Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 65-year-old man was admitted to our hospital because of thirstyness and left lower abdominal pain. On admission, he was found to have urolithiasis, renal insufficiency (BUN: 73 mg/dl, Crt: 4.4 mg/dl), and hypercalcemia (13.2 mg/dl). Chest X-ray films and computed tomograms showed enlargement and calcification of the hilar lymph nodes, and thickened interlobar fissures in both lungs. Levels of angiotensin converting enzyme (30.2 IU/l) and 1.25 (OH)2VitD3 (66.4 pg/ml) were elevated. Histologic examination of the specimen obtained from transbronchial lung biopsy showed non-caseous epithelioid cell granulomas. Because the level of parathyroid hormone was normal and no malignancies were detected, a diagnosis of sarcoidosis was made. Treatment with extracorporeal shock wave lithotripsy, transurethral lithotomy, saline infusion, and prednisolone (30 mg/day) alleviated the urolithiasis, renal insufficiency, and hypercalcemia. After discharge, the patient was followed up and given prednisolone therapy. About 1 month after the prednisolone dose had been tapered to 15 mg/day, the patient experienced dyspnea and facial and pedal edema. Because congestive heart failure was diagnosed, he was re-admitted to our hospital for a second time. Although he was then placed on intensive therapy, he died of ventricular tachycardia associated with sarcoidosis of the heart.
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PMID:[Sarcoidosis with hypercalcemia, urolithiasis, renal insufficiency, and heart failure]. 1048 65

Unexplained hypercalcemia has been increasingly recognized in cats since 1990. In some instances, hypercalcemia has been associated with calcium oxalate urolithiasis, and some affected cats have been fed acidifying diets. We studied the laboratory findings, clinical course, and treatment of 20 cats with idiopathic hypercalcemia. Eight (40%) of the cats were longhaired and all 14 cats for which adequate dietary history was available had been fed acidifying diets. Clinical signs included vomiting (6 cats), weight loss (4 cats), dysuria (4 cats), anorexia (3 cats), and inappropriate urinations (3 cats). Hypercalcemia was mild to moderate in severity. and serum parathyroid hormone concentrations were normal or low. Serum concentrations of phosphorus, parathyroid hormone-related peptide, 25-hydroxycholecalciferol, and calcitriol were within the reference range in most cats. Diseases commonly associated with hypercalcemia (eg, neoplasia, primary hyperparathyroidism) were not identified despite thorough medical evaluations and long-term clinical follow-up. Azotemia either did not develop (10 cats) or developed after the onset of hypercalcemia (3 cats), suggesting that renal failure was not the cause of hypercalcemia in affected cats. Seven of 20 cats (35%) had urolithiasis, and in 2 cats uroliths were composed of calcium oxalate. Subtotal parathyroidectomy in 2 cats and dietary modification in 11 cats did not result in resolution of hypercalcemia. Treatment with prednisone resulted in complete resolution of hypercalcemia in 4 cats.
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PMID:Idiopathic hypercalcemia in cats. 1111 Mar 84

