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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Analysis is carried out of the clinical, pathomorphological and immunological characteristic of lupus nephropathy in 62 patients, 56 females and 6 males. A series of new investigation methods were used for that purpose. An early tendency towards kidney involvement in the course of LED is established and in 22 of the patients (36%) the renal symptoms have been the first clinical manifestations of the basic illness. Lupus nephropathy progresses most often with a nephrosis syndrome (in 66.1% of the patients), rarely pure and not combined with hypertension and/or with renal insufficiency. The pathomorphological changes are rather multiform but in the majority of the cases almost all structural elements of glomerules and the rest of the renal tissue are affected. The clinical picture severity, histopathological changes and nephropathy evolution course were established to be distinctly dependent on the course acuteness of the basic morbid process. The importance of the detailed study of the clinico-morphological and immune characteristic of lupus nephropathy upon the timely diagnosis. Proper treatment and the prognosis assessment of the illness is stressed upon.
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PMID:[Clinical morphological and immunological characteristics of lupus nephropathy]. 7 Aug 87

In healthy subjects with normal renal function beta2-microglobulin (beta2m) is constantly produced in the body. It is eliminated almost exclusively by the kidneys, predominantly by glomerular filtration but possibly also by some direct uptake from the blood. After glomerular filtration more than 99,9% of excreted protein is reabsorbed in the kidney tubules where it is catabolized. The main factor, influencing on the serum level of beta2m is the GFR. Determination of S-beta2m appears to be more effective than analysis of S-creatinine for the detection of a slightly reduced GFR. A relatively high S-beta2m, in comparison with the GFR, may be seen in e.g. malignant proliferative disorders and SLE. This indicates an increased production of the protein. An entirely free passage over the glomerular membranes is not likely for beta2m in healthy subjects but the sieving coefficient might approach 1,0 in renal disease. The increased glomerular elimination of the protein could then possibly be counterbalanced by an increased synthesis, which should explain the pronounced relationship at a log/log scale between S-beta2m and the GFR. An increased excretion of beta2m in the urine is a sensitive indicator of proximal tubular dysfunction in many clinical conditions. In marked renal insufficiency there is, however, an obligatory 100-1 000-fold increase of the normal excretion, not related to the kind of renal disorder. In studies of the protein precautions are necessary to avoid degradation of the protein, in urine with a low pH.
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PMID:The serum level and urinary excretion of beta2-microglobulin in health and renal disease. 8 68

Since 1970 in 27 out of 46 patients with the diagnosis of systemic lupus erythematosus (SLE) a renal biopsy could be taken. The morphological outcome was followed in 14 patients with a total of 18 repeated biopsies. By light- and electron microscopy renal involvement was demonstrable in all patients. Four histologic subgroups could be differentiated: Mesangio-proliferative (MESLN, 14), focal proliferative (FLN, 6), diffus proliferative (DLN, 6), and membranous lupus nephritis (MLN, 1). Some biopsies demonstrated linear deposits with IgG/IgA-specificity. 2/27 patients only showed a clinical deteriorating course with progressive renal insufficiency despite steroid or steroid-azathioprine therapy. One patient with DLN died in terminal renal failure. The morphological follow-up showed an unfavourable course in 3/14 patients only. One MESLN demonstrated a transition to DLN, one DLN an increase of proliferative lesions and a second DLN focal and local sclerosis. In our experience renal involvement in SLE can adequately characterised and controlled by repeated be clinico-pathological correlations an aggressive therapeutic regimen is not indicated and can be avoided.
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PMID:[Clinico-pathological correlations in lupus nephritis with reference to therapeutic and prognostic aspects (author's transl)]. 38 73

Sixty six patients with lupus nephropathy with hypertonic syndrome are examined. In patients with latent (inactive) lupus glomerulonephritis hypertonic syndrome developed 3--8 months after the initiation of the corticosteroid treatment, advancing with fluctuations, in some of the patients the arterial pressure being normalized after the discontinuation of that treatment. In patients with chronic active lupus glomerulonephritis without nephrotic syndrome, the hypertension develops before the initiation of the corticosteroid treatment, fluctuating at the beginning, and gradually assumes a stable character 3--5 months after the beginning of such treatment, sometimes with a malignant course and rapid development of renal insufficiency. The hypertonic syndrome advances most severely and malignantly in chronic lupus glomerulonephritis with nephrotic syndrome and is resistant to the active antihypertensive treatment. In 18, out of 25, such patients, the hypertonic syndrome is manifested in parallel with nephropathy before the inclusion of the cortocosteroid treatment. The grave and malignant course of the hypertonic syndrome is associated with the peculiarities of the clinical form and histomorphological type of that lupus nephropathy. In the patients with nephrosclerosis, the hypertonic syndrome is with a gradually progressing evolution, in parallel with the progress of the renal insufficiency.
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PMID:[Symptomatic arterial hypertension in lupus nephropathy]. 43 52

