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1.
Cornea ; 12(5): 406-12, Sept. 1993.
Artigo em Inglês | MedCarib | ID: med-8216

RESUMO

We found corneal lesions of West Indian punctate keratopathy in 128 of 2,048 patients examined in a general eye clinic in Grenada, West Indies. Of these 125 were Black, two were Indians (Hindu), and one a White female. The lesions occured in asymptomatic persons with no history of trauma or recurrent erosions. Males were affected more than females, and older adults more than children. The condition was usually unilateral but occasionally bilateral, with one to four lesions in the intrapalpebral fissure in a paracentral location. The lesions were round, discrete, white to yellowish-gray dots 0.2-0.6 mm in size located at the level of the epithelial basement membrane and Bowman's layer. No vascularization nor other anterior membrane disorders were observed. Corneal biopsies of 11 patients were studied by histopathologic and immunoperoxidase techniques. Histopathology revealed areas of lipid positive material in Bowman's layer and adjacent corneal stroma. The epithelium showed basal cell edema, degeneration, and irregular thickening of the basement membrane. Immunoperoxidase studies did not contribute any new information about these lesions (AU)


Assuntos
Humanos , Masculino , Feminino , Doenças da Córnea/patologia , Doenças da Córnea/epidemiologia , Doenças da Córnea/etnologia , Opacidade da Córnea/epidemiologia , Opacidade da Córnea/etnologia , Substância Própria/patologia , Técnicas Imunoenzimáticas , Recém-Nascido , Pessoa de Meia-Idade , Membrana Basal/patologia , Pré-Escolar , Adulto , Idoso , Idoso de 80 Anos ou mais , Índias Ocidentais/epidemiologia
2.
West Indian med. j ; 42(suppl.2): 1, July 1993.
Artigo em Inglês | MedCarib | ID: med-5529

RESUMO

The morphological changes in both insulin-dependent and non-insulin-dependent diabetes mellitus (IDDM and NIDDM) are indistinguishable. The earliest pathological changes are enlarged glomeruli due to hypertrophy seen mainly in IDDM patients. There is also an increase in total volume of both basement membrane (BM) and capillary lumen. A second peak of glomerular hypertrophy occurs late in the disease when overt pathological changes are established. At this, many glomeruli are comprised and the open, functioning glomerulii will show a three-fold increase in size. The pathognomonic change in diabetic nephropathy is nodular glomerulosclerosis or nodular intercapillary glomerulosclerosis (Kimmelstiel-Wilson lesion) which is characterised by enlargement of mesangium due to increase in mesangial matrix. This is associated with diffuse thickening of the capillary wall which is due to increased BM material. A diffuse lesion may be considered specific after ruling out all the other causes of thickened BM, i.e. immune-complex glomerulonephritis, anti-glomerular basement membrane antibody disease, etc. The exudative and capsular drop lesions are not specific for diabetes mellitus but can be considered to be highly suggestive lesions. There is hyaline arteriolosclerosis, involving both afferent and efferent arterioles. The only pathognomonic tubular lesion (Armanni-Ebstein lesion) is a rare finding, and is found in the straight portion of the proximal convoluted tubules in which tubular cells contain glycogen. The patients with the nephropathic syndrome may show lipid-filled proximal tubules. In the late stages, there are non-specific atrophic changes with thickening of the basement membrane. There are no specific gross features of the kidney in diabetes mellitus. It may be enlarged, normal or granular contracted. The subscapular surface may either be finely or coarsely granular with focal depressed scars. The cut surface may show thinning of the cortex, loss of the corticomedullary junction and prominent blood vessels. Papillary necrosis is uncommon (AU)


Assuntos
Humanos , Diabetes Mellitus/patologia , Circulação Renal , Diabetes Mellitus Tipo 1 , Diabetes Mellitus Tipo 2 , Glomerulonefrite Membranosa/sangue , Hipertrofia , Nefropatias Diabéticas , Mesângio Glomerular , Complexo Antígeno-Anticorpo , Arteriosclerose , Membrana Basal , Necrose Papilar Renal
3.
Lancet ; 336(8729): 1472-4, Dec. 15 1990.
Artigo em Inglês | MedCarib | ID: med-15797

