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)

A clinicopathological study of 206 Indian children with nephrotic syndrome showed a primary renal cause in 195 (96%), of which 77% were boys. In 126 children (96 boys, 30 girls) onset of the disorder occurred before the age of 5 years. Renal biopsy showed minimal lesions in 150 patients (77%); in 85 of these biopsy was done 3 months to 16 years after onset of the nephrotic syndrome. Significant renal histological abnormalities in 45 cases were labelled as mesangiocapillary 8, mesangioproliferative 4, proliferative with extensive crescents 2, membranous 3, focal segmental glomerulosclerosis 9, focal global glomerulosclerosis 2, advanced nonspecific 8, and mild proliferative 9. Nephritic manifestations were mainly associated with significant renal lesions, which were more frequently encountered when the onset of disease was after the age of 5 years. Clearance of proteinuria with corticosteroid therapy was practically confined to patients with minimal or mild renal histological changes. Our findings suggest that the pattern of idiopathic nephrotic syndrome in Indian children is similar to that reported from Western countries.
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PMID:Nephrotic syndrome in indian children. 0 Sep 73

The effect of acute experimentally induced renal failure after intramuscular injection of glycerol on serum and urine GGTP, LAP and AP activities was studied in 30 rabbits. High doses of glycerol caused shock, myolysis and hemolysis, leading to acute renal insufficiency. Serum urea and creatinine levels significantly increased, there was proteinuria, and significant decrease in 24-hr diuresis, glomerular filtration, and urinary urea excretion. The changes in LAP and AP activities were significant, and in GGTP-nonsignificant. In the urine GGTP and LAP increased significantly, and AP nonsignificantly. Urinary excretion of AP increased significantly, and GGTP and LAP nonsignificantly. The highest activity and urinary excretion of GGTP and LAP were observed on the 2nd day, and of AP--on the 5th day of renal failure.
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PMID:Nephron function in acute glycerol-induced renal insufficiency in rabbits. 0 78

The kidney is one of the target organs involved as a consequence of the systemic complications seen in drug abusers. This may manifest itself in one of the following forms: acute hepatitis with modest proteinuria (less than 2 Gm. per day); bacterial endocarditis with hematuria, azotemia, and a focal or diffuse glomerulonephritis; the nephrotic syndrome with focal mesangial sclerosis and diffuse interstitial nephritis often pursuing a fulminant course terminating in uremia; acute renal failure secondary to rhabdomyolysis and myoglobinuria; polyarteritis nodosa with renal involvement; and obstructive uropathy secondary to fungus ball in the urinary tract.
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PMID:Renal complications of drug addiction. 1 1

NZB/NZW F1 female mice were treated with the immunosuppresive enzyme L-asparaginar antibodies, diminished deposition of gamma-globulins in kidneys, significantly delayed the onset of proteinuria, and reduced deaths from nephritis. These effects were associated with reduction of cellular IgM antibody synthesis to both T-dependent and T-independent antigens, but the graft-versus-host reaction was not affected. After several weeks of therapy, antibodies against Asnase appeared in the circulation, the effect on antibody synthesis was lost, ANA and anti-DNA appeared, followed by proteinuria and deaths from nephritis. Therefore Asnase proved to be an effective therapy in NZB/NZW mice, but its usefulness was limited by the appearance of inactivating antibodies.
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PMID:Effect of altered lymphocyte function on immunologic disorders in NZB/NZW mice. 1 1

Immunologic mechanisms of proteinuria were investigated in guinea pigs (GP) injected with sheep antiserum (NTS) to GP glomerular basement membrane (GBM). Linear deposition of sheep gamma 1 and gamma 2 IgG led to a prompt but transient (36 hr) increase in albumin excretion from control values of 0.026 +/- 0.013 mg/hr to maximal values of 26+/-12.1 mg/rh at six hours without detectable histologic or electron microscopic changes except for decreased staining for glomerular polyanion and epithelial cell foot process fusion. GBM permeability to anionic ferritin was not increased during proteinuria. Anti-GBM antibody deposits did not fix GP C3 or C4 in vivo or in vitro. NTS-induced proteinuria was the same in guinea pigs that were normal, greater than 95% depleted of C3 through C9, genetically deficient in C4, and depleted of circulating polymorphonuclear leukocytes (PMN). Prior administration of antihistamines, steroids, azathioprine, colchicine, indomethacin, heparin, aprotinin (Trasylol), and niridazole also failed to reduced proteinuria. Initial proteinuria subsided by 36 hr, did not recur despite linear deposition of GP gemma 1 and gemma 2 after day seven, and antibody to GMB-bound sheep globlin. In the GP nephrotoxic nephritis model, anti-GBM antibody deposits apparently mediate increased permeability to albumin by a currently undefined mechanism which is independent of complement, PMN, and other know mediators of inflammation.
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PMID:Complement-independent nephrotoxic nephritis in the guinea pig. 1 57

