Results 171 to 180 of about 85,166 (213)
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On Treating Glomerulonephritis
Archives of Internal Medicine, 1979A patient seeks treatment for hematuria and proteinuria and undergoes diagnostic examination that excludes urologic lesions and does not reveal characteristic findings of specific renal diseases, such as acute poststreptococcal glomerulonephritis. To clarify further the nature of the disease, a renal biopsy is performed.
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Arginase in Glomerulonephritis
Nephron Experimental Nephrology, 2000Arginase metabolizes <i>L</i>-arginine to <i>L</i>-ornithine and urea. Two arginase isoforms, AI (liver arginase) and AII (ubiquitously expressed, functions unknown), have been identified. It is clear that arginases potentially have important roles in addition to urea generation for high concentrations are present at ...
S N, Waddington, V, Cattell
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Postinfectious Glomerulonephritis
Advances in Anatomic Pathology, 2012Postinfectious glomerulonephritis (PIGN) is an immunologically mediated glomerular injury triggered by an infection. Poststreptococcal glomerulonephritis (PSGN) is a classic example of PIGN with diffuse proliferative and exudative glomerular histology, dominant C3 staining and subepithelial "humps." Only the nephritogenic streptococcal infections cause
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New England Journal of Medicine, 1998
D E, Hricik, M, Chung-Park, J R, Sedor
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D E, Hricik, M, Chung-Park, J R, Sedor
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The Indian Journal of Pediatrics, 1999
Acute glomerulonephritis (AGN) manifests with abrupt onset of hematuria, facial edema, hypertension and impairment of renal function. The commonest form of AGN in developing countries is that following a beta hemolytic streptococcal infection where the glomerular injury is mediated by deposition of immune complexes. In the usual patient with moderately
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Acute glomerulonephritis (AGN) manifests with abrupt onset of hematuria, facial edema, hypertension and impairment of renal function. The commonest form of AGN in developing countries is that following a beta hemolytic streptococcal infection where the glomerular injury is mediated by deposition of immune complexes. In the usual patient with moderately
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