Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been found that polycystic kidney (ADPKD) is often associated with gout. On the other hand, there are reports describing that the hyperuricemia (HU) seen in ADPKD corresponds to a reduction in renal function. We investigated the uric acid metabolism in 44 patients with ADPKD (age, 50 +/- 12.8 years; CCR, 50.5 +/- 41.1 ml/min) at our hospital. From among these 44 patients, 14 with a CCR of 80 ml/min were selected. Their data for uric acid metabolism were compared against those from the previous year's studies on various disease types (114 normal subjects, 70 with membranous nephropathy, 175 with IgA nephritis, 122 with gout, 137 with asymptomatic hyperuricemia, and 42 with diabetes mellitus). Among the 44 patients with ADPKD, the serum uric acid (SUA) was 7.7 +/- 1.9 mg/dl and HU affected 28 (63.6%). The incidence of gouty arthritis was also high (6 patients, 13.6%), revealing a positive correlation between SUA and CCR. Compared with membranous nephropathy and IgA nephritis, ADPKD exhibited an accentuated increase in SUA associated with a reduction in CCR. It is believed that this represents a factor for a high incidence of complications of hyperuricemia and gouty arthritis in ADPKD in contrast to other diseases. However, no increase in the production of uric acid was noted in ADPKD.
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PMID:A study of uric acid metabolism and gouty arthritis in patients with polycystic kidney. 833 99

Autosomal dominant polycystic kidney disease (ADPKD) is the most common of the inherited renal cystic diseases and constitutes 10% of the end stage kidney disease population. ADPKD is caused by PKD1 and PKD2 gene mutations in 85% and 15% of the cases respectively. Its high prevalence and negative impact on health outcomes fostered efforts to explain pathophysiologic pathways of cyst formation in kidneys. Among these are increased apoptosis, unopposed proliferation of tubule cells, impaired polarization and planar cell polarity, impaired cAMP pathway, cilier dysfunction, activated mTOR pathway, increased tumor necrosis factor-alpha (TNF-alpha) production. Many drugs have been tried in an attempt to halt cystogenesis in some point. Despite success to some extent in experimental studies, none reached clinical armamentarium yet. Colchicine, originally extracted from Colchicum autunale, is an anti-inflammatory drug that has been in continuous use for more than 3000 years. It has been used successfully to prevent attacks of familial mediterranien fever and amyloidosis, to treat gout and pseudogout attacks for a few decades. Colchicine principally is a microtubule inhibitor, thus prevents cell migration, division, and polarization. It also has anti-apoptotic, anti-proliferative and anti-inflammatory effects and down-regulates (TNF-alpha) receptors. As can easily be seen, many of the effects of colchicine have pathophysiologic counterparts in ADPKD. Thus, we hypothesized that colchicine would be beneficial to prevent or at least delay cyst formation in ADPKD patients. Indirect evidence also support our hypothesis, in which taxol and paclitaxel, other two microtubule inhibitors, were shown to delay cyst formation in experimental models of ADPKD. To our opinion, despite its narrow therapeutic index, widespread experience makes colchicine a suitable candidate for prolonged clinical use, should experimental studies show any benefit in ADPKD.
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PMID:Colchicine treatment in autosomal dominant polycystic kidney disease: many points in common. 1976 12