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 middle-aged man with idiopathic membranous nephropathy, who developed chronic renal failure, received a cadaver renal allograft. Two months later, massive, persistent proteinuria developed. A biopsy specimen of the allograft showed changes characteristic of membranous nephropathy and identical to those present in the patient's own kidney. The criteria for recurrence of glomerulonephritis in renal allografts are met in this case.
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PMID:Recurrence of idiopathic membranous nephropathy in a renal allograft. 109 95

We describe a case of membranous nephropathy in a patient with pulmonary, splenic and hepatic sarcoidosis. The patient was asymptomatic, and edema was absent notwithstanding the proteinuria (over 8.0 gm/100 ml daily). Prednisone cleared the pulmonary and splenic complications, but the proteinuria, although diminished, persisted. Adjunctive therapy with cyclophosphamide caused further diminishment of the proteinuria. We have reviewed the relationship between the nephropathy and the sarcoidosis and suggest that a causal relationship exists between the two diseases.
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PMID:Membranous glomerulopathy in a patient with sarcoidosis. 110 20

Sixty-six patients of all ages whose renal biopsy appearances satisfied strict criteria for the histopathological diagnosis of membranous nephropathy were studied and followed for a mean of 5-4 years (range 1 to 20 years). From initial investigation seven patients were found to have associated neoplasia, and in two patients the condition followed treatment with a mercurial diuretic and gold. One patient was Australia antigen positive. Two patients developed renal vein thrombosis, but in both this appeared to follow not precede their nephrotic syndrome. In the remaining 56 patients there was no associated factor. During the follow-up period, approximately one-quarter of the patients (15) died, nine from renal failure; one-quarter (10) had a persistent nephrotic syndrome, another one-quarter (15) proteinuria of lesser degree. The final one-quarter (16) are now in complete remission. The prognosis of the 54 patients with an initial nephrotic syndrome was poorer than the 12 with lesser proteinuria and no oedema at onset; five of 11 children were in complete remission when last seen. All but one of the nine patients who developed terminal chronic renal failure 4 to 18 years from onset had an unremitting nephrotic syndrome, eight of the 10 currently alive with a persistent nephrotic syndrome have reduced renal function. Renal functional deterioration did not occur in the absence of proteinuria. There was only slight correspondence between the stage of biopsy appearance, glomerular filtration rate at time of biopsy, time of the biopsy from apparent onset, or status at last follow-up. Staging is therefore of limited prognostic value. Twenty-two patients were treated with corticosteroids for 2 to 36 months; we detected no short or long-term benefit when compared to patients not so treated.
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PMID:Membranous nephropathy. Long-term follow-up and association with neoplasia. 117 11

Membranous nephropathy (MN) accounts for about 20 percent of cases of the nephrotic syndrome. The importance of renal biopsy in establishing the diagnosis is emphasized. In the great majority of MN patients, no etiologic factor can be discerned. In a significant minority, MN appears to be a manifestation of sarcoidosis, diabetes, lupus, syphilis, malaria, or toxicity from heavy metals or drugs. In some cases the "cause" is neoplasia (including lymphoma) or a viral infection. Massive proteinuria, hypoproteinemia and edema are the principal manifestations of MN, finally resulting in renal failure. Treatment consists chiefly of diet and diuretic drugs. In the more pronounced cases, corticosteroids may have a favorable effect and in very resistant cases, cyclophosphamide is indicated. Judicious use of these modalities if often associated with the diminution or disappearance of the clinical signs of MN.
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PMID:Membranous nephropathy: an overview. 120 87

Experimental evidence suggests that barriers to glomerular filtration of macromolecules exist at the glomerular basement membrane itself and at the level of the epithelial cell and epithelial slit pores. The distribution of negatively charged glomerular sialoprotein (GSP) at the latter site and the reduction in histochemical staining for GSP reported in several clinical and experimental glomerular diseases suggest a role for this material in the regulation of glomerular permeability. Alternatively, reductions in GSP associated with proteinuria may reflect only epithelial cell swelling consequent to the proteinuria. The sequence of subepithelial immune complex deposition, epithelial cell swelling and foot process fusion, alterations in histochemical staining for GSP, and development of proteinuria was studied in 12 Lewis rats biopsied weekly during development of autologous immune complex (Heymann) nephropathy. Deposition of IgG was detectable 3 weeks after antigen injection by immunofluorescence. Electron-dense deposits were first seen by electron microscopy coincident with the appearance of complement at week 4. Proteinuria began at 6 to 8 weeks, 3 to 5 weeks after detectable immune complex deposition. Proteinuric animals had marked subepithelial immune complex deposition and extensive epithelial cell swelling and foot process fusion. Despite these changes, there was no detectable reduction in staining for GSP until week 14, 6 to 8 weeks after onset of proteinuria. Reductions in GSP apparently do not play a role in altering glomerular permeability early in autologous immune complex (Heymann) nephropathy, and proteinuria and epithelial cell swelling can be present in this model without detectable changes in GSP. These findings suggest that early alterations in GSP reported in some other proteinuric disorders may be of pathogenetic significance rather than simply a reflection of changes in epithelial cell morphology secondary to proteinuria. In this experimental model of membranous nephropathy, immunofluorescence was more sensitive than electron microscopy in the early detection of immune deposits.
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PMID:Autologous immune complex nephropathy. I. Sequential study of immune complex deposition, ultrastructural changes, proteinuria, and alterations in glomerular sialoprotein. 124 22

