Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Erythropoiesis and immunity are evaluated in (C57BL/6xDBA/2) F1 mice with immune complex glomerulonephritis induced by GVHR as compared to the genetically determined models of systemic lupus erythematosus. Elevated content of serum blood antinuclear antibodies, polyclonal activation during early disease periods, immune complex deposition in kidney tissues indicate the presence of the autoimmune syndrome in (C57BL/6xDBA/2)F1 mice, similar to that in mice with genetic lupus nephritis. The findings of a decrease of CFUs on days 5 and 8 at early times of disease, a reduction of hematocrit in combination with the enhancement of stem cell proliferation on the 6th-7th month of disease, an increase of the absolute leukocyte count and relative monocyte count in the peripheral blood of diseased mice may attest to the depression of stem cell differentiation in erythropoiesis and to the enhancement of stem cell differentiation in granulocyto-monocytopoiesis, that needs, however, further research and confirmation.
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PMID:[Indicators of erythro- and immunopoiesis in the development of autoimmune disease induced by graft vs host reaction]. 180 66

Patients with diffuse, proliferative lupus nephritis (DPLN) were subjected to differential solute clearances (n = 22) and serial renal biopsy (n = 11) before and again after 6-12 mo of immunosuppressive therapy. Glomerular sieving of dextrans of graded size was analyzed with a heteroporous membrane model. This revealed active DPLN to be associated with 1) a reduction of overall pore density accompanied by a 53% depression of glomerular filtration rate (GFR), and 2) appearance of a subset of large, nondiscriminatory pores, which accounted for the observed nephrotic level of proteinuria. Morphometric analysis of biopsy tissue provided evidence of reduced filtration surface area due to global or segmental occlusion of capillary loops in glomerular tufts. Activity of DPLN resolved posttreatment. A computed increase in pore density was associated with a 24% increment in GFR; a marked reduction in the fraction of shuntlike pores was accompanied by a parallel reduction of proteinuria into a subnephrotic range. Repeat biopsy revealed diminished glomerular cellularity, fewer immune deposits, and an ensuing increase in the fraction of tuft area occupied by patent loops. Epithelial filtration slit frequency also increased. Neither functional nor structural recovery was complete, however. Residual pore density approximated only 23-35% of that in healthy controls, and corresponding shuntlike pores were threefold more prominent. We conclude that severe DPLN is only partially reversible by current modalities of treatment and that the ensuing residual injury is far more severe than suggested by conventional tests of renal function.
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PMID:Extent of glomerular injury in active and resolving lupus nephritis: a theoretical analysis. 203 58

The relationship between serologic tests and renal histologic change over time was examined in 55 patients with lupus nephritis. After a median interval of 40 months on various immunosuppressive drug regimens, C3 complement levels were improved in 78% of patients and anti-DNA levels were improved in 85%. Comparison of initial and followup renal pathology showed that the activity index of the biopsy improved in 82%, while the chronicity index worsened in 71% of patients. Normalization of C3, but not anti-DNA levels, was associated with a lowering of the activity index on repeat biopsy. Prolonged depression of serum C3 levels was associated with a trend (p = 0.066) towards worsening of the chronicity index, but the change in chronicity index showed no relationship to the duration of elevated anti-DNA. Our studies indicate that abnormal levels of C3 complement are predictive of the degree of persistently active glomerular disease, but that duration of abnormal C3 or anti-DNA are less consistent predictors of the acquisition of chronic, irreversible renal lesions.
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PMID:Lupus nephritis: association between serology and renal biopsy measures. 325 18

In 35 initially normotensive patients with chronic glomerulonephritis and lupus nephritis (including 27 patients with nephrotic syndrome; NS), blood pressure (BP), urinary sodium excretion, plasma renin activity (PRA), plasma aldosterone level (PA), urinary aldosterone excretion (Au and blood volume were measured before and during prednisolone treatment. In 7 patients (all with NS) steroid-induced hypertension has developed. The patients prone to develop hypertension were hypervolemic nephrotics with initial depression of PRA, PA, Au, and severe sodium retention. In these patients prednisolone did not produce diuresis of natriuresis nor did it decrease proteinuria. In normo- and hypovolemic patients prednisolone produced significant diuresis and natriuresis and failed to induce hypertension. Thus, two types of response to prednisolone could be observed in patients with NS.
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PMID:Steroid-induced hypertension in patients with nephrotic syndrome. 328 84

