Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the method of concanavalin A (Con a) inducible suppressor activity the peripheral mononuclear cells (PMC) of 17 patients with Mesangial IgA nephritis, 13 patients with idiopathic mesangial proliferative glomerulonephritis but with no IgA deposits on immunofluorescence (Non-IgA nephritis) and 18 healthy subjects were studied. DNA synthesis was measured by incorporation of 3H Thymidine. The mean suppression index (S.I.) of 0.94 +/- 0.08 (SEM) in the IgA nephritic patients was significantly different from that of the non-IgA nephritic patients (0.67 +/- 0.05) (P less than 0.01) as well as the group of normal healthy controls (0.64 +/- 0.05) (P less than 0.0025). The data show that patients with IgA nephritis have abnormal suppressor cell function and suggest an autoimmune basis in the pathogenesis of IgA nephritis.
 ...
PMID:Loss of concanavalin A induced suppressor T-lymphocyte function in patients with mesangial IgA nephritis. 646 97

We studied prostaglandins and kallikrein urinary excretion in 14 children with acute poststreptococcal glomerulonephritis within 48 hours of hospital admission (period A), and again, 4-6 weeks later, when they were clinically recovered (period B). Seventeen apparently healthy children were studied as controls. The results (mean +/- SEM) indicate that PGE2 urinary excretion (ng/kg/day) was diminished during both periods of study (control group = 2.06 +/- 0.43, patients = period A 0.91 +/- 0.28 [P less than 0.02], period B 0.92 +/- 0.21 [P less than 0.02]). PGF2 alpha urinary excretion (ng/kg/day) was also suppressed during period A, but not during period B when large individual variability existed (control group = 7.10 +/- 1.07, patients period A 3.56 +/- 0.66 [P less than 0.001], period B 10.51 +/- 5.01 [NS]). Kallikrein urinary excretion (EU/kg/day) was also depressed during the acute phase and remained low during convalescence (control group = 0.492 +/- 0.1, patients period A 0.143 +/- 0.044 [P less than 0.001], period B 0.265 +/- 0.093 [P less than 0.02]). There was no difference in PGE/PGF ratio between controls and patients in the periods of study (control 0.328 +/- 0.055, period A 0.395 +/- 0.144, period B 0.384 +/- 0.128). Urine volume (ml/day) was lower in period A (582 +/- 75.8) but comparable in period B (1020 +/- 140.2) and control children (1210 +/- 80.2). No correlation could be found between the urinary excretion of PGE2, PGF2 alpha and kallikrein with any of the following parameters: urinary or serum sodium and potassium, serum or urinary osmolality, Cosm, urine flow, plasma renin activity, plasma or urinary aldosterone, hypertension or fluid retention.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Urinary excretion of prostaglandins (PGE2 and PGF2 alpha) and kallikrein in acute glomerulonephritis. 658 Sep 82

Idiopathic crescentic glomerulonephritis is associated with a 70% to 80% incidence of end-stage renal failure. Oral corticosteroid therapy in combination with immunosuppressive agents or anticoagulants has not altered the prognosis of this disease. We have seen five adults with idiopathic crescentic glomerulonephritis and treated them with intravenous methylprednisolone. Before therapy, the average serum creatinine concentration was 7.4 +/- 1.3 mg/dL (chi-square +/- SEM). This value declined to 2.0 +/- 0.48 mg/dL within 4 weeks. All patients continue to maintain stable renal function over an average follow-up period of 19 months (range 1.5 to 36 months). These data suggest that a prospective controlled trial of this therapy is warranted in the management of this entity.
 ...
PMID:Pulse methylprednisolone therapy in idiopathic, rapidly progressive glomerulonephritis. 736 54

