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)

Antireflux surgery was performed in five patients with vesicoureteral reflux at a time when renal insufficiency was present. Notable proteinuria was present in four of the patients, and a kidney biopsy specimen showed glomerular lesions in one. Despite the eradication of reflux and of infection, all five patients continued to have progressive renal insufficiency culminating in renal failure. Vesicoureteral reflux nephropathy may include a glomerulopathy leading to progressive glomerular sclerosis. Antireflux surgery would not alter this ongoing process and therefore would not halt progressive renal failure.
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PMID:Irreversible renal failure following vesicoureteral reflux. 75 14

The light- and electron microscopic changes in the glomeruli of the rat's kidney have been investigated in the course of ageing and after subtotal nephrectomy, constriction of the renal vein, and intoxication by N-nitrosomorpholine. In spite of the fact that four different experimental models have been used, identical changes were always found in the glomeruli. Morphologically they consisted of a diffuse thickening of the glomerular basement membrane and of an increase in the mesangial matrix without a proliferation of the glomerular cells. Despite this thickening of the glomerular basement membrane, functionally an increased permeability of the glomerular capillaries for macroproteins could be observed, shown by a moderate proteinuria. For these morphological changes the term "glomerulosclerosis" is suggested; they are interpreted as a non-specific, non-inflammatory reaction of the glomerulus to an impairment caused by a number of varied influences. From the study of the formal pathogenesis of the glomerulosclerosis presented here one can conclude that in the individual experimental models the same result has been achieved in different ways. One possibility in the development of glomerulosclerosis is an increased production of the components of the basement membrane and of the mesangial matrix. This is the pathway which appears to be followed after nephrectomy. Another possibility is a slowing down of the breakdown of both the matrix and the membrane. This seems to be the case in the glomerulosclerosis occuring in the course of ageing, and after hypoxic and toxic changes. It could be accounted for by a functional disturbance of, presumably, the mesangial cells responsible for the breakdown of the basement membrane and of the matrix. On the other hand, one may have to consider a primary alteration of the macromolecules of these structures, as is already known from studies of the, chemically closely related, collagen. The light- and electron microscopic studies of the normal and of the altered glomeruli have led to certain conclusions concerning the origin and the fomation of the glomerular basement membrane and the mesangial matrix. In order to widen the scope of the studies, additional autoradiographic investigations with 3H-proline and 3H-leucine have been performed in ultrathin and semithin sections of the rat's glomeruli. The results of the studies presented here suggest that of the three cell types of the glomerulus the visceral epithelial cells (podocytes, "Deckzellen") may participate on the formation of the glomerular basement membrane, whereas the mesangial cells appear to be responsible for the synthesis of the mesangial matrix.
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PMID:[On the pathogenesis of the glomerulosclerosis ultrastructural and autoradiographic investigations on the rat kidney (author's transl)]. 79 Aug 31

The present studies examined the pathogenesis of focal glomerular sclerosis in aging rats. A marked difference in development of the lesion was noted between males and females, and strain variability was an important factor. Increased glomerular basement membrane permeability with loss of selectivity unrelated to changes in glomerular sialoprotein occurred with aging and was accompanied by increasing proteinuria. Noncomplement-fixing mesangial deposits of rat IgM were present after 1 month of age and were also found in lesser amounts in germfree rats. Fluoresceinated eluates of rat kidneys did not have antibody activity against rat serum or tissue antigens. There was no evidence for a pathogenetic role of IgM deposits. Rat IgG, IgA, IgE, C3, and fibrin were occasionally found in sclerotic areas. Analysis of multiple histologic sections revealed a close correlation between aging and glomerular pathology, with a poor correlation between tubular damage and aging. Glomerular damage appeared to be the initial event leading to tubular damage. Indirect evidence suggests that a relative thymic deficiency may play an important role in the pathogenesis of the lesion.
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PMID:Spontaneous glomerular sclerosis in aging Sprague-Dawley rats. I. Lesions associated with mesangial IgM deposits. 79 8

