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)

Chronic renal insufficiency was produced surgically in Fischer 344 rats in order to evaluate the effects of enflurane anesthesia in animals with impaired renal function. Three groups of rats were anesthetized with enflurane: a control group without impairment of renal function (n = 7); a group with minimal impairment of renal function (n = 6); and a group with moderately severe renal impairment (n = 9). Another group of rats with moderately severe renal impairment (n = 8) was anesthetized with halothane. Two hours of anesthesia resulted only in mild transient depression of urea clearance in all groups. Six hours of anesthesia resulted in a 5 to 10 ml/day increase of urinary output in all groups and small increases in urea nitrogen levels in both groups with moderately severe renal impairment. Deterioration of the model was noted late in the experiment; at sacrifice, animals that had been anesthetized with enflurance and four with halothane had terminal renal failure. The morphological lesion in both groups was similar, resembling glomerulonephritis. Thus, there was no difference in the renal response to enflurane or halothane anesthesia among rats with chronic renal insufficiency.
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PMID:Renal effects of enflurane anesthesia in Fischer 344 rats with pre-existing renal insufficiency. 49 Mar 24

A patient with hereditary angio-oedema (HAO) developed mesangiocapillary glomerulonephritis (MCGN) under observation. HAO is characterized by an inherited defect of complement-deficiency of C1 esterase. MCGN is often associated with another complement abnormality which leads to depression of serum C3 and there is some evidence that the complement abnormality precedes the nephritis. The coincidence of these two rare diseases in the present patient, and in one previously described, suggests that other complement abnormalities may predispose to the development of MCGN.
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PMID:Hereditary angio-oedema with mesangiocapillary glomerulonephritis. 59 84

Thirty-three nephrotic patients were studied for IgG-subclass levels in matched pairs of serum and urinary specimens. Levels in the serum were compared with those found in the sera of non-nephrotic control children and normal adults. Results have shown an asymmetric depression in the serum level of certain IgG subclasses in some patients with minimal-change nephrotic syndrome, focal glomerulosclerosis, and proliferative glomerulonephritis, indicating that the urinary loss of IgG alone cannot account for the low blood levels of this immunoglobulin class in these conditions.
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PMID:Asymmetric depression in the serum level of IgG subclasses in patients with nephrotic syndrome. 89 Oct 26

A new procedure, plasma fibrinogen chromatography, has been utilized, together with other blood coagulation assays, to quantify fibrin formation in 43 children with acute poststreptococcal glomerulonephritis (AGN) from the time of hospitalization until recovery. During the prediuretic phase of AGN, significant evidence for substantial increase in fibrin formation (intravascular coagulation) included gross increase in plasma high molecular weight fibrinogen complexes (HMWFC), the development of either hypo- or hyperfibrinogenemia and gross depression of coagulation factor XIII concentration and of alpha2-macroglobulin concentration. During the diuretic phase of the disease, these abnormalities regressed and evidence of enhanced plasma fibrinolytic activity, documented by an increase in fibrinogen first derivative, was detected. Concomitantly, urinary excretion of fibrin(ogen) degradation products (FDP) underwent substantial increase. With disease recovery, which occurred in all children, urinary FDP excretion ceased and all coagulation findings normalized.
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PMID:Pathophysiological response of the blood coagulation system in acute glomerulonephritis. 99 77

The present report outlines the clinical features of a 2-year-old boy who following varicella developed purpura of the lower extremities, transient gastrointestinal bleeding and glomerulonephritis. The triad of symptoms suggests Schonlein-Henoch Syndrome, but coagulation studies and renal biopsy did not confirm this, and varicella is thought to be the cause of the complications. Therapy with corticosteroids and azathioprine had only a minor effect on the nephritis but caused depression of serum IgG and specific antibody resulting in reinfection or reactivation of varicella.
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PMID:Varicella followed by glomerulonephritis. Treatment with corticosteroids and azathioprine resulting in recurrence of varicella. 108 27