As part of a larger study of serial complement profiles in glomerulonephritis plasma C3 and C4 concentrations were measured using commercially available immunodiffusion plates. A total of 303 samples were obtained from 128 patients suffering from forms of nephritis associated with hypocomplementaemia-namely, lupus nephritis, mesangiocapillary glomerulonephritis (M.C.G.N.), and acute glomerulonephritis.These simple measurements of C3 and C4 gave clinically useful information. In lupus nephritis C3 and C4 generally correlated and C4 concentrations were more often and more profoundly depressed than C3 concentrations. Neither C3 nor C4 concentrations alone correlated well with the antinuclear factor titre.In both acute glomerulonephritis and M.C.G.N. the C3 concentrations were frequently lower than 20% of normal (which was never the case in patients with lupus), while the C4 concentration was usually normal and was almost never depressed in the absence of C3 depression. This suggests activation of complement at the C3 level by the "bypass" pathway in acute nephritis as well as in M.C.G.N., though both may be operating in some patients. In acute glomerulonephritis but not in M.C.G.N. C3 concentrations returned to normal within eight to 12 weeks.The two varieties of M.C.G.N. identified by the site of the deposits in the capillary glomerular walls differed in their C3 levels. In 10 patients with intramembranous dense linear deposits the C3 was always low over very long periods of time, rising in three out of four patients only after transplantation and immunosuppression. Other patients with M.C.G.N., in contrast, often showed normal C3 concentrations. Concentrations of C4 did not differ in either group, being normal in 80% of samples from all types.
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PMID:Plasma C3 and C4 concentrations in management of glomerulonephritis. 420 Apr 78

To determine whether patients with systemic lupus erythematosus (SLE) and active nephritis have more profound defects in cellular immune responses, we studied cell-mediated immunity (CMI) in 12 patients with lupus nephritis (LN) and 11 patients with chronic mesangial proliferative glomerulonephritis (CGN) without renal insufficiency. The LN patients had a significant depression in CMI, characterized by impaired delayed hypersensitivity skin reactivity to keyhole limpet haemocyanin (KLH), decreased percentage of T cells and diminished lymphocyte transformation to phytohaemagglutinin (PHA). The levels of concanavalin A (Con A)-induced suppressor cell activity (SCA) were significantly lower in LN patients compared with those in normal controls and those in CGN patients. The levels of all CMI parameters for the 6 LN patients with the nephrotic syndrome (NS) were significantly more decreased when compared with those of the 6 LN patients without NS. In contrast, the CMI levels in CGN patients with or without NS did not differ from normal subjects. These findings may lend further insight into the understanding of the immunoregulatory defect in LN.
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PMID:Defective cellular immune responses in lupus nephritis. 648 92

Intraplatelet and plasma serotonin levels were measured in 269 samples from 44 patients with systemic lupus erythematosus (SLE) and clinical nephritis. The intraplatelet serotonin levels were depressed and the plasma serotonin levels were raised in lupus nephritis. There was a strong correlation between both lowered intraplatelet serotonin concentration and raised plasma "serotonin", and the overall clinical activity of the disease. This correlation was also observed in the majority of individual patients studied serially; the platelet serotonin levels correlated with both clinical and immunological tests. Serotonin uptake by platelets was significantly diminished, but there was no correlation between serotonin uptake and platelet serotonin levels. There was, however, a correlation between the amount of platelet-aggregating material in the serum and depression of intraplatelet serotonin. This study provides further evidence of in vivo platelet activation in SLE nephritis, and provides a measure of the activation in relation to the clinical and immunological activity of the disease.
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PMID:Platelet and plasma serotonin in glomerulonephritis. III: The nephritis of systemic lupus erythematosus. 742 90

