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)

Analgesic abuse is a major public health hazard in Australia, and analgesic nephropathy with consequent terminal renal failure is the underlying cause in 20% of the patients requiring dialysis and transplantation. Analgesics are invariably taken in the form of compounds and mixtures. In the aspirin-phenacetin-caffeine (APC) mixture, aspirin appears to be the major nephrotoxic agent and phenacetin appears to play a secondary and synergistic role. The renal disease associated with abuse of analgesics is characteristic and is part of a much wider clinical syndrome, the analgesic syndrome, which includes peptic ulcer disease (35%), anemia (60 to 90%), hypertension (15 to 70%), ischemic heart disease (35%), psychological and psychiatric manifestations, pigmentation, and possible gonadal- and pregnancy-related effects. The primary lesion in analgesic nephropathy is renal papillary necrosis (RPN), and this is a nephrotoxic effect common to all nonsteroid antiinflammatory agents. The most important factor in the management of patients with analgesic nephropathy is the cessation of analgesic abuse, and this leads to improvement and stabilization of renal function. A small proportion of patients will, however, deteriorate in relation to accelerated hypertension, persistent proteinuria, ischemic heart disease, and complications leading to nephrectomy. Patients with analgesic nephropathy are poor risk patients and have a poor prognosis, even after dialysis and transplantation.
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PMID:Analgesic nephropathy: etiology, clinical syndrome, and clinicopathologic correlations in Australia. 36 34

The authors developed the special enzyme immunoassay technique for the detection of the urinary antitrombin III (AT-III) levels. Sensitivity of the method was 7.8 ng/ml. The study lasted for 2 hrs. The levels of AT-III were studied in the circadian human urine in health, in physiological and nephropathy-complicated pregnancy, as well as in patients with gastroduodenal ulcer-induced bleeding. There was a 34.1-fold increase in the urinary AT-III levels in pregnant females with Stages II-III nephropathy and a 17.3-fold increase in those who sustained the resection of the stomach, which could be explained by proteinuria and abnormal resorption of AT-III in the proximal tubules of the kidney.
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PMID:[The determination of the concentration of antithrombin III in the urine]. 227 59

Translational research (TR) can be defined as research where a discovery made in the laboratory (bench) can be applied in the diagnosis, treatment or prevention of a disease. Examples of medical discoveries contributing to translational medicine (TM) include the isolation of insulin by Banting (Nobel Laureate, 1923), the discovery of penicillin by Alexander Fleming (Nobel Laureate, 1945) and recently the discovery of the role of bacterium Helicobacter pylori in the causation of gastritis and peptic ulcer by Marshall and Warren (Nobel Laureates, 2005). Clinical research (CR) would be a more appropriate term for the bulk of research work undertaken by doctors. CR embraces both clinical based and laboratory-based research. The terminology "bedside to bench" applies more to CR as opposed to "bench to bedside" in the case of TR. But regardless of who does it, as long as the discovery can be translated to the bedside and results in improvement in patient care it can be considered a contribution to TM. Our work spans a 30-year period, involving laboratory-based research, clinical trials and genomics of IgA nephritis (Nx). This is a series of work to elucidate the pathogensis and therapy of IgANx. Plasma beta-thromboglobulin (BTG) an in-vivo index of platelet aggregation and anti-thrombin III increase due to a constant thrombogenecity resulting from platelet degranulation formed the basis for anti-platelet and low-dose warfarin therapy. A study of the natural history of IgANx revealed 2 courses, a slowly progressive course with end-stage renal failure (ESRF) at 7.7 years and a more rapid course at 3.3 years. Triple therapy (cyclophosphamide, persantin and low-dose warfarin) delayed progression to ESRF by about 8 years and for some patients up to 20 years. Documentation of abnormal suppressor T cell function provided the basis for immune therapy. Four patterns of proteinuria were present in IgANx and it is the quality and not so much the quantity of proteinuria which determined the prognosis. Low molecular weight proteinuria was a bad prognostic marker. A controlled therapeutic trial using ACEI/ATRA showed that therapy decreases proteinuria, improves renal function and converts non-selective to selective proteinuria. Subsequent work confirmed that it was the ATRA, not the ACEI which contributed to improved renal function. Individual anti proteinuria response to ATRA varies depending on ACE gene polymorphism. We found that the II genotype of the ACE gene was renoprotective and patients with this genotype had significantly reduced incidence of ESRF compared to those with the DD genotype. Patients responsive to ATRA therapy can retard progression to ESRF by up to 32 years. Mild renal failure can be reversed with possible regression of glomerulosclerosis because of glomerular remodelling by ATRA.
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PMID:3rd College of Physicians' lecture--translational research: From bench to bedside and from bedside to bench; incorporating a clinical research journey in IgA nephritis (1976 to 2006). 1710

A number of studies has confirmed that the epidemiology of Helicobacter pylori (H. pylori) is changing worldwide, with a decrease especially in developed Countries. Nevertheless, since this Gram-negative bacterium infects almost 50% of the world's population, it remains a global problem. Beyond its role in the pathogenesis of the main gastroduodenal diseases, including gastritis, peptic ulcer and gastric cancer, H. pylori has been suspected to be involved in several extra-gastroduodenal disorders. Patients with chronic kidney disease (CKD) present gastric mucosal injuries and dyspepsia more often than the general population. However, the reported relationship between CKD and H. pylori infection is conflicting. In fact, in this population these conditions have a multifactorial pathogenesis and H. pylori infection could play a limited role in their development. Nevertheless, while it seems that the prevalence of the bacterium is lower in patients with CKD than in controls, H. pylori has been shown to be associated to an increased occurrence of proteinuria in patients with type 2 diabetes mellitus. This narrative review analyzes the results of recent literature in this field with particular focus on data reported by meta-analyses.
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PMID:The relationship between Helicobacter pylori and chronic kidney disease: update 2020. 3262 70