thromboxane-b2 and Nephrotic-Syndrome

To observe the clinical effect of Modified Taohong Siwu Decoction (MTSD) in treating pediatric intractable nephropathy (PIN).. Ninety-five cases of PIN were divided into 2 groups at random. The 60 cases in the treated group were administered with MTSD and the 35 patients in the control group were treated with heparin. The clinical therapeutic effect and levels of thromboxane B2(TXB2) and 6-keto-prostaglandin F1 alpha before and after treatment were observed.. The total effective rate of the treated group was 81.7%, which was similar to that in the control group (80.0%, P > 0.05). The levels of TXB2 and TXB2/6-ketoprostaglandin F1 alpha ratio were higher in both groups of patients as compared with those of the healthy control (P < 0.01), After treatment, the two criteria were significantly improved in the two groups, as compared with those before treatment, the difference was significant (P < 0.01), while in comparson between the treated and the control group, no significant difference was found (P > 0.05).. MTSD has good effect in treating PIN, it could improve the metabolic unbalance of thromboxane and prostacyclin.

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Child; Child, Preschool; Drug Therapy, Combination; Drugs, Chinese Herbal; Female; Heparin; Humans; Male; Nephrotic Syndrome; Phytotherapy; Thromboxane B2

To explore the mechanism of Buyang Huanwu Decoction (BHD) in treating primary nephrotic syndrome (PNS).. Based on the treatment of prednisone acetate and cytoxan, two groups of PNS patients were treated with aspirin and persantin (western medicine group, 35 patients) and BHD and western medicine (TCM-WM group, 35 patients) respectively. The effect on anticoagulation was observed and compared. Plasma levels of thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6-Keto-PGF1 alpha), endothelin (ET), calcitonin gene related peptide (CGRP) were determined before and after treatment, and at the time of reducing dose and turning to maintenance dose of prednisone. The therapeutic effect of the two groups were also observed. Another group of 30 healthy person was established for control.. The difference of TXB2, 6-Keto-PGF1 alpha, ET, CGRP between patients and healthy persons was very significant before treatment (P < 0.001). Above-mentioned 4 parameters improved synchronously with the clinical improvement in the therapeutic course and they were better in the TCM-WM group than those in the western medicine group (P < 0.001) and the complete remission rate of the former group was also higher than that of the latter (62.9% vs 37.1%, chi 2 = 4.63, P < 0.05).. BHD could improve the therapeutic effect in treating PNS through the mechanism of improving TXB2, 6-Keto-PGF1 alpha, ET and CGRP levels.

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Calcitonin Gene-Related Peptide; Drug Therapy, Combination; Drugs, Chinese Herbal; Endothelins; Female; Humans; Male; Middle Aged; Nephrotic Syndrome; Prednisone; Thromboxane B2

Platelet function was studied in 56 children with nephrotic syndrome, 33 were on oral prednisolone (P) treatment (group 1), while 23 were in early (< 6 months) remission (group 2): 12 on P (group 2a) and 11 not on P (group 2b), and there were 18 controls (group 3). The following tests were used: platelet aggregation with collagen in a laser rheoaggregometer; adenosine triphosphate (ATP) release: during aggregation with luciferin-luciferase in a lumiaggregometer; thromboxane B2 (TXB2) release: by radioimmunoassay; platelet cAMP concentration: by binding assay. The changes in plasma cholesterol (C) and triglycerides (TG) were compared with the platelet aggregation results. Patients in group 1 and 2 exhibited significantly higher aggregability, TXB2 release and ATP release in response to collagen than those in group 3 (p < 0.01), but there was no difference between groups 1 and 2 or groups 2a and 2b. Some differences were observed between the histological groups. Patients with IgA and SLE nephropathy displayed higher aggregability than those with minimal change nephrotic syndrome in remission (p < 0.05). The highest level was in membranous nephropathy. The platelet cyclic adenosine monophosphate (cAMP) concentration was significantly lower in groups 1 and 2 than in group 3 (p < 0.001). No differences were observed between groups 1 and 2 or between groups 2a and 2b. Plasma C and TG levels did not show any correlation with the platelet aggregation.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adenosine Triphosphate; Adolescent; Blood Platelets; Child; Child, Preschool; Cholesterol; Cyclic AMP; Female; Humans; In Vitro Techniques; Male; Nephrotic Syndrome; Platelet Aggregation; Prednisolone; Thromboxane B2; Triglycerides