Neuraminidase (NA) is an enzyme produced by several microorganisms, which is capable of liberating sialic acid from glycoproteins and modifying cellular adhesion mechanisms. NA is considered a virulence factor in some bacterial species and has been implicated in the pathogenesis of acute poststreptococcal glomerulonephritis, a disease in which glomerular leukocyte infiltration is a prominent feature. We examined the effect of NA on kidney infiltration by neutrophils (PMN), T lymphocytes (TL) and monocyte-macrophages (MM). Intravenous injection of NA resulted in an early increase in the number of PMN (1 hr, 3.42 +/- 0.19 cells/cgs, mean +/- SEM; 3 hr, 3.63 +/- 0.13; 6 hr, 2.9 +/- 0.24; controls, 1.53 +/- 0.18; P < 0.001) and MM (1 hr, 3.49 +/- 0.16; 3 hr, 4.02 +/- 0.2; 6 hr, 3.88 +/- 0.27; controls 1.43 +/- 0.14; P < 0.001) in the glomeruli, while TL increased later (24 hr, 2.29 +/- 0.14; 48 hr, 2.4 +/- 0.2; 72 hr, 2.16 +/- 0.15; controls 0.7 +/- 0.07; P < 0.001). PMN and TL were also increased in the interstitium (up to ninefold for PMN and up to threefold for TL). Following i.v. injection of 51Cr-labeled NA-treated leukocytes, renal radioactive uptake was significantly increased at all times tested (percent radioactivity/gram of tissue after PMN injection, 3 hr, 5.57 +/- 0.46, mean +/- SEM; 12 hr, 5.38 +/- 0.77; 60 hr, 6.51 +/- 1.1; controls, 1.26 +/- 0.17, 1.75 +/- 0.25, and 2.46 +/- 0.08, respectively; P < 0.001 in each case.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Neuraminidase promotes neutrophil, lymphocyte and macrophage infiltration in the normal rat kidney. 753 44

The use of cyclosporin A (Cy A) in idiopathic nephrotic syndrome, particularly lesions of focal segmental glomerular sclerosis, is controversial. A retrospective study of 10 adult patients with nephrotic syndrome treated with Cy A was performed. Histological diagnosis was established in all patients: focal segmental glomerular sclerosis (n = 6), focal global sclerosis (n = 1), mesangial proliferative glomerulonephritis (n = 1), focal proliferative glomerulonephritis (n = 1) and minimal change disease (n = 1). All patients had previously received immunosuppressive therapy (duration of steroids 1-76 months; 35.0 +/- 12.1, mean +/- SEM). Cy A in a dose of 3-5 mg/kg/day, reduced proteinuria from 16.85 +/- 6.67 to 3.37 +/- 1.48 g/24 hours (P = 0.008), with an associated increase in serum albumin from 15.2 +/- 2.6 to 34.3 +/- 2.5 g/l (P < 0.001). In six patients steroid therapy was discontinued. Cy A was well tolerated for up to 5 years. There was no significant nephrotoxicity. In conclusion, Cy A was effective treatment of refractory idiopathic nephrotic syndrome, including those cases with focal segmental glomerular sclerosis.
 ...
PMID:Cyclosporin A in refractory idiopathic nephrotic syndrome: 5 years clinical experience. 787 Jun 36

Renal function recovery (RFR) is a rare event in patients with end-stage renal disease (ESRD). Although some predictive factors have been described, there are still unresolved questions. We have analyzed the Canadian Organ Replacement Register data for the 1981 to 1989 period to assess the incidence and factors predictive of RFR in a large ESRD population as well as the outcome after recovery. Renal function recovery was defined as the interruption of renal replacement therapy (RRT) for more than 3 months. Patients on RRT for < or = 45 days were excluded. Of 14,318 registered ESRD patients, 342 (2.4%) experienced RFR after 8.9 +/- 0.5 months of RRT (mean +/- SEM); 52.3% of the recoveries occurred within 6 months of initiating RRT, while 23.7% were only observed after 12 months or more. By Cox regression, patients within the following diagnostic groups had a significantly higher rate of RFR than those with primary glomerulonephritis, who are considered to comprise the reference group: myeloma (relative rate [RR] = 6.00; P < 0.001), drug-induced disease (RR = 4.21; P < 0.001), vascular/hypertensive disease (RR = 2.60; P < 0.001), and systemic disease (RR = 2.58; P < 0.001). Inversely, patients with polycystic kidneys (RR = 0.06; P = 0.004) and diabetic patients (RR = 0.56; P = 0.024) had a lower rate of RFR than those with glomerulonephritis. Men younger than 45 years had a lower rate of RFR than older men and women of all ages (P < or = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Renal function recovery in end-stage renal disease. 837 35

