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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ultrastructural alterations of glomerular anionic sites were studied in biopsy specimens from 34 patients with IgA nephropathy using polyethyleneimine (PEI). Prominent common findings in the glomeruli of the patients were few PEI particles in electron dense deposits in the mesangial and subepithelial area and marked reduction in glomerular anionic sites covered with deposits. The anionic sites of the glomerular basement membrane (GBM) and epithelial cell surface coat (ESC) appeared unaltered in the patients with hematuria and/or mild proteinuria. But in patients with proteinuria in the nephrotic range, focally discrete loss of anionic sites in the lamina rara externa (LRE) was seen and the number of anionic sites of the ESC were decreased with retraction of the foot processes. The anionic sites of the lamina rara interna showed much less change in these patients. Subepithelial deposits were often seen concomitantly with focal loss of anionic sites in the LRE at the site of the deposits, but subendothelial deposits had little influence on the anionic sites of the neighboring GBM. The anionic sites of GBM that showed focal thinning with small GBM projections were appreciably decreased in number, but those in split GBM were not decreased. These results suggest that either loss of the negative charge on the glomerular capillary wall associated with subepithelial immune deposition or morphological changes of the GBM contribute to the progression of proteinuria in IgA nephropathy.
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PMID:Ultrastructural alterations of glomerular anionic sites in IgA nephropathy. 292 Apr 73

To elucidate the morphological basis of glomerular haematuria, morphometric analysis of the glomerular basement membrane (GBM) and lamina densa (LD) was performed on silver impregnated samples for electron microscopy. The cases studied consisted of 3 groups: group A, normal controls, being from donors for kidney transplantation; group B, haematuric; and group C, non-haematuric cases with isolated proteinuria. Qualitative analysis revealed that gap formation, splitting, segmental and diffuse thinning of the GBM occur preferentially in haematuric cases. The morphometry of the GBM and LD yielded increased mean values of the GBM and of LD thickness in groups B and C. The coefficient of variation (CV, SD/mean) for the GBM and LD, however, was the highest in group B among the 3 groups, suggesting the most irregular GBM and LD in group B. In addition, CV was significantly higher in cases with splitting, segmental attenuation and gap of the GBM than cases without. The findings suggest that the irregularity of the GBM rather than its mean thickness is clearly associated with splitting and ultimately with haematuria via the gaps produced.
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PMID:Alterations of glomerular basement membrane relevant to haematuria. 313 75

Recently the appearance of deformed polymorphous erythrocytes in the urinary sediment has been described as characteristic of glomerular bleeding. We studied 30 patients with histologically confirmed glomerular disorders and 25 patients with urological diseases and with hematuria. In the sediment of 10 ml urine 200 erythrocytes were counted under phase-contrast microscopy and evaluated relative to their morphology. The number of glomerular erythrocytes was expressed as a percentage. In all groups of glomerular disorders (mesangial-proliferative, membranous and membrano-proliferative glomerulonephritis, focal segmental glomerulosclerosis, glomerulonephritis of systemic disease, thinning of the glomerular basement membrane) the percentage of glomerular erythrocytes varied widely between 2 and 100%. In 7 cases less than 10% of glomerular erythrocytes were found. There was no correlation between the percentage of glomerular erythrocytes and the degree of renal insufficiency, hematuria or proteinuria. On the other hand, in patients with hematuria from the lower urinary tract, erythrocytes were uniformly non-glomerular in shape (95-100%). We conclude that 10-20% or more of glomerular erythrocytes in the urinary sediment are a good indicator of glomerular disease, whereas lower figures do not definitely rule out a glomerular origin for hematuria.
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PMID:[Diagnosis of glomerular and non-glomerular erythrocyturia using phase contrast microscopy of the urine sediment]. 331 Feb 12

