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)

Two types of experimental GN induced by immunological procedures. Heymann-type AIC-GN and NTN, were treated with anticoagulant agents. Dipyridamole, aspirin, ticlopidine or batroxobin was administered either to rats with AIC-GN for 14 to 28 days or to NTN rats 2 days prior to injection with NTS and 14 to 21 days thereafter. A significant decrease in the amount of urinary protein was observed only in rats treated with 12.5 to 50.0 mg/kg dipyridamole daily, whereas no significant decrease in proteinuria was observed in either AIC-GN or NTN rats treated with the other agents. Histopathologically, no improvement in the light and electron microscopic findings was noted in AIC-GN rats treated with these agents, even with dipyridamole. On the other hand, in NTN rats, light and electron microscopic study of the kidneys from rats sacrificed 30 to 60 min after NTS injection revealed that platelet aggregation and inflammatory changes in the glomeruli were remarkable reduced in rats pretreated with 56.4 mg/kg aspirin or 50.0 mg/tg triclopidine daily, but no difference in the renal lesions between rats treated with aspirin or triclopidine and control animals were observed 2 weeks after NTS injection. No histological improvement was observed in rats pretreated with dipyridamole. It would be reasonable to conclude from these results that the favorable effect of dipyridamole on proteinuria is not related to its antiplatelet activity and that platelet aggregation is not essential to the development of renal lesions in rat AIC-GN and NTN. (J Lab Clin Med 99:428, 1982.)
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PMID:Effects of various antiplatelet drugs and defibrinating agent on experimental glomerulonephritis in rats. 646 69

Chronic kidney disease is a progressive condition that results in significant morbidity and mortality. Because of the important role the kidneys play in maintaining homeostasis, chronic kidney disease can affect almost every body system. Early recognition and intervention are essential to slowing disease progression, maintaining quality of life, and improving outcomes. Family physicians have the opportunity to screen at-risk patients, identify affected patients, and ameliorate the impact of chronic kidney disease by initiating early therapy and monitoring disease progression. Aggressive blood pressure control, with a goal of 130/80 mm Hg or less, is recommended in patients with chronic kidney disease. Angiotensin-converting enzyme inhibitors and angiotensin-II receptor antagonists are most effective because of their unique ability to decrease proteinuria. Hyperglycemia should be treated; the goal is an AIC concentration below 7 percent. In patients with dyslipidemia, statin therapy is appropriate to reduce the risk of cardiovascular disease. Anemia should be treated, with a target hemoglobin concentration of 11 to 12 g per dL (110 to 120 g per L). Hyperparathyroid disease requires dietary phosphate restrictions, antacid use, and vitamin D supplementation; if medical therapy fails, referral for surgery is necessary. Counseling on adequate nutrition should be provided, and smoking cessation must be encouraged at each office visit.
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PMID:Chronic kidney disease: prevention and treatment of common complications. 1557 Oct 58

While the pathophysiology of chronic disorders varies there are three basic mechanisms - inflammation, oxidative stress and endothelial dysfunction - that are common in many chronic diseases. However, the failure of these mechanisms to work synchronously can lead to morbidity complicating the course of many chronic diseases. We analyzed data of 178 patients from cohorts with selected chronic diseases in this quasi-experimental study. Endothelial dysfunction was determined by flow-mediated dilatation (FMD) and asymmetric dimethylarginine (ADMA) levels. Serum ADMA, high sensitive C-reactive protein (hs-CRP), serum PTX3, malondialdehyde (MDA), Cu/Zn-superoxide dismutase (Cu/Zn-SOD), glutathione peroxidase (GSH-Px) levels and FMD were studied in baseline and after 12 weeks of Morinda citrifolia (anti-atherosclerotic liquid- AAL), omega-3 (anti-inflammatory capsules- AIC) and extract with Alaskan blueberry (anti-oxidant liquid- AOL). Stepwise multivariate regression analysis was used to evaluate the association of FMD with clinical and serologic parameters. Serum ADMA, MDA, PTX3, hsCRP and albumin levels, and proteinuria were significantly decreased while CuZn-SOD, GSH-Px and FMD levels were significantly increased following AAL, AIC and AOL therapies. The FMD was negatively correlated with serum ADMA, MDA, PTX3, and hsCRP levels and positively correlated with CuZn-SOD and eGFR levels. ADMA and PTX3 levels were independently related to FMD both before and after AAL, AIC and AOL therapies. Our study shows that serum ADMA, MDA, PTX3 levels are associated with endothelial dysfunction in patients with selected chronic diseases. In addition, short-term AAL, AIC and AOL therapies significantly improves a number of parameters in our cohort and can normalize ADMA, PTX3, hsCRP and MDA levels.
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PMID:The Effect of Corrected Inflammation, Oxidative Stress and Endothelial Dysfunction on Fmd Levels in Patients with Selected Chronic Diseases: A Quasi-Experimental Study. 3248 98