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 term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy. 164 77

Severe secondary hyperparathyroidism is still observed at present in 5-10% of haemodialysis patients. It requires surgical correction. Fifty-eight haemodialysis patients had neck surgery and their 222 parathyroid glands analysed. The individual gland weight was comprised between 22 and 3880 mg (mean +/- SEM, 689 +/- 62 mg). Mean total parathyroid gland weight per patient was comprised between 2 and 3 g. Schematically, 4 types of gland architecture could be distinguished: diffuse hyperplasia alone; diffuse hyperplasia associated with incipient nodule formation; hyperplasia with pronounced nodule formation; and nodule formations alone. Total gland weight was significantly higher for the latter two histological forms than for the former suggesting transformation with time of pure hyperplasia to nodular hyperplasia. Patients with chronic pyelonephritis had a mean gland weight higher than that of patients with chronic glomerulonephritis (3308 +/- 498 mg versus 1824 +/- 358 mg, p less than 0.01). No relation was found between total gland weight and plasma calcium, phosphate or alkaline phosphatases. However, a weak relation existed between total gland weight and plasma immunoreactive parathyroid hormone. In addition, a negative relation was observed between highest prior plasma aluminium and gland weight when considering only patients with a gland weight less than 2000 mg. Parathyroid gland aluminium content was significantly higher in haemodialysis patients than in nonuraemic patients with primary hyperparathyroidism. A direct relation was found between parathyroid gland and bone aluminium. In conclusion, in haemodialysis patients with evolving hyperparathyroidism initially diffuse gland hyperplasia appears to be associated progressively with nodule formation. Circulating immunoreactive parathyroid hormone is positively related to total gland weight.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hyperparathyroidism secondary to renal insufficiency: anatomo-clinical relations and the potential role of an aluminum overload]. 648 74

Chronic renal failure associated with hypercalcemia and hypophosphatemia was diagnosed in 6 horses. The renal lesions in 5 of the horses were classified as chronic glomerulonephritis and in the sixth, as chronic interstitial nephritis/pyelonephritis. There was no evidence of primary hyperparathyroidism or pseudohyperparathyroidism, thus suggesting that hypercalcemia associated with advanced renal failure in horses is related to a unique role of the equine kidney in calcium homeostasis.
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PMID:Paradoxic hypercalcemia and hypophosphatemia associated with chronic renal failure in horses. 706 1