Humoral and cellular immune mechanisms are thought to be involved in various forms of vasculitis and glomerulonephritis. Recent clinical and experimental results point to a role of cytokines in ANCA-positive vasculitides. We analyzed tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and interleukin-2 receptors (IL-2R) in renal biopsies and in plasma from 22 patients with Wegener's granulomatosis and microscopic polyangiitis. Kidney biopsies were examined by immunocytochemistry, polymerase chain reaction and in situ hybridization. Immunoreactive TNF-alpha, IL-1 beta and/or IL-2R positive infiltrating cells were observed in 21 of 22 biopsies. TNF-alpha, IL-1 beta and IL-2R staining was evident in the interstitium and at periglomerular and perivascular sites. The number of positive cells was markedly increased in biopsies with active lesions. Positive cells were also present in cellular and fibrocellular crescents, surrounding tuft necrosis and in the walls of arteries and arterioles with acute vasculitic lesion. Some tubular epithelial cells stained for TNF-alpha and IL-1 beta. TNF-alpha, IL-1 beta and IL-2R positive infiltrating cells correlated with the presence of histologically active renal lesions. The evaluation of TNF-alpha and IL-1 beta expression at the mRNA level assessed by the polymerase chain reaction demonstrated specific transcripts for TNF-alpha and IL-1 beta in all six cases analyzed. In situ hybridization studies showed an increased expression of mRNA for TNF-alpha and IL-1 beta in infiltrating mononuclear cells, in epithelial cells of Bowman's capsule and in some tubules, predominantly of patients with active renal lesions. The results at the mRNA level correlated with the immunocytochemical findings. Compared to healthy individuals higher TNF-alpha plasma levels were observed in patients with vasculitis (34.4 +/- 16.6 pg/ml (SEM) vs. 1.9 +/- 0.7 pg/ml in controls; P < 0.01). All patients presented a marked increase in sIL-2R plasma levels (3512 +/- 485 U/ml vs. 397 +/- 21 U/ml in healthy controls; P < 0.001). IL-1 beta was not detected in most plasma samples. Elevated TNF-alpha and sIL-2R plasma levels were related to active renal lesions. Our study clearly demonstrates that in ANCA-positive vasculitis TNF-alpha and IL-1 beta are produced in situ by activated infiltrating mononuclear cells and resident renal cells. Intrarenal localization of cytokine producing cells and the correlation between cytokine production and histological signs of activity suggest that TNF-alpha and IL-1 beta are important locally acting mediators in the vasculitic/glomerulonephritic process.
 ...
PMID:In situ production of TNF-alpha, IL-1 beta and IL-2R in ANCA-positive glomerulonephritis. 845 68

Bovine heart cardiolipin specifically inhibits platelet aggregation induced by PAF in vitro. In the past we have reported that patients with primary glomerulonephritis have increased PAF levels in plasma (Iatrou et al., 1995b). In this work we investigate the existence of cardiolipin in the blood of end-stage renal patients due to primary glomerulonephritis and we study its implication in the biological study of PAF. Lipids from blood samples of end-stage renal patients were extracted, fractionated onto silicic acid column and onto High Performance Liquid Chromatography (HPLC) cation exchange column. PAF fraction was removed and phospholipids were separated from the rest lipid fraction with current counter distribution and furthermore fractionated onto HPLC silica column. The results show: 1. cardiolipin is present in the blood of end-stage renal patients. 2. Blood cardiolipin specifically inhibits PAF-induced aggregation in washed rabbit platelets. 3. Scatchard plot analysis of PAF binding, in the presence of unlabelled PAF and in the presence of cardiolipin, shows that rabbit platelets possess two different types of binding sites. One of which is saturable and of high affinity, kD = 0.103 +/- 0.03 nM (SEM, n = 3) with 337 +/- 94 binding sites per platelet for PAF and kD = 0.087 +/- 0.02 nM with 371 +/- 92.7 binding sites per platelet for cardiolipin while the other one has almost infinite binding capacity. 4. Blood cardiolipin competes [3H]PAF binding in rabbit platelets. This work shows that cardiolipin exists in the blood of end-stage renal patients and specifically inhibits PAF-induced aggregation as well as PAF binding in rabbit platelets. The possible implication of the biological actions of cardiolipin in the anticardiolipin-antiphospholipid syndrome is also discussed.
 ...
PMID:Blood cardiolipin in haemodialysis patients. Its implication in the biological action of platelet-activating factor. 862 43

