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)

Five patients (median age 63 years) with severe crescentic glomerulonephritis had acute renal failure (median plasma creatinine 930, range 690-1390). Following induction of immunosuppressive treatment all patients achieved recovery of adequate renal function (median creatinine 440, range 290-570 mumol/l). After 3-6 months of continuous remission, all patients, despite stable renal function developed increasing proteinuria (median 4.4 g/24 h, range 3.2-6.1), and enalapril (5-20 mg per day) was substituted or introduced as antihypertensive therapy. Immunosuppression was not altered. After 1 year, renal function remained stable in four patients and plasma creatinine increased initially in one patient before becoming stable: proteinuria was reduced substantially in all patients to a median of 0.8 g/24 h, range 0.2-1.3). Patients with severe crescentic glomerulonephritis may develop persistent or increasing proteinuria despite successful treatment of acute disease. We have used enalapril to reduce proteinuria and maintain function in such patients.
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PMID:Effect of enalapril on proteinuria and renal function in patients with healed severe crescentic glomerulonephritis. 179 92

The presented material consists of 9 postoperative patients' investigations. Interstitial nephritis was diagnosed in them after histological examination. Seven patients had a chronic disease, 2--acute disease. The revealed possible predisposing factors were: a prolonged use of analgetics, contact with formalin and typographical dyes, systematic alcohol usage, frequent catarrhal diseases with long-term fever, a history of acute renal destructive process. The clinical picture of patients with chronic interstitial nephritis was characterized by long periods of temperature elevation, small changes in blood counts, weakness, pain in the lumbar region. In urine analyses: moderate microhematuria, leukocyturia, proteinuria. There were signs of early damaged renal tubular functions. Antiinflammatory therapy was ineffective so the patients were operated on for various indications. During the operations there were severe macroscopic renal cirrhotic deteriorations. 2 patients underwent nephrectomy, 15 intraoperative biopsy. Histologically there were revealed: signs of interstitial tissue various cirrhotic changes in hydrops and lymphoplasmacytic infiltration with tubular compression and dystrophic changes. The following complex therapy including nonsteroid antiinflammatory agents, in some cases corticosteroids, desensitizing and antihistaminic remedy allowed one to achieve alleviation of the process.
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PMID:[Interstitial nephritis in urological practice]. 187 26

The clinical presentation, initial laboratory and renal biopsy findings, and subsequent clinical course were studied and compared in 128 children with Henoch-Schoenlein (HS) nephritis and in 206 children with IgA nephropathy. The clinical and pathological findings of the two conditions were similar. After a mean follow-up period of 5 years, 72 patients (56%) with HS nephritis and 67 (32%) with IgA nephropathy showed no demonstrable abnormality, 29 (23%) with HS nephritis and 103 (50%) with IgA nephropathy had minor urinary abnormalities, 7 (5%) with HS nephritis and 26 (13%) with IgA nephropathy had heavy proteinuria and/or hypertension, and 20 (16%) with HS nephritis and 10 (5%) with IgA nephropathy had developed chronic renal failure. A worse outcome was significantly associated with the more severe clinical presentations and more severe glomerular changes by light microscopy in HS nephritis, whereas there was no relationship between the severity of clinical presentation and glomerular changes and prognosis in IgA nephropathy. These findings suggest that HS nephritis is an acute disease and prognosis is associated with the severity of glomerular changes at onset, while IgA nephropathy is a chronic, slowly progressive glomerular disease.
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PMID:Henoch-Schoenlein nephritis and IgA nephropathy in children: a comparison of clinical course. 359 38

On the assumption that increased urinary lysozyme concentration (;lysozymuria') indicates tubular proteinuria and therefore impaired tubular function, urinary lysozyme has been estimated in acute disorders where transient disturbances of renal function might be expected, in cases diagnosed clinically as extrarenal uraemia, and in a few examples of acute renal disease. Reversible lysozymuria occurred with hypokalaemia, postoperative ;collapse', electrolyte depletion, severe extrarenal infection, acute pyelonephritis, the nephrotic syndrome, after a few apparently uncomplicated surgical operations, and very transiently after ventricular fibrillation abolished by DC shock. There was no lysozymuria with severe uraemic heart failure, aspirin and paracetamol poisoning, or severe jaundice, nor in two cases of acute glomerulonephritis. Although lysozymuria may occasionally be useful in the clinical diagnosis of acutely disordered renal function, the results suggest that its value is limited; on the other hand, they have provided information on renal pathophysiology in acute disease.
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PMID:Lysozymuria and acute disorders of renal function. 470 97

