Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392525 (nephrolithiasis)
 2,669 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For assessing the risk of adverse complications of surgery the group of 130 patients with post-operational hypoparathyroidism was analysed. Surgical hypoparathyroidism has been diagnosed in 51% of operated on thyroid gland patients. Laryngeal nerves have been damaged in 46.6% of patients. The injury to laryngeal nerves has been irreversible in 2/3 of patients, and reversible in the remaining 1/3. Cataract, nephrolithiasis and vitamin D3 intoxication have been observed in some cases before surgery. Their incidence increased in severe surgical hypoparathyroidism. Osteoporosis of the spine has been diagnosed in 49% of patients including some with vertebral fractures. No correlation between the degree of spine osteoporosis and diagnosis before surgery, number of operations on thyroid gland, and type of therapy has been noted. The symptoms of hypercalcemia have been diagnosed in 5 patients out of which hypercalcemia has been transient in 2 patients, and lasted for 1-5 months in the remaining 3 patients. The results of 7,873 analyses of mineral metabolism have been assessed. Hypocalcemia has been found in 38.4%, hypercalcemia in 1.6%, hypomagnesemia in 25.7%, hyperphosphatemia in 41.5%, decreased alkaline phosphatase serum activity in 28.7%, and hypercalciuria in 22.4% of cases. Surgical hypoparathyroidism is frequently accompanied by surgical hypothyroidism and injury to the recurrent laryngeal nerves.
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PMID:[Postoperative hypoparathyroidism: risk of complications]. 166 68

Increased levels of serum alkaline phosphatase (ALP) (E.C.3.1.3.1.) were observed in 25 patients with various urological conditions involving the kidneys: malignancy, complicated nephrolithiasis, and surgical and percutaneous manipulations. Other possible sources for increased ALP level, mainly hepatic and osseous, were excluded by history, laboratory tests, and liver and bone imaging. Studies of isoenzymes of ALP did not show a distinctive pattern. ALP levels returned to the normal range by treating the underlying lesions involving the kidney: nephrectomy, complete removal of stones, or removal of nephrostomy. The increase in serum ALP activity may be derived from the injury to the brush border membrane of the renal tubular cells. Renal function impairment and contrast media induced nephrotoxicity may also be responsible for the increased serum ALP. Serum ALP may be a marker for involvement of the kidneys in pathological processes and an indicator of complete treatment. This clinical observation is worthy of further study.
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PMID:Increased serum alkaline phosphatase activity: a possible indicator of renal damage. 177 5

Treatment with 1,25-(OH)2D3 (calcitriol) was compared with placebo in a double-blind, randomized, parallel clinical trial of 24 months' duration. Subjects were white women with postmenopausal osteoporosis. The study was completed by 15 patients who received placebo and 12 patients who received calcitriol. Positive slopes were observed in the active treatment group for total body calcium, bone mineral content of the radius, bone mineral density of the lumbar spine, and radiographic absorptiometry of the middle phalanges. In contrast, negative slopes were observed for the bone mineral measurements in the placebo group. Measurement of urinary hydroxyproline and of serum alkaline phosphatase and osteocalcin suggested that the mechanism of action of 1,25-(OH)2D3 involved reduction of bone resorption. Hypercalciuria occurred regularly and preceded hypercalcemia by about 2 weeks. A decline in creatinine clearance was observed in two patients, one of whom had nephrolithiasis on sonography. Calcitriol is effective in preventing bone loss, but must be used with caution.
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PMID:Role of calcitriol in the treatment of postmenopausal osteoporosis. 218 76

A 14-year-old Turkish boy had severe rickets that had been clinically evident since he was 2 years of age. When he was 5 years of age, he had normal serum calcium and phosphorus levels and increased alkaline phosphatase activity. Treatment with modest dosages of vitamin D (5000 U/d for 3 weeks) resulted in hypercalcemia. At 10 years of age, high-dose vitamin D (40,000 U/d) plus phosphorus (1.1 g/d) therapy for 20 days resulted in symptomatic nephrolithiasis. When, 14 years of age, he had normocalcemia, hypophosphatemia, increased alkaline phosphatase activity, and normal circulating parathyroid hormone concentration. Levels of 25-hydroxyvitamin D were normal but those of 1,25-dihydroxyvitamin D were markedly increased. Rickets and osteopenia were evident on radiographs, and osteomalacia was present on trabecular bone obtained at biopsy. Balance study results showed increased intestinal absorption of calcium and phosphorus, hypercalciuria, and increased urinary phosphorus excretion. This patient manifests an unusual form of hypophosphatemic rickets in which hypercalciuria is a cardinal feature. In contrast with most varieties of hypophosphatemia, this disorder is characterized by appropriately increased production of 1,25-dihydroxyvitamin D in response to hypophosphatemia. It is recommended that urinary calcium excretion be assessed in all patients with hypophosphatemic rickets so that appropriate therapy will be instituted.
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PMID:Hypercalciuric hypophosphatemic rickets, mineral balance, bone histomorphometry, and therapeutic implications of hypercalciuria. 278 97