Following acceptance to a renal dialysis therapy program, 13 patients underwent serial examination of the serum complement system for periods of 6 to 12 months. Serum levels of C3 and C4 were examined at monthly intervals before the first dialysis of each month. The patients suffered from various primary renal diseases, including glomerulonephritis, obstructive uropathy with chronic pyelonephritis, nephrosclerosis and chronic nephropathy of undetermined nature. Levels of serum C3 were depressed at some time during the study period in all patients. Serum C4 levels were normal. The depression of serum C3 levels was significant and prolonged in nine patients. There seemed to be no relationship between the nature of the basic disease and the depression of serum C3 levels. Caution should be exercised in attributing depressed C3 levels to a particular type of underlying renal disease in patients on renal dialysis.
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PMID:Levels of serum complement components in patients undergoing renal dialysis. 114 Sep 50

To assess the subacute toxicity of 6-amidino-2-naphthyl 4-[(4,5-dihydro-1H-imidazol-2-yl)amino] benzoate dimethanesulfonate (FUT-187) a 13 week subacute toxicity study by gavage was done in Cynomolgus monkeys at dosage levels of 0, 15, 45 and 135 mg/kg/day. Deaths were seen in the 135 mg/kg/day group; with associated debility. The animals that died had high plasma levels of FUT-187. Little weight gain was seen in the 135 mg/kg/day group. There were no clear treatment related effects on ophthalmoscopy or electrocardiography or on hematological, biochemical or urinalysis. There were no effects noted at necropsy or on histopathology and the causes of death for each of the 3 animals that died were suppurative glomerulonephritis, bone marrow depression and possible gavage injury respectively. The no-effect level for toxicology was considered to be 45 mg/kg/day.
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PMID:The evaluation of 6-amidino-2-naphthyl 4-[(4,5-dihydro-1H-imidazol-2-yl)amino] benzoate dimethanesulfonate (FUT-187) by oral administration in cynomolgus monkeys in a 13 week subacute toxicity study. 129 20

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

Sixty patients with chronic renal failure (CRF) were studied for the rates of lipid peroxidation (LPO), the state of the antioxidative system (AOS) as well as for the morphofunctional state of biomembranes in renal tubules measured by excretion of low-molecular compounds tested in urine x by means of proton nuclear magnetic resonance spectroscopy. The control group numbered 35 patients with glomerulonephritis free of functional disturbances in the kidneys. The increased values of malonic dialdehyde levels in red blood cells and blood serum and those of diene conjugates in red blood cell membranes provide evidence for a significant increase of the LPO levels. Furthermore, depression of the AOS was revealed, manifested by the decreased levels of blood serum alpha-tocopherol as well as by unstable levels of superoxide dismutase in red blood cells. In the presence of the high LPO levels significant tubular dysfunctions were progressing, parallel with aggravation of renal function. Disturbances detected in excretion and reabsorption of amino acids (leucine, alanine, glycine, valine, histidine), thin organic acids and ketone bodies in CRF patients point to the existence of disturbances in tubular membranes. Tubular dysfunction appears to be caused by the disturbances of the biomembrane morphofunctional states induced by the high levels of free radical oxidation as well as by the AOS function failure.
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PMID:[Free radical oxidation and tubular dysfunctions in patients with chronic kidney failure]. 194 50

In Brown-Norway (BN) rats mercuric chloride induces an autoimmune disease characterized by an increase in serum IgE concentration, and by the production of anti-glomerular basement membrane antibodies responsible for a glomerulonephritis with a heavy proteinuria. (i) This disease results from a B-cell polyclonal activation probably due to frequent anti-class II T cells. (ii) The self limitation observed in this model is associated with both a decrease in the frequency of anti-class II T cells and the emergence of CD8+ T cells able to suppress these autoreactive T cells. (iii) In Lewis (LEW) rats which do not develop autoimmunity, HgCl2 provokes the appearance of non-antigen-specific CD8+ T cells responsible for a depression of T-cell functions. The aim of this work was to test the effect of treatment with an anti-CD8 monoclonal antibody (MoAb) in both BN and LEW rats. Anti-CD8 MoAb-treated rats were effectively depleted in CD8+ T cells. However, neither the induction nor regulation phases of mercury-induced autoimmunity were modified in BN rats. Mercury-induced immunosuppression in LEW rats was abrogated; however, depletion in CD8+ T cells did not allow the disease to occur in that strain. Finally, CD8 depletion induced in normal BN rats the appearance of rare anti-class II T cells showing that these cells are normally present in that strain but negatively controlled by suppressor T cells.
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PMID:Role of CD8+ T cells in mercury-induced autoimmunity or immunosuppression in the rat. 213 55


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