To determine whether an "atherogenic" diet (excess of cholesterol and neutral fat) induces pathological calcification in various organs, including the kidney, and abnormal oxalate metabolism, 24 male Sprague-Dawley rats were fed either normal lab chow (controls, n = 12) or the cholesterol- and fat-rich experimental diet (CH-F, n = 12) for 111 +/- 3 days. CH-F rats developed dyslipidemia [high blood levels of triglycerides, total, low-density lipoprotein (LDL)-, very low-density lipoprotein (VLDL)-, high-density lipoprotein (HDL)-bound cholesterol, total phospholipids], elevated serum total alkaline phosphatase and lactate dehydrogenase (LDH) levels, in the absence of changes in overall renal function, extracellular mineral homeostasis [serum protein-corrected total calcium, magnesium, parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D)], plasma glycolate and oxalate levels. There was a redistribution of bone calcium and enhanced exchange of this within the extraosseous space, which was accompanied by significant bone calcium loss, but normal bone histomorphometry. Liver oxalate levels, if expressed per unit of defatted (DF) dry liver, were three times higher than in the controls. Urinary glycolate, oxalate, calcium and total protein excretion levels were elevated, the latter showing an excess of proteins > 100 kD and a deficit of proteins > 30-50 kD. Urinary calcium oxalate supersaturation was increased, and calcium phosphate supersaturation was unchanged. There were dramatically increased (by number, circumference, and area) renal calcium phosphate calcifications in the cortico-medullary region, but calcium oxalate deposits were not detectable. Electron microscopy (EM) and elemental analysis revealed intratubular calcium phosphate, apparently needle-like hydroxyapatite. Immunohistochemistry of renal tissue calcifications revealed co-localization of phospholipids and calcium phosphate. It is concluded that rats fed the CH-F diet exhibited: (1) a spectrum of metabolic abnormalities, the more prominent being dyslipidemia, hyperoxaluria, hypercalciuria, dysproteinuria, loss of bone calcium, and calcium phosphate nephrocalcinosis (NC); and (2) an interaction between calcium phosphate and phospholipids at the kidney level. The biological significance of these findings for the etiology of idiopathic calcium urolithiasis in humans is uncertain, but the presented animal model may be helpful when designing clinical studies.
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PMID:Nephrocalcinosis and hyperlipidemia in rats fed a cholesterol- and fat-rich diet: association with hyperoxaluria, altered kidney and bone minerals, and renal tissue phospholipid-calcium interaction. 1122 20

A 12-year-old girl was admitted to ward because of persistent left flank pain, vomiting, and hematuria. A stone was located at the ureteropelvic junction of the left kidney, as determined by means of abdominal sonography. Metabolic investigation for a renal stone revealed that she had hypercalcemia, hypophosphatemia, and hypercalciuria. Hyperparathyroidism was diagnosed based on the hypercalcemia and inappropriately elevated serum parathyroid hormone level. A parathyroid adenoma was successfully diagnosed by using thallium/technetium subtraction parathyroid scanning. Extracorporeal shock wave lithotripsy was performed to treat the renal stone, and the parathyroid adenoma was successfully removed. The patient's postoperative course was uneventful. This case is presented because urolithiasis and hyperparathyroidism are rare in children. Metabolic evaluation is mandatory in children with a renal stone. Further investigation for the hyperparathyroidism should be performed if hypercalcemia associated with hypercalciuria is documented.
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PMID:Urolithiasis and primary parathyroid adenoma: report of one case. 1498 62

Hypoparathyroidism, deafness and renal dysplasia (HDR) syndrome is an autosomal dominant disorder characterized by hypoparathyroidism, sensorineural deafness and renal dysplasia. Herein, we report a case of HDR syndrome associated with nephrocalcinosis and distal renal tubular acidosis. A 34-year-old woman was admitted to investigate recurrent stone formation and bilateral nephrocalcinosis. As a 3-year-old child, she had been diagnosed with HDR syndrome without chromosome evaluation. She had spontaneous stone passages on several occasions. On laboratory examination, serum calcium and intact parathyroid hormone at lower levels. Urinary citrate excretion was extremely low at 51.6 mg/day. On an ammonium chloride loading test, complete distal renal tubular acidosis was proved. To prevent the nephrocalcinosis from deteriorating, she was given potassium-sodium citrate. Since administration, she has not experienced spontaneous stone passage or renal colic. Nephrocalcinosis and recurrent urolithiasis will strongly affect renal prognosis in this case and we consider that citrate medication is an effective therapy in avoiding progress of her nephrocalcinosis.
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PMID:Case of hypoparathyroidism, deafness and renal dysplasia (HDR) syndrome associated with nephrocalcinosis and distal renal tubular acidosis. 1751 29

