Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To discover the biochemical alterations occurring in the first 24 hours of acute pancreatitis (PA), we made an experimental study using rats. We used 90 animals in which necrosis and hemorrhage were induced by closing the choledochus. Animals underwent evolutive periods of 1, 2, 3, 4, 5, 6, 12, 18 and 24 hours. They were sacrificed and plasma (to determine amylase, lipase, creatinine and calcium), urine (amylase and creatinine), ascitic and pleural liquid (amylase and lipase) were obtained from 6 animals of each evolutive period. We made a post-mortem study of the pancreas of three animals of each subgroup. There was a significant increase in the amylasemia from the third hour (p less than 0.005) and of plasmatic lipase from the first hour (p less than 0.0001). Creatinine values remained in normal range and calcemia fell after the sixth hour (p less than 0.001). There was an increase in amylase concentration in urine and in ascitic and pleural liquids, and of the lipase in the last two. These changes correlated with the duration of the disease and with the histologic changes of the gland, which consist in edema, acinar necrosis, vasculitis and hemorrhage, which are present from the first hour and increase as time passes.
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PMID:[Biochemical and functional changes in experimental acute pancreatitis in the rat]. 248 Jun 23

In this retrospective study, we analyzed clinical laboratory, and pathologic variables to determine their value in predicting survival and survival free of renal failure for 170 consecutive patients with idiopathic renal vasculitis and glomerulonephritis evaluated during a 15 year period. Of the 170 patients, 108 had focal segmental necrotizing glomerulonephritis alone (FSNGN), 33 had FSNGN and small-artery vasculitis, and 29 had FSNGN and medium-sized artery vasculitis. Considerable overlap of clinical, laboratory, and pathologic findings existed among the three groups. Overall patient survival was 81% at one year, 61% at five years, and 44% at ten years, significantly less than expected survival. Overall survival free of renal failure, by definition, was lower than patient survival. There were no differences among these three groups in patient survival or survival free of renal failure. Multivariate analysis identified leukocytosis and serum creatinine level as independent predictors of patient survival and survival free of renal failure. In addition, univariate analysis identified age and hypertension as significant risk factors but did not add independent predictive value for these two end points. In patients with serum creatinine levels less than 4 mg/dl, the effect of increasing levels of leukocyte count was significantly associated with poorer outcomes for both patient survival (P = 0.006) and survival free of renal failure (P = 0.024). Outcomes for these two end points were worse for patients with lower serum creatinine levels (less than 4.0 mg/dl) and high leukocyte counts (greater than 16,000/mm3) than for those with serum creatinine levels greater than or equal to 4.0 mg/dl.
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PMID:Risk factors in idiopathic renal vasculitis and glomerulonephritis. 260 Dec 60

The prognostic markers in 87 consecutive patients with lupus nephritis who underwent renal biopsy are reported for five clinically relevant long-term outcomes--renal insufficiency, renal failure, death due to renal systemic lupus erythematosus, death due to non-renal SLE and death due to SLE, both renal and non-renal. We have demonstrated that a number of previously neglected or rarely studied predictors were important prognostic markers. These included the duration of renal disease before biopsy, overall severity of SLE, as well as the presence of vasculitis, hypertension or a comorbid ailment. Furthermore, the study confirms the predictive importance of serum creatinine, 24-h urinary excretion of protein, C3, and of the activity and chronicity indices on biopsy. However, overall a simple measure of tubulointerstitial disease was the best predictor obtained from biopsy. Prognostic models based on clinical data alone were developed for each of the five outcomes. The models amplify our clinical understanding of lupus nephritis. Markers of renal severity were most important in predicting renal outcomes such as renal insufficiency and renal failure. Prognostic factors less directly related to renal disease (comorbidity and vasculitis) were important predictors of fatality. A marker of immunologic disease activity (C3) was a valuable predictor for many of the outcomes. Thus markers of disease severity reflecting organ damage due to SLE and other comorbid conditions could be combined with markers of immunologic activity to predict a variety of outcomes of relevance to a clinician. When biopsy data obtained by light or electron microscopy were evaluated for their ability to add new predictive information to the clinical models, only a limited value for biopsy was noted. It is likely that this reflected the close correlational relationships between clinical and biopsy variables, the strong clinical models generated, and the inclusion in the clinical models of the previously neglected clinical variables, duration of renal disease before biopsy and the presence of vasculitis or comorbid disease.
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PMID:The clinical and renal biopsy predictors of long-term outcome in lupus nephritis: a study of 87 patients and review of the literature. 269 9

Twenty five patients with renal vasculitis presenting over an eight year period were reviewed. Ten had microscopic polyarteritis, 6 classic polyarteritis, 5 overlap syndrome, 2 Churg-Strauss syndrome and 2 Wegener's granulomatosis. Clinical features included hypertension, pulmonary involvement, neurological involvement and arthralgia. Serum creatinine was over 500 umol/l in 13 patients, 10 of whom required dialysis. Visceral angiography was positive in 80% of those studied, Focal and segmental necrotising glomerulonephritis was the commonest renal lesion. Treatment consisted of corticosteroids and cytotoxic agents in most cases. Plasmapheresis was used for rapidly progressive renal failure, severe pulmonary haemorrhage or cerebral vasculitis. Improvement or stabilisation of renal function was seen in 68% of patients treated. There were 4 early deaths and one late death. The diagnosis, histology, treatment and outcome of renal vasculitis is discussed. The importance of early diagnosis and treatment is emphasised in this potentially reversible cause of acute renal failure.
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PMID:Systemic vasculitis with renal involvement--a review. 269 9