It is possible to differentiate the proteinuria of glomerulonephritis by means of microelectrophoresis in polyacrylamide-gradient gels. The advantages of this method (quick, cheap, concentration of the urine not required) led to its introduction into clinical use. Upon separating the urinary proteins according to their molecular weight and form, four patterns of proteinuria may be differentiated: low molecular, intermediate and high molecular. Those forms of glomerulonephritis which show constant morphological and clinical findings (e.g. minimal proliferative glomerulonephritis, mesangioproliferative glomerulonephritis with crescents) can be related to one of the four patterns of proteinuria, whereas the pattern of proteinuria in other forms of glomerulonephritis (e.g. (peri-)membranous glomerulonephritis, mesangioproliferative glomerulonephritis) are dependent on the phase of the disease.
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PMID:[Differentiation of the proteinuria by microelectrophoresis in continuous polyacrylamide-gradient gels (author's transl)]. 124 1

This is a case report of a 35-year-old female who showed a relatively short clinical course of severe liver cirrhosis and proteinuria. On light microscopical studies of autopsy material, besides active postnecrotic type liver cirrhosis, typical membranous glomerulonephritis was found. Immunofluorescent study disclosed not only clustered HBsAg (hepatitis type B surface antigen) in occasional hepatic cells but also beaded granular type deposition of HBsAg, IgG, IgM, IgA and complement C3 along renal glomerular basement membrane (GBM). Electron microscopical study disclosed multiple particulated material in occasional inclusion bodies of hepatic cells and in subepithelial and subendothelial dense deposits along the GBM. Enzymatic immunoelectron microscopical study confirmed these particles especially along the GBM being HBsAg themselves. It was concluded that HBsAg-Ab (antibody) complex was the pathogenetic factor responsible for the glomerular change of this particular case. Although HBsAg and Ab were examined to be negative in serum throughout the patient's clinical course, the possibility of the presence of circulating HBsAg-Ab complex in serum was discussed.
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PMID:Membranous glomerulonephritis associated with active liver cirrhosis both involved by HBs antigen. 127 84

A patient with hydatid cyst of the presented stunted growth, normal renal function and no significant proteinuria. The radiological abdominal investigation disclosed, besides the hydatid cyst, horseshoe kidneys. Renal biopsy was performed during surgery. Immunofluorescence (direct and indirect) and immunoperoxidase studies revealed glomerular deposits of hydatid antigen and its corresponding antibody. A grade I immune complex type of membranous glomerulonephritis, without significant clinical signs, was diagnosed in association with the hepatic hydatid disease.
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PMID:[Hepatic hydatidosis with glomerular involvement: report of a case]. 130 57

Patients with heavy proteinuria have an increased incidence of venous thrombosis and coronary heart disease (CHD). They also exhibit perturbations in lipoprotein metabolism. Lipoprotein (a) (Lp(a)) predisposes to CHD; it may also promote intravascular thrombosis since it contains apolipoprotein (a), which could act as a competitive inhibitor of plasminogen activation. We have measured the concentration of serum Lp(a) in 10 men with proteinuria due to idiopathic membranous nephropathy (IMN), in eight men with a similar diagnosis but who were in remission, and in 103 healthy men. Serum Lp(a) levels were significantly elevated in the men with active IMN, having a median value of 31.3 (range 3.2-75.0) mg/dl, whereas they were 8.4 (3.4-31.5) mg/dl in the patients in remission, which was similar to the value of 11.3 (< 0.8-87.4) mg/dl found in the healthy controls. Lp(a) is unique in containing an apolipoprotein which is a giant mutant of plasminogen and it is thus possible that the high circulating levels of Lp(a) contribute to the vascular morbidity associated with proteinuria by promoting thrombosis or atherogenesis or both.
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PMID:Serum lipoprotein (a) in men with proteinuria due to idiopathic membranous nephropathy. 133 76

Membranous nephropathy is a histological appearance which indicates a particular immunopathogenesis, but may have many basic aetiologies and is probably not a single disease. It is predominantly an appearance seen in middle-aged and elderly individuals, and in general has a slow progression over years or even decades towards remission or renal impairment in almost equal proportions. An aggressive search for associated disease is worthwhile, and one should wait to see what the evolution of proteinuria and renal function may be. If a progressive course becomes evident, then a trial of treatment with corticosteroids is worthwhile, but if this is ineffective, a more aggressive approach involving the use of alkylating agents may be justified. Cyclosporin does not appear to have a major effect in the majority of patients, and intravenous gammaglobulin is under evaluation at the moment with some encouraging results. The best treatment regime remains to be determined.
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PMID:Membranous nephropathy and its treatment. 133 86


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