Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nephrogenic fibrosing dermopathy (NFD) is a novel fibrosing disorder of the skin with characteristic histopathology. It affects patients with impaired renal function and appears to be independent from the type of kidney disease. Its aetiopathology is unknown and presently no standard therapy exists. We report a patient with systemic lupus erythematosus (SLE) and glomerulonephritis who developed diffuse indurated erythematous plaques covering nearly the entire legs and trunk. She had never received dialysis. The second patient suffered from SLE and antiphospholipid syndrome related thrombotic glomerulopathy. After 10 weeks of haemodialysis she developed the same skin condition. To the best of our knowledge, these are the first reports of NFD occurring in patients with SLE.
Lupus 2004
PMID:Nephrogenic fibrosing dermopathy in two patients with systemic lupus erythematosus. 1546 93

Studies of late renal allograft biopsies focus on chronic damage investigated by light microscopy (LM). We evaluated the use of immunohistochemistry (IH) as applied in the routine study of transplant glomerulopathies. Among renal transplants in 1985 - 1997, 129 were identified where a graft biopsy had been obtained 6 months or more after transplantation, studied by LM and IH and the original renal disease was known. IH results were evaluated in relation to glomerular LM findings and the original diagnosis. The risk of graft loss in relation to recurrent and de novo glomerulopathy was evaluated. By LM, 69 biopsies (53%) showed glomerulopathy, mesangial sclerosis only in 26, proliferative changes in 15, membranous in 15 and combined membranous and proliferative in 13. By IH, 46 biopsies (36%) stained positive with IgM and/or complement only and 24 with immune complexes including IgA and/or IgG. Seven biopsies (5.4%) showed glomerular disease by IH in spite of normal LM. Recurrence was diagnosed in 22 grafts; 12 had IgA nephropathy, 3 had SLE, 6 other immune complex nephritides and 1 systemic vasculitis. Twenty-eight biopsies (22%) with proliferative and/or membranous glomerulopathy lacked clear connection to the original renal disorder. More than half of these had deposits of IgM and C3 only. The further graft survival was significantly reduced in the presence of de novo glomerulopathy by LM, relative risk 2.0 (confidence interval 1.1 - 3.8) in a Cox-proportional hazards analysis also including serum creatinine and Banff chronic allograft nephropathy (CAN) grade, p = 0.03. In conclusion, transplant glomerulopathy should be separated from recurrence. De novo glomerulopathy is frequent and ominous.
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PMID:Renal allograft glomerulopathy and the value of immunohistochemistry. 1552 58

A series of patients with systemic lupus erythematosus (SLE) and proteinuria were studied to determine whether nephrotic-range proteinuria was associated with diffuse epithelial cell foot process effacement in the absence of peripheral glomerular immune aggregate deposition. Biopsies from patients with known or suspected SLE and a histologic diagnosis of (1) normal by light microscopy, (2) mesangial proliferative glomerulonephritis, or (3) focal segmental glomerulosclerosis were studied. Biopsies were excluded when they demonstrated endocapillary proliferation or necrosis by light microscopy or electron-dense glomerular basement membrane deposits by electron microscopy. Patients were required to fulfill four of 11 American Rheumatologic Association criteria for the diagnosis of SLE, and proteinuria could not be associated with nonsteroidal anti-inflammatory drug use. Eighteen biopsies were studied, eight from patients with nephrotic-range proteinuria (>/=3 g/d) and 10 from patients with non-nephrotic proteinuria. The time from diagnosis of SLE to biopsy was shorter for nephrotic patients that for nonnephrotic patients. Seven of eight biopsies from nephrotic patients demonstrated at least 80% foot process effacement, whereas no biopsy from a nonnephrotic patient exhibited >20% effacement. There were no other significant pathologic differences between the nephrotic and nonnephrotic patients. The single common morphologic feature associated with nephrotic proteinuria was diffuse visceral epithelial cell foot process effacement. It is concluded that the development of nephrotic-range proteinuria in patients with SLE without peripheral immune aggregate deposition or endocapillary proliferation on renal biopsy is more likely a manifestation of SLE than the coexistence of idiopathic minimal-change glomerulopathy and SLE.
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PMID:Glomerular podocytopathy in patients with systemic lupus erythematosus. 1554 64