Three children with primary hyperparathyroidism, confirmed at operation, are reported. The generalized skeletal changes with pathological fractures are leading in two of them, necessitating a long-term orthopedic treatment. Big solitary adenomas were found at operation. The disease, in the third child, had the course of nephrolithiasis. Hyperplasia of all four parathyroid bodies with light cells was established at operation. The biochemical deviations are typical in all three children undergone operations: hypercalcemia, hypophosphatemia, elevated alkaline phosphatase with increased excretion of calcium and phosphorus in urine.
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PMID:[Primary hyperparathyroidism in childhood and adolescence]. 710 84

A total of 19 patients with active nephrolithiasis, 14 patients with non-active nephrolithiasis and 17 healthy subjects were examined under standardized intake of calcium, phosphorus, purine and protein. In patients with both active and non-active renal stone disease the following abnormalities were found: elevated plasma levels of PTH and osteocalcin, increased activity of the bone isozyme of alkaline phosphatase, low plasma levels of phosphate and increased urinary excretion of calcium and oxalic acid. These abnormalities were more marked in patients with active than non-active nephrolithiasis. No correlation was found between plasma PTH levels and parameters of bone turnover as well as calciuria and oxaluria. Results presented in this paper suggest that (a) Smith's criteria of active renal stone disease are of minor pathogenetic and therapeutic value and (b) patients with active nephrolithiasis differ from non-active renal stone formers by more elevated oxaluria and markers of bone turnover and more marked abnormalities in calcium-phosphate metabolism related parameters.
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PMID:Markers of bone turnover in patients with nephrolithiasis. 941 56

Although the number of patients with primary hyperparathyroidism (pHPT) has increased since biochemical screening came to be widely employed, few data are available concerning the clinical analysis of Japanese patients. We therefore tried to determine the recent clinical and biochemical state of Japanese patients with pHPT. Clinical and biochemical data were analyzed in a series of 103 pHPT patients who had been hospitalized in Kobe University Hospital during a 17 year period from 1979 to 1995. The data were obtained from the hospital records and additionally from information through questionnaires performed in 1995. Patients were 29 males and 74 females. The average ages at diagnosis were 53.4 +/- 16.0 (SD) year-old and 53.9 +/- 15.2 year-old, respectively. The major clinical symptoms were nephrolithiasis (35.9%), thirst/polyuria (33.0%), easy fatigability (20.4%) and back pain/lumbago (16.5%), but 19.4% of the patients were asymptomatic. Out of 87 cases who received parathyroidectomy, 10 (11.5%) were diagnosed with parathyroid carcinoma. Age- and sex-corrected bone mineral density (BMD) of the radius was significantly lower in the group with back pain/lumbago than in the group without the symptom. Similarly, radial BMD was lower in the group with a high serum alkaline phosphatase value. Patients with nephrolithiasis had a lower urinary calcium/creatinine ratio (UCa/ UCr; 0.305 +/- 0.188 mg/mg) than the patients without nephrolithiasis (0.400 +/- 0.160 mg/mg). This inconsistent result suggests that some important factors except urinary calcium would contribute to urinary stone formation in pHPT. Our data mostly agreed with previous reports on a Caucasian population except for a relatively high prevalence of parathyroid carcinoma, but the negative correlation between nephrolithiasis and urinary calcium was not easily explicable. This finding should be confirmed by analyzing a larger number of cases.
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PMID:Clinical and biochemical presentation of primary hyperparathyroidism in Kansai district of Japan. 944 96

Twenty male Wistar rats, weighing 150 g, were placed in metabolic cages on a 30% sucrose diet for 7 days, before allocation to two groups: a control group (n = 5) and a lactose group (n = 15). They received respectively a 30% sucrose diet or a 30% lactose diet for 8 weeks, each containing 0.67% calcium and 0.38% phosphorus. After 4 (T1) and 8 (T2) weeks, the serum calcium (Ca) and citrate levels were significantly (P < 0.01) higher in rats fed the lactose diet. Serum alkaline phosphatase activity was increased in the lactose group (P < 0.01) at T1 and T2. The lactose-rich diet induced an increase in urinary Ca excretion at T1 and T2; citrate excretion was only enhanced at T2 (P < 0.001). No difference between the two groups was observed in urinary oxalate (Ox) excretion or creatinine clearance. Crystalluria analysis revealed a marked number (>300/mm3 at T1 and T2) of calcium oxalate dihydrate crystals (COD) in rats fed the lactose-rich diet, whereas no COD crystals were observed in sucrose-fed control rats at any time point. The formation of COD crystals in lactose-fed rats was related to an increase in calcium oxalate (CaOx) product (pCaOx), which was respectively 12.6 vs 3.9 at T1 and 10.5 vs 1.8 at T2, and an increase in CaOx ratio (Ca/Ox), which was 99.1 vs 7.5 and 67.5 vs 18.5 at T1 and T2, respectively. The high pCaOx and Ca/Ox ratios in the lactose group were due to hypercalciuria, in agreement with the number and the type of crystals. The present experimental model confirms that the ingestion of a 30% lactose diet increases urinary Ca excretion without changing urinary Ox excretion and shows for the first time that it induces a stable and marked crystalluria composed of COD. Such a non-nephrotoxic and stable model is of interest for the study of CaOx crystal formation secondary to hypercalciuria, and thus afterwards eventually for CaOx nephrolithiasis.
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PMID:A stable animal model of diet-induced calcium oxalate crystalluria. 953 98

