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)

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

An outbreak of urolithiasis that doubled the annual mortality rate of chickens in a large flock of table-egg-layers is described. Despite the presence of a large unilateral urolith and/or severe renal atrophy, the layers often maintained active egg production and apparent homeostasis until a small urolith blocked the ureteral flow from the contralateral kidney. This terminal episode appeared to produce acute obstructive renal failure, rapidly developing visceral gout (visceral urate deposition), uremia, and death. The atrophy observed appeared to be acquired and progressive. Histologic features in the kidneys were acute to chronic glomerulonephritis, interstitial nephritis, and pyelonephritis. Epizootiologic and microbiologic studies indicated that a combination of infectious and noninfectious mechanisms may have been involved. Causative roles for calcium-phosphate imbalance, infectious bronchitis (IB), Newcastle disease (ND), and adenovirus or reovirus infections could be neither excluded nor confirmed. Contributory factors may have been spray ND-IB and other vaccinations of 15-week-old ND-IB-susceptible pullets, water deprivation, shipping stress, Mycoplasma synoviae infection, immune complex disease, and mycotoxins.
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PMID:Epizootiology, pathology, and microbiology of an outbreak of urolithiasis in chickens. 672 98

In a series of investigation to elucidate the roles of chemical substances in the atrophic process of nephron in chronic pyelonephritis (CPN), two protease inhibitors (PI) and enterobacterial antigen were examined by immunofluorescence (IF). Alpha-antitrypsin (alpha 1AT) was always found in the sclerotic glomerular tuft (GT) and along the thickened Bowman's capsule (BC) as well as the thickened tubular basement membrane (TBM) in every atrophic nephron of CPN. Antithrombin III (AT III) was always found along the inside of thickened TBM in every atrophic nephron, but not found in the sclerotic GT nor along the thickened BC. No enterobacterial antigen was present in the sclerotic GT, thickened BC, and thickened TBM. Therefore, alpha 1AT and AT III seem to play significant roles in the process of atrophy of nephrons as a different factor from the persistence of enterobacterial antigen which has been considered to be one of the progressive factors of CPN. At III was easily dissociated from the thickened TBM after the incubation in warm (37 degrees C) 0.01 M phosphate buffered saline of various pH (pH 4.0, pH 7.2 or pH 10.0) and cold (4 degrees C) or warm (37 degrees C) 0.75 M hydrazine solutions of the same pH, while alpha 1AT was not dissociated from the atrophic nephrons after the incubation in all solutions. These results may imply different processes of deposition between the two PI in the atrophic nephrons.
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PMID:Alpha 1-antitrypsin and antithrombin III in atrophic nephrons of chronic pyelonephritis. 680 52

The patient, a 30-year-old woman, was admitted to Itoh Hospital in February, 1979 for hyperthyroidism. She had a history of pyelonephritis and recurrent urinary tract infection. Laboratory data on admission revealed overt hyperthyroidism (T3: 405 ng/dl, T4: 22.5 micrograms/dl and T3U: 57.--%), severe hypercalcemia of 12.6 mg/dl and hypercalciuria. The PSP excretion and GFR were both decreased. Serum c-PTH was nondetectable. As the thyroid function improved, there was a gradual decrease and later normalization of plasma calcium, phosphate and urinary calcium excretion. When subtotal thyroidectomy was performed on October 19, 1979, hypertrophy of the parathyroid gland was not demonstrated. In comparison with 98 other hyperthyroid patients, the pathogenesis of hypercalcemia was discussed. In conclusion, hypercalcemia in the patient, T. Y., was regarded as a kind of disequilibrium hypercalcemia which resulted from a combination of increased bone turnover and decreased calcium excretion by the kidney.
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PMID:A case report on disequilibrium hypercalcemia in hyperthyroidism. Comparison of calcium metabolism with other patients with hyperthyroidism. 717 16

Magnesium ammonium phosphate calculi developed in the urinary bladders and urethras of four of five offspring of Miniature Schnauzer parents with recurrent struvite urolithiasis. Calculi were detected by radiograhy when the dogs were 12 to 15 months old. Males and females were affected. A significant number of urease-producing staphylococci were identified in the urine of three of four dogs before urolith formation, and in one dog after urolith formation. The dogs were evaluated until they were 26 months old. Serum concentrations of calcium, phosphorus, and magnesium were inside usual limits throughout the study. Abnormalities that might predispose to urinary tract infection were not identified by radiography or necropsy studies. In one dog, bladder calculi recurred after surgical removal of multiple cystoliths. In another, urethral obstruction and acute generalized pyelonephritis induced a lethal uremic crisis. Gross and microscopic lesions, detected after necropsy of all dogs with uroliths, were typical of bacterial infection.
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PMID:Struvite urolithiasis in a litter of miniature Schnauzer dogs. 740 90

Spontaneous urinary calculus was observed in only 27% of female LEW rats among nine inbred strains maintained in the Institute for Animal Experimentation. The condition occurred between 3 and 9 weeks of age with loss of weight, enlargement of the os urethral externum, anuria and general marasmus. All of the affected rats died from anuria 3 to 4 days after the onset. The affected rats had one to ten infected stones or many fine crystals of sand, which consisted of magnesium ammonium phosphate, in the urinary bladder and/or urethra. Analysis of microorganisms revealed that Corynebacterium renale, known as a causative agent of bovine pyelonephritis, was the most probable candidate for producing infection stones. This is the first report that the rat is spontaneously infected with C. renale. This could be a useful animal model for human urinary calculus and also for C. renale infection in the field of veterinary science.
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PMID:Spontaneous urinary calculus in young LEW rats caused by Corynebacterium renale. 805 21

