Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bone status, calcium and phosphate metabolism were prospectively evaluated in 98 renal transplant recipients with stable renal function. Aseptic necrosis of bone was found in 30 patients, leading to arthroplasty in 12 patients. Plasma parathyroid hormone and nephrogenic cyclic adenosine monophosphate (cAMP) values were greater and the duration of pre-transplant chronic renal failure longer in patients with aseptic necrosis of bone than in those who were not affected. Cumulative oral corticosteroid doses and the number of acute rejection episodes treated by intravenous methylprednisolone pulses were similar in patients with or without aseptic necrosis of bone. Hyperparathyroidism was confirmed histologically in 14 patients, comprising 4 cases of adenoma and 10 of diffuse hyperplasia. Serum parathyroid hormone correlated positively with serum creatinine (r = 0.47; P less than 0.001) and with cumulative corticosteroid dose (r = 0.30; P less than 0.003). This study suggests that hyperparathyroidism is a factor in the pathogenesis of aseptic bone necrosis. The frequency and severity of bone necrosis may be decreased by early detection and treatment of post-transplant hyperparathyroidism.
Nephrol Dial Transplant 1989
PMID:Aseptic necrosis of bone following renal transplantation: relation with hyperparathyroidism. 254 Apr 58

Persistent hypercalcaemia developed in a 26-year-old man after rhabdomyolysis-induced acute renal failure. Although several serum parathyroid values were normal following recovery of renal function, primary hyperparathyroidism was suspected after 9 months of prolonged hypercalcaemia. A single parathyroid adenoma was removed and serum calcium as well as serum parathyroid hormone returned to normal values. The persistence of increased serum calcium concentrations after rhabdomyolysis-induced acute renal failure should lead one to consider other causes of hypercalcaemia, and particularly primary hyperparathyroidism.
Nephrol Dial Transplant 1986
PMID:Parathyroid adenoma causing persistent hypercalcaemia after rhabdomyolysis-induced acute renal failure. 311 Jun 63

This review discusses the impact of molecular genetics on the diagnosis and prognosis of renal cell tumours as well as the genetic changes in renal cell tumours associated with von Hippel-Lindau disease and end-stage kidney disease. The use of molecular techniques enables the division of renal cell tumours into genetically and biologically well defined entities. The new classification system distinguishes between papillary renal cell tumours, including papillary renal cell adenoma and papillary renal cell carcinoma, nonpapillary renal cell carcinoma, chromophobe renal cell carcinoma and renal oncocytoma. The advantage of the new classification system is that genetic markers, in contrast to the tumour phenotype, are constant during tumour progression and allow a precise diagnosis even from a small biopsy specimen.
Nephrol Dial Transplant 1996
PMID:Molecular genetics of human renal cell tumours. 904 31

Clonal analysis has shown that in renal hyperparathyroidism (2-HPT), parathyroid glands initially grow diffusely and polyclonally after which the foci of nodular hyperplasia are transformed to monoclonal neoplasia. There is a great deal of information about genetic abnormalities contributing to the tumourigenesis of parathyroid neoplasia in primary hyperparathyroidism. It is speculated that allelic loss of the MEN1 suppressor gene and overexpression of cyclin D1 induced by rearrangement of the parathyroid hormone gene may be the major genetic abnormality in sporadic parathyroid adenoma but not in 2-HPT. The pathogenesis of 2-HPT, abnormality of the Ca2+-sensing receptor (CaR) gene and the vitamin D receptor gene may possibly contribute to parathyroid tumourigenesis in 2-HPT. However, this is not yet clear and heterogeneous and multiple genetic abnormalities may be responsible for the progression of secondary parathyroid hyperplasia.
Nephrol Dial Transplant 1999
PMID:Mechanism of parathyroid tumourigenesis in uraemia. 1004 55

