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)

The female patient initially showed the acquired type of total lipoatrophy at about 8 years of age. At 12 years of age, the onset of diabetes mellitus was speculated from advanced pyodermia and dedentition. At 29 years of age, glucosuria was found, and she developed proteinuria, ascites, and pretibial edema. The physical examination revealed: hepatosplenomegaly, complete absence of subcutanous fat, cutaneous xanthomas, and emaciated facies with pronounced zygomatic arches. Diabetic retinopathy was revealed in the ophthalmological examination, and nephropathy was evident in renal biopsy specimens. She also had peripheral diabetic neuropathy. No adipose tissue was found in the mesenterium under peritoneoscopy. The hepatic biopsy specimen revealed advanced portal liver cirrhosis. Laboratory findings included: hyperlipidemia, elevation of BMR without evidence of hyperthyroidism, impaired renal function, and undetected anti-insulin antibodies and anti-insulin antibodies. Endocrinological examinations revealed normal value, except for an impaired hGH response in the arginine test. C-peptide immunoreactivity was high. Her condition was fairly well controlled by 140 units of insulin injection daily.
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PMID:Lipoatrophic diabetes. Report of a case. 15 92

Three groups of female (NZB X NZW)F1 hybrid mice were treated with an intermittent regimen of dactinomycin (actinomycin D), 3.5 microgram. daily. Median survival was doubled in two of the groups and increased by more than 75 per cent in the third. Most of the treated animals never had significant proteinuria. When kidneys from 14 treated mice, which died between the ages of 11 and 20 months, were examined by light and fluorescence microscopy, most showed the lesions of normal aged CBA and C57BL/6 mice, some expansion of the mesangial matrix and increased cellularity, consistent with deposition of immunoglobulins and complement components in the mesangium, generally sparing the capillary loops. Four of the 14 animals, three of them long-lived, had advanced renal glomerular disease. These data indicate that dactinomycin, by whatever therapeutic mechanism, permits very extended survival of B/W female mice, the large majority of them without significant renal disease.
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PMID:Dactinomycin treatment of murine lupus erythematosus. I. Renal disease and longevity. 15 31

Glomerular deposits of immunoglobulin A (IgA) (and immunoglobulin G [IgG]) has been described in IgA-nephropathy (Berger's disease), in anaphylactoid purpura, and systemic lupus erythematosus. The pathogenesis of mesangial IgA deposits in these disease states is unclear. Circulating immune complexes have been speculated to be involved although their existence in blood in IgA nephropathies have never been reported. We describe a 53-year-old man who presented with a petechial rash in lower extremities accompanied by painful swelling of left ankle and wrist. Polyclonal elevation of IgA and IgG in serum was found, along with cryoglobulins containing IgA and IgG (rheumatoid factor positive). After two years, hematuria, mild proteinuria, and active urinary sediment developed and renal biopsy revealed focal proliferative changes. Immunofluorescence revealed predominantly mesangial deposits of IgA and IgG but no IgM nor complement. This experience suggests that circulating complexes consisting of IgA and IgG may lead to renal lesions presenting clinically and histologically in a way similar to that commonly seen in IgA nephropathies.
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PMID:Case report: mesangial IgA-IgG deposition in mixed cryoglobulinemia. 15 12

NZB x OUW F1 hybrid mice were treated with thiamphenicol at 25, 50 and 250 mg/kg/day from the time of their first positive antinuclear antibody test until their death. Untreated mice fed the same diet served as controls with body weight, mortality and renal disease patterns conforming to published reports of the biology of the BW mice. Regular testing of urine and bloodm and detailed postmortem examinations showed (a) that with increasing drug dose levels heavy proteinuria was almost eliminated and blood urea concentrations significantly lowered; (b) that in treated and untreated mice moderate to severe anaemia developed, apparently unrelated to the degree of uraemia; (c) that changes in renal function did not correlate with antinuclear antibody activity, nor did the drop in packed cell volume correlate with fixed or free circulating antierythrocyte autoantibody positivity; (d) that histological analysis of renal changes showed that at the highest dose level glomerular lesions were minimal. Thus the prolonged treatment with thiamphenicol reduced the severity of the spontaneous renal disease and resulted in a significant extension of lifespan.
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PMID:Thiamphenicol and lupus nephritis. The effects of long-term therapy on kidney function and pathology: a pilot study. 15 49

Lesions of glomerular nephropathy were found in 5 cases of acute trichinosis, characterized by a low proteinuria and hematuria as well as by moderate deficit of the renal function. Renal biopsy revealed lesions of proliferative glomerulitis, while immunofluorescence examination showed granular deposits of IgG and beta1-C-globulin on basement membranes. Serum complement was reduced. These observations suggest an immunological mechanism in the development of the glomerular nephropathy during acute trichinosis.
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PMID:Trichinous nephropathy. 15 33

