Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ovarian hyperstimulation syndrome (OHSS) is still a difficult diagnostic and therapeutic problem. OHSS is associated with significant hypertrophy of the ovaries associated with the loss of the intravascular fluid to the third space which results in hypovolaemia, oliguria, electrolyte imbalance, and a rise in haematocrit. The endogenous OHSS is rare. Most often OHSS appears as a complication of induction of ovulation. The fundamental issue in pathophysiology of OHSS is an increase of capillary permeability which results in the leakage of fluid to the third space. The vascular endothelial growth factor--VEGF--is considered to be the factor directly responsible for the processes involved. The most common are the mild and moderate forms of the syndrome. The severe form of OHSS is a life-threatening condition. The following symptoms may be present: ascites, pleural and pericardial effusion, oliguria, dyspnoea with tachypnoe, tachycardia, adult respiratory distress syndrome, renal failure, venous thrombosis, ischaemic stroke, haemorrhage from a ruptured ovary. Therapy should be based on the correction of hypovolaemia, hypotension and oliguria. Antithrombotic prophylaxis is an integral part of the OHSS management. Some interesting attempts have been undertaken to re-infuse the protein-rich ascites fluid directly to the systemic circulation, so called continuous auto-transfusion system of the ascites (CATSA).
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PMID:[The ovarian hyperstimulation syndrome--diagnostic criteria, management procedures]. 1737 30

Podocyte loss in adults leads to glomerulosclerosis. However, the impact of podocyte loss on glomerulogenesis and the development of the kidney as a whole has not been directly studied. Here, we used a podocyte-specific Cre transgene to direct the production of diphtheria toxin (DTA) inside podocytes during nephrogenesis. Affected podocytes underwent translational arrest and apoptosis, leading to oliguria, proteinuria, hematuria, interstitial hemorrhage, and perinatal death. Glomerular cell-cell interactions were disrupted, even before overt podocyte apoptosis. VEGF production by podocytes was greatly decreased, and this was associated with reduced endothelial fenestration and altered glomerular vascular architecture. In addition to these glomerular anomalies, embryonic podocyte ablation also led to structural changes and increased apoptosis in proximal tubules. The collecting ducts, however, only showed molecular changes that are likely an indirect effect of the greatly reduced urine flow. Although podocyte loss significantly impacted the development and maintenance of the vasculature both inside and outside the glomerulus, our results suggest that there is a lack of long-range signaling from deep-seated, mature glomeruli to the differentiating cells in the outer nephrogenic zone. This study illustrates the tight integration of various cell types in the developing kidney and shows that the impact of podocyte loss during development is much greater than that in adults. This study also shows the specificity and effectiveness of a genetically controlled podocyte ablation system in mice where the additional readily available tools can further expand its applications.
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PMID:Ablation of developing podocytes disrupts cellular interactions and nephrogenesis both inside and outside the glomerulus. 1884 18