Eight (two men, six women) cases of adult thin basement membrane syndrome were studied to clarify the clinicopathological characteristics of the disease. The average age at the time of biopsy was 40 years. All the patients had persistent microscopic haematuria, normal renal function, and normal blood pressure, with the exception of one who was hypotensive. Most of them had persistent or transient proteinuria. Renal symptoms were found in four families, although no relative had Alport's syndrome. Renal biopsy findings observed by light and immunofluorescence microscopy did not indicate any important abnormalities, but extensive diffuse thinning of the glomerular basement membrane, ranging from 153 to 213 nm, was a constant finding by electron microscopy. All the patients retained stable renal function at the time of final follow up, indicating a benign prognosis of the syndrome.
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PMID:Thin basement membrane syndrome in adults. 355 66

Peripheral glomerular capillary walls were studied in 26 cases of IgA nephropathy by means of the transmission electron microscope. Ultrastructural abnormalities were identified in 11 cases (42%). Abnormalities of the glomerular basement membrane (GBM) were the most frequent change which consisted of localized thinning, lamination, irregular thickening, disruption, membranolysis and aneurysmal dilatation of the GBM. Subendothelial electron dense deposits were seen. Necrosis and detachment of the podocytes from the GBM were also encountered. The changes were correlated with the clinical findings at the time of diagnosis which showed a significant correlation of these peripheral glomerular capillary wall lesions with proteinuria. With light microscopy, crescents were significantly more frequently seen in the cases showing the ultrastructural capillary wall abnormalities than those without. This observation suggested that local peripheral glomerular capillary wall damage was an important factor in the pathogenesis of the extracapillary lesions in IgA nephropathy.
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PMID:Peripheral glomerular capillary wall lesions in IgA nephropathy and their implications. 639 13

Six hundred and twenty-five patients with diabetes mellitus were studied by standardised clinical methods, resting and exercise electrocardiography (ECG) and digitised echocardiography to determine the prevalence of coronary and non-coronary heart disease. Clinical evidence of coronary artery disease (angina and infarction) was present in 110 (18 per cent) normotensive patients. Hypertension (blood pressure greater than 165/95 mmHg) was present in 172 (27 per cent) of whom 32 had cardiac symptoms. Heart failure or left ventricular dilatation was seen in 18 of whom 11 had either hypertension or coronary artery disease and six asymptomatic patients had unexplained ventricular hypertrophy. Echocardiograms in 245 of 290 asymptomatic patients with normal ECG showed that relaxation was prolonged (p less than 0.001) and mitral valve opening delayed (p less than 0.001) from normal especially in those with severe microangiopathy (proliferative retinopathy and/or heavy proteinuria). The peak rates of cavity dimension increase and posterior wall thinning were reduced from normal (both p less than 0.001) and patients with severe microangiopathy had the most marked changes. Redivision of these 245 diabetics by abnormalities of left ventricular function showed that 147 had normal function in whom only one of 23 (random 15 per cent sample) had a positive exercise ECG. Prolonged relaxation or delayed mitral valve opening alone (a nonspecific abnormality) was present in 41 and only three of 28 had a positive exercise ECG. Thirty-one had delayed mitral valve opening with inco-ordinate relaxation (abnormalities very suggestive of coronary artery disease) of whom 20 of 29 had a positive exercise ECG. Twenty-six had delayed mitral valve opening with slow cavity dimension increase or wall thinning (without hypertrophy) of whom 21 of 25 had a negative exercise ECG. This is a relatively specific abnormality similar to that found in left ventricular hypertrophy. Coronary artery disease is common in symptomatic and asymptomatic forms in diabetes mellitus. Non-coronary left ventricular diseases, such as dilation and hypertrophy, are probably no more common in diabetics than non-diabetics. A small number of diabetics with severe microangiopathy had abnormal relaxation and reduced peak rate of dimension increase or wall thinning which may represent left ventricular disease due to microangiopathy.
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PMID:A prospective study of heart disease in diabetes mellitus. 670 23

