!). Irrigation for instance with Renacidin ; when using a nephrostomy-tube, one can start 5 days after the operation. It is important to look for fever and flank pain. Especially useful in cases with small residual stones. Reduction of phosphate excretion in urine ( Shorr -regimen). Some aluminium combinations reduce the intestinal phosphate absorption as a result of the formation of a nonabsorbable aluminium-phosphate combination. This can be combined with a low calcium- and phosphate diet. In several publications good results are shown. Also when using a less rigid regimen, satisfactory results are seen: decrease of the phosphate excretion from 30 to 17 mmol/24 h (own investigation). Urease-inhibitors result in a lower urine-pH and a decrease of the ammonium-concentration. there are only a few publications with results, but AHA seems able to reduce the stone size in 24% of the patients. Ad II. This stone is concerning formation and treatment much like the calcium oxalate stone. In case of an alkaline urine one must look for primary hyperparathyroidism and renal tubular acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Conservative therapy of phosphate calculi]. 653 26

The urinary citrate excretion was examined in patients with nephrolithiasis who were categorized on the basis of different physiologic or metabolic abnormalities. A wide prevalence of low citrate excretion (hypocitraturia) was observed, with over one half of our patients with stones exhibiting it. Hypocitraturia was found in all patient categories except primary hyperparathyroidism and hyperuricosuric calcium oxalate nephrolithiasis. As expected, hypocitraturia was present in renal tubular acidosis and in enteric hyperoxaluria. However, urinary citrate was also low in absorptive and renal hypercalciurias, and in patients in whom an acid-base disturbance was clearly excluded.
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PMID:Low urinary citrate excretion in nephrolithiasis. 682 13

Diagnostic evaluation was conducted on 34 patients with a single episode of renal stone formation. Absorptive hypercalciuria as disclosed in 55.9 per cent (23.5 percent type I and 32.4 per cent type II), renal hypercalciuria in 11.8 per cent, primary hyperparathyroidism in 2.9 per cent, hyperuricosuric calcium oxalate nephrolithiasis in 8.8 per cent and no metabolic abnormality in 20.6 per cent. Compared to the group with recurrent stone formation the group with a single stone episode had just as severe biochemical abnormalities or laboratory results, such as hypercalciuria and exaggerated calciuric response to oral calcium load in absorptive hypercalciuria, high fasting urinary calcium and cyclic adenosine monophosphate in renal hypercalciuria, hyperuricosuria in hyperuricosuria calcium oxalate nephrolithiasis and low urine volume in no metabolic abnormality. The results suggest that the same physiological and environmental disturbances characterize stone formation in patients with a single stone episode as in those with recurrent stone formation and indicate the need for diagnostic evaluation.
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PMID:Should patients with single renal stone occurrence undergo diagnostic evaluation? 708 82

A 9-year-old castrated male domestic shorthair cat with dysuria, anorexia, vomiting, and lethargy was admitted to the veterinary teaching hospital. A large, firm mass was palpable in the ventral cervical region. Hypercalcemia, azotemia, and nonregenerative anemia were evident on serum biochemical analysis and CBC, and multiple uroliths were detected by abdominal radiography. At necropsy, light microscopy of the ventral cervical mass revealed a parathyroid adenocarcinoma. Light microscopy of sections of the kidneys revealed multifocal, chronic, lymphocytic/plasmacytic, tubulointerstitial nephritis, as well as moderate multifocal acute tubular necrosis. On quantitative analysis, the uroliths were composed of calcium oxalate. Determination of serum calcium concentration is indicated in cats with calcium oxalate urolithiasis to aid in detection of primary hyperparathyroidism.
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PMID:Calcium oxalate urolithiasis in a cat with a functional parathyroid adenocarcinoma. 775 34

The dietary habits of renal stone formers appear to differ from those of the general population. Renal stone formers seem to eat more oxalate, more flesh protein and less vegetable fibres than their normal counterparts. Often their urine volume is low. These are environmental factors which govern nephrolithiasis. Subtle underlying defects are detected not infrequently in these patients; for example, medullary sponge kidneys, abnormally structured macromolecular inhibitors of calcium oxalate crystallization (nephrocalcin and Tamm-Horsfall protein), incomplete distal renal tubular acidosis, deficient activation of pyridoxine, defective intestinal absorption of citrate, excessive production of interleukin-1 by monocytes, subtle primary hyperparathyroidism, heterozygosity for cystinuria, and, discovered more recently, abnormal chloride channels along the nephron. Many of these defects are inheritable, but carriers of the trait are not always active stone formers. The opinion forwarded in this review is that combinations of the environmental and of the underlying or genetic defects are required to trigger renal stone disease.
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PMID:Genetic versus environmental factors in renal stone disease. 882 32