SLE nephritis is usually a slow process that may lead to renal failure many years after its first presentation. Success of different therapeutic modalities in preventing renal failure is therefore evaluated and compared only after many years of treatment. Lately, this conservative philosophy has been challenged with the acknowledgment of collapsing glomerulopathy (CG), a recent recognized clinical-pathological entity, characterized by rapidly progressive renal failure. Despite this ominous description we present an unusual case of a patient who presented with systemic lupus erythematosus (SLE) and clinical and pathological findings of CG, who completely remitted several weeks after commencing immunosuppressive therapy with intravenous cyclophosphamide and prednisolone.
Lupus 2005
PMID:Hyperacute renal failure as the initial presentation of systemic lupus erythematosus. 1586 22

We present the case of a 69-year-old man with nephrotic syndrome and renal insufficiency, who developed lobular glomerulonephritis. An electron microscopy examination of a renal biopsy showed microtubular structures of 24 nm in diameter in the subendothelial space and the paramesangial area. These deposits were PAS-positive and Congo red-negative, and revealed predominantly positive staining for kappa light chain. There was no evidence of diseases with highly organized glomerular deposits, such as amyloidosis, cryoglobulinemia, systemic lupus erythematosus or paraproteinemia. Therefore, the patient was diagnosed to have immunotactoid glomerulopathy (ITG). During a seven-year course he has not developed any disease known to be associated with organized glomerular immune deposits. Hence, we believe ITG occurred as a primary glomerular disease in this case. We also highlight cases of ITG with microtubular deposits that have been reported in Japan, compare these cases to previous reports, and show that the characteristics of the Japanese cases are male predominance; a high incidence of membranoproliferative glomerulonephritis (MPGN); a low incidence of monoclonal gammopathy and hematological malignancies and a higher incidence of hypocomplementemia.
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PMID:Immunotactoid glomerulopathy with microtubular deposits, with reference to the characteristics of Japanese cases. 1590 96

Renal electrolyte disorders, acute renal failure, and a variety of chronic renal diseases are common in HIV-infected patients. Glomerular disorders include IgA nephropathy, cryoglobulinemia, amyloidosis, and a lupus-like immune complex glomerulopathy. The most attention has been focused on collapsing glomerulopathy associated with nephrotic syndrome and progressive renal failure, which appears to be unique for patients with HIV/AIDS, called HIV-associated nephropathy (HIVAN), and it occurs predominantly in African American patients. Investigations in humans and in a transgenic mouse model reveal direct infection of renal epithelial cells by HIV and toxic cellular and immunologic processes mediated by HIV glycoproteins as the principal pathophysiology of HIVAN. Highly active antiretroviral treatment may be associated with an improved renal outcome and even reversal of kidney disease in some patients. Treatment with angiotensin-converting enzyme inhibitors may avert progression of HIVAN to end-stage kidney disease and result in superior patient and kidney survival as compared with untreated patients.
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PMID:HIV-associated renal disorders: recent insights into pathogenesis and treatment. 1609 Dec 56

Collapsing glomerulopathy is a severe form of glomerular injury, closely associated with HIV infection, characterized by the collapsing feature of glomerular damage with frequent tubulointerstitial involvement and rapid progression to terminal renal failure. The etiopathogenesis in non-HIV infected patients remains obscure. We reported a patient whose diagnosis of collapsing glomerulopathy (CG) and systemic lupus erythematosus (SLE) was done simultaneously and described the diseases characteristics suggesting that SLE could be an etiologic factor for the induction of this glomerulopathy, clinical evolution and treatment.
Lupus 2005
PMID:Can systemic lupus erythematosus be the cause of collapsing glomerulopathy? 1630 82

