Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-three patients with chronic hereditary nephritis, obtained from 23 unrelated families, were evaluated with respect to clinicopathologic features. Renal tissue was examined by light microscopy in 25 cases, immunofluorescence in 19 cases, and electron microscopy in 16 cases. The light microscopic findings varied, and foam cells were present in only four cases. Immunofluorescence was negative in all but four cases, and in these the immunomicroscopic pattern was compatible with the findings of end stage glomeruli and hyaline arteriolar sclerosis. Although electron microscopy uniformly showed marked thinning or splitting of the glomerular basement membrane, parallel splitting of the glomerular basement membrane with interposition of electron dense granular particles was seen in only eight cases. Association of glomerular basement membrane splitting with granular particles was observed in four of six patients with IgA nephropathy, in two patients with benign familial hematuria, and in a normal kidney donor. Eleven patients, seven men and four women, had chronic renal failure requiring dialysis. Of five patients who received renal allografts, three are alive, with post-transplant survival ranging from 24 to 70 months. The other two died of septicemia.
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PMID:Chronic hereditary nephritis. A clinicopathologic study of 23 new kindreds and review of the literature. 39 12

To clarify the incidence of thin basement membrane disease (TMD) among the patients with idiopathic asymptomatic hematuria and/or proteinuria, in 217 serious renal biopsies (children 85, adults 132) were studied with clinical and morphometric analysis. TMD used is defined as follows: 1) Glomerulus in minor abnormalities; 2) GBM less than or equal to 200 nm in width, with more than 20% in total glomerular capillary surface; 3) Absence of significant immunoglobulins or complement components. Out of 217 patients 93% had either IgA nephropathy (55%), normal glomeruli (21%) or TMD (17%). TMD consisted of 22% in children and 14% in adults. Remained 15 consisted of non-IgA mesangial proliferative glomerulonephritis (6 cases), incomplete foot process disease (5), membranous nephropathy (2), membranoproliferative glomerulonephritis (1), and unclassified (1). Patients with TMD were found mostly (71%) in younger age less than 20 years old. Out of the patients with TMD, 38% had renal abnormality in the family history, but remainders were sporadic. The common urinary abnormality in TMD was microscopic hematuria occasionally with mild proteinuria (95%), while proteinuria only was rare (5%). Outcome of TMD was favorable prognosis with normal renal function. TMD was histologically divided into 2 groups; diffuse type (GBM thinning was more than 50% in the capillary surface) (19 cases; 51%), and focal type (it was less than 50%) (18 cases; 49%). The incidence of those family history was 64% and 15%, respectively (p less than 0.05). It was concluded that TMD was a popular disorder in patients with asymptomatic hematuria and/or proteinuria and it may expect 17% in incidence.
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PMID:[Thin basement membrane disease in patients with asymptomatic hematuria and/or proteinuria: a clinicopathological study]. 187 54

Thin-basement-membrane nephropathy, also called benign recurrent hematuria, is characterized by diffuse thinning of the glomerular basement membrane and by hematuria. To determine the incidence of thin-basement-membrane nephropathy among patients with idiopathic hematuria, we conducted a prospective study in the nephrology units of three large hospitals in the Netherlands. Eighty normotensive adults without azotemia underwent renal biopsy because of recurrent macroscopic hematuria (n = 26) or persistent microscopic hematuria (n = 54). Idiopathic IgA nephropathy was found in 27 of the 80 patients. Light microscopical examination showed that 42 patients had normal renal tissue. The remaining 11 patients had mesangioproliferative glomerulonephritis (n = 5), interstitial nephritis (n = 3), or focal global glomerulosclerosis (n = 3). Tissue from the 42 patients whose renal biopsy specimens were normal when examined with light microscopy was analyzed morphometrically with electron microscopy to determine the thickness of the glomerular basement membrane. Two subsets of patients were identified by this analysis. In 18, thin-basement-membrane nephropathy was found (mean basement-membrane thickness [+/- SE], 191 +/- 28 nm; normal, 350 +/- 43 nm); all but one of these 18 patients had microscopic hematuria, which persisted during follow-up (median duration, 50 months). (Of the 54 patients who presented with microscopic hematuria, 17 [31 percent] had thin-basement-membrane nephropathy.) The thickness of the glomerular basement membrane was normal in the other 24 patients (361 +/- 69 nm); during follow-up, hematuria disappeared in all 13 of these patients who had macroscopic hematuria, and hematuria resolved in 5 of the 11 patients who had microscopic hematuria. We conclude that in patients with persistent microscopic hematuria, the incidence of thin-basement-membrane nephropathy is similar to that of idiopathic IgA nephropathy. Morphometric analysis of the thickness of the glomerular basement membrane should be included in the workup of adults with persistent microscopic hematuria that is not of urologic origin.
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PMID:Thin-basement-membrane nephropathy in adults with persistent hematuria. 290 74

