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)

Human beta-2 microglobulin (beta-2 M) is released into body fluids as a result of cell turnover, excreted by the kidney, and catabolized in the proximal tubule. Urinary excretion rates constitute a sensitive index of renal tubular function. The beta-2 M urine-to-serum ratio was measured in 25 patients with primary hyperparathyroidism (15 preoperative and 10 treated conservatively) in addition to 20 age- and sex-matched control subjects. The ratio was found to be significantly higher in both the operative and the conservatively managed groups compared to controls (p less than 0.05, Mann-Whitney U test). After surgical excision of a single parathyroid adenoma in the 15 operative cases, the beta-2 M urine-to-serum ratio fell to normal limits. These preliminary findings indicate that the urine-to-serum beta-2 M ratio may be of value in detecting change in renal function in asymptomatic patients with hyperparathyroidism. Further studies are indicated to establish whether these subtle changes are associated with long-term morbidity.
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PMID:The beta-2 microglobulin urine-to-serum ratio: an early marker of renal dysfunction in primary hyperparathyroidism. 331 60

Long-Evans (Eker) rats carry a mutation that predisposes them to develop spontaneous renal cell tumors of two morphologic patterns: solid chromophilic masses or cystic lesions lined by eosinophilic cells. Previous studies have suggested that these tumors arise from the proximal tubules. In the present study, lectin-binding characteristics and cytokeratin expression of various stages of hereditary rat renal epithelial neoplasia were examined to localize the portion of the nephron from which tumors arise. Lectin-binding histochemistry has been used as a marker of cell surface glycoprotein expression, thought to be important in the differentiation of benign from malignant epithelial lesions and in the determination of their cell of origin. The presence or absence of keratin intermediate filaments in the rat nephron has been used to identify nephron segments. The polyclonal antibody to high- and low-molecular-weight cytokeratin stained the cells of the collecting ducts but not the proximal or distal tubules. Binding to the proximal tubules by the lectins Conavalia ensiformis (Con A), Dolichas biflorus, Ricinus communis (RCA-1), and Triticum vulgare and to the distal tubules by Con A, RCA-1, Arachis hypogaea (PNA) with and without neuraminidase, and the antibody for cytokeratins was demonstrated. The lectin binding and cytokeratin staining patterns of rat hereditary renal cell carcinoma, adenoma and the preneoplastic lesions of atypical tubules and hyperplasias suggest that cystic adenomas arise from the distal nephron, principally the collecting duct, whereas the solid atypical tubules, hyperplasias, and adenomas arise from the proximal nephron, principally the proximal tubule.
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PMID:Preneoplastic and neoplastic lesions of rat hereditary renal cell tumors express markers of proximal and distal nephron. 748 12

Metanephric adenoma is a rare renal neoplasm that is histologically and clinically unique. We found this neoplasm in a 54-year-old woman. This large, well-circumscribed, solid, tan tumor showed histologic similarity to developing metanephric tubular epithelium. It is composed of uniformly small epithelial cells forming tubules. Immunohistochemical evaluation showed that the tumor cells express proximal tubule marker URO-2 and wt1 gene protein product, commonly expressed in Wilms' tumors. Ultrastructurally, the epithelial cells were characterized by the presence of cilia on the luminal side and were resting on an abundant basement membrane. Cytogenetic analysis showed normal female karyotype. The unique features of metanephric adenoma should be clinically and pathologically recognized because of its invariably benign course.
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PMID:Metanephric adenoma: histology, immunophenotype, cytogenetics, ultrastructure. 868 36

Cell proliferation rate and apoptosis were examined in archival kidneys from young, middle-aged, and old male F344 rats. Immunohistochemical expression of proliferating cell nuclear antigen (PCNA) and apoptosis were quantified in the same cell populations of the proximal tubule epithelium. A total of 79 kidneys from 40 rats were examined. There was a progressive increase in cell proliferation rates in rats from 4 and 6-10 months of age. In 23-month-old rats, proliferative activity appeared to be reduced. No age-related variations in apoptotic indices were found. One of the 16 rats aged 23 months had a tubular cell adenoma. In the tumor-affected kidney, cell proliferation rate was dramatically higher than in the contralateral kidney as well as in all the other kidneys examined. This high proliferative activity was not balanced by variation in cell death.
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PMID:Age-related cell proliferation and apoptosis in the kidney of male Fischer 344 rats with observations on a spontaneous tubular cell adenoma. 1112 94

