Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intense proteinuria in rats bearing a functioning pituitary tumor MtT SA5 was considered to be evoked by overproduction of albumin due to elevated serum growth hormone (GH). The present study revealed a striking reduction of proteinuria by bilateral adrenalectomy. Supplementation for about 6 weeks with glucocorticoids to adrenalectomized tumor-bearing rats again induced marked proteinuria, but supplementation with mineralocorticoids failed to augment proteinuria. An analysis of systemic blood pressure and renal blood flow did not yield any conclusive result. In spite of an assumption that glucocorticoids enhance GH production of the tumor based on the presence of glucocorticoid receptor in the tumor tissue, no difference was found in serum GH levels between glucocorticoid- and mineralocorticoid-supplemented adrenalectomized rats. The mechanism remains to be clarified, but modification of glomerular permeability or a change in glomerular hydraulic pressure by glucocorticoids might be considered.
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PMID:Reduction of proteinuria by adrenalectomy and its restoration by glucocorticoids in rats bearing functioning pituitary tumor. 236 33

Intensive proteinuria accompanied by marked renal enlargement occurs in rats bearing functioning pituitary tumor MtT SA5. Urinalysis showed that protein excretion was up to 700 mg/day, and that the excreted protein consisted mostly of albumin. However, serum total protein and albumin levels remained almost unchanged. Histological examination revealed glomerular lesions, hyaline casts in the tubules, and proliferation of the tubular epithelium. The glomerular lesions consisted of accumulation of proteinaceous material in the subcapsular space; its organization and formation of fibrous crescents was with or without epithelial crescents. Electron microscopy revealed loss of foot processes and accumulation of absorption droplets in glomerular epithelial cells. Removal of the tumor resulted in a rapid reduction in urinary protein excretion. However, proteinuria persisted for at least 4 weeks after tumor removal with levels of approximately one-fourth of those before tumor removal. Histological changes of the kidneys resolved to some extent but damage still remained in the glomerular epithelial cells 4 weeks after tumor removal. Although proteinuria in animals bearing functioning pituitary tumors has long been implicated in hyperprolactinemia, the present study suggests that proteinuria in tumor-bearing rats is a control mechanism for overproduction of albumin in the liver stimulated by elevated serum growth hormone since hyperalbuminemia and possibly the hyperfibrinogenemia would cause the elevation of blood viscosity, resulting in thrombosis, unless control mechanisms were present. This proteinuria may serve for studies of glomerular permeability disorders as a model for homologous protein-overload proteinuria.
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PMID:Proteinuria induced by transplantable rat pituitary tumor MtT SA5. Model for homologous protein-overload proteinuria. 371 38

A case of systemic lupus erythematosus (SLE) complicated with hypopituitarism after steroid pulse therapy is reported. A 46-years-old-female with a history of SLE starting in 1975 was admitted to our hospital in February 1991 for lupus nephritis. Steroid pulse therapy, 1000 mg methyl-prednisolone for 3 successive days as one therapy unit, was administered. Proteinuria improved remarkably, however, general fatigue and headache appeared 2 weeks after initiation of therapy. Endocrinological examination revealed hypopituitarism including the levels of TSH, FSH, GH and ACTH. The secretion of FSH and LH gradually improved after replacement therapy of dried thyroid. MRI examination of the brain revealed an empty sella. It is known that pituitary tumor, cerebrovascular accident and autoimmune lymphocytic hypophysitis cause hypopituitarism. In this case, it is unlikely that the pulse therapy may be responsible for the infarction of the anterior pituitary artery furthermore, there has been no articles describing such incidence after steroid pulse therapy. This case may be indicative of a very rare case in which the empty sella might have been exacerbated by the pulse therapy in the causation of hypopituitarism.
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PMID:[Hypopituitarism associated with empty sella after steroid pulse therapy in a patient with SLE]. 814 29

We report the case of 19-year-old woman with cyclical Cushing's disease, in whom plasma adrenocorticotropin (ACTH) was secreted periodically after her first pregnancy. Since the 33rd week of pregnancy, hypertension and proteinuria became clinically remarkable. She gave normal birth at 36th week of pregnancy; however she continued to gain body weight even after delivery and developed typical Cushingoid features. Her ACTH secretion lacked normal daily fluctuation but exhibited periodic change during 1-year observation, showing 119 pg/ml, 34.6 pg/ml and 115 pg/ml at the 4th, 7th and 13th months after delivery. Plasma ACTH levels were increased by corticotropin releasing hormone and metyrapone, while low-dose dexamethasone suppressed cortisol secretion. Gel filtration analysis of the patient's plasma detected big ACTH molecules being eluted with a peak of authentic 1-39 ACTH. Cranial magnetic resonance imaging revealed a 1-cm pituitary mass in right cavernous sinus. The pituitary tumor was removed by transsphenoidal surgery at 13th month after delivery and was pathologically compatible with ACTH-producing pituitary adenoma by immunohistochemistry. This case includes clinically rare subsets of Cushing's syndrome showing periodic ACTH secretion and aberrant ACTH molecules.
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PMID:Periodic secretion of adrenocorticotropin in a patient with Cushing's disease manifested during pregnancy. 1600 22