The present series comprises 2086 consecutive patients who were studied in a stone clinic during a period of 15 years. Each patient was subjected to a comprehensive protocol including a fully biochemical investigation. Calcium stones were by far the commonest accounting for 61% of cases; infection, uric acid/calcium oxalate and cystine stones accounted respectively for 24%, 8%, 5% and 2%. Nephrolithiasis was more prevalent in males with the male to female ratio 1:0.76, on the other hand infection stones were more frequent in females with the male to female ratio 1:1.6. The peak age incidence of renal calcium stones occurred in the third to fifth decades, although about 3.4% reported onset of disease in the first and second decades of life. The onset of cystine stones was always in the first and second decades, while uric acid stones affected older patients. Renal stones were recurrent in about 50% of cases. In a retrospective analysis it was found the interval to first recurrence to be less than 5 years in about half patients. The cystine and uric acid groups had the highest rate of recurrence. In patients with calcium stones a definite metabolic or mechanical cause for their stones was found respectively in 8.2% and 10.1%. Particularly primary hyperparathyroidism was revealed in 2.8%. A metabolic defect could be found in 54% of the patients with idiopathic calcium stones. In these patients with idiopathic calcium stones the prevalence rate of hypercalciuria was 33%. In patients with uric acid stones and with mixed uric acid/calcium oxalate stones a definite metabolic cause for their stones was found respectively in 9.5% and 4.1% whereas an underlying disease of the urinary tract was diagnosed respectively in 8.5% and 6.2%. In patients with struvite stones the incidence of persistent infection was 46% (Proteus 18%). In this group the presence of an underlying disease of the urinary tract was diagnosed in 18.8% whereas a definite metabolic disease was demonstrated in 8.5%, a urinary risk factor for metabolic stone disease in 42% and a previous episode of metabolic stone disease in 33%.
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PMID:Clinical observations on 2086 patients with upper urinary tract stone. 893 17

Although underlying metabolic abnormalities do not differ fundamentally in patients with either first or recurrent nephrolithiasis and 35% of patients with a first event may have to face a recurrence 5 years later, extended metabolic investigations in patients with a first renal calculus should be restricted to particular, exceptional cases. However, in patients with a first calculus basic investigations with respect to specific causes for a concrement such as primary hyperparathyroidism, incomplete renal-tubular acidosis, recurrent urinary tract infection and cystinuria are mandatory. This includes, in addition to a laboratory investigation of blood and urine after a 2-hour-fasting period, analysis of the stone and a urography. The extended metabolic investigation in patients with recurrences or a first occurrence in a patients with a risk constellation includes evaluation of the most important lithogenic (calcium, oxalate, phosphate, uric acid) and inhibiting components (citrate) in the 24-hour urine, in patients with cystine calculi quantitation of cystine. A metabolic investigation should never be undertaken in the hospital or under standardized diet, but always under accustomed, unrestricted nutrition. At least 2 urine samples should be investigated from each patient, preferably not prior to 3-4 months after the event when homeostasis of the patient is restored analogously to the onset of concrement development.
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PMID:[Nephrolithiasis--rational etiological assessment]. 915 99

In recurrent calcium stone formers interfering factors or changes in receptor sensitivity may alter the interrelationships among calcium-regulating hormones, and hormonal behavior often does not fit with the theoretical assumptions. The vitamin D system appears to have the most important metabolic and clinical effects. Abnormal up-regulation of the synthesis of calcitriol and the consequent parathyroid hormone (PTH) suppression can induce hypercalciuria. Consequently, the hypocalciuric effect of thiazide would be caused by an enhanced response to PTH and by a reduction in 1,25(OH)2-vit D. A negative role of vitamin D on the skeleton has been observed in the presence of a negative calcium balance. Moreover, vitamin D also plays a role in urine oxalate excretion. PTH seems not to be directly stimulated in hypercalciuria and recurrent calcium nephrolithiasis, and patients with hyperparathyroidism and recurrent calcium nephrolithiasis show a similar degree of bone demineralization, irrespective of the presence of absence of the so-called 'primary hyperparathyroidism.' Calcitonin plays a contributory role in the pathogenesis of recurrent calcium nephrolithiasis that seems to be strictly related to dietary calcium intake. A higher sensitivity of thyroid C cells, particularly in absorptive hypercalciuric patients, could be related to the pathogenesis of hypercalciuria and contribute to its persistence.
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PMID:Calciotropic hormones and nephrolithiasis. 938 31


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