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)

Percutaneous renal biopsies from 56 patients with systemic lupus erythematosus were studied to determine the relationship between renal function and the light microscopic, electron microscopic and immunofluorescent antibody findings. The glomerular lesions were classified into 5 major groups: diffuse membranoproliferative glomerulonephritis (34%), diffuse proliferative glomerulonephritis (26.8%), membranous nephropathy (12.5%), minimal lesion ('nil') and minimal lesion with increased mesangial matrix and/or cells (21.4%) and focal and segmental glomerulonephritis (5.3%). Minimal lesions and focal and segmental glomerulonephritis were invariably associated with normal renal function. Patients with moderate to severe renal involvement and the nephrotic syndrome had predominantly diffuse membranoproliferative and diffuse proliferative glomerulonephritis. Membranous nephropathy was associated with moderate renal involvement and the nephrotic syndrome in 50% of cases. Patients with pure mesangial electron dense deposits had normal renal function or mild renal involvement when the deposits were heavy. Moderate and heavy subepithelial, and intramembranous/subepithelial deposits were associated with moderate to severe renal involvement and the nephrotic syndrome. Renal involvement was most severe with heavy subendothelial deposits. Cytoplasmic tubuloreticular structures measuring approximately 18 to 20 nm in diameter and 80 to 100 nm in length were found in 93% of all biopsies, but bore no relationship to the renal function of the patients. Anti-Hu-IgG fluorescent deposits were found in all the renal biopsies; in 81.3% these were associated with less heavily stained deposits of immunoglobulin IgA, IgD and IgM. Early complement components Clq and C4 were utilized in the complement pathway of activation. Pure mesangial fluorescent deposits were associated with normal renal function or mild proteinuria. Diffuse granular and lumpy deposits along the capillary loops were usually associated with moderate to severe renal involvement and the nephrotic syndrome. In the present series of cases, there was a good correlation between renal function of patients with systemic lupus erythematosus and the glomerular lesions as determined by light, electron microscopic and immunofluorescent microscopic findings.
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PMID:Lupus nephritis: correlation between light, electron microscopic and immunofluorescent findings and renal function. 78 52

The third component of complement (C3) was measured in the urine of 98 patients with a variety of renal diseases. Renal biopsy was performed on 83 of the patients and examined by light, electron, and immunofluorescence microscopy. Urinary C3 was detected in cases of membranous glomerulonephritis, mesangiocapillary glomerulonephritis, rapidly progressive glomerulonephritis, and renal amuloidosis. It was not detected in minimal lesion glomerulonephritis; in cases of proliferative glomerulonephritis it was detected only in those showing histological evidence of a progressive lesion. Concentrations were low or undetectable in cases of non-immunological renal diseases. There was a good correlation between urinary C3 concentrations and the deposition of C3 in glomerular capillary walls, as seen by immunofluorescence microscopy, and there was no correlation with the degree or selectivity of proteinuria. Urinary C3 excretion appears to be an accurate indicator of continuing activity of disease. It is suggested that the presence of C3 in urine is due to complement fixation by immune complexes in glomerular capillary walls, and that urinary C3 estimations have potential applications in the study of glomerulonephritis.
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PMID:Significance of urinary C3 excretion in glomerulonephritis. 78 6

Eighty-one adult patients with the idiopathic nephrotic syndrome were treated with prednisone, 60 to 120 mg, on alternate days. Treatment was continued with diminishing drug doses for up to 10 years. Biopsy specimens were categorized as showing lipoid nephrosis 36 per cent, focal sclerosis 12 per cent, diffuse proliferative 22 per cent and membranous nephropathy 30 per cent. Patients with systemic causes of the nephrotic syndrome were excluded. Proteinuria decreased to normal or to less than or equal to 3 g with a greater than or equal to 50 per cent decrease from base line in 83 per cent of the patients with lipoid nephrosis, 30 per cent of the patients with focal sclerosis, 50 per cent of the patients with diffuse proliferative nephritis and 71 per cent of the patients with membranous nephropathy. Improvement occurred in those with focal sclerosis, diffuse proliferative nephritis and membranous nephropathy only after prolonged treatment (14 to 15 months). Stable or improved renal function occurred in 97 per cent of those with lipoid nephrosis, 50 per cent of those with focal sclerosis, 73 per cent of those with diffuse proliferative nephritis and in 83 per cent of those with membranous nephropathy. Death or dialysis occurred in 12 per cent of the patients, and complications coincident with treatment occurred once every 12 patient years. Compared to other series of patients with the idiopathic nephrotic syndrome, therapy of our patients with prolonged alternate day steroids resulted in (1) decreased protein excretion, (2) maintenance of good renal function and (3) decreased number of complications of therapy.
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PMID:Therapy of the idiopathic nephrotic syndrome with alternate day steroids. 83 92