Camostat mesilate, a developed derivative of gabexate mesilate for oral use, was administered in a daily dose of 600 mg for 4 weeks to 17 patients with heavy proteinuria due to various nephropathies. Five patients had glomerulonephritis (3 patients with IgA nephropathy, one each with membranoproliferative GN and membranous nephropathy) and 3 had systemic vasculitis. These patients had been treated with glucocorticoid, cyclophosphamide, anticoagulants, and dipyridamole. Five patients had diabetic nephropathy and had been treated with conventional therapy including angiotensin converting enzyme inhibitors. Two cases with benign nephrosclerosis, one with Alport syndrome, and the rest with end-stage renal failure of undetermined cause were also included in this study. Urinary protein decreased promptly within 2 weeks (from 5.2 +/- 0.7 to 3.5 +/- 0.5, mean +/- SE, p less than 0.005), and serum total protein and albumin levels increased significantly. Serum creatinine levels did not change. Decreases in urinary protein excretion of more than 50% were observed in five out of eight patients with glomerulonephritis or systemic vasculitis, two out of five with diabetic nephropathy, and one with chronic renal failure. However, urinary protein excretion values remained at the same level in two patients with benign nephrosclerosis and a patient with Alport syndrome. We suggest that camostat mesilate caused a change in glomerular capillary permeability for macromolecules through its inhibitory effects on the kallikrein-kinin system, complement system, coagulation system, and platelet function, which contributed to the treatment of the various nephropathies.
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PMID:Effect of camostat mesilate on heavy proteinuria in various nephropathies. 279 62

In the last 10 years we have evaluated 63 patients with acute crescentic rapidly progressive glomerulonephritis (AC-RPGN), 46 of whom received pulse methylprednisolone (PM). The groups consisted of patients with no immune deposits, immune complexes, vasculitis, and antiglomerular basement membrane (anti-GBM) disease. Seventy-nine percent of non-anti-GBM patients improved versus 25% of unpulsed, p less than 0.005; 70% stopped dialysis (D) versus none of unpulsed, p less than 0.009; creatinine decreased from 8.6 before to 2.7 mg/dl after PM, p less than 0.05. Percent crescents and oligoanuria did not influence PM results, but did with conventional therapy (prednisone, cytotoxics, anticoagulants, supportive treatment). Seventeen percent of anti-GBM patients improved, none stopped D. In anti-GBM patients, serum creatinine less than 6 mg/dl was associated with a favorable response to PM, p = 0.045. Twenty-one percent of responding patients lost function at 19.8 months. The long-term response for non-anti-GBM patients was 62%. Patients with low chronicity on biopsy had shorter duration of disease (p = 0.006) and 92% initial, 85% long-term improvement; those with high chronicity had an immediate 71%, and 36% long-term response rate, p less than 0.02. Thus, PM is effective and appears superior to conventional therapy in treatment of non-anti-GBM AC-RPGN.
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PMID:Methylprednisolone therapy for acute crescentic rapidly progressive glomerulonephritis. 280 84

Renal biopsies from 50 patients with segmental necrotizing glomerulonephritis (SNGN) were divided into three groups on the basis of initial clinical information: (group A) Wegener's granulomatosis (WG)--14 patients; (group B) SNGN without renal vasculitis (RV)--21 patients; and (group C) SNGN with RV--15 patients. Renal biopsy findings did not distinguish the SNGN in WG from non-WG patients. However, focal endocapillary proliferation was more common in non-WG groups B (48%) and C (33%) than in WG (7%). In addition, GBM deposits of both IgG and C3 were present in 35% of biopsies in group B and 33% in group C in comparison to only 7% in WG. Glomerular fibrin deposition was common in all groups (54% group A, 70% group B, and 100% group C), suggesting that coagulation plays a role in the development of SNGN. Histologic parameters of severity and chronicity of the SNGN were inconsistent predictors of outcome, although an increased percentage of crescents in the non-WG groups correlated with a poorer prognosis. Chronic renal failure developed in 46% of group A patients, 65% group B, and 73% group C. After clinical follow-up, 15 patients had WG, 15 patients had documented or suspected systemic vasculitis (SV), and idiopathic SNGN was present in 20 patients. Sixty-six percent of patients with SV had RV, and 62% of biopsies with RV were from patients with SV. Chronic renal failure developed in 78% of patients with idiopathic SNGN and 57% patients with SV. These findings confirm that SNGN carries a poor prognosis, independent of its association with WG or SV. Fourteen of the 15 WG patients were treated with alkylating agents, and the development of chronic renal failure appeared to be related to delays in diagnosis and therapy. In the non-WG groups, presentation in acute renal failure with high serum creatinine and long duration of symptoms was predictive of development of chronic renal failure. Therapy in the non-WG patients consisted of alkylating agents (seven patients), steroids (20 patients), and dialysis only (seven patients). The seven non-WG patients treated with alkylating agents had clinical responses similar to WG patients, and cyclophosphamide therapy appeared to be most beneficial to patient outcome. Results of this retrospective study stress the importance of early diagnosis and, although based on small numbers of patients, suggest that aggressive chemotherapy should be recommended for SNGN, independent of its association with biopsy-proven WG or documented SV.
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PMID:Segmental necrotizing glomerulonephritis: diagnostic, prognostic, and therapeutic significance. 286 53