Forty-one patients with systemic lupus erythematosus and glomerulonephritis were studied in a randomized drug trial. Thirteen patients received prednisone only (Group 1), 16 received oral cyclophosphamide and oral azathioprine (1 mg/kg body weight . d of each initially) (Group 2), and 12 were given boluses of intravenous cyclophosphamide (0.5 to 1.0 g/m2 body surface area every 3 months) (Group 3). The mean observation period was 42 months (range 1 to 6.5 years). Renal function deteriorated in four of 12 patients in Group 1 and three of 27 patients in Groups 2 and 3 (p = 0.114). By life-table analysis, 86% of the entire group survived 5 years after entry to the study. Marked hypertension, fluctuating changes in serum creatinine, erratic changes in levels of antibody to DNA, reduced C3 levels, increasing proteinuria or sustained hematuria, and flares of extrarenal disease activity occurred more commonly in Group 1. Infectious complications were not commoner in Groups 2 and 3. We conclude that any marginal benefits produced by the programs tested cannot be shown in this class of patients without markedly increasing the sample size. Our current studies involve more vigorous treatment of patients with more acute disease and less treatment during prolonged periods of relatively good health.
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PMID:Alternative modes of cyclophosphamide and azathioprine therapy in lupus nephritis. 704 43

The hemolytic-uremic syndrome (HUS) is an acute disorder, characterized by the triad of microangiopathic hemolytic anemia, nephropathy and thrombocytopenia. The great majority of patients are children, usually under 4 years of age, although adults can be affected. The onset is abrupt and usually follows gastroenteritis or upper respiratory infection. Later, clinical manifestations based on the triad, such as pallor, jaundice, edema, hypertension and purpura soon develop. The urinary output is reduced and the urine may appear dark yellow or tea-colored. Laboratory tests of peripheral blood show severe hemolytic anemia associated with fragmented red blood cells and thrombocytopenia, usually below 50,000/microliters. The blood urea nitrogen, serum creatinine and lactate dehydrogenase concentrations are elevated. Proteinuria and microscopic hematuria, which are indicative of active glomerular damage are also seen. Profound understanding of these manifestations is sufficient to permit an early diagnosis of HUS.
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PMID:[Diagnosis and clinical features of hemolytic uremic syndrome]. 843 21

Puumala hantavirus-induced nephropathia epidemica (NE) is an important cause for an acute reversible renal failure in Scandinavia, European Russia, and the Balkans. The characteristic histopathological renal finding is an acute tubulointerstitial nephritis. Mild to massive proteinuria, hematuria, and a rise in the serum creatinine level are typically seen. The pathogenetic mechanisms of NE kidney failure are incompletely understood. Therefore we studied the infiltrating cell populations and local expression of cytokines and growth factors in the kidney during the acute disease. Results of the histological and immunohistological studies of eight kidney biopsies show mild to moderate interstitial infiltration of lymphocytes, plasma cells, monocytes/macrophages, and polymorphonuclear leukocytes, mainly eosinophilic granulocytes and neutrophils. An increased expression of the cytokines tumor necrosis factor-alpha, transforming growth factor-beta, and platelet-derived growth factor was seen at the same sites mainly in the peritubular area of the distal nephron. Concomitantly also at the same locations expression of the endothelial adhesion molecules ICAM-1, VCAM, and PECAM was seen. Light microscopic changes in tubuli were common. Interestingly, despite the often massive transient proteinuria, no marked changes were seen in the glomeruli of NE kidneys. No evidence of Puumala virus was found in the kidney biopsies.
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PMID:Cytokines, adhesion molecules, and cellular infiltration in nephropathia epidemica kidneys: an immunohistochemical study. 859 83