To determine the utility of magnetic resonance imaging (MRI) of the brain in diagnosing active neuropsychiatric disease in systemic lupus erythematosus (NP-SLE), a prospective study of 51 hospitalized systemic lupus erythematosus (SLE) patients during 64 separate episodes of suspected NP-SLE was initiated. In addition to standard hematology, chemistry, and serological tests, the workup included MRI in all patients. A computed tomographic scan of the brain was obtained in patients enrolled in the first year of the study. Of the 64 neuropsychiatric episodes, 42 were attributable to NP-SLE and 22 were attributed to causes other than SLE. Neuropsychiatric complaints unrelated to lupus included depression (n = 6), seizures (n = 5), headache (n = 3), altered mental status (n = 2), aseptic meningitis (n = 2), cardiovascular accident (n = 2), transient ischemic attack (n = 1), and vertigo (n = 1). The MRI was abnormal in 34 of 64 (53%) episodes. MRI abnormalities were more common in patients with focal neurological deficits (19/26) than in those without focal findings (15/38; P = .008) and in patients with nephritis (19/24) than in those without renal disease (15/40; P = .002). MRI abnormalities were as frequent in NP-SLE (25/42) as in cases with non-NP-SLE-related causes (9/22). Periventricular increased signal (PIS) was a frequent MRI finding (10/64). Enlargement of the prepontine cistern, an MRI finding not previously described in NP-SLE, was seen (14/64). Both findings were associated with the presence of hypertension and lupus nephritis. PIS similar to that seen in our patients has been described in otherwise healthy elderly individuals with risk factors for stroke, suggesting that vascular abnormalities may be important in the etiology of these lesions. In conclusion, abnormalities in brain MRI occur frequently in NP-SLE, especially in patients with focal neurological deficits. However, the presence of similar MRI abnormalities in SLE patients with neuropsychiatric symptoms and findings with non-SLE-related causes limits the specificity of the MRI for diagnosing NP-SLE.
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PMID:Magnetic resonance imaging of the brain in neuropsychiatric systemic lupus erythematosus. 851 97

The diversity of clinical presentations of lupus nephritis parallel the diversity of pathologic lesions seen in the kidneys of patients with SLE. Renal manifestations range from asymptomatic hematuria or proteinuria to overt nephritic and nephrotic syndromes, rapidly progressive glomerulonephritis, and chronic renal failure. Subclinical nephropathy both during presentation and during monitoring of disease activity is frequently missed because of the notorious unreliability of routine screening urinalyses performed in high-throughput clinical pathology laboratories. Requisitions for urine microscopy should be flagged for special attention in patients at risk for lupus nephritis. Depression of classic complement pathway components and high titers of anti-DNA, anti-nucleosome, or anti-Clq antibodies identify patients are increased risk of renal involvement or flares of nephritis. Several disease activity and damage indexes are available, but they are mostly used in clinical research setting and none has achieved wide use for standard clinical practice.
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PMID:Clinical presentation and monitoring of lupus nephritis. 1573 84

The pathogenesis of calciphylaxis, which has a rising incidence in the chronic dialysis population and a high mortality rate, is poorly understood. Abnormalities in the calcium-phosphorus-parathyroid axis are clinically related to calciphylaxis, but alone, they cannot explain this condition. Here, we present two patients who had chronic inflammatory conditions and hyperparathyroidism and who developed calciphylaxis. A 41-year-old white woman on hemodialysis following scleroderma, hepatitis C, liver transplant, and failed kidney transplant, developed progressive ulcerative lower extremity calciphylaxis lasting more than 3 years. She had evidence of severe hyperparathyroidism and elevated serum C-reactive protein (CRP). A 39-year-old white woman on continuous ambulatory peritoneal dialysis for 6 years for renal failure secondary to lupus nephritis, with sustained lupus activity during the dialysis period, developed rapidly progressing ulcerative calciphylaxis of the lower and upper extremities not responding to adequate treatment of hyperphosphatemia and hyperparathyroidism. Her condition culminated in death within 2 months of the appearance of the skin lesions. Her serum CRP was elevated on a sustained basis before the development of the calciphylaxis and rose to a very high level after appearance of the skin lesions. Inflammation may assist in the development of calciphylaxis through depression of serum levels of fetuin-A, an endogenous inhibitor of calcification that is also a negative acute-phase reactant. The interactions between inflammation-mediated changes in the levels of endogenous inhibitors of calcification and abnormalities in calcium-phosphorus metabolism merit intensive study in the future as potential mechanisms of calciphylaxis.
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PMID:Association between calciphylaxis and inflammation in two patients on chronic dialysis. 1698 64


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