The tests for the detection of intravascular coagulation and of secondary fibrinolysis performed in 79 patients with systemic lupus erythematosus and 30 patients with other collagenoses were positive in over 63% of the cases. A highly significant correlation was found between the presence of fibrinolytic degradation products (FDP) and the incidence of nephropathy and renal insufficiency, as well as between the presence of fibrin monomers (Godal's ethanol-gelification test) and the evolutive signs of the primary disease (fever, accelerated ESR).
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PMID:Pathogenic role of intravascular coagulation in immune diseases. 59 17

The female predominance among patients with systemic lupus erythematosus and the protective effects of androgens in the murine lupus model prompted us to assess the androgenic status of 12 men with the disease. Save for minor abnormalities explained by treatment or renal insufficiency, normal serum testosterone, luteinizing hormone, and follicle stimulating hormone levels were found. Hypogonadism or androgen deficiency was not evident.
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PMID:Androgenic status of males with systemic lupus erythematosus. 73 97

Two patients with long-standing systemic lupus erythematosus were found to have persistent hyperkalemia. The hyperkalemia could not be explained by renal insufficiency, oliguria, diminished distal sodium delivery, acidemia, or hemolysis. After sodium depletion, urinary aldosterone excretion and plasma aldosterone concentration rose appropriately. No increase in urinary potassium excretion or decrease in serum potassium concentration was noted after fludrocortisone acetate, furosemide, or acetazolamide plus sodium bicarbonate. We conclude that these patients have a primary defect in renal tubular potassium secretion that may be related to an immune complex interstitial nephritis.
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PMID:Impaired renal tubular potassium secretion in systemic lupus erythematosus. 84 84

Fifteen patients with spontaneous systemic lupus erythematosus (SLE) have been phenotyped by determination of plasma isoniazid (INH) half-life. Seven patients had signs of renal insufficiency. Of the 15 patients, 13 were slow and only 2 rapid acetylators. No correlation was found between the plasma INH half-lives and the renal function. Thus, there is the same marked predominance of slow acetylators in patients with spontaneous SLE as in patients with the drug-induced SLE-like syndrome.
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PMID:Spontaneous systemic lupus erythematosus and acelylator phenotype. 84 61

A 22-year-old woman with systemic lupus erythematosus complicated by mild renal insufficiency and severe systemic hypertension inadvertently received an excessive amount of clonidine hydrochloride. In association with a presumed toxic level of clonidine in the serum, the patient developed abnormalities of cardiac conduction, including 2:1 atrioventricular block, complete heart block, 3:2 Wenckebach block, and first-degree atrioventricular block. The transient nature of these abnormalities, with the return of normal conduction upon the cessation of therapy with clonidine, implicates this drug as being capable of producing high-grade atrioventricular block at toxic levels.
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PMID:Cardiac toxicity of clonidine. 92 17

This study demonstrates that in systemic lupus erythematosus (SLE), the presence of immune complexes on the glomerular basement membrane (GEM) does not invariabley result in histological and/or functional lesions of the kidney. Among a group of 29 lupus patients, six subjects were selected for thorough investigation, because their renal function was normal or only slightly altered though they had suffered from SLE for 20 months to 18 years. All patients had antinuclear factor, anti-native-DNA antibody and a low level of complement; 3 had anti-denatured-DNA antibody, 2 had denatured DNA-anti-denatured-DNA circulating complexes and 3 had anti-RNA-protein antibody. Kidney biopsies disclosed either no histological lesion or minimal changes in five of them and diffuse proliferative glomerulonephritis in one. By contrast, using the immunofluorescent technique, granular deposits containing the third component of complement (C3) were found on the GBM of all patients; IgG was present in 5 cases, IgM in 3, fibrinogen in two cases and around the tubules of one. Electron microscopy confirmed the presence of subendothelial and mesangial deposits. Our results also showed a good correlation between the importance of deposits and the presence of denatured DNA-anti-denatured-DNA circulating complexes. From the data obtained in these 6 cases as well as in the 23 other patients of the group, 3 categories of lupus patients could be distinguished with regard to kidney involvement: 1) patients with insignificant histological lesions, no immune deposits and essentially normal function; 2) patients with definite histological lesions, immune deposits and renal insufficiency and 3) patients with few if any histological lesions and little functional impairment contrasting with important immune deposits. The resistance of some patients to the mephrotoxic effects of immune deposits shows that lupus nephritis depends on intricate pathogenic mechanisms and suggests that these are possible antagonized by "protective" factors.
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PMID:Immune complex deposits in systemic lupus erythematosus kidney without histological or functional alterations. 114 88


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