RESUMO

In a study of the pathogenesis of the oedema of kwashiorkor the ultrastructure of the kidneys from 6 children was examined shortly after they died from oedematous malnutrition. There was a generalised effacement of the glomerular epithelial cells onto the basement membrane. The filtration slits that remained were narrowed. The picture was similar to that seen in minimal-change nephrotic syndrome-but none of the children had albuminuria. The degree of effacement was statistically related to treatment with gentamicin. The findings suggest that there is a defect in the anionic charge of the glomerular basement membrane in oedematous malnutrition, that the membrane charge is more easily neutralised by cations such as gentamicin, and that, because proteinuria is not a feature of oedematous malnutrition, the proteinuria in other conditions associated with glomerular epithelial cell effacement (eg, minimal-change nephrotic syndrome) is due to something more complex than simple loss of charge.(AU)


Assuntos
Humanos , Lactente , Glomérulos Renais/ultraestrutura , Kwashiorkor/patologia , Membrana Basal/ultraestrutura , Edema/tratamento farmacológico , Edema/etiologia , Edema/patologia , Gentamicinas/uso terapêutico , Kwashiorkor/complicações , Kwashiorkor/tratamento farmacológico , Microscopia Eletrônica , Análise de Regressão
4.
West Indian med. j ; 37(suppl): 50, 1988.
Artigo em Inglês | MedCarib | ID: med-6575

RESUMO

In an attempt to quantify the immuno-histochemical properties of the glomerular basement membrane (GBM), monoclonal antibodies (mAbs) were prepared against heparin sulphate Proteoglycan (HSPG). The HSPG was isolated from bovine glomerulae. Enzyme-linked immuno-sorbent assays (ELISA) and immunoblotting demonstrated that the mAbs reacted with HSPG. Indirect immuno-fluorescence showed that the mAbs stained renal basement membranes (BMs) and BMs in other organs of normal bovine and human tissues in patterns typical of HSPG. Immuno-inhibition studies, and immuno-blotting of heparin lyase digested HSPG, indicated that the mAbs recognizes HSPG core protein. Human kidney biopsies revealed interesting patterns of staining for HSPG. For instance, in kidney biopsies from patients with acute post-streptococcal glomerulonephritis, intact linear staining for HSPG was noted despite abnormal pathological processes shown by widened capillary loops. On the other hand, in membranous and in diffuse proliferative lupus glomerulonephritis, loss of HSPG staining was demonstrated at sites of immuno-deposition of IgG or C3; whereas, increased staining for HSPG was seen in areas of newly formed GBM. Extensive loss of HSPG was seen in areas of glomerular sclerosis and necrosis. In biopsies from patients with minimal change glomerulonephritis and mesangio-proliferative lupus glomerulonephritis, a normal linear GBM distribution of HSPG was noted. The study demonstrates that immunological injury to the HSPG component of the GBM of the kidneys plays an aetiological role in the pathogenesis of proteinuria in man (AU)


Assuntos
Humanos , Anticorpos Monoclonais , Membrana Basal/imunologia , Rim/patologia , Proteoglicanas/imunologia , Trinidad e Tobago , Ensaio de Imunoadsorção Enzimática , Imunoensaio de Fluorescência por Polarização
5.
Clin Nephrol;4(5): 198-201, Nov. 1975.
| MedCarib | ID: med-10573

RESUMO

Membranous glomerulonephropathy with crescents. A case is reported in which typical histological features of idiopathic membranous glomerulonephropathy co-existed with atypical glomeruli showing cellular epithelial crescents in addition to diffuse basement-membrane thickening. These features were seen in a renal biopsy specimen taken during rapidly progressive deterioration of renal function in a patient previously known to have mild ankle edema for four years


Assuntos
Humanos , Pessoa de Meia-Idade , Feminino , Glomérulos Renais/patologia , Glomerulonefrite/patologia , Membrana Basal/ultraestrutura , Epitélio/citologia , Epitélio/patologia , Epitélio/ultraestrutura , Glomérulos Renais/ultraestrutura
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