The transcription factor c-Jun regulates the expression of genes involved in proliferation and inflammation in many cell types but its role in human renal disease is largely unclear. In the current study we investigated whether c-Jun activation is associated with human renal disease and if c-Jun activation regulates pro-inflammatory and pro-fibrotic genes in renal cells. Activation of c-Jun was quantified by scoring renal expression of phosphorylated c-Jun (pc-Jun) in control human renal tissue and in biopsies from patients with various renal diseases (diabetic nephropathy, focal glomerulosclerosis, hypertension, IgA nephropathy, membranous glomerulopathy, minimal change disease, membranoproliferative glomerulonephritis, systemic lupus erythematosus, acute rejection, and Wegener's granulomatosis); this was correlated with parameters of renal damage. Furthermore, we studied the functional role of c-Jun activation in human tubular epithelial cells (HK-2) stimulated with TGF-beta. Activated c-Jun was present in nuclei of glomerular and tubular cells in all human renal diseases, but only sporadically in controls. Across the diseases, the extent of pc-Jun expression correlated with the degree of focal glomerulosclerosis, interstitial fibrosis, cell proliferation, kidney injury molecule-1 (Kim-1) expression, macrophage accumulation, and impairment of renal function. In HK-2 cells, TGF-beta induced c-Jun activation after 1 h (+40%, p < 0.001) and 24 h (+160%, p < 0.001). The specific c-Jun N-terminal kinase (JNK) inhibitor SP600125 abolished c-Jun phosphorylation at all time points and blunted TGF-beta- or BSA-induced procollagen-1alpha 1 and MCP-1 gene expression in HK-2 cells. We conclude that in human renal disease, the transcription factor c-Jun is activated in glomerular and tubular cells. Activation of c-Jun may be involved in the regulation of inflammation and/or fibrosis in human renal disease.
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PMID:Glomerular and tubular induction of the transcription factor c-Jun in human renal disease. 1789 46

Epidemiological data of renal diseases is population-based and have great geographic variability. Due to the lack of a national renal data registry system, there is no information on the prevalence rate, and clinical and laboratory features of various glomerulo-nephritidis (GNs) in Iran. In a retrospective cross sectional study, we analyzed 462 adult renal biopsies in Tehran, Iran. We determined the prevalence rate and the frequency of different clinical and laboratory findings in patients with different GNs. We also compared our results with the reports from other countries. There were 267 (57.8%) males and 195 (42.2%) females. The mean (+/- SD) age was 33.6 +/- 15.7 (range, 13-75) years. A total of 55 biopsies, which had revealed pathologies other than GNs, were excluded. Among the remaining 407 biopsies, membranous glomerulopathy (MGN) was the most common GN (23.6%), followed by IgAN (13.5%), membranoproliferative GN (MPGN) (11.5%), systemic lupus nephritis (SLE-GN) (10.6%), focal and segmental glomerulosclerosis (FSGS) (10.3%), and minimal change disease (MCD) (9.8%). Our study shows that MGN is the most common form of GN, followed by IgAN, MPGN, SLE-GN, FSGS and MCD in adult patients in Iran. A multi-center study with a larger sample size is needed for more comprehensive data in Iranian population.
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PMID:Prevalence and clinical findings of biopsy-proven glomerulonephritidis in Iran. 1795 43

In the present work general characteristics and occurrence of TLR receptors have been presented. The participation of TLR receptors in kidney pathology in experimental models in the course of urinary system infection, acute renal failure and interstitial fibrosis has been discussed. In addition, the importance of TLRs in various forms of glomerular nephritis and in haemodialytic patients as well as in postrenal-transplant patients has been shown. It is believed that in lipopolysaccharide-induced renal failure in the course of infections caused by Gram negative bacteria TLR4 plays a fundamental role. In the event of damage of renal tubular epithelial cells by mechanical, toxic, or ischemic factors activation of TLRs induces inflammatory processes leading to acute renal failure. In the course of progressive fibrosis of renal interstitial tissue TLR 2 and 4 receptors are stimulated, which results in the fact that immunological and structural cells of renal tissue release chemokines and cytokines, which causes increased inflow of leucocytes and intensification of interstitial nephritis and progressive fibrosis. The study on experimental models on mice MLR (mixed lymphocyte reaction) with genetically conditioned lupus-like disease showed that, CpG-DNA stimulation as a TLR 9 specific agonist intensifies inflammatory symptoms in mice. Similarly in apoferritin induced glomerulopathy (model of immune complex disease) CpG-DNA nucleotide increased glomerulopathy symptoms. It has been proved that activation of mechanisms of inherent immunity through TLR4 receptors affects the frequency and intensity of acute rejections in human organ transplantations. Incidence of acute kidney and lung [transplant rejections was significantly lower in recipients with mutated variants of Toll-like receptor 4 (TLR-4 Asp 299Gly and TLR-4-Tyr399-IIe).
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PMID:[Toll-like receptors (TLR) in the pathogenesis of kidney diseases]. 1836 25


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