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)

Although the precise etiologic incitant of the minimal lesion idiopathic nephrotic syndrome of childhood is not known, it is likely that a host mechanism mediates the permeability alterations of the glomerular capillary wall resulting in massive proteinuria. As a first step in examining the possibility that local kinin release may account for the proteinuria in this disorder, two parameters of the plasma kinin-generating system, plasma prekallikrein and kallikrein inhibitor, were assayed during 27 nephrotic episodes in 21 corticosteroid-responsive children. Plasma kallikrein was assayed by means of its esterase activity on a synthetic arginine ester substrate, N-alpha-tosyl-L-arginine methyl ester (TAMe), after activation of Hageman factor by kaolin. This activity, after subtraction of spontaneous arginine esterase activity (i.e., TAMe esterase activity measured in plasma not exposed to kaolin) is derived from prekallikrein. Plasma prekallikrein activity in 11 normal children was 99.6 +/- 2.9 mumol TAMe hydrolyzed/ml plasma/hr (mean +/- SEM). Kallikrein inhibitor was quantified in arbitrary units. Kallifrein inhibitor activity in 11 normal children was 0.94 +/- 0.04 units. During the overt nephrotic syndrome, before initiation of intensive daily corticosteroid treatment, mean values were: prekallikrein, 58.5 +/- 7.24 mumol/ml/hr; and kallikrein inhibitor, 0.35 +/- 0.06 units. After corticosteroid-induced remission occurred, mean values were: plasma prekallikrein, 118.6 +/- 3.2 mumol/ml/hr; and kallikrein inhitor, 0.78 +/- 0.03 mumol/ml/hr. Both parameters were again assayed in 14 of the 21 children after complete cessation of corticosteroid treatment. Plasma prekallikrein was normal, 99.6 +/- 4.8 mumol/ml/hr; but kallikrein inhibitor was still somewhat depressed, 0.84 +/- 0.03 units. A subset of 9 patients had marked depression of plasma prekallikrein to levels less than 20 mumol/ml/hr and essentially undetectable inhibitor activity. Serum alpha-2 macroglobulin was elevated in nephrotic patients: mean value during relapse, 862 +/- 29 mg/100 ml; during corticosteroid-maintaining remission, 615 +/- 29 mg/100 ml. After cessation of corticosteroids, mean serum level was 481 +/- 20 mg/100 ml. The proportional reduction of plasma prekallikrein and kallikrein inhibitor suggested that an enzyme-inhibitor complex formed in vivo, perhaps at a local site of activation in proximity to the glomerular basement membrane. These data suggest that the plasma kinin-generating system may be the host effector mechanism subserving the increased glomerular capillary permeability in the minimal lesion nephrotic syndrome of childhood.
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PMID:A study of the plasma kinin-generating system in children with the minimal lesion, idiopathic nephrotic syndrome. 5 8

A patient with nephrotic syndrome in association with partial lipodystrophy is reported. The features of partial lipodystrophy are well recognized and the renal lesion is a mesangiocapillary glomerulo-nephritis of a dense deposit type with an associated depression of C3. This type of kidney involvement is becoming increasingly recognized as common in the syndrome of partial lipodystrophy.
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PMID:Partial lipodystrophy with nephrotic syndrome. 66 98

We have studied sodium retention during volume expansion in rats with autologous immune complex nephropathy (AICN), a model of nephrotic syndrome (NS) in which GFR after volume expansion was not different from that in adjuvant-injected controls (C). AICN rats developed heavy proteinuria (298 +/- 27 vs. less than 10 mg/day), hypoalbuminemia (2.14 +/- 0.15 vs. 3.08 +/- 0.12 g/100 ml) and hypercholesterolemia (181 +/- 22 vs. 58 +/- 4 mg/100 ml). After saline, there were no significant differences in blood pressure (119 +/- 2 vs. 114 +/- 2 mm Hg), renal plasma flow (4.9 +/- 0.41 vs. 4.1 +/- 0.28 ml/min), inulin clearance (1.37 +/- 0.06 vs. 1.55 +/- 0.10 ml/min), or SNGFR (47 +/- 2 vs. 53 +/- 4 nl/min). Sodium excretion, however, was significantly lower in NS rats (4.7 +/- 1.1 vs. 9.2 +/- 1.2 muEq/min). Proximal sodium reabsorption was decreased in NS rats (35 +/- 2 vs. 41 +/- 2%, 2.5 +/- 0.2 vs. 3.3 +/- 0.2 nEq/min). Sodium delivery into the loop, however, was equal in NS and C, since the slightly lower filtered load in NS rats offset the depression in proximal reabsorption. Sodium reabsorption by the loop and by the distal convoluted tubules were equal in NS and C. Thus, sodium delivered into the cortical collecting ducts was the same in both groups (0.33 +/- 0.17 vs. 0.34 +/- 0.07 nEq/min; 4.5 +/- 0.6% of filtered sodium vs. 4.4 +/- 0.3%). The percent of filtered sodium excreted in the urine, however, was significantly lower in the NS rats, 2.18 +/- 0.48% vs. 4.0 +/- 0.58%. We conclude that antinatriuresis in this model of NS is determined beyond the superficial late distal convoluted tubule. The inability to excrete the sodium load during volume expansion is due to either enhanced reabsorption by the collecting duct or to abnormal function in deep nephrons.
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PMID:Renal sodium retention during volume expansion in experimental nephrotic syndrome. 75 Jun 93