While cyclosporine A (CsA) is an effective therapy for nephrotic syndrome, it has nephrotoxic side effects. We compared the anti-proteinuric effects and nephrotoxicity in rats with passive Heymann nephritis (PHN) of CsA and mycophenolate mofetil (MMF).. PHN was induced in female Wistar rats. Two treatment groups consisting of 8 rats each received either 25 mg of CsA or 25 mg of MMF/kg body weight/day and were compared with untreated controls. Kidney function and proteinuria were monitored over 4 weeks. Western blots were used for densitometric analysis of renal cyclooxygenase-2 (COX-2) protein expression. Thromboxane B2 (TxB2) and 6-keto-PGF(1alpha) were determined by radioimmunoassays (RIAs) in renal tissue and urine.. Rats with PHN exhibited a marked proteinuria of 12.76 +/- 4.42 vs. 0.73 +/- 0.28 mg/24 h (p < 0.01) and showed increased glomerular concentrations of TxB2 and 6-keto-PGF(1alpha) (992.6 +/- 216.9 and 1,187.0 +/- 54.2 pg/mg protein, respectively) compared with healthy controls (595 +/- 196.17 and 729 +/- 297.84, respectively) and a strongly induced COX-2 protein expression. CsA and MMF treatment reduced PHN-related proteinuria to 2.10 +/- 1.47 and 1.47 +/- 7.2 mg/24 h, respectively. In rats with PHN, CsA induced a significant deterioration of renal function and enhanced urine excretion of thromboxane A2, paralleled by a significant, twofold increase in COX-2 protein expression and renal prostaglandins. By contrast, MMF treatment in rats with PHN was not nephrotoxic and had no effect on prostaglandin production. COX-2 protein expression under MMF was suppressed.. While the antiproteinuric efficacy of MMF and CsA in PHN was comparable, the absence of nephrotoxicity might favor MMF in the treatment of nephrotic syndrome. The CsA-induced increase in COX-2 expression and COX-2-dependent prostacyclin may indicate a mechanism that compensates nephrotoxicity in the diseased and CsA-exposed kidney.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Blotting, Western; Cyclooxygenase 2; Cyclosporine; Enzyme Inhibitors; Female; Glomerulonephritis; Mycophenolic Acid; Nephrotic Syndrome; Rats; Rats, Wistar; Thromboxane B2

In order to examine the intracellular thromboxane A2 (TXA2) signal transduction system in platelets of patients with nephrotic syndrome, we measured the levels of TXA2 metabolites in urine and blood and platelet calcium ion level as a result of STA2, an analog of STA2 (9,11-dimethylmethano-11,12-methano-TXA2) stimulation, and obtained the following results: (1) In pediatric patients with nephrotic syndrome, urinary thromboxane B2 (TXB2) and 11-dehydro-TXB2 excretion were signficantly higher in the onset and relapse groups compared to the remission and control groups. (2) The blood 11-dehydro-TXB2 level in the onset group was significantly higher than those in the remission and control groups. (3) Platelet calcium concentrations due to STA2 stimulation were significantly increased in the onset, relapse and remission groups compared to the control group. These findings suggest activation of the TXA2 signal transduction system in platelets of pediatric patients with nephrotic syndrome.

Topics: Blood Platelets; Calcium; Child; Child, Preschool; Female; Humans; Male; Nephrotic Syndrome; Thromboxane A2; Thromboxane B2

For the purpose of clarifying the changes occurring in thromboxane (TX)A2 metabolism in the platelet of nephrosis patients, we investigated the changes in platelet sensitivity to TXA2 and the changes in TXA2 production in pediatric patients with nephrotic syndrome (N.S.) using STA2 which is an analogue of TXA2 and ONO 3708 which is a TXA2 receptor antagonist. The subjects investigated in the present study consisted of 11 cases with initial onset of N.S. (onset group), 15 relapse patients (relapse group) and 15 children with N.S. without any recurrence in the past 6 months (remission group) as well as 25 normal children (control group). The results were as follows: (1) Platelet aggregation attributable to STA2 stimulation was enhanced at the onset and relapse of N.S. (2) Sensitivity to TXA2 was enhanced in the platelets of patients in the relapse group. (3) Though some demonstrated enhanced platelet sensitivity to TXA2, while others in the onset group did not, enhanced sensitivity was observed in all the patients along with an improvement in hypoalbuminemia. (4) The amount of daily urinary excretion of TXB2 and 11-dehydro-TXB2 in the onset group and relapse group was increased in comparison with the status in the remission group and control group. The above results demonstrated enhanced platelet sensitivity to TXA2 and increased biological production of TXA2 in patients with N.S., suggesting that TXA2 metabolism in the platelet is deeply involved in the pathophysiology of N.S.