The selectivity of proteinuria has been determined immunochemically at least 4 times over periods of 3 years or more in 27 children and adolescents who had been investigated by renal biopsy. Variations of the selectivity outside the limits of experimental error were observed in 14 patients, in 8 of whom there was a progressive decline. Six of these 8 had focal and segmental glomerular lesions, including one case of Alport's syndrome, and 2 had proliferative glomerulonephritis. Two different anomalies of relative IgG clearance were noted: in proliferative glomerulonephritis there was a constantly low clearance, and in focal glomerulosclerosis an elevated clearance increasing with time. Indirect evidence suggests that the latter may be due to the presence of low molecular weight IgG fragments in serum and urine.
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PMID:The significance of variation in the selectivity of proteinuria. 80 62

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

The case is presented of a young man who, after prolonged intravenous narcotic administration, developed subacute bacterial endocarditis involving the aortic valve, and rapidly progressive glomerulonephritis. After treatment of and recovery from renal failure, persistent proteinuria was shown to be caused by focal glomerulosclerosis. The association of these lesions with "mainlining" is reviewed.
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PMID:Renal and cardiac complications of drug abuse. 99 44

Renal biopsies from 10 patients staining predominantly for immunoglobulin A are reviewed. Historically, nine of 10 patients were less than 32 years of age; they all presented with either microscopic or gross hematuria. The initial creatinine clearances demonstrated good function in all patients; only one patient experienced a progressive decline in the creatinine clearance. Similarly, proteinuria was mild. The light and electron microscopic findings presented a variable pattern, including a group with changes confined to the mesangium, another group also having glomerular basement membrane changes, and one patient with severe, progressive glomerular sclerosis. Immunogluorescence demonstrated large amounts of IgA predominantly within the mesangium but occasionally involving the peripheral capillary loops. Serum IgA levels were elevated in six of eight patients tested, and two of five patients had elevated nasal IgA concentrations. These data suggest that there is an immunologic entity, IgA glomerulonephritis, characterized by the above clincial findings in association with elevated serum and occasionally nasal IgA levels, but that the pathologic findings are highly variable. Neither the mechanism nor the particular pathogenetic significance of the raised IgA levels is presently known. The similarities of this entity to the reported findings in anaphylactoid purpura are mentioned.
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PMID:Immunoglobulin A glomerulonephritis: a clinicopathologic study. 108 41

Immunofluorescence studies of rat kidneys from 3-24 mo. of age demonstrated deposition of immunoglobulins, predominately IgM, within the glomerular mesangium by age 3 mo. Immunoglobulins eluted in acid buffer, did not fix complement, were not associated with inflammatory changes, and increased markedly with the onset of proteinuria at about 12 mo. Rats 24 mo. old also had mesangial deposits of IgG and fibrin. No basement membrane deposits were seen, and autoantibodies to antigens in normal kidney, liver, spleen, and skeletal muscle were not demonstrable in serum or eluates of kidneys from aged animals. The focal and segmental glomerular sclerosis which develops in aged rats does not appear to be mediated by glomerular deposition of auto-antibody or immune complexes. Mesangial accumulation of macro-molecular material, perhaps as a consequency of the age-associated increase in glomerular permeability, may contribute to the development of the glomerular sclerosis of aging in the rat by impairing mesangial phagocytic or clearing mechanisms rather than through immunologically mediated tissue injury.
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PMID:The immunopathology of the aging rat kidney. 110 3

From two groups of diabetics, i.e. an "invesitgation-group" of 40 cases and a "comparison-group" of 55 cases, the following characteristics of a state preliminary to proliferative diabetic retinopathy are resulting: early commencing of angiopathy by means of proteinuria (nephropathy), progression of retinopathy (pre-stage), pronounced progressiveness of the accompanying nephropathy and arterial hypertension, and finally uncommon diabetic heredo-familiarity. They all permit permature conclusion on proliferative retinopathy (and glomerulosclerosis).
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PMID:[Pre-conditions of proliferative diabetic retinopathy (author's transl)]. 114 87

33 cases of chronic glomerulonephritis who responded unsatisfactorily to treatment with indomethacin alone were treated in addition with a low dose of cyclophosphamide. The five patients with focal glomerulosclerosis responded poorly. The remaining 28 patients showed a statistically significant improvement in renal function and proteinuria.
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PMID:Treatment of chronic glomerulonephritis with a combination of indomethacin and cyclophosphamide. 120 60


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