Three cases are described showing a seasonal exacerbation of their nephrotic syndrome in association with an atopic trait and grass pollen allergy. The first patient has a history of four consecutive seasonal relapses each requiring steroid therapy. Following a course of desensitization injections he has now been free of relapse for 3 consecutive years. The second patient has also had a recurrent steroid-sensitive nephrotic syndrome often associated with the pollen season and allergic rhinitis. In this patient a course of cyclophosphamide has reduced his tendency to relapse. The third patient who has been on continuous prednisone therapy shows a seasonal increase in proteinuria. Serum changes in the first two patients include: a seasonal rise in total and grass pollen specific IgE; the continued presence of grass pollen specific IgG throughout the year but with a reduction during the pollen season in association with a more pronounced fall in the total IgG level; a depression in the C3 level in association with each major relapse; a mild rise in the I-K titre and a positive result in the Clq test for circulating complexes. A renal biopsy performed on the first patient when in relapse showed minor histological changes only and IgG, IgM, IgA, IgD, IgE, C3 and fibrinogen were undetectable by immunofluorescent examination. The probable mechanism for the development of proteinuria in these patients is discussed.
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PMID:Seasonal nephrotic syndrome. Description and immunological findings. 80 95

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

Cancer chemotherapy with anthracyclines, of which doxorubicin (DX2) is the main representative, is limited by cardiomyopathy developing in animals and patients after cumulative dosing. The toxicity is probably related to free radical formation by the anthracycline as well as its metabolites with concomitant O2.- and .OH generation resulting in lipid peroxidation and subsequent membrane damage. An in vitro model is required to investigate the individual contribution of each metabolite to cardiotoxicity. For in vivo studies, the species of choice is the mouse because it lacks the DX-induced nephrotic syndrome seen for instance in rats and rabbits. Thus, isolated mouse heart muscle was chosen as an in vitro model. To characterize the model, we used l-isoprenaline/dl-propranolol and metacholine/atropine to measure the beta-adrenergic and the muscarinic responses of (spontaneously beating) right and (paced) left atrium. Dose response curves (n greater than or equal to 4) were highly reproducible: pD2,iso = 8.0 +/- 0.3 (left) and 8.5 +/- 0.4 (right); pD2,met = 6.7 +/- 0.1 (left) and 6.2 +/- 0.3 (right). Propranolol as well as atropine behaved as competitive antagonists, with pA2-values of 8.4 +/- 0.2/8.5 +/- 0.2 (l/r) and 9.1 +/- 0.1/9.1 +/- 0.2 (l/r), respectively. These values corresponded to those obtained with other organ preparations. We tested the effect of DX in two ways: a) by measuring the direct inotropic and chronotropic effect during 60 minutes of incubation with 10-100 microM DX in the organ bath, and b) by determining the remaining beta-adrenergic response to l-isoprenaline after the incubation period. Both variables turned out to be equally affected. For paced left atria an IC50 (causing 50% depression of contractile force) of 35 microM was determined. Right atria stopped beating at concentrations above 50 microM, thus hampering IC50 determination. The results indicate that anthracyclines exert an effect not related to receptor integrity, but directly to the functionality of heart muscle. To check whether radical stress can be involved in the observed negative inotropic effect, incubations with xanthine/xanthine oxidase (to produce reactive oxygen species) were performed. A pronounced negative effect on mouse atrial contraction was indeed observed. However, initially a positive inotropic effect accompanied by an increased resting tension were seen. It can be concluded that mouse atrium can be used as a model to compare anthracyclines and their metabolites with regard to their acute cardiotoxic effects.
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PMID:Isolated mouse atrium as a model to study anthracycline cardiotoxicity: the role of the beta-adrenoceptor system and reactive oxygen species. 216 63