We report three cases of urolithiasis associated with sarcoidosis and reviewed the Japanese published reports. All cases had hypercalcemia, hyperuricemia, hypercalciuria and renal dysfunction. A serum level of 1,25-(OH)2D3 was elevated and intact parathyroid hormone (PTH) was decreased. Stone components were predominantly calcium oxalate. Abnormal calcium metabolism is a well-known feature of sarcoidosis and the reported prevalence of urolithiasis in patients with sarcoidosis was 1.3-14.0% in the English published reports. However, urolithiasis associated with sarcoidosis is uncommon in Japan and we could find only 16 documented cases including ours. Abnormal calcium metabolism is caused by an increase in serum concentration of 1,25-(OH)2D3, which is derived from endogenous overproduction in the pulmonary macrophages. If patients with urolithiasis have abnormal calcium metabolism, renal impairment and suppression of PTH, the possibility of sarcoidosis should be considered for a differential diagnosis. Also, it should be emphasized that the presence or developing of urolithiasis is to be monitored during follow up of patients with sarcoidosis.
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PMID:Three cases of urolithiasis associated with sarcoidosis: a review of Japanese cases. 1788 Mar

The parathyroid glands secrete parathyroid hormone (PTH), which is important for maintaining calcium homeostasis. Parathyroid gland hyperplasia and subsequent hyperparathyroidism can occur secondary to chronic renal failure in dogs, resulting in significant alterations in calcium metabolism. Renal secondary hyperparathyroidism is a complex, multifactorial syndrome that involves changes in circulating levels of calcium, PTH, phosphorus, and 1,25-dihydroxycholecalciferol (calcitriol). An increased PTH level can have deleterious effects, including soft tissue mineralization, fibrous osteodystrophy, bone marrow suppression, urolithiasis, and neuropathy. Dietary phosphorus restriction, intestinal phosphate binders, and calcitriol supplementation may slow the progression of renal disease and decrease PTH concentrations in animals with secondary hyperparathyroidism; however, the prognosis for these animals is guarded to poor.
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PMID:Renal secondary hyperparathyroidism in dogs. 1974 44

A case of oxyphil cell adenoma of parathyroid is presented. A 82-year-old woman complained of back pain. Left hydronephrosis, elevated serum calcium-parathyroid hormone and a nodule in the right neck suggested functioning parathyroid adenoma. Resected adenoma (15 mm x 10 mm x 5 mm) was exclusively composed of oxyphil cell. Production of parathyroid hormone by oxyphil cells was confirmed by immunohistochemistry. This case was found to be the smallest parathyroid oxyphil cell adenoma hitherto reported that caused urolithiasis.
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PMID:[Functioning oxyphil cell adenoma of parathyroid diagnosed with ureteral stone]. 1980 May 55

From the analysis of various urinary constituents and the estimation of serum parameters, it is now possible to identify the risk factors responsible for or contributing for stone formation metabolic factor included calcium, oxalate, uric acid, citrate and pH. Environmental factors where total volume, sodium, phosphate and magnesium. Urinary citrate and magnesium found to be lower in stone formers. The levels of serum parameters like calcium, sodium and intact parathyroid hormone (IPTH) is higher than normal. Where as potassium and magnesium is found to be lower than normal. Higher level of IPTH is associated with primary hyperparathyroidism and is related with stone formation in-patient with urolithiasis. Serum levels of phosphorus, uric acid and Creatinine found to be normal.
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PMID:Twenty four hours urine and serum biochemical parameters in patients with urolithiasis. 2067 1

Primary hyperparathyroidism (PHPT) is a disease to cause calcium, phosphorus, bone metabolism abnormality by the over secretion of parathyroid hormone (PTH) . A rise of PTH brings hypercalcemia, hypophosphatemia, and clinical symptoms include a recurrent urolithiasis, a letter of psychoneurosis, a gastrointestinal ulcer and bone resorption. It is the object disease of the clinical study that is important as one of the causes of urolithiasis in the urology department domain now because most of symptom type PHPT is renal stone types although it is a border domain with the internal secretion surgery, and the disease is often discovered at the urology department.
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PMID:[Diagnosis and treatment of urolithiasis with primary hyperparathyroidism]. 2196 Feb 29


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