Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute aortic thrombosis associated with spinal cord infarction in a 47-year-old man with nephrotic syndrome is described. He was admitted to our hospital presenting with the nephrotic syndrome. Renal biopsy revealed mild mesangial proliferative glomerulonephritis. The urinary protein excretion rate transiently decreased after the start of treatment with prednisolone, but it increased again and was followed by the development of the signs and symptoms of spinal cord infarction, which was diagnosed by magnetic resonance signal abnormalities, and then symptoms of ischemia in the lower limbs. Digital subtraction angiography revealed an obstruction at the bifurcation of the abdominal aorta. Emergency thrombectomy was performed, and the arterial blood flow was reestablished. Laboratory data on the fibrinocoagulation system showed a hypercoagulable state. In this case, fibrinocoagulation abnormalities due to the nephrotic syndrome led to the hypercoagulable state, and dehydration might have triggered the thrombotic complication.
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PMID:Acute aortic thrombosis associated with spinal cord infarction in nephrotic syndrome. 139 31

Seventy donor kidneys for transplant were studied with light microscopy (LM), electron microscopy (EM) and immunofluorescence (IM) for C3, C4, Clq, IgG, IgA, IgE, IgM, and antifibrin; the samples were taken just before transplanting the allograft kidney. Glomerular changes were found in 35.7% of apparently normal living donors: 9 cases showed relative glomerular ischemia with an irregular basal membrane (12.9%); 5 cases showed a diffusely widened basal membrane without antecedents of hyperglycemia (7.1%); in one case (1.4%) there was a lesion similar to type 1 mesangio-capillary glomerulonephritis with C3++, IgG++, IgA+, and IgM+; in another case (1.4%) there were scant isolated C3 glomerular, subepithelial deposits with indentation of the basement membrane of the immunocomplex type with a microhematuria which was demonstrated only after donation, and in 9 cases (among them two pairs of siblings) there were mesangial IgA and mesangial electron-dense deposits compatible with Berger's disease (12.9%). None of these glomerulopathies were evident under LM.
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PMID:Morphological findings in 70 kidneys of living donors for renal transplant. 214 95

A 3-year-old child with minimal change nephrotic syndrome (MCNS) developed an acute hypertensive encephalopathy characterized by coma, focal seizures, right hemiparesis, global aphasia and cortical blindness. Episodic hypertension and seizures persisted for 24 h despite intervention with antihypertensive and anticonvulsant therapy. Clinical suspicion of cortical blindness was confirmed by visual-evoked potential studies. CT scans performed 14 and 21 days after the acute episode demonstrated symmetric occipital white matter lucencies compatible with ischemia and/or associated edema. Hypertensive encephalopathy with cortical blindness and symmetric white matter hypodense lesions visualized on CT scan have recently also been described in eclampsia of pregnancy. This report documents an unusual acute hypertensive encephalopathy in childhood MCNS, unassociated with membranoproliferative glomerulonephritis, or progressive focal glomerulosclerosis.
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PMID:Acute hypertensive encephalopathy in minimal change nephrotic syndrome. 225 60

Samples from 103 kidneys donated for transplant were studied under light microscopy (LM), electron microscopy (EM) and immunofluorescence (IM, with C3, C4, C1q, IgG, IgA, IGE, IgM and antifibrin) just before transplantation. Seven kidneys were obtained from a cadaver (CK). Glomerular damage attributed to perfusion (perfusion glomerulopathy) was present in 4 cases. Glomerular changes in apparently healthy donors were present in 33% of cases: minor glomerular lesions, such as type I collagen fibers in the mesangial matrix (3 cases); uniform widening of the basal membrane without prior evidence of diabetes (4); relative glomerular ischemia with basal membrane irregularities (9). Major lesions were found in 17.5% of kidneys: IgA mesangial deposits compatible with Berger's disease (9, including 2 pairs of siblings); dense mesangial deposits suggesting the same process (6); subacute bacterial endocarditis glomerulopathy with IgG++, C1q+ and IgM+ (1, a CK); a type I mesangio-capillary glomerulonephritis with C3++, IgG++, IgA+ and IgM+ (1); subpedicelar and transmembranous isolated glomerular deposits of the immune complex type (1, complicated with microhematuria after donation). None of these glomerulopathies was demonstrated by LM, hence the use of EM and IM is essential for diagnosis.
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PMID:[A morphologic study of 103 kidneys donated for renal transplantation]. 251 71

To evaluate the influence of hypertension on human glomerulonephritis, 200 biopsies from 74 patients with Iga nephropathy were examined. Chosen for this study were 28 hypertensive patients and 46 normotensive subjects during an observation period of 3.84 +/- 2.17 years, which extended from the first to the last biopsy. In a comprehensive analysis, the following findings were observed: Glomerular sclerosis was analyzed semiquantitatively and estimated as "glomerular index" (GI). Interstitial volume (IV) was determined by the point-counting method. Mesangial electron dense deposits (MDD) and arteriolar hyaline change (HC) were also analyzed semiquantitatively. Arterial fibroelastic intimal thickening was analyzed morphometrically and estimated as the luminal "occlusive rate" (OR). These morphological parameters including their serial changes were compared between the hypertensives and the normotensives. The serial changes in GI and IV from the first to the last biopsy were significantly greater in the hypertensives than in the normotensives. Both OR and HC, including their serial changes, were significantly higher in the hypertensive subjects. In the study of MDD and its serial changes, no difference was apparent between the two groups. In the study of OR and HC, there was no correlation observed with GI. Our observations show that hypertension accelerates the progression of both glomerular and vascular sclerosis in case of human glomerulonephritis and suggests that this acceleration cannot only be explained by ischemia-related factors resulting from vascular sclerosis.
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PMID:Hypertension-related aggravation of Iga nephropathy: a statistical approach. 321 69