Characteristics of the membranous lesion are usually the capillary wall thickening in morphology and the clinical manifestation of a nephrotic syndrome. As entities of such a lesion the following types of glomerulonephritis (GN) could be considered: (peri-) membranous GN, garland type of postinfectious GN, and membranoproliferative (MP) GN. The morphological, especially the electronmicroscopical observations relative to separate immune deposit locations in the capillary wall--subendothelial, intramembranous, subepithelial--are the basis to differentiate the diseases as entities. The characteristic finding of the (peri-) membranous GN is the presence of subepithelial immune deposits along the capillary walls, which are separated by "spikes" and later on are incorporated into the basement membrane, while some of the deposits became rarefied; on the other hand, new subepithelial deposits can be observed when the disease of the most common idiopathic form starts again after a period of remission.--The deposits of the garland type of the postinfectious GN--the disease is more often a chronic progressive process than the other types of postinfectious GN--are in a subepithelial location. In contrast to the former the deposits vary in size and number and only some capillary walls are affected.--In type I of the MPGN the immune deposits are located mainly in a subendothelial position, often together with a mesangial interposition in such a manner, that the capillary wall has the appearance of "double contour" histologically. The most striking change of type II is the presence of dense deposits in the lamina densa of the capillary basement membrane ("dense deposit GN"). In type III of MPGN the deposits are located in all three positions of the capillary wall--subendothelial, intramembranous, subepithelial--and the lamina densa is markedly disrupted (little or no affinity for silver in thin sections after silver impregnation). Concerning the entity of the 3 types of MPGN, the depression of serum complement and the complement activating C3-nephritis factor are persistent features of type II, while these findings are obvious only in 50% of type I and III-diseases.
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PMID:[Clinical pathology of the glomerulus--from phenomenon to entity. The membranous lesion]. 248 36

We have studied a girl seven and a half years old with a renal disease manifested by proteinuria and nephrotic syndrome combined with initial macroscopic hematuria normal blood pressure and persistent depression of the complement C3 levels with the complement activating gamma globulin (C3 Nef) present in serum. The anatomopathological study showed findings of membranoproliferative glomerulonephritis type II with intramembranous deposit (dense deposit disease). An unusual association with partial lipodystrophy was present in this case. A follow-up of five years, and a few considerations about etiopathogenic theories were presented.
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PMID:[Partial lipodystrophy and membranoproliferative glomerulonephritis. Apropos of a case]. 267 78

To determine whether the hypogammaglobulinemia of childhood nephrotic syndrome is characterized by symmetric depression of the IgG subclasses, the authors compared the IgG subclass concentrations in nephrotic patients in relapse versus remission. The authors used a highly sensitive monoclonal antibody-based enzyme immunoassay that allows quantitation with comparable precision of all four subclasses. They analyzed 28 sera obtained from 22 nephrotic patients during relapse (n = 16) and/or remission (n = 12). The mean ages of the two groups were similar. IgG1 and IgG2 were significantly decreased during relapse compared with remission, whereas IgG3 and IgG4 were not significantly different. This pattern of asymmetric depression of IgG subclasses supports a cause other than urinary losses in the pathogenesis of this abnormality.
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PMID:IgG subclasses in children with nephrotic syndrome. 275 Jul 9

We describe a 10 year old patient admitted to the Children's Hospital of Buffalo with hypocomplementemia associated with steroid responsive minimal change nephrotic syndrome. The sibling also had a low serum C3 concentration and all family members studied had C3 slow phenotypes. Factor I levels were at the lower limit of normal in the patient and his brother. Functional assays for CH50, total hemolytic C3 and serum concentration of C2, C4-C9 and factors B and H were all within normal limits. This case confirms that a depressed serum complement level can occur in minimal change nephrotic syndrome and indicates that this depression could represent a preexisting inherited rather than an acquired deficiency. The findings are consistent with the presence of a null or hypomorphic C3 slow allele in hypocomplementemic family members. Additional studies are needed to resolve the association between the inherited partial C3 deficiency and minimal change nephrotic syndrome.
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PMID:Hereditary partial deficiency of the third component of complement associated with minimal change nephrotic syndrome. 315 40


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