The clinical and histopathological features of 37 patients with idiopathic membranous nephropathy are presented. Males were four times as commonly affected as females and the age at presentation ranged from nine to 70 years. The period of observation varied from three months to 23 years. Twenty-eight patients (76 percent) presented with the nephrotic syndrome and nine patients (24 per cent) presented with non-nephrotic proteinuria. At the end of the study, of the patients presenting with the nephrotic syndrome, seven (25 per cent) were in remission, seven (25 per cent) remained nephrotic, nine (32 per cent) showed only proteinuria and five (18 per cent) were dead or on dialysis. Altogether eight patients (28 per cent) developed renal failure. The nine patients who presented with non-nephrotic proteinuria appeared to do better, and none developed renal failure. The occurrence of spontaneous remission makes assessment of benefit from immunosuppressive therapy difficult. However, analysis of our data and a review of the literature suggest that in this condition oral prednisone, cyclophosphamide and azathioprine have no significant therapeutic properties. Histological assessment confirmed the occurrence of mild (Grade 1) changes in patients biopsied soon after presentation, and tubular atrophy increased with the duration of illness. Immunofluorescence confirmed deposition of mainly IgG and complement. Repeat biopsies in 14 patients showed no histological improvement and remission was not accompanied by resolution of histological abnormalities.
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PMID:Idiopathic membranous nephropathy. 86 73

Twenty-eight patients with SLE and distinct, well-defined renal morphologic lesions of membranous nephropathy were followed up for 4 years. These patients comprised approximately 8% of the patients evaluated for SLE during a 12-year period. The patients with membranous lupus nephropathy had typical systemic features of SLE, and most of them had positive LE cell tests and ANA, low serum complement concentrations, and mildly elevated serum antinative DNA levels. Proteniuria and microscopic hematuria were usually discovered years after systemic symptoms of SLE had developed, Only two patients had slowly progressive renal failure, and most patients continued to have proteinuria. Prednisone treatment did not influence either proteinuria or renal function. In only one patient, the renal character of the disease changed drastically, demonstrating membranoproliferative glomerulonephritis. Six patients died (21%); most of these died of cardiovascular illnesses. The relatively benign and stable renal course of membranous lupus nephropathy in patients with otherwise typical SLE suggests that the renal pathogenesis is different from that of proliferative lupus nephritis.
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PMID:Membranous lupus nephropathy: a clinicopathologic study. 91 91

Four patients with rheumatoid arthritis developed heavy proteinuria after five to 12 months of treatment with D-penicillamine. Light microscopy of renal biopsy samples showed minimal glomerular capillary wall thickening and mesangial matrix increase, or no departure from normal. Electron microscopy, however, revealed subepithelial electron-dense deposits, fusion of epithelial cell foot processes, and evidence of mesangial cell hyperactivity. Immunofluorescence microscopy demonstrated granular capillary wall deposits of IgG and C3. The findings were similar to those in early membranous glomerulonephritis, differences being observed however in the results of staining for the early-acting complement components C1q and C4. It is tentatively concluded that complement was activated by the classical pathway.
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PMID:Immunopathology of penicillamine-induced glomerular disease. 95 Jun 31

Twelve cats were used to study autolytic changes in glomerular morphology and compare these with lesions of naturally occurring feline renal disease. The 12 cats had normal clinical, urinary, and blood features. One kidney (0-hour control) was excised immediately after a given cat was euthanatized, and portions of it were prepared for light and electron microscopy. The opposite kidney (autolytic) remained in situ for selected postmortem intervals, up to 24 hours, at which time it was similarly processed. Renal tissues from 4 additional cats (3 with proteinuria and 1 with diabetes mellitus) were processed and examined for comparison. Zero-hour control kidneys had the following mean quantitations: renal weight was 9.9 g; glomerular diameter, 83 mum; number of cells per glomerulus in 1-mum section was 63; and diameter of cell nuclei was 6.3 mum for mesangial, 6.7 mum for visceral epithelial, and 6.4 mum for endothelial. In comparison with 0-hour control kidneys, autolytic kidneys had increased weight and glomerular diameter, but the diameter of cell nuclei decreased. Basement membrane thickness and glomerular cell numbers did not differ between 0-hour control and autolytic kidneys. Kidneys from 4 diseased cats had increased glomerular diameter and glomerular basement membrane changes characterized by hyalin thickening and dense deposits. These changes are compatible with a lesion diagnosis of membranous glomerulonephritis.
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PMID:Feline glomeruli: morphologic comparisons in normal, autolytic, and diseased kidneys. 96 8

