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)

Seventy-two adults with the nephrotic syndrome without renal insufficiency had a membranous type of renal histology on biopsy. These patients were randomly allocated to at least eight weeks of alternate-day treatment with prednisone or placebo in a multicenter study. Deterioration of glomerular filtration rate was significantly more rapid in placebo-treated than in prednisone-treated patients, and ultimately 10 of 38 given placebo but only one of 34 given prednisone were in renal failure (creatinine more than 5 mg per deciliter [440 mumol per liter]) or dead (P less than 0.02). In male patients and in those with nonselective initial proteinuria, there was a trend (not reaching statistical significance) toward more rapid deterioration of renal function. Age, admission blood pressure, serum creatinine, daily total protein excretion, and severity of histologic changes did not predict the subsequent course. We conclude that a short course of alternate-day prednisone therapy was beneficial in our group of patients with idiopathic membranous nephropathy.
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PMID:A controlled study of short-term prednisone treatment in adults with membranous nephropathy. Collaborative Study of the Adult Idiopathic Nephrotic Syndrome. 38 20

A patient with membranous nephropathy (MN) received a renal allograft from his brother. The allograft functioned immediately but nephrotic range proteinuria developed seven days after transplantation in the absence of any signs of rejection. Renal function deteriorated five weeks after transplantation due to ureteric obstruction. Nephrostomy drainage resulted in the return of renal function to normal and demonstrated that the allograft was the source of the nephrotic range proteinuria. An open renal biopsy of the allograft performed at the same time revealed the presence of recurrent MN. The recipient was investigated in an attempt to identify possible humoral immune mechanisms that may explain this very rapid recurrence of MN.
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PMID:Rapid recurrence of membranous nephropathy in a related allograft. 38 8

Different types of urinary protein excretion may be recognized by determination of the proteins molecular weight. Beside chromatography different electrophoretic procedures have been applied to urinary proteins to study the underlying renal disease. The various zone electrophoreses separate merely by surface charge, proteins however covered by sodium dodecyl sulfate (SDS) migrate according to their molecular radius. So by SDS-polyacrylamide electrophoresis (SDS-PAe) macromolecular proteinurias (Mr 60,000- greater than 300,000 daltons) due to glomerular damage may be distinguished from micromolecular forms (Mr 10,000-70,000 d) due to tubular dysfunction. By densitometric quantitation of the separated Ig and transferrin an index of the glomerular selectivity is obtained, i.e. the capacity of the glomerular system, to retain serum proteins of a Mr above 150,000 d. By this procedure proliferative and degenerative glomerulopathies may be distinguished from minimal change disease, focal glomerular sclerosis and early membranous nephropathy; serial determinations of this selectivity index in the latter two disease entities show a gradual deterioration of glomerular protein handling with time. A glomerular proteinuria of even "physiological" quantity has been proved as early sign of renal involvment in systemic diseases; it may be detected earlier as for example the retinopathy in juvenile diabetics. Micromolecular proteinurias also occur at least in two forms: the typical tubular proteinuria (MW 10,000-70,000 d) is associated with acute or chronic severe tubular dysfunction as in interstitial nephritis and acute kidney failure; rejection episodes of kidney transplants lead to transient tubular proteinurias, too. The second form of micromolecular proteinuria (Mr 40,000-70,000 d) has been found frequently in association with a glomerular in diabetic and hypertensive glomerulosclerosis. By measuring clearances of the microproteins, the proteinuria with this pattern could be established as form independant from glomerular and tubular proteinurias. The constancy of the two micromolecular proteinurias led to the hypothesis of at least two selective mechanism of tubular protein resorption. SDS-PAe additionally allows the differentiation of extrarenal proteinurias, as caused by overflow, paraproteins, postrenal Ig-secretion or bleeding etc. In comparing clinical and in part histological data of about 2,000 patients suffering from kidney diseases the analysis of urinary proteins by this method has been proved as valuable non-invasive tool for diagnosis and follow-up.
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PMID:Diagnostic significance of SDS-PAA-electrophoresis of urinary proteins: different forms of proteinuria and their correlation to renal diseases. 44 75

During gold therapy a patient with rheumatoid arthritis developed nephrotic syndrome, and a patient with juvenile chronic arthritis proteinuria. Electron microscopic examination of bioptic specimens of the kidneys revealed in both instances membranous glomerulonephritis with typical epimembranous deposits and intracellular gold inclusions. Immunofluorescent examination performed only in the second patient revealed that the deposits in the wall of the glomerular capillaries contain IgG which suggests an immunocomplex mechanism of the development of the renal disease, induced very probably by chrysotherapy.
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PMID:Gold nephropathy in rheumatoid arthritis and in juvenile chronic arthritis. 53 99

A total of 163 Japanese children (90 boys and 73 girls, ranging in age from 3 to 15) with proteinuria and/or hematuria were studied for renal histopathology using biopsy materials by light microscopy, electron microscopy, and immunofluolescence method. Eleven patients were diagnosed as membranous nephropathy (MN) while the other 152 patients had various renal diseases other than MN. All patients with MN did not have any known predisposing of associated caused. Hepatitis B virus surface antigen (HBsAg) in the serum, as determined by a reversed passive hemagglutination method (RPHA), was positive in 100% of the patients with MN, while it was positive in 4.6% of the patients with other renal diseases. The difference was statistically significant. Of the 11 mothers of the children with MN, six were positive for HBsAg, and one of the remaining 2 was positive for antibody to HGsAg (anti-HBs) and another was not examined. These findings suggest that MN among Japanese children are mainly, if not exclusively, caused by hepatitis B virus (HBV) and that the virus is transmitted from the mother to child in most instances. In each case of HBsAg-associated glomerulonephritis reported, HBsAg was detected, by immunofluorescence, in the glomeruli, with a distribution similar to that of immunoglobulins. However deposits of HBsAg could not be demonstrated in the glomeruli of the 9 patients with MN studied. Pathogenic immune complexes in the glomerular lesions with subepithelial deposits have been shown to weigh less than 1 million daltons. Since the intact 20-nm HBsAg has a molecular weight of more than 2.4 million daltons, probably most immune complexes containing it would be very large and rapidly cleared by the reticuloendothelial system. Therefore, this failure to detect glomerular staining with anti-HBs antiserum may mean that MN is caused by some other antigen, of a lower molecular weight, associated with HBV, but not necessarily by HB surface antigen.
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PMID:[Etiology of membranous nephropathy in children: Association between membranous nephropathy and hepatitis B virus infection (author's transl)]. 54 9

