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)

The mechanism of the increased renal clearance of amylase and the amylase to creatinine clearance ratio (CAM/CCR) in acute pancreatitis remains controversial with both renal tubular dysfunction and altered glomerular permeability being invoked as explanations. To differentiate between these mechanisms, we investigated the quantity and character of protein excretion in 10 patients with pancreatitis. For a short period of time, seven of 10 patients had mild proteinuria with a mean protein excretion rate of 230 +/- 154 mg/24 hr. Proteinuria decreased in 9/9 survivors to 17 +/- 18 mg/24 hr. Albumin excretion rate initially was minimally increased in 10/10 patients with a mean of 61 +/- 40 mg/24 hr, decreasing during recovery in 8/9 survivors to 10.9 +/- 10.4 mg/24 hr (P less than 0.01). Electrophoresis of urine obtained during the acute phase consistently showed a low molecular weight proteinuria pattern that cleared with recovery. Twenty-one of 22 urinary samples with an elevated CAM/CCR had a low molecular weight protein pattern. All the above findings can be explained by alterations in renal tubular reabsorption of proteins without changes in glomerular permeability. In 2/4 patients a low molecular weight protein was present in urine specimens from the acute phase that was not present in highly concentrated urine specimens from the recovery period. This raises the possibility that an abnormal low molecular weight protein enters the serum in acute pancreatitis, which, after glomerular filtration, produces the renal tubular malfunction found in acute pancreatitis.
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PMID:Urine protein excretion in acute pancreatitis. 243 Oct 86

The aetiology of the primary systemic vasculitides remains obscure. Recent years have seen significant advances in our understanding of inflammation and in particular the role of and interaction between the vascular endothelium, mediators and immune effector cells. This has helped to further elucidate those specific processes relevant to vasculitis which result in endothelial cell damage. In Wegener's granulomatosis and microscopic polyarteritis the evidence favours an autoimmune inflammatory response characterised by specific mediators in which the endothelium is both target and active participant. Current treatment of these disorders with combinations of corticosteroids and cytotoxics is highly effective in inducing remission. However, long-term use of this therapy is potentially toxic and there remains also a significant risk of relapse. It is hoped that increased understanding of the pathogenesis of systemic vasculitis will enable more specific, less toxic and more effective therapies to be defined. Jayne et al. have suggested a beneficial effect of intravenous pooled normal human immunoglobulin (IVIG) in patients with ANCA-positive vasculitis. In vitro studies have shown that IVIG contains antiidiotypic antibodies to ANCA and AECA, capable of inhibiting the binding of these autoantibodies to their autoantigens. In vivo, IVIG may also provide the immunoregulatory elements needed for the idiotype network and control of the autoimmune repertoire. Mathieson et al. successfully used monoclonal antibodies to T cells (Campath-H directed against CDw52) in a patient with ANCA-negative dermal lymphocytic vasculitis. Monoclonal antibodies to CAMs have been used in human renal transplant rejection and reduced the inflammation and proteinuria in animal models of anti-glomerular basement membrane disease. In vasculitis, the therapeutic use of specific anti-CAM antibodies may result from further definition of the role of CAMs. Increased understanding of the pathogenesis of systemic vasculitis is likely to provide the basis for the use of more specific immunotherapies in the future.
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PMID:Mechanisms of endothelial cell injury in vasculitis. 799 43

In an earlier study, we showed that feeding CLA immediately after weaning prolonged survival of NZB/W F1 mice after onset of proteinuria. In the present study, the feeding of CLA was delayed until mice had developed proteinuria. Thirty NZB/W F1 mice were fed a regular rodent chow after weaning. Urine samples were collected to detect proteinuria. Once a mouse was proteinuria positive, it was then randomly assigned to a 0.5% CLA supplement semipurified diet or a control diet (supplement 0.5% corn oil). The next proteinuria positive mouse was then assigned to the opposite diet to which the first mouse was assigned. Mice fed the control diet lost 25% more body weight (13.0 g) than mice fed the CLA diet (9.7 g). Moreover, CLA-fed mice survived an average 1.7-fold longer (148 d) than mice fed the control diet (89 d) after the onset of proteinuria. This follow-up study confirmed that dietary CLA had a beneficial effect in the autoimmune NZB/W F1 mouse. In summary, the cachectic symptom of systemic lupus erythematosus was decreased by dietary CLA and survival days were increased over control group.
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PMID:Dietary CLA decreased weight loss and extended survival following the onset of kidney failure in NZB/W F1 mice. 1266 15