Management of secondary hyperparathyroidism is difficult because of the interrelationship of parathyroid hormone, calcium and phosphorus. This study was carried out to assess the efficacy of intravenous administration of alfacalcidol once weekly versus twice weekly in patients with severe hyperparathyroidism. Twenty-one hemodialysis patients with intact parathyroid hormone >88 pmol/L were divided into two groups. Eleven patients (Group 1) were given a once-weekly alfacalcidol intravenously for 12 weeks. The starting dose was 4 microg which was increased or decreased by 1 microg per week. Ten patients (Group 2) were given twice-weekly alfacalcidol intravenously for 12 weeks. The starting dose was 2 microg twice weekly which was increased or decreased by 0.5 microg/dose. The dose was increased or decreased according to serum calcium and phosphorus levels. Serum calcium, phosphorus and alkaline phosphatase levels were measured weekly and intact parathyroid hormone every 4 weeks. Intact parathyroid hormone reduced significantly (P = 0.0001) from 128.12 +/- 35.42 pmol/L to 82.93 +/- 65.20 pmol/L and from 113.74 +/- 40.83 pmol/L to 64.24 +/- 35.17 pmol/L after 4 weeks in Groups 1 and 2, respectively. After 4 weeks alkaline phosphatase declined significantly (P = 0.0001) from 146.0 +/- 57.3 IU/L to 116.0 +/- 45.6 IU/L in Group 1 and from 139.0 +/- 45.1 IU/L to 116.6 +/- 38 IU/L in Group 2. There were no significant differences in serum levels of calcium, phosphorous or their product. Interestingly, an adenoma disappeared in one patient from Group 1, and out of two adenomas, one disappeared from another patient in the same group. These results indicate that intravenous alfacalcidol once weekly is safe and effective in suppressing high parathyroid hormone in hemodialysis patients.
Ther Apher Dial 2008 Apr
PMID:Intravenous alfacalcidol once weekly suppresses parathyroid hormone in hemodialysis patients. 1838 62

The study of thyroid nodules in hemodialyzed patients using ultrasonography has been described in a limited number of reports. The thyroid glands of 143 patients with end-stage renal disease on hemodialysis were examined by ultrasonography using frequency probes. Although a goiter (thyroid volume > 20 mL) was observed in only 20 patients (14%), nodular lesions of the thyroid gland were more frequent and found in 85 patients (59.4%), especially in female patients (42 patients, 72.4%). The etiology of thyroid nodular lesions was as follows: cyst in 43 (30.0%), adenomatous goiter in 14 (9.8%), adenoma in 11 (7.7%), hypoechoic lesion in 17 (11.9%), and intrathyroid calcification in 8 (5.6%). Ultrasound-guided fine-needle aspiration cytology was performed in 5 patients, but no abnormal cells were found. Compared to patients without nodules, the age was higher in patients with cysts (54 +/- 15 vs. 63 +/- 13 years; P < 0.05) and hypoechoic lesions (70 +/- 13 years; P < 0.05). The serum thyroglobulin level was higher in patients with adenomatous goiters (26 +/- 28 vs. 148 +/- 166 ng/mL; P < 0.05). The thyroid volume was greater in patients with adenomatous goiters (14.2 +/- 5.7 vs. 19.0 +/- 7.3 mL; P < 0.05) and adenomas (18.2 +/- 6.7 mL; P < 0.05). In conclusion, patients undergoing hemodialysis frequently develop thyroid abnormalities and ultrasonography is a useful imaging modality to identify these lesions.
Ther Apher Dial 2010 Jun
PMID:Ultrasonographic detection of thyroid nodules in hemodialysis patients in Japan. 2060 86

The goal of the pharmacological therapy in secondary hyperparathyroidism (SHPT) is to reduce serum levels of parathyroid hormone and phosphorus, to correct those of calcium and vitamin D, to arrest or reverse the parathyroid hyperplasia. However, when nodular hyperplasia or an autonomous adenoma develops, surgery may be indicated. We reviewed the literature with the aim of defining if the echographic criteria predictive of unresponsiveness of SHPT to calcitriol therapy are valid also in the cinacalcet era and if drug therapy may reverse nodular hyperplasia of parathyroid gland (PTG). The responsiveness to therapy and regression of the nodular hyperplasia of PTG remains an open question in the calcimimetic era as well as the cutoff between medical and surgical therapy. Prospective studies are needed in order to clarify if an earlier use of cinacalcet in moderate SHPT might arrest the progression of parathyroid growth and stabilize SHPT.
Ther Apher Dial 2018 Feb
PMID:Parathyroid Nodular Hyperplasia and Responsiveness to Drug Therapy in Renal Secondary Hyperparathyroidism: An Open Question. 2898 Jul 61