This study supports the concept that primary necrotizing and crescentic glomerulonephritis is a kidney-limited form of polyarteritis nodosa. Thirty-four patients with necrotizing and crescentic glomerulonephritis were divided into three groups based on the presence or absence of systemic vasculitis as determined by clinical or histologic criteria. Laboratory studies demonstrated elevated erythrocyte sedimentation rates, anemia, mild eosinophilia, hematuria, and proteinuria in patients in each group; there were no significant differences in these data between the groups, however. Complement levels and antinuclear antibody screens were normal. Mean serum creatinine levels were markedly elevated but fell by a factor of two following therapy. There was a higher morbidity in the patients with kidney-limited disease. This was attributable to a higher percentage of these patients' having no symptoms and presenting for medical care only after they were in chronic renal failure. Most patients not experiencing chronic renal failure were treated with cyclophosphamide and prednisone, which seemed effective in this retrospective study.
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PMID:Clinical and pathologic features of polyarteritis nodosa and its renal-limited variant: primary crescentic and necrotizing glomerulonephritis. 288 Jul 91

To evaluate the diagnostic usefulness of gallium 67 scintigraphy in glomerular disease, 45 patients with various glomerulopathies, excluding lupus nephritis and renal vasculitis, were studied. Persistent renal visualization 48 hours after the gallium injection, a positive scintigram, was graded as + (less than), ++ (equal to), and +++ (greater than) the hepatic uptake. Positive scintigrams were seen in ten of 16 cases of focal segmental glomerulosclerosis, six of 11 cases of proliferative glomerulonephritis, and one case of minimal change, and one of two cases of membranous nephropathy; also in three of six cases of sickle glomerulopathy, two cases of diabetic neuropathy, one of two cases of amyloidosis, and one case of mild chronic allograft rejection. The 25 patients with positive scans were younger than the 20 with negative scans (31 +/- 12 v 42 +/- 17 years; P less than 0.01), and exhibited greater proteinuria (8.19 +/- 7.96 v 2.9 +/- 2.3 S/d; P less than 0.01) and lower serum creatinine values (2 +/- 2 v 4.1 +/- 2.8 mg/dL; P less than 0.01). The amount of proteinuria correlated directly with the intensity grade of the gallium image (P less than 0.02), but there was no correlation between the biopsy diagnosis and the outcome of the gallium scan. It was concluded that gallium scintigraphy is not useful in the differential diagnosis of the glomerular diseases under discussion. Younger patients with good renal function and heavy proteinuria are likely to have a positive renal scintigram regardless of the underlying glomerulopathy.
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PMID:Gallium 67 scintigraphy in glomerular disease. 319 76

We phenotyped with monoclonal antibodies (MAb) the cellular infiltrates in kidneys of patients with rapidly progressive glomerulonephritis (RPGN) responsive (R) or nonresponsive (NR) to pulse methylprednisolone therapy (PM)-eight anti-GBM, six no immune deposits, three immune complex, two vasculitis, and one proliferative GN. There were glomerular, periglomerular, crescentic, and interstitial T and T-cell subsets. Few interstitial and no glomerular B and NK cells were observed. TH cells were much more common than TS. Phenotypes were quantitatively evaluated in 221 nephritic and 32 control glomeruli. T and/or TH cells were positively correlated with M phi, r = 0.30 to 0.74, P less than 0.05 to 0.0005. Although differences in phenotypes were observed, these differences were insufficient to distinguish between subtypes. Analysis of R and NR revealed no relationship to percent crescents, entry serum creatinine, oliguria, or need for dialysis. NR was related to presence of anti-GBM disease, P = 0.001, as was ability to stop dialysis, 0 of 7 GBM versus 9 of 10 other, P less than 0.001. Mild infiltrates of lymphocytes and M phi correlated with R, P less than or equal to 0.02. R had fewer numbers of TH and M phi in glomeruli, P = 0.0001, in crescents, P less than 0.02, and total TH and M phi compared to NR, P less than 0.001. Crescentic and total TH/S ratios were lower in NR than R, P less than 0.05. These findings demonstrate that components of the cell-mediated immune (CMI) system are present by MAb analysis, that subtypes cannot be differentiated by CMI constitution, and R to PM is related to intensity and composition of CMI involvement. Independence of the CMI system relative to anti-GBM disease remains to be clarified.
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PMID:T-cells and macrophages in rapidly progressive glomerulonephritis: clinicopathologic correlations. 350 99


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