Glomerulonephritis proteinuria

Brown, muddy granular casts (highly indicative of ATN) Proteinuria (glomerulonephritis or allergic interstitial nephritis) Eosinophiluria (acute interstitial nephritis)... 

Wada T, Tomosugi N, Naito T, et al. Prevention of proteinuria by the administration of anti-interleukin 8 antibody in experimental acute immune complex-induced glomerulonephritis. J Exp Med 1994 180 1135-1140. 

Penicillamine onset may be seen in 1 to 3 months, and most responses occur within 6 months. Early adverse effects include skin rash, metallic taste, hypogeusia, stomatitis, anorexia, nausea, vomiting, and dyspepsia. Glomerulonephritis may occur, which manifests as proteinuria and hematuria. Penicillamine is usually reserved for patients who are resistant to other therapies because of the rare but potentially serious induction of autoimmune diseases (e.g., Goodpasture s syndrome, myasthenia gravis). 

GL/- White cells in urine proteinuria microscopic or gross hematuria nonspecific urogenital findings abnormal menses glomerulonephritis. 

Nephrotic syndrome is characterized by proteinuria and edema due to some form of glomerulonephritis. The resulting fall in plasma protein concentration decreases vascular volume, which leads to diminished renal blood flow. This in turn causes secondary aldosteronism characterized by Na and water retention and K+ depletion. Rigid control of dietary Na is essential. Therapy of the nephrotic syndrome using a thiazide (possibly with a K -sparing diuretic) to control the secondary aldosteronism, is a useful initial approach to treatment Since nephrotic edema is frequently more difficult to control than cardiac edema, it may be necessary to switch to a loop diuretic (and spironolactone) to obtain adequate diuresis. 

Signs and symptoms of gold toxicity, the primary serious reaction, include decreased Hgb level, decreased granulocyte count (less than 150,000/mm ), proteinuria, hematuria, stomatitis, blood dyscrasias (anemia, leukopenia WBC count less than 4000/mm, thrombocytopenia, and eosinophilia), glomerulonephritis, nephrotic syndrome, and cholestatic jaundice. 

The mechanism of massive proteinuria is obviously different in each primary glomerulonephritis (Cl). 

Masuyama H, Suwaki N, Nakatsukasa H, Masumoto A, Tateishi Y, Hiramatrsu Y. Circulating angiogenic factors in preeclampsia, gestational proteinuria, and preeclampsia superimposed on chronic glomerulonephritis. Am J Obstet Gynecol 2006 194 551-556. 

Kawasaki et al. (1992) induced crescentic glomerulonephritis with a small dose of nephrotoxic serum in WKY rats, which was characterized by the early infiltration of CD8 positive cells in glomeruli. In vivo depletion of CD8 positive cells completely prevented proteinuria and crescent formation. 

Proteinuria occurs in about 7% of patients using bucillamine (1). Less often, nephrotic sjmdrome can develop (5-9). Microscopically there is membranous glomerulonephritis, with diffuse fine granular precipitation of IgG and C3 around the capillary walls, electron-dense deposits at the subepithehal side of the basement membrane and effacement of foot processes. 

A review of 15 other available reports of renal insufficiency and proteinuria in patients with chronic myeloid leukemia or other malignancies confirmed that the histological spectrum of renal lesions associated with interferon alfa is varied, and includes membranous glomerulonephritis, minimal change glomerulonephritis, acute interstitial nephritis, hemolytic-uremic sjmdrome, and thrombotic microangiopathy. Renal comphcations were reversible in nine patients three patients had persistent proteinuria, and four had persistent renal dysfunction, of whom three required chronic hemodialysis. Two-thirds of the patients developed renal comphcations within 1 month of treatment with interferon alfa, and one-third had received a relatively low dosage of interferon alfa (9-15 MU/week). 

Some degree of renal damage occurs in about 10% of patients taking tiopronin (1-3,5,6). As with penicillamine, proteinuria can progress to nephrotic syndrome (13,14). Biopsy may show minimal change membranous glomerulonephritis and granular depositions of IgG and C3 (13,15). 

Fusion inhibitors are a new class of agents approved in the management of HIV infection. They bind to surface proteins on T-lymphocytes and prevent entry of the HIV virus. The only fusion inhibitor currently approved for use is enfuvirtide. Nephrotoxicity has not been reported with enfuvirtide, however, one patient with a previous history of proteinuria and hematuria was described to have developed membranoprolif-erative glomerulonephritis [158]. The cause and effect relationship of this event and the use of the fusion inhibitor remain unclear. 

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