Using ethylene glycol (EG) and vitamin D3 as crystal-inducing diet (CID) in rats, we investigated the effect of the dosage of EG on the generation of chronic calcium oxalate (CaOx) nephrolithiasis. We collected weekly 24 hour urines and measured herein the amount of oxalate, calcium, glycosaminoglycans (GAG's), creatinine, protein, alkaline phosphatase (AP), gamma-glutamyl transpeptidase (gamma-GT), and N-acetyl-beta-glucosaminidase (NAG). The potential of these urines to inhibit crystal growth and agglomeration was also evaluated. After four weeks, the kidneys were screened by histology and radiography for the presence of CaOx crystals and the amount of kidney-associated oxalate was biochemically measured. Using 0.5 vol.% EG, only a part of the rats showed CaOx deposition in the renal cortex and/or medulla, without obvious differences between Wistar and Sprague-Dawley (SD) rats. If a dietary EG concentration of 0.75, 1.0, or 1.5 vol.% was used, the amount of kidney-associated oxalate was proportionally higher and CaOx crystal formation was consistently found in all rats. Most crystals were encountered in the cortex, whereas in the medulla and the papillary region, crystals were only occasionally detected. From these data, we conclude that in the chronic rat model, based on EG and vitamin D3, a consistent deposition of CaOx crystals is obtained using a EG concentration of at least 0.75%.
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PMID:Experimental nephrolithiasis in rats: the effect of ethylene glycol and vitamin D3 on the induction of renal calcium oxalate crystals. 981 34

Nephrolithiasis is a common disorder and a significant problem because of incidence, recurrence and severe consequences. Stone disease is a surgical as well as a medical problem. Major progress has been made recently in understanding the pathophysiological disturbances responsible for stone formation as well as in the techniques of stone removal. The introduction of extracorporeal shock wave lithotripsy has considerably reduced the need for surgery. Improvements in methods of kidney stone removal have not diminished the need for the application of an effective prophylactic program. The internist should take a complete history of stone events (number, composition, location and outcome of stone event), family history of stones, dietary habits (focusing on the consumption of animal protein, salt and dairy products), medications and physical examination. Radiopaque stones should be documented by plane X-ray films. Ultrasonography should be used to image calculi that are nonopaque, and to easily distinguish them from masses such as tumour or blood clot. Computed tomography is also an excellent method for imaging nonopaque renal calculi but higher cost and radiation exposure are disadvantages [2]. Crystallographic analysis is the essential diagnostic procedure. If available, previous stones should also be examined. "In stone disease, everything is measurement. What the laboratory cannot tell you, you will not know; what it tells you in error, you will not correct by using your instincts, your medical experience, or your art [3]". Reliable diagnostic protocols are available for the identification of different causes of stones. The complexity of protocols depend on the severity of nephrolithiasis. Patients with a single stone episode undergo simple protocol, and extensive detailed protocol is used for patients with recurrent stone disease, or patients at increased risk. Simple protocol, besides the already mentioned history of stone events, radiographic investigation and crystallographic analysis, includes serum urea, creatinine, uric acid, sodium, calcium, phosphorus and protein levels, urinary pH and volume, urine samples for culture and urinary calcium, uric acid, oxalate and citrate. Extensive metabolic evaluation includes simple protocol, determination of serum levels of alkaline phosphatase, parathyroid hormone, thyroxin, magnesium. A 24-h collection of urine specimen is analysed for urea, creatinine, uric acid, calcium, phosphate, sodium, magnesium, oxalate and citrate. Extensive protocol includes specialized evaluation tests [5]. Urinary acidification test is important for detecting distal renal tubular acidosis. Two 24-h urine specimens are collected while the patient is on the regular diet. The patient is then placed on a restricted diet (400 mg of calcium and 100 mEq of sodium) for a week, and another 24-h urine sample is collected. After that fasting and calcium load tests are performed (Sheme 1). Fasting urinary calcium is used to detect renal calcium leak, and calciuric response to oral calcium load provides an indirect measure of intestinal calcium absorption. Diagnostic criteria for major forms of stone disease [8] are presented in Table 1. There are some still unsolved questions: does time after passage of stones or urological intervention influence the frequency of urine abnormalities that can be detected; are there differences in 24-h urine composition between weekdays and weekends: what is the prevalence of the most important urinary risk factors of recurrent idiopathic calcium nephrolithiasis: do male patients differ from females with respect to urinary risk factors or recurrent idiopathic calcium nephrolithiasis? [7].
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PMID:[Functional evaluation in patients with kidney calculi]. 986 14


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