A patient with biopsy documented acute poststreptococcal glomerulonephritis and arteritis recovered completely with supportive therapy. Illness was preceded by group A streptococcal pharyngitis. At the time of presentation, serum creatinine concentration was 11.5 mg/dl. Serum cryoglobulins containing IgG and C3 were present. The first biopsy, performed during the acute illness, contained glomeruli with typical features of acute PSGN. Medium-sized arteries had extensive necrosis and leukocytic infiltration, and contained IgG, C3, and fibrin. Glomerular filtration rate returned to normal within three weeks; proteinuria cleared by three months, and microscopic hematuria by 11 months. Renal biopsy one year later showed minimal mesangial hypercellularity and no arteritis.
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PMID:Necrotizing arteritis in acute poststreptococcal glomerulonephritis: report of a recovered case. 1 62

We report epidemiologic, clinical, laboratory, and biopsy findings in 14 cases of nephropathia epidemica. The patients were between 19 and 49 years of age. The onset of the disease was characterized by high fever, nausea, headache, backache, abdominal pain, proteinuria, oliguria, hematuria, and uremia. The symptoms subsided rapidly during the polyuria phase, which followed the oliguria stage. Because of renal failure, hemodialysis was required in eight cases. Edema of eyelids, conjunctival injection and hemorrhages, transitory myopia, and acute glaucoma were the most common eye abnormalities. Renal biopsy specimens showed glomerular changes, with mild swelling of the epithelial cells of Bowman's capsule, thickening of the basement membrane of glomerular capillaries, glomerular adhesions, inflammatory cell infiltration, leukocytoclasis and hemorrhages in the interstitium, and eosinophilic hyaline degeneration and vacuolization of the epithelial cells of the proximal tubuli.
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PMID:Nephropathia epidemica. The Scandinavian form of hemorrhagic fever with renal syndrome. 1 20

Renal tubular and glomerular functions were evaluated in 35 consecutive patients with multiple myeloma and were correlated with changes in renal histopathology and myeloma protein patterns. All nine patients without Bence Jones proteinuria had CCr greater than 50 ml/min. In contrast 16/26 patients with Bence Jones proteinuria had CCr less than 50 ml/min and the magnitude of the Bence Jones proteinuria correlated well with the degree of renal insufficiency. Frequent abnormalities in renal tubular acidifying and concentrating ability were observed only in patients with Bence Jones proteinuria and occurred in the absence of significant reductions of glomerular filtration rate. Severely deranged renal histology was seen only in patients with Bence Jones proteinuria and consisted primarily of tubular atrophy and degeneration; glomeruli appeared normal. These data suggest that Bence Jones proteins exert a direct nephrotoxic effect at the tubular level with resultant tubular dysfunction and tubular atrophy. Glomerular filtration rate remains relatively preserved despite the significant abnormalities of tubular function. Although obstructing tubular casts were observed only in patients with severely impaired glomerular filtration rate, many patients with similarly impaired renal function had no evidence of such casts. Instead, tubular atrophy and degeneration correlated best with renal dysfunction.
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PMID:Renal function in patients with multiple myeloma. 2 82

Heroin addiction is associated with several severe and occasionally fatal renal complications. Acute renal failure consequent to rhabdomyolysis and myoglobinuria, when treated supportively, carries a good prognosis. Staphylococcal or other bacterial septicemia may in itself prove fatal and is associated with a proliferative immune complex, acute glomerulonephritis, which generally follows the course and prognosis of septicemia. The necrotizing angiitis reported in heroin addicts still is largely undefined. Focal and segmental glomerular sclerosis is the most common pathologic finding in the syndrome of heroin-associated nephropathy (HAN). Typically, HAN presents with massive proteinuria and progresses rapidly to renal failure. Presumptive evidence supports the premise that heroin or its vehicles elicits immunologically mediated renal damage. The antigen still is unidentified. Removing the antigenic challenge by stopping heroin injection apparently interdicts the progression of renal disease. Renal transplantation can be effectively accomplished in patients with HAN without early recurrence if patients discontinue the use of heroin.
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PMID:Renal consequences of narcotic abuse. 2 85

Takayasu's disease is a nonspecific arteritis of unknown cause with predilection for the aortic arch and its branches; approximately 20% of those affected are children or adolescents, predominantly females. The purpose of this article is to report the case of a young girl in which the mode of presentation was microscopic hematuria and proteinuria. Subsequently, aortic valvular insufficiency developed and there was evidence of aortitis in the thoracic and abdominal aorta, as well as in the arch. All functional and anatomical cardiac derangements were documented by ultrasound and angiocardiography. Renal biopsies showed progressive glomerular involvement characterized by focal and segmental glomerulonephritis. It is postulated that a common immunologic mechanism was responsible for the aortic and glomerular lesions.
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PMID:Takayasu's arteritis associated with glomerulonephritis. A case report. 3 Oct 83


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