Renal apical chloride-base exchangers are essential to electrolyte and acid-base homeostasis. Different functional isoforms of apical anion exchangers have been identified in kidney proximal tubule and cortical collecting duct. Included amongst these are the following: chloride-formate, chloride-oxalate, and chloride-hydroxyl exchangers in proximal tubule; and chloride-bicarbonate exchanger in cortical collecting duct. Chloride-formate exchange, which was first identified in kidney proximal tubule, works in parallel with the apical sodium-hydrogen exchanger, and is thought to reabsorb the bulk of luminal chloride. Despite numerous studies, the molecular identities of apical chloride-base exchangers have remained unknown. Recent studies have identified a new class of anion exchangers, including pendrin (encoded by the PDS gene) and downregulated in adenoma (DRA, encoded by the DRA gene). Pendrin is expressed in the kidney, whereas DRA is not. Functional studies indicate that pendrin can function in chloride-formate and chloride-base exchange modes. It is unlikely that pendrin is the apical chloride-formate exchanger in the kidney proximal tubule. However, it is the only molecule that has been shown to mediate chloride-formate exchange. In the present review, recent studies regarding the renal distribution and membrane localization of pendrin, and its functional properties, including its roles in chloride reabsorption and base excretion, are addressed.
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PMID:Molecular physiology of the renal chloride-formate exchanger. 1149 64

Primary aldosteronism (PA) is the most common cause of endocrine hypertension. PA is most frequently presented as moderate to severe hypertension, but the clinical and biochemical features vary widely. The aim of our study was to identify genetic variants that influence the phenotype of patients with PA. We hypothesized that genetic variants potentially affecting aldosterone production (aldosterone synthase, CYP11B2), renal proximal tubule reabsorption (alpha-adducin), or the mechanisms of counterbalance leading to vasodilatation and sodium excretion (bradykinin B(2)-receptor, B(2)R) could influence the clinical and biochemical characteristics of patients with PA. We studied three polymorphisms of these genes (C-344T of CYP11B2, G460W of alpha-adducin, and C-58T of B(2)R) in 167 primary aldosteronism patients (56 with aldosterone-producing adenoma and 111 with idiopathic hyperaldosteronism). B(2)R and alpha-adducin genotypes were strong independent predictors of both systolic and diastolic blood pressure levels; plasma renin activity and aldosterone also play a marginal role on BP levels. Body mass index, age, sex, and CYP11B2 genotype displayed no significant effect on the clinical parameters of our population. In particular, alpha-adducin and B(2)R polymorphisms accounted for 13.2% and 11.0% of the systolic and diastolic blood pressure variance, respectively. These data suggest that genetic variants of alpha-adducin and the bradykinin B(2)-R influence the blood pressure levels in patients with primary aldosteronism.
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PMID:Blood pressure in patients with primary aldosteronism is influenced by bradykinin B(2) receptor and alpha-adducin gene polymorphisms. 1210 46

The worldwide increase in the incidence of metabolic syndrome correlates with marked increase in total fructose intake in the form of high-fructose corn syrup, beverage and table sugar. Increased dietary fructose intake in rodents has been shown to recapitulate many aspects of metabolic syndrome by causing hypertension, insulin resistance and hyperlipidaemia. Recent studies demonstrated that increased dietary fructose intake stimulates salt absorption in the small intestine and kidney tubules, resulting in a state of salt overload and thus causing hypertension. The absorption of salt (sodium and chloride) in the small intestine is predominantly mediated via the chloride/base exchangers DRA (Down Regulated in Adenoma) (SLC26A3) and PAT1 (Putative Anion Transporter 1) (SLC26A6), and the Na(+) /H(+) exchanger NHE3 (Sodium Hydrogen Exchanger3) (SLC9A3). PAT1 and NHE3 also co-localize on the apical membrane of kidney proximal tubule. Luminal fructose stimulated salt absorption in the jejunum and kidney tubules, responses that were significantly diminished in PAT1 null mice. These studies further demonstrated that Glut5 (SLC2A5) is the major fructose-absorbing transporter in the small intestine (and kidney proximal tubule) and plays an essential role in the systemic homeostasis of fructose. Increased dietary fructose intake for several weeks upregulated the expression of NHE3, PAT1 and Glut5 in the intestine and resulted in hypertension in wild-type mice, a response that was almost abolished in PAT1 null mice and abrogated in Glut5 null mice. This article will discuss the interaction of Glut5 with salt-absorbing transporters and review the role of dietary fructose in enhanced salt absorption in intestine and kidney as it relates to the pathogenesis of hypertension in metabolic syndrome.
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PMID:Dietary fructose, salt absorption and hypertension in metabolic syndrome: towards a new paradigm. 2114 27