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

Renal biopsy specimens from 163 patients with IgA nephropathy were examined by electron microscopy to clarify the significance of gaps of the glomerular basement membrane (GBM) in IgA nephropathy. Gaps of the GBM were observed in 21 cases. In 1 case the capillary lumen was partially filled with fibrin-like materials, basement membrane-like materials, and epithelial cells, and in 6 cases wide gaps of the GBM were observed. In 10 cases the gaps of the GBM were covered by epithelial and/or endothelial cells, and in 4 cases spherical microparticles were seen at the gaps of the GBM. Microscopic hematuria of less than 5 red blood cells per high-power field of vision at the time of biopsy was less frequently observed in patients with gaps of the GBM than in patients without (p less than 0.05). Marked local thinning or splitting of the GBM and electron-dense deposits or spherical microparticles on peripheral capillary walls were more frequently observed in patients with gaps of the GBM than in those without (p less than 0.001, less than 0.005, less than 0.05, and less than 0.001, respectively).
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PMID:Ultrastructural study of gaps of the glomerular basement membrane in IgA nephropathy. 355 13

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

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

From a series of 333 renal biopsies examined by immunofluorescence microscopy, 231 specimens corresponded to primary glomerulonephritis unassociated with systemic diseases. Of those 231 biopsies, 39 had diffuse mesangial deposits of IgA (16.8%). Thirty cases of IgA nephropathy had one to several glomeruli in the Epon-embedded tissue. All cases showed mild to moderate increase of mesangial cells and matrix. Mesangial deposits were present in all cases; subendothelial (5/30), intramembranous (3/30), and subepithelial (10/30) deposits wee also found. Occasional dense granular deposits involved the basement membrane of the capsule of Bowman (1/30) and the subendothelial region of some extraglomerular arterioles (2/30). Thinning (6/30) and splitting (4/30) of the glomerular lamina densa appeared focally in some cases.
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PMID:IgA nephropathy: an ultrastructural study. 726 25

To elucidate the morphological basis of glomerular hematuria in IgA nephropathy, morphometric analysis of GBM alterations was performed by electron microscopy in 73 cases of IgA nephropathy. These cases were divided into 2 groups by the degree of hematuria. The IgA (1) groups (52 cases) showed 1-30 Red Blood Cells (RBC)/hpf in urinary sediment and the IgA (2) group (21 cases) showed 30 or more RBC/hpf. The GBM alterations were observed in 67% of IgA nephropathy patients. Splitting and focal thinning of GBM were more frequent in the IgA (2) group than in the IgA (1) group. The gap was not associated with the degree of hematuria, but when accompanying splitting, it was with the degree of hematuria. It was concluded that most IgA nephropathy patients had GBM alterations, and splitting of the lamina densa, focal thinning of GBM, and a gap with splitting, which was associated with the degree of hematuria.
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PMID:[Electron microscopy study on alterations of glomerular basement membrane in IgA nephropathy]. 823 Aug 13

We examined kidney biopsy specimens obtained from 40 adult patients with isolated hematuria to determine the renal pathology and the incidence of thin glomerular basement membrane nephropathy (TGBMN). Light microscopy showed minor glomerular abnormalities in 26 patients (65%), focal and segmental lesions in 3 patients (8%), and mild diffuse proliferative glomerulonephritis in 11 patients (28%). Immunofluorescence microscopy showed IgA nephropathy (IgA-N) in 16 patients (40%), in whom no progressive lesions were identified. We measured the glomerular basement membrane (GBM) thickness using electron microscopy, and TGBMN was identified in 4 patients (10%). Our results suggest that IgA is a major pathological finding in adult patients with isolated hematuria. GBM thinning does not appear to be a major cause of glomerular hematuria.
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PMID:Isolated hematuria in adults: IgA nephropathy is a predominant cause of hematuria compared with thin glomerular basement membrane nephropathy. 888 79


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