Of 90 patients with membranous nephropathy proved by biopsy, 8 (8.9%) had pre-existing rheumatoid arthirtis. Four of these eight patients received systemic treatment with gold. Two others received only token amounts of gold. In two patients who received gold, the renal lesions did not occur until months after discontinuance of gold therapy. We found that clinically significant renal lesions (lesions associated with proteinuria) in patients with rheumatoid arthritis were more likely to be membranous nephropathy than occult amyloidosis or adult lipoid nephrosis. The membranous lesion in patients with rheumatoid arthritis may be difficult to identify by light microscopy, and, although special strains can be helpful, the pathology is frequently sufficiently subtle to require immunofluorescence and electron microscopy for definitive diagnosis. We postulate that chrysotherapy may not be the cause of membranous nephropathy in patients with classic rheumatoid arthritis in whom gold has been used. Whether it merely exacerbates a lesion already present in these patients, or whether it plays little or no role in the development of membranous nephropathy is an unsettled question. Our data lead to think that RA can induce MN and that gold is not the primary inciting agent.
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PMID:Membranous nephropathy in patients with rheumatoid arthritis: relationship to gold therapy. 66 57

The initial clinical and histologic renal findings and the subsequent course of 90 patients with SLE were evaluated in a study of the natural history of lupus nephropathy. Initial renal biopsy revealed focal glomerulonephritis in 32 patients, diffuse glomerulonephritis in 47, membranous nephropathy in seven and minimal changes in four. Forty-one patients were rebiopsied three months to five years later; ten of 15 patients with focal glomerulonephritis showed progression to diffuse glomerulonephritis or membranous nephropathy, whereas changes in morphologic pattern were less common in the other types of lupus nephropathy. There was no difference between the patients with the focal lesion who progressed and those who did not in age, sex distribution, duration of SLE prior to biopsy, renal function, and serological studies; however, the patients with progression initially had more proteinuria, higher histologic activity on light microscopy, and more intensive glomerular electron-dense deposition. Focal lupus glomerulonephritis progresses frequently to diffuse glomerular involvement. Certain clinical and morphologic findings at initial evaluation may help to predict future progression in the course of lupus nephropathy.
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PMID:Changing histopathology patterns in lupus nephropathy. 69 93

The diagnosis by inferior vena cavography of right renal vein thrombosis with extension into the vena cava was made in a 33 year old man with idiopathic membranous glomerulonephritis and multiple pulmonary emboli. After one year of continuous anticoagulant drug therapy with heparin and coumadin, venography showed absence of clots in the vena cava and therapy was discontinued. Proteinuria in excess of 4 g/24 hr continued. Six months later pulmonary emboli recurred and venography again demonstrated large clots in the vena cava and right renal vein. The potential for recurrence of renal vein thrombosis and pulmopnary embolism in the presence of active renal diseases is thus demonstrated.
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PMID:Recurrent renal vein thrombosis consequent to membranous glomerulonephritis. 69 97

Seven adult patients with idiopathic nephrotic syndrome and with a glomerular histology considered normal but with ultrastructurally provable membranous glomerulonephritis (MNG) were studied. The glomerular lesions were found to represent all ultrastructural evolutionary phases (A,B, and C) of MGN. In patients with serial biopsies, the membranous lesion seemed to have passed through all of its evolutionary phases towards healing (C) without developing spikes or thickening of the glomerular basement membrane (GBM), i.e., the traditional light microscopic characteristics of MGN. This evolution was associated with a benign clinical course. The membranous lesions were associated with a vacuolization visible in obliquely or tangentially cut segments of the GBM in silver-stained paraffin sections. This alteration seemed to be created by irregularities of the argyrophilic lamina densa of the GBM and not by subepithelial deposits, as suggested previously. All seven patients had a remission of the nephrotic syndrome which appeared to be spontaneous and not drug-induced. The amount of proteinuria correlated with the ultrastructural phase of MGN and with the intensity of immunofluorescent staining. In one patient, the latter became negative.
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PMID:Nonprogressive, histologically mild membranous glomerulonephritis appearing in all evolutionary phases as histologically "early" membranous glomerulonephritis. 75 Jun 96

Treatment of membranous nephropathy and the nephrotic syndrome with 2 mg/kg/day of indomethacin resulted in prompt and sustained reduction in urinary protein excretion and the loss of edema fluid, which allowed the withdrawal of diuretic therapy and liberalization of salt intake. The reduction in proteinuria was paralleled by a decrease in urinary prostaglandin E (PGE) and F (PGF) levels. Plasma PGE and PGF levels did not change appreciably. Withdrawal of indomethacin therapy resulted in an increase in urinary protein and urinary PGE excretion. Reinstitution of therapy resulted in reductions in both values. Indomethacin may provide a useful means of reducing proteinuria and controlling edema in some patients with the nephrotic syndrome.
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PMID:Indomethacin and the nephrotic syndrome. 76 92


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