The renal allograft is host to a number of injuries and all its structural components are prone to damage. The glomeruli respond to these varied stimuli in many ways. The fibrinoid necrosis, thrombosis, and polymorphonuclear cell exudation that accompany hyperacute or accelerated rejection are well-recognized. The transplant may also be afflicted by forms of de novo or recurrent glomerulonephritis. Apart from these, there are other patterns of reaction. The mesangium is often the site of a rapidly reversible change; it expands readily. Arterial changes initiate ischemia and collapse of glomerular capillary spaces. Glomerulitis accompanies cases of acute rejection, but when seen as a predominant feature, usually antedates chronic rejection. Heavy proteinuria may be associated with profound alterations in the peripheral capillary basal lamina including irregular thickening, interposition of mesangial cell cytoplasm, and lamellation. Allografts with these glomerular changes eventually fail.
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PMID:Glomerular changes in renal allografts. 351 May 33

An epidemic of nephritis occurred among soldiers in World War I, predominantly those in the trenches. Characterized by the sudden onset of albuminuria, hypertension, edema, and dyspnea, atypical features such as bronchitis, an evanescent course, low early mortality, and frequent relapses distinguished it from poststreptococcal glomerulonephritis. Pathologic features included glomerular ischemia, capillary thrombi, endocapillary proliferation, and frequently epithelial crescents, suggesting an underlying vasculitis. The cause was not established, but a postinfectious, possibly postviral, etiology seems most plausible. Trench nephritis was the major nephrologic problem of World War I, accounting for 5% of medical admissions and more than 10% of military hospital bed occupancy at that time.
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PMID:Trench nephritis: a retrospective perception. 351 20

The glomerular ultrastructure was retrospectively reviewed from 45 renal transplant biopsies with the clinical and light microscopic diagnosis of acute rejection (25 cases) and chronic rejection (20 cases). Three grades of morphologic alteration were ultrastructurally defined. In acute rejection, capillary lumenal obliteration with endothelial cell hypertrophy and cellular infiltration were interpreted as the local glomerular expression of the endothelial vascular alterations of acute humoral rejection and were correlated with a poor graft survival. Graft nephrectomy was necessary in 9 of 11 patients with grade III glomerulopathy. In chronic rejection, thickened basement membranes and increased amount of mesangial matrix were considered the result of ischemia. The degree of ultrastructural glomerular alterations in chronic rejection did not correlate with graft survival. Urine protein values were consistently elevated, although poorly correlated with the severity of glomerular alterations. Recurrent glomerulonephritis was not documented in any case. We concluded that the glomerular alteration in acute rejection is a component of acute humoral rejection and that the degree of glomerulopathy in acute rejection is a good predictor of the graft survival.
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PMID:Glomerulopathy in acute and chronic rejection: relationship of ultrastructure to graft survival. 635 20

In this analysis of 43 patients with IgA nephropathy, renal morphology was correlated with clinical data. Gross hematuria and mild proteinuria were typical among younger patients. Among older individuals the clinical spectrum was wider. A comparison with data previously obtained from the normal population indicated that disease-related glomerular sclerosis was present in 1/3 of initial biopsy specimens. The prevalent pattern of glomerular sclerosis was that of global tuft collapse, the type of sclerosis known to result from ischemia. Intrarenal vascular sclerosis was present in 1/3 of initial biopsies. Follow-up specimens from 6 patients showed progression of glomerular sclerosis, vascular sclerosis or both. Hypertension occurred in over 1/4 of patients. It is proposed that progressive renal damage in IgA nephropathy may not be solely immunologically mediated. Glomerular sclerosis may also be mediated by vascular sclerosis, or alterations in intrarenal hemodynamics in glomerulonephritis may have a direct damaging effect on both the glomerulus and the intrarenal vasculature.
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PMID:Intrarenal vascular sclerosis in IgA nephropathy. 714 32

A comparison has been made of the percentage of sclerotic glomeruli found in normal subjects and in 31 patients 6 months to 15 years after an episode of acute poststreptococcal glomerulonephritis (PSGN). The findings establish that a greater than expected incidence of glomerular sclerosis occurs in the course of PSGN. The pattern of glomerular sclerosis frequently was that of contracted collapsed tufts, one known to result from ischemia. In the majority of specimens with significant glomerular sclerosis, there was co-existent vascular sclerosis (arterioles and/or prearterioles), and the incidence of both glomerular and vascular sclerosis increased with time from onset of PSGN. Intrarenal vascular sclerosis may thus be of major importance in the genesis and progression of glomerular sclerosis in PSGN.
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PMID:Role of intrarenal vascular sclerosis in progression of poststreptococcal glomerulonephritis. 736 16


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