Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urinary cyclic AMP excretion per 24 h or per g creatinine in primary hyperparathyroidism (1 degrees HPT) has been evaluated by several authors with conflicting results. In 50 patients with 1 degrees HPT, 25 patients with secondary (2 degrees) HPT and 35 healthy control persons we determined urinary cyclic AMP per 24 h or per g creatinine. These parameters did not satisfactorily discriminate patients from controls, especially when glomerular filtration rate (GFR) as determined by creatinine clearance was reduced. Since urinary cyclic AMP is derived from plasma by glomerular filtration and from kidney by tubular production-the amount of tubules is reflected by GFR-the cyclic nucleotide was related to GFR. In controls urinary cyclic AMP correlated better with GFR than with creatinine excretion. Additionally, in 45 of 50 patients with 1 degrees HPT and in all with 2 degrees HPT, urinary cyclic AMP/GFR was raised. In 1 degrees HPT serum levels of parathyroid hormone correlated closer with urinary cyclic AMP/GFR than with urinary cyclic AMP/g creatinine. The ratio cyclic AMP/GFR decreased to normal or subnormal values after removal of adenomatous or hyperplastic glands in 1 degrees HPT and during infusion of calcium in 2 degrees HPT. In 50 patients with renal lithiasis caused by diseases other than 1 degrees HPT (anatomical variations, pyelonephritis, immobilization after tetraplegia) the ratio cyclic AMP/GFR was not raised. Urinary cyclic AMP/GFR, therefore, reflects parathyroid hormone excess more reliably than cyclic AMP/g creatinine.
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PMID:Hyperparathyoidism: influence of glomerular filtration rate on urinary excretion of cyclic AMP. 19 82

Bone morphological parameters of renal osteodystrophy such as abundance of osteoid surface, osteoid seam width index, calcification fronts, osteoclast activity and trabecular bone volume were studied in 71 patients on maintenance hemodialysis and compared with bone densitometry, laboratory and clinical data. Increased osteoclast activity (hyperparathyroidism) was by far the most common bone morphological finding. Patients with chronic pyelonephritis or polycystic kidney disease had more than double the amount of osteoid than patients with chronic glomerulonephritis. The trabecular bone volume seemed to be increased in most patients in contrast to the cortical bone volume which was decreased, judged from bone densitometry and previously from X-ray. Despite that patients with polycystic kidney disease were older, their trabecular volume was larger than in patients with glomerulonephritis. The bone mineral content evaluated by bone densitometry was low in most patients, and more associated with bone morphological signs of osteomalacia than with secondary hyperparathyroidism. Serum phosphate (S-PO4) and serum parathyroid hormone (S-PTH) seemed to discriminate better between osteomalacia and secondary hyperparathyroidism than serum alkaline phosphatase (S-Alk. phosph.), which was elevated in both groups. Patients who had been bilaterally nephrectomized were no more abnormal than other patients, and they had lower S-Alk. phosph. The abundance of osteoclasts was found to be a predictor of future development of clinical secondary hyperparathyroidism.
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PMID:Studies of bone morphology, bone densitometry and laboratory data in patients on maintenance hemodialysis treatment. 397 74

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

Bone mineral content (BMC) was measured annually over a three year period in 31 consecutive patients on maintenance hemodialysis (HD). No patient had received treatment with vitamin D derivatives, anticonvulsants or corticosteroids, nephrectomy or a renal transplant. Initial median BMC value in per cent of sex and age matched normal mean was significantly decreased to 91.0% (P less than 0.01), indicating bone mineral loss in chronic renal failure prior to HD. During HD a highly significant fall in mean BMC (in per cent of initial value) continued to 95.1%, 92,7% and 90.8% after 1, 2 and 3 years, respectively, with no influence of age, sex or initial BMC value. The interindividual variation in BMC changes, however, was considerable: the BMC loss over 3 years exceeded 10% in 13 (42%) patients ("rapid losers") while 12 (39%) patients had a BMC loss below 5%, or no loss at all. The "rapid loser" group had significantly higher serum levels of parathyroid hormone and alkaline phosphatases and, moreover, developed a lower serum phosphate and calciumXphosphorus product than the other group of patients ("slow losers"). The mean BMC loss over 3 years of HD was pronounced and significant (P less than 0.02) in patients with chronic pyelonephritis (9.8%) and polycystic kidney disease (14.2%), but much smaller, and not significant, in patients with chronic glomerulonephritis (4.8%). It is concluded that a selection of patients with a high degree of bone mineral loss during HD is not possible by means of sex, age, initial BMC, biochemical parameters, or diagnosis (2 patients with chronic glomerulonephritis appeared to be "rapid losers"). For that purpose a high-precision BMC method is mandatory.
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PMID:Bone mineral content in patients on prolonged maintenance hemodialysis: a three year follow-up study. 664 Oct 32

Fifty-eight patients on intermittent haemodialysis underwent parathyroidectomy because of severe secondary hyperparathyroidism. Mean individual parathyroid gland weight was 689 +/- 62 (SEM) mg. Mean total gland weight per patient was between two and three grams. Increasing nodule formation within hyperplastic glands appeared to develop with increasing time of duration of hyperparathyroidism. Patients with chronic pyelonephritis had a higher gland weight than those with chronic glomerulonephritis. A direct relationship was found between gland weight and circulating immunoreactive parathyroid hormone, but an inverse relationship between gland weight and plasma aluminium concentration. The higher the parathyroid gland aluminium, the higher was the bone aluminium concentration.
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PMID:Secondary hyperparathyroidism in chronic haemodialysis patients: a clinico-pathological study. 665 93

Hydrocortisole, parathyroid hormone (PTH), and calcitonin were radioimmunoassayed in the blood of patients with chronic pyelonephritis. Hydrocortisone content decreased at the early stages of nephrosclerosis before renal failure, and hypercalcitoninemia was developing. In chronic renal insufficiency hydrocortisone level normalized, hypercalcitoninemia augmented, and PTH level in the blood plasma increased. Disorders of these substances metabolism are believed to be one factor in the pathogenesis of pyelonephritic nephrosclerosis. Measurements of blood hydrocortisone and calcitonin in patients with chronic pyelonephritis can be used for early diagnosis of nephrosclerosis before its clinical manifestation as chronic pyelonephritis. Such measurements will help objectively assess the activity of the sclerotic process, timely begin proper treatment, and predict the disease course and outcome.
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PMID:[Hydrocortisol, parathyroid hormone and calcitonin in blood of patients with chronic pyelonephritis and nephrosclesosis]. 947 16

Blood plasma content was studied of hydrocortisone, parathyroid hormone (PTH) and calcitonin in patients with chronic pyelonephritis (ChP) using methods of radioimmunologic and immunoenzymatic analyses. ChP patients had marked alterations of blood plasma levels of hydrocortisone, PTH and calcytonin, with the reduced levels of hydrocortisone and hypercalcitoninamia being noted during the early stages of nephrosclerosis. It is suggested that hydrocortisone and calcitonin content in blood of ChP patients might be used as indicators of state of the endocrine mechanisms controlling the renal connective tissue metabolism during the early stages of nephrosclerosis. The above measure will also be helpful in the assessment of activity of the sclerotic process in the kidneys, prognosis of the outcome of the medical condition, and development of treatment options of adequate pathogenetic therapy.
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PMID:[Hormonal disorders in patients with chronic pyelonephritis with nephrosclerosis and kidney failure]. 962 41