Indentations of the glomerular basement membrane were observed by light microscopy in ultrathin Epon-embedded serial sections from the renal biopsies of patients who had membranous glomerulonephritis, minimal change glomerulonephrits, acute or resolving exudative glomerulonephritis and focal glomerulonephrits, interstitial nephritis, amyloidosis, rheumatoid arthritis, or ankylosing spondylitis. In patients with membranous glomerulonephritis, acute or resolving exudative glomerulonephritis, amyloidosis, or rheumatoid arthritis, the occurrence of indentations in the glomerular basement membrane differed significantly from that in controls. The presence of indentations did not correlate with proteinuria, hematuria, leukocyturia, arterial hypertension, or with the nephrotic syndrome or its treatment with steroids. Examination of alternate serial sections by light and be electron microscopy showed that the indentations that were light microscopically visible corresponded to craters on the epithelial surface of the glomerular basement membrane seen in the electron microscope. These craters contained protruding portions of the epithelial cells, extracellular electron-lucent material or electron-dense amorphous or striated membranous material. They were often surrounded by spikelike protrusions of the lamina densa. These indentations might represent solitary remnants of former subepithelial deposits.
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PMID:Indentations of the glomerular basement membrane in renal diseases. A light and electron microscopic study on ultrathin serial sections. 97 63

The renal tubular epithelial antigen (Tub-Ag) of rats was solublized by Pronase and purified by gel filtration and acrylamide gel electrophoresis. Purified Tub-Ag was a glycoprotein with S20,W value of 8.4. Utilizing radiolabeled Tug-Ag, a sensitive radioimmunoassay for Tub-Ag and homologous antibody (anti-Tub-Ag) was developed. Tub-Ag activity associated with a protein of the same molecular size was demonstrated in the serum, as well as in Pronase extracts of all the organs tested, including kidney, liver, lung, spleen, intestine, stomach, and heart. The physiochemical properties of the Tub-Ag of rats and its distribution were essentially the same as the Tub-Ag of humans, which had been found in immune deposits in the kidney of some patients with idiopathic membranous glomerulonephritis. Rats were immunized with the purified Tub-Ag emulsified in Freund's complete adjuvant and followed for Tub-Ag and anti-Tub-Ag in the serum, as well as for proteinuria and immunohistological changes in the kidney. Serum Tub-Ag dropped sharply after 20 days, when anti-Tub-Ag appeared in the circulation. Persistent, massive proteinuria appeared still later, more than 30 days after injection, when anti-Tub-Ag disappeared and Tub-Ag reappeared in the serum of some of those rats. In others, anti-Tub-Ag in the serum persisted throughout the observation period of 90 days. The pathology of the kidney of the rats with proteinuria was that of a typical membranous glomerulonephritis; thickening of glomerular capillary walls with granular deposits of gamma-globulin and Tub-Ag was observed. On the basis of these results, Tub-Ag in the serum, probably released from cellular membranes of various organs as a physiological metabolite, is considered to maintain the pathological process in the kidney by providing the antigen continuously to form immune complexes.
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PMID:The pathogenesis of experimental membranous glomerulonephritis induced with homologous nephritogenic tubular antigen. 99 27

Renal biopsies of 23 heroin addicts who presented with the nephrotic syndrome were examined by light and electron microscopy. The majority of patients (14) showed focal segmental glomerular sclerosis on light microscopy, four patients showed "minimal change", and two were classified as "focal global sclerosis." In one case focal mesangial proliferation was the outstanding feature; one patient had diabetic glomerulosclerosis; and one had mesangiocapillary glomerulonephritis and dysproteinemia. Visceral epithelial swelling and proliferation were present in 14 patients on light on light microscopy. Electron microscopy showed distinct podocyte changes consisting of loss of foot processes, vacuolization, and cytoplasmic degeneration; focal separation of podocytes from basement membranes was found in 11 of 18 cases. In some instances a few electron-dense deposits were present in the mesangium. Membranous nephropathy was not encountered, although it occurs in 30 to 40% of unselected adult nephrotic individuals. Of 15 patients followed for 2 months to 5 years, one died of heroin overdose, eight went into renal failure, two improved, and four continued to have proteinuria. It is concluded that nephrotic syndrome of heroin addicts is most often associated with focal segmental glomerular sclerosis and occasionally with minimal change disease or focal global sclerosis. Conceivably these three conditions represent different phases of one disease process, although different reactions to heroin or its various vehicles and contaminants cannot be excluded. The morphologic resemblance to experimental aminonucleoside and N,N'-diacetylbenzidine-induced nephrosis suggests a possible toxic origin.
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PMID:Glomerular morphology in nephrotic heroin addicts. 99 59


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