Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostanoids belong to the growing family of eicosanoids, which are all derived from arachidonic acid. Prostanoids act as modulators and mediators in a large spectrum of physiological and pathophysiological processes within the kidney. On the one hand, the potent vasoconstrictor and platelet-aggregating thromboxane (TX) A2 is involved in the pathophysiology of a variety of glomerular diseases, such as haemolytic-uraemic syndrome and immune-mediated glomerulopathies. Prostaglandin (PG) E2, on the other hand, interferes with tubular electrolyte and water handling. Clinical data support the hypothesis that this member of the prostanoid family contributes to the pathophysiology of Bartter's syndrome, hyperprostaglandin E syndrome, idiopathic hypercalciuria and renal diabetes insipidus. Both prostanoids, TXA2 and PGE2, are involved in the pathophysiology of obstructive uropathies. The physiological and protective role of renal vasodilator prostanoids (PGI2 and PGE2) has been studied during treatment with non-steroidal anti-inflammatory drugs. Part of the pharmacological effects of frusemide and converting enzyme inhibitors is mediated by PGI2 and PGE2. The role of renal prostanoids in cyclosporine toxicity is still equivocal. Future investigations on the physiological and pathophysiological role of renal prostanoids will have to consider the multiple interactions between prostanoids on the one hand, and classical hormones and other mediators (e.g. cytokines) on the other hand.
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PMID:Prostanoids in paediatric kidney diseases. 191 Nov 54

Renal and systemic prostanoid activity was assessed in various renal tubular disorders, using mass spectrometric determination of urinary excretion rates of primary prostaglandins (PGE2, PGF2 alpha, PGI2, and TXA2) and their systemically produced index metabolites. Only PGE2 levels (normal range: 2.0-16.4 ng/h per 1.73 m2) are elevated in Bartter syndrome (median: 43.4, range: 6.7-166.3), nephrogenic diabetes insipidus (46.2, 12.1-1290), Fanconi syndrome (96.6, 19.3-135.5), and in a complex tubular disorder in premature infants (40.7, 22.3-132.1), for which the term hyperprostaglandin E syndrome has been introduced. In this disorder with a Bartter-syndrome-like tubulopathy, the systemic features of the disease such as fever, diarrhoea and osteopenia with hypercalciuria were associated with increased systemic PGE2 activity. In most patients the urinary excretion rate of the systemic index metabolite of PGE2 (PGE-M) was markedly elevated (1028, 285-4709; normal range: 104-664 ng/h per 1.73 m2). Hypercalciuria per se was associated neither with increased renal nor with systemic PGE2 hyperactivity. Most problems in infants with hyperprostaglandin E syndrome could be controlled by long-term indomethacin treatment in contrast to the moderate and partial effect of this treatment in patients with Fanconi syndrome. Thus increased PGE2 synthesis plays a major role in the pathogenesis of hyperprostaglandin E syndrome, while in Fanconi syndrome PGE2 hyperactivity in the kidney is a secondary event and only aggravates the water and electrolyte wastage.
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PMID:Role of prostaglandins in hyperprostaglandin E syndrome and in selected renal tubular disorders. 315 22