We examined the functional role of interleukin (IL)-1 in mesangial cell proliferation during rat anti-Thy-1 nephritis by blocking its action with IL-1 receptor antagonist (IL-1ra). Anti-Thy-1 nephritis was induced by intravenous injection of 5 mg/kg OX-7 IgG (day 0) into inbred Wistar rats. Groups of animals (n = 9) were implanted with a micro-osmotic pump on day -1, which delivered 25 micrograms/hour human recombinant IL-1ra or saline continuously until the rats were killed at day 6, the peak of mesangial cell proliferation. Immunostaining showed that IL-1 was expressed by mesangial cells during disease. IL-1ra treatment did not affect the mild, but significant, proteinuria seen after OX-7 injection. Compared with saline treatment, IL-1ra treatment reduced mesangial cell proliferation (decreases 24% P < 0.05), glomerular hypercellularity (decreases 29%; P < 0.05), and glomerular macrophage accumulation (decreases 20%; P < 0.05). However, IL-1ra treatment had no effect on glomerular IL-1 beta mRNA expression and caused only a small reduction in the high levels of glomerular expression of platelet-derived growth factor-beta protein (decreases 6%; P < 0.05). IL-1ra caused a modest reduction in the marked up-regulation of glomerular transforming growth factor-beta 1 mRNA expression on day 6 (decreases 26%; P < 0.05), although urinary excretion of this factor was unaffected. Interestingly, IL-1ra treatment had relatively little effect upon glomerular deposition of laminin, fibronectin, and collagen type IV seen in this acute disease. In conclusion, this study has 1) demonstrated that IL-1 is expressed by mesangial cells in vivo, 2) demonstrated that IL-1 is a mesangial cell growth factor in experimental mesangioproliferative nephritis, and 3) suggests that IL-1 has little or no fibrogenic activity in mesangial matrix deposition.
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PMID:Role of interleukin-1 in mesangial cell proliferation and matrix deposition in experimental mesangioproliferative nephritis. 921 40

The injection of rabbit antidog-placenta serum in 11 dogs resulted in an acute nephritis which was fatal within a month in 4, progressed to a chronic disease in 5, and healed in 2 animals. The nephritis produced in 5 dogs by the injection of rabbit antidog-kidney serum was comparable to that following the injection of antiplacenta serum. The manifestations of the acute disease included edema, hypertension, proteinuria, cylindruria, hematuria, nitrogen retention, hypoalbuminemia, hypercholesterolemia, increased erythrocyte sedimentation rate, and anemia. The non-fatal chronic nephritis was characterized by proteinuria, cylindruria, and hematuria. With the onset of renal failure elevation of the blood urea nitrogen again occurred. Antiplacenta serum did not cause abortion when injected into pregnant dogs, nor did pregnancy modify the subsequent development of nephritis.
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PMID:Glomerulonephritis produced in dogs by specific antisera. I. The course of the disease resulting from injection of rabbit antidog-placenta serum or rabbit antidog-kidney serum. 1327 92

In the classic form of hemolytic uremic syndrome associated with toxins of gram-negative enterobacteria, mortality in the acute stage has been lower than 5% since 1978 (data from the Nephrology Committee, Argentine Society of Pediatrics). Children usually die because of severe involvement of the central nervous system, intestine, or myocardium and its complications, or because of intercurrent infection. Treatment in this phase is supportive, and efforts should be put into prevention of infection by Shiga-like toxin-producing enterohemorrhagic Escherichia coli. Of the 95% who survive, approximately one third is at risk for having chronic sequelae. Motor, sensory, or intellectual deficits, intestinal strictures, myocardial infarctions, or diabetes are infrequent. The more-frequent chronic renal lesion is characterized by the hyperfunction of nephrons remaining after the acute necrotizing lesion, which leads to progressive scarring, and not by persistence or recurrence of the microangiopathic process. Three courses of progression to end-stage renal failure have been described. Children with most severe forms do not recover from acute renal failure and enter directly into a dialysis and transplantation program. A second group recovers renal function partially, with persistent proteinuria and frequently hypertension; progression to end-stage renal failure occurs in 2 to 5 years. The third group may recover normal serum creatinine and creatinine clearance, with persistent proteinuria. They are at risk of progressing to chronic renal failure and end-stage renal disease after more than 5 years, and sometimes as late as 20 years, after the acute disease. Treatment should aim at preventing the mechanisms associated with progressive renal scarring. Transplantation is indicated in this form of hemolytic uremic syndrome, because there is little, if any, risk of recurrence, and the prognosis is similar to that of transplantation for other diseases.
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PMID:Long-term course and mechanisms of progression of renal disease in hemolytic uremic syndrome. 1601 85


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