Big renin, a relatively inactive renin which possesses a molecular weight larger than that of normal plasma or renal renin, has been demonstrated by gel filtration in certain human plasma, tumor extracts, and amniotic fluid. Big renin was not present in normal plasma or kidney extracts. Plasma from 3 hypertensive patients with nephropathy contained chiefly big renin. Varying proportions of both big and normal renin activity were present in plasma of other patients with hypertension and proteinuria. The renin present in amniotic fluid, which increased in activity following exposure to acid pH, was shown to be big renin in two patients. Large amounts of circulating big renin apparently can cause hypertension in patients with Wilms' tumors. Furthermore, the relatively inactive big renin may replace normal plasma renin in some patients, resulting in low plasma renin activity.
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PMID:Occurrence of big renin in human plasma, amniotic fluid and kidney extracts. 16 87

This investigation was initiated to study and correlate the clinical and ultrastructural aspects of glomerulonephritis induced in the laboratory mouse by the intraperitoneal injection of a sublethal dose of murine cytomegalovirus. An attempt was made to ascertain the pathogenesis of the glomerular changes and the resultant viremia. Murine cytomegalovirus infection caused an acute transient glomerulonephritis in young female mice of the HA/ICR strain. Mice that survived a sublethal inoculation of homogenized infected gland developed transient proteinuria and excreted tubular casts. The murine cytomegalovirus infection resulted in a glomerular lesion that was selective for the mesangial cell. After entering the mesangial cell by phagocytosis the virus replicated in the nucleus and was excreted into the channel of the mesangial matrix, with extension toward the periphery of the capillary loop and adjacent to the urinary space. Virus particles were rarely found in the glomerulus after the 5th day of infection and chronic renal disease was not observed.
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PMID:Murine cytomegalovirus glomerulonephritis: clinical and ultrastructural observations. 18 Aug 54

Glomerular epithelial slit alterations and their relation to proteinuria have not been studied in detail in New Zealand Black/White (NZB/W) mice. The kidneys of proteinuric and nonproteinuric female NZB/W mice and normal Swiss albino mice were perfusion-fixed with tannic acid-glutaraldehyde and studied by light and electron microscopy. Semiquantitative studies were performed on full montages of glomeruli enlarged 10,000 times. Fine structural alterations of the epithelial slits, with emphasis on the slit diaphragm, were studied on semiserial thin sections. Proteinuric NZB/W mice with features of membraneous nephropathy exhibited: (1) wedging of electron-dense deposits below the slit diaphragm, (2) enlargement and distortion of interpedicel spaces, (3) displacement, folding, and stacking of slit diaphragms, (4) formation of occluding junctional complexes in residual slits, and (5) variable loss of foot processes. Similar alterations were not observed in controls or nonproteinuric NZB/W mice, including animals having complexes inglomerular mesangia but not in epithlialslits. These studies show that in NZB/W mice, abnormal protein excretion is associated with structural modification of the slit pore and suggest a role for such a component in the process of protein ex
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PMID:An ultrastructural study of the glomerular slit diaphragm in New Zealand black/white mice. 18 54

Plasma proteins cross the glomerular basement membrane in inverse proportion to their molecular dimension; molecules larger than serum albumin are completely excluded from the glomerular filtrate. This filtration, which is purely passive, also depends of the electrical charge of the proteins; negatively charged proteins are indeed repelled by the negatively charged layer of sialogylcoproteins present along the outer surface of the epithelial cell membrane and extending to the glomerular basement membrane. The filtered proteins are selectively absorbed by the proximal tubular cells and are hydrolyzed by lysosomal enzymes. This results in a renal catabolism of proteins the importance of which depends on their ability to cross the glomerular barrier. In renal disease, proteinuria results either from an increased permeability of the glomerular basement membrane (selective or non-selective glomerular proteinuria) or from a diminished tubular reabsorption of normally filtered proteins of low molecular weight (tubular proteinuria).
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PMID:[Current concept of the mechanism of proteinuria]. 19 41

Nephropathy with proteinuria is an occasional complication of gold therapy for rheumatoid arthritis and is considered to be due to an immune hypersensitivity reaction. Three patients are described in whom the structural changes typical of gold nephropathy were demonstrated by electron microscopy of renal biopsies. There was early membranous glomerular nephropathy with multiple sub-epithelial deposits of immune complexes. In one case these were shown by immunofluorescence to contain IgG and complement. Proximal tubules contained characteristic dense granular intracytoplasmic gold inclusions, best demonstrated by electron microscopy of unstained sections.
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PMID:Gold nephropathy. 20 7


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