Previous reviews of hematuria in children and adolescents have included patients with proteinuria and other renal functional abnormalities such as hypertension and reduced GFR. We report the clinico-pathological correlations in 76 pediatric patients, aged 3 to 19 years, who underwent a renal biopsy because of isolated hematuria during the 10-year period, 1972 to 1981. All specimens were examined by light and electron microscopy and immunofluorescence techniques. The overall prevalence of abnormal renal histology was 56%. The vast majority (41 of 43) of the abnormal biopsy specimens could be classified into four distinct histological categories: (1) Alport syndrome (N = 9); (2) IgA nephropathy (N = 8); (3) thinning of the glomerular basement membrane (N = 17); (4) vascular C3 staining (N = 7). The children were divided into three clinical subgroups (1) isolated microscopic hematuria ( IMH ), N = 42; (2) IMH plus a family history of hematuria in a first degree relative, N = 15; and (3) IMH plus at least one episode of gross hematuria, N = 19. A significant graded increase in the likelihood of obtaining an abnormal renal biopsy was demonstrated (X2 = 10, P less than 0.007) from groups one to three. Sex, age at onset, or duration of hematuria were not associated with an increased proportion of histopathologic abnormalities. These findings indicate that the yield of a renal biopsy in children with isolated hematuria can be predicted accurately from specific clinical characteristics.
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PMID:Isolated hematuria in children: indications for a renal biopsy. 672 31

In 32 patients from 27 families affected with hereditary neophropathy (Alport syndrome) the glomerular basement membranes were examined electron microscopically and the percentage of characteristically split and thin basement membrane portions was determined. The clinical course was more severe in males which corresponded with a higher rate of basement membrane alterations: on an average in males 61% split and 6% thin but only 18% split and 21% thin in females. The splitting lesion increased with age in males but not so in females. There were also indications for a possible positive correlation of the splitting lesion and the grade of proteinuria. Compared with the splitting lesion basement membrane thinning seemed to be of minor importance.
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PMID:Hereditary nephropathy (Alport syndrome): correlation of clinical data with glomerular basement membrane alterations. 739 44

Long-term study of 21 PNH patients revealed an unexpectedly high incidence of functional and anatomic renal abnormalities. Most patients demonstrated varying degrees of hematuria and proteinuria distinct from hemoglobinuria. Evaluation of renal function revealed hyposthenuria, abnormal tubular function, and declining creatinine clearance. Radiologically these patients had enlarged kidneys, cortical infarcts, cortical thinning, and papillary necrosis which were confirmed by autopsy studies. Hypertension developed in eight patients. Urinary tract infection was uncommon. The renal findings bear striking similarity to those of sickle cell anemia. Contrary to the usual opinion, out studies clearly showed evidence of widespread renal pathology in PNH most likely due to repeated microvascular thrombosis similar to the venous thrombosis involving other organs in this disorder.
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PMID:The kidneys in paroxysmal nocturnal hemoglobinuria. 744 17

We measured the thickness of the glomerular basement membrane (GBM) in 48 rheumatoid arthritis (RA) patients with proteinuria and/or hematuria and studied its relationship to clinical features of RA. Ten cases with minor glomerular abnormalities, renal cancer, donor of renal transplantation, were studied as controls. Secondary glomerular diseases and hereditary thin basement membrane disease (TBMD) were excluded. Mean GBM thickness was 289 +/- 74 nm (mean +/- SD) in RA patients, which was significantly thinner than that of control group (342 +/- 38 nm) (p < 0.01). Mean GBM thickness were 276 +/- 72 nm and 336 +/- 68 nm in RA patients with and without gold sodium thiomalate (GST) treatment, respectively (p < 0.05). Mean GBM thickness of RA patients without GST and controls were not different statistically, but RA patients with GST had significantly thinner GBM, compared with controls (p < 0.01). The mean thickness of GBM were also 274 +/- 69 nm and 344 +/- 72 nm in RA patients with and without hematuria, respectively (p < 0.01). According to these results, we suspect that the thinning of GBM in RA patients may be related to GST treatment.
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PMID:An ultrastructural study of glomerular basement membrane in rheumatoid arthritis patients with urinary abnormalities. 755 19


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