Recent studies in the experimental proliferative glomerulonephritis (GN) indicate that apoptosis is the major mechanism that mediates the resolution of glomerular hypercellularity during the repair process of experimental GN. The role of apoptosis during progressive GN, however, has not yet been well understood. We have, therefore, examined the role of apoptosis during the progression of experimental crescentic GN to end-stage renal failure. A progressive model of antiglomerular basement membrane GN was induced in Wistar-Kyoto rats with a single injection of anti-rat glomerular basement membrane antibody. Renal function and histologic studies were performed chronologically from Day 0 to Week 8 after disease induction. The incidence of apoptosis in glomeruli as well as glomerular crescents was examined during the progression of crescentic GN to end-stage kidney disease. Many leukocytes infiltrated glomeruli from the early phase of GN, and severe necrotizing and mesangiolytic glomerular damage was observed from Day 5 to Week 3. After glomerular damage, mesangial hypercellularity with mesangial cell proliferation and extracellular matrix accumulation began with crescent formation. Thereafter, glomerular inflammation continued with marked extracellular matrix accumulation until Week 4, and the renal function deteriorated. The proliferative glomerular lesions subsequently progressed to sclerotic lesions and eventually to chronic renal failure in Week 8. Although the number of proliferating cells and infiltrating leukocytes slowly decreased, glomerular inflammation resolved with scar formation as mesangial sclerosis. Significant apoptosis was present from Day 7 (mean +/- SEM, 0.53 +/- 0.12 cells/glomerular cross-section) and gradually increased in number with the proliferating lesions as glomerular inflammation continued. Moreover, apoptosis increased during the resolution of the glomerular inflammation, and many apoptotic cells were present in the sclerotic lesions in Week 8 (1.97 +/- 0.27 cells/glomerular cross-section). As glomerular inflammation subsided, cellular crescents progressed to fibrous crescents with a reduction of cellularity by Week 8, and apoptosis increased significantly within these lesions. These findings indicate that apoptosis plays an essential role in the resolution of intra- and extraglomerular inflammation and in the elimination of glomerular cells within the scarring regions for progressive crescentic GN. The regulation of the apoptotic phenomenon during crescentic GN may be important in the progression of glomerular inflammation and the development of pathologic glomerular sclerosis.
 ...
PMID:Apoptosis in progressive crescentic glomerulonephritis. 864 89

Neutrophils (PMNs) and their toxic contents can injure glomeruli, but to date their fate in glomerulonephritis has been unknown. We studied glomerulonephritis induced in rats by formation of concanavalin A (Con A)/anti-Con A immune complexes on glomerular endothelial cells. PMN infiltration, which was almost exclusively confined to the lumen of glomerular capillaries, was transient, peaking at 4 hours, with only 9.0 +/- 4.1% (mean +/- SEM) of the maximum remaining at 24 hours. There was clear evidence of PMN apoptosis leading to phagocytosis in situ by intraluminal macrophages. However, the kinetics of leukocyte infiltration and PMN apoptosis, the preferential location at 24 hours of apoptotic PMNs within occluded capillary loops, and tracking of radiolabeled PMNs all indicated that in situ phagocytic clearance after apoptosis was the fate of a minority of PMNs, amounting to no more than one-fifth of the peak infiltrating load. Instead, the majority of infiltrating PMNs (72.9 +/- 3.1%) had emigrated from inflamed glomeruli by 24 hours, apparently returning to the circulation. We conclude that PMN emigration from inflamed glomeruli is a hitherto unrecognized mechanism for regulation of PMN-mediated glomerular injury.
 ...
PMID:Neutrophil fate in experimental glomerular capillary injury in the rat. Emigration exceeds in situ clearance by apoptosis. 900 38


<< Previous 1 2 3 4 5 Next >>