Urinary tract infections (UTIs) are associated with approximately 27% of premature births. Escherichia coli is the most frequent causal agent of UTIs and expresses virulence factors, including surface adhesins that recognize specific host tissue receptors. We have reported that E. coli Dr adhesin recognizes decay-accelerating factor as the host tissue receptor and that these receptors are increased during pregnancy. Induction of pathogenesis is a cumulative effect of the host-pathogen relationship involving specific host factors and virulence characteristics of the invading organism. Recently, an experimental model of chronic pyelonephritis has been developed with E. coli bearing Dr adhesin (E. coli Dr(+)) in nonpregnant lipopolysaccharide hyporesponder C3H/HeJ mice. In this study, we investigated the role of E. coli Dr(+) on the outcome of pregnancy in C3H/HeJ mice. Groups of pregnant mice were infected with E. coli Dr(+) or its isogenic mutant which does not bear the Dr adhesin (E. coli Dr(-)) by urethral catheterization. Nearly 90% of pregnant mice infected with E. coli Dr(+) delivered preterm (before 90% gestation) compared to 10% of mice infected with E. coli Dr(-) and none of the mice treated with phosphate-buffered saline (PBS). Also, there was a significant reduction in fetal birth weight in the E. coli Dr(+)-infected group compared to the E. coli Dr(-)- and PBS-treated groups (P = 0.003). This experimental model of E. coli Dr(+)-induced preterm delivery in mice may help in understanding the molecular mechanisms involved in UTI-induced preterm labor involving bacterial adhesins.
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PMID:Experimental gestational pyelonephritis induces preterm births and low birth weights in C3H/HeJ mice. 1053 Dec 54

We identified 40 pediatric patients with urolithiasis. There were 27 boys and 13 girls. Initial symptoms were abdominal pain, with or without microscopic hematuria in 40% of the cases, and urinary tract infection/pyelonephritis in 25% of the cases. Stones were made of struvite (35% of the cases), calcium-phosphate (25%) or calcium-oxalate (20%). The high prevalence of struvite stones reflects the importance of urinary tract infection a major cause of urolithiasis in that specific age group. Hypercalciuria was the most common urinary biochemical abnormality, found in more than 50% of the children. In the absence of a spontaneous passage of the stone, extra-corporeal shock wave lithotripsy represents an excellent therapeutic option. This article emphasizes the importance of stone analysis and extensive biochemical investigations in children with urolithiasis, in order to avoid recurrence and potential progression towards chronic renal failure.
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PMID:[Urinary calculi epidemiology in children]. 1549 64

Milk of calcium is a viscous colloidal suspension of calcium carbonate, calcium phosphate, or calcium oxalate, or a mixture of these compounds. The calcific material gravitates to the dependent portion of a cystic cavity. Crescent- or hemisphere-shaped calcium density with a sharp horizontal upper border at the milk of calcium-clear fluid interface confirms the diagnosis. Bilateral milk of calcium in the renal pelvis or in dilated calyces is very rare and has not been reported in patients with spinal cord injury. A 63-year-old male patient with T-10 paraplegia presented with recurrent urinary tract infections. X-ray of the kidneys, taken with the vertical beam while the patient lay supine, revealed a poorly defined opacity overlying the lower pole of the right kidney. Findings on ultrasonography of the kidneys were interpreted as a large, staghorn-type calculus in the dilated lower pole calyx of the right kidney. Because x-ray of the kidneys showed a poorly defined opacity overlying the lower pole of the right kidney, milk of calcium was suspected, and computed tomography (CT) of the kidneys was performed. Calcific debris with horizontal layering in the lower pole calyces of both kidneys was seen; this confirmed the diagnosis of milk of calcium. A 62-year-old female patient with C-7 tetraplegia underwent ileal conduit urinary diversion. Subsequently, she developed calculi in the right kidney, which were treated with shock wave lithotripsy. Follow-up x-ray revealed faintly opaque shadows with indistinct margins in the region of both kidneys. Intravenous urography showed cortical thinning at the upper poles and blunting of the calyces, suggestive of chronic pyelonephritis. The right renal pelvis was bulky, and bilateral renal calculi were diagnosed during ultrasonography; however, the presence of faintly radio-opaque shadows with indistinct margins raised suspicions of renal milk of calcium. A CT scan of the kidneys, which was performed in the supine and subsequently in the prone position, revealed gravity-dependent layering of calcific material in the pelves of both kidneys and in the midpole calyces of the right kidney, thus confirming the diagnosis of milk of calcium. In conclusion, CT scan of the kidneys confirmed the diagnosis of bilateral renal milk of calcium, a very rare entity in patients with spinal cord injury. Awareness of typical and unique features of milk of calcium during imaging enables physicians to recognize renal milk of calcium and to differentiate it from nephrolithiasis, thereby avoiding unwarranted interventions such as shock wave lithotripsy or endoscopic procedures.
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PMID:Bilateral renal milk of calcium masquerading as nephrolithiasis in patients with spinal cord injury. 1766 Jan 62


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