Topics: Adolescent; Blood Platelets; Child; Child, Preschool; Female; Humans; Male; Nephrotic Syndrome; Platelet Aggregation; Recurrence; Serum Albumin; Thromboxane A2; Thromboxane B2

Topics: Humans; Hypercholesterolemia; Nephrotic Syndrome; Platelet Aggregation; Pravastatin; Serum Albumin; Thromboxane B2

Plasmic and urinary TXB2 and 6-Keto-PGF1 alpha of 87 patients of nephrotic syndrome (NS) and 25 healthy subjects were measured by RIA, and the influence of Yiqi Huoxue Jiedu decoction (YHJ) and corticosteroid on above-mentioned parameters was investigated.. Plasmic and urinary TXB2 as well as the ratio of TXB2/6-K-PGF1 alpha of both types of NS increased (P < 0.01-0.05). The plasmic TXB2 of II type was higher than that of I type of NS (P < 0.01), 6-K-PGF1 alpha increased as well (P < 0.05). After treatment, plasmic and urinary TXB2 of both types of NS were remarkably lower (P < 0.01), while urinary 6-K-PGF1 alpha increased significantly (P < 0.05). In comparing with pre-treatment investigation, the plasmic 6-K-PGF1 alpha of II type was reduced (P < 0.05). It was shown that YHJ would inhibit the synthesis of TXA2 and regulate the TXA2-PGI2 balance. YHJ was markedly effective in producing TXB2 and 6-K-PGF1 alpha increase, its therapeutical effects was better to patients with Yin Deficiency and both Qi-Yin Deficiency, but not so well with Yang Deficiency Syndrome.

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Cyclophosphamide; Drugs, Chinese Herbal; Female; Humans; Male; Middle Aged; Nephrotic Syndrome; Prednisone; Thromboxane B2; Yin Deficiency

In accordance with the results of examining 40 children with nephrotic and mixed glomerulonephritis, it has been established that in the pathogenesis of the nephrotic syndrome of paramount importance is imbalance of the output of renal prostanoids, manifesting in the predominance of the vasopressor and proaggregate fraction--thromboxane A2 and in the deficiency of its antagonist prostacyclin that exerts a protective action on glomerular filtration. Sodium and water retention in patients with the nephrotic syndrome favours an increase of the content of antidiuretic hormone and plasma renin activity.

Topics: 6-Ketoprostaglandin F1 alpha; Child; Circadian Rhythm; Dinoprost; Dinoprostone; Humans; Nephrotic Syndrome; Renin-Angiotensin System; Thromboxane B2; Vasopressins; Water-Electrolyte Balance

Renal vasoconstriction has been implicated as a major contributing factor for the nephrotoxic effects of cyclosporine. In an attempt to assess the relative contribution of thromboxane (Tx), the effects of coadministering CsA with the selective Tx synthetase inhibitor, Dazmegrel (DAZ) (Pfizer, Inc.), were determined. Rats were treated orally with 50 mg/kg of DAZ plus 50 mg/kg of CsA and various indicators of nephrotoxicity and efficacy were assessed. Animals treated with CsA + DAZ had a normalization of renal TxB2 synthesis as compared with animals treated with CsA alone (160 vs. 338 pg/ml). Kidney proximal tubule damage following CsA treatment alone was also reduced in animals coadministered DAZ, as indicated by reduced urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) (9.7 vs. 14.1 U/g creatinine) and by histological examination of kidney sections. However, DAZ did not affect blood levels of CsA nor its efficacious activity in a model of experimental allergic encephalomyelitis (EAE). These studies suggest a major role of elevated thromboxane production in the acute nephrotoxic effects of CsA and demonstrate a reduction in this toxicity by DAZ without altering CsA's efficacious activity.

Topics: Acetylglucosaminidase; Amino Acid Sequence; Animals; Chromatography, Gel; Chromatography, High Pressure Liquid; Creatinine; Cyclosporine; Drug Antagonism; Encephalomyelitis, Autoimmune, Experimental; Imidazoles; Kidney; Kidney Tubules, Proximal; Male; Molecular Sequence Data; Nephrotic Syndrome; Rats; Rats, Inbred F344; Thromboxane B2; Thromboxane-A Synthase; Vasodilator Agents

The administration of the aminonucleoside of puromycin (PAN) to rats causes the nephrotic syndrome that is associated with an acute decline in renal function, and an interstitial infiltrate. We examined whether essential fatty acid deficiency (EFAD), which inhibits macrophage infiltration in glomerulonephritis, affects PAN-induced renal dysfunction. Both control and EFAD rats developed proteinuria that resolved over 28 d. After PAN administration, there was a prominent infiltration of macrophages in rats fed a normal diet. The infiltrate was prevented by the EFAD diet. The absence of a macrophage interstitial infiltrate was associated with a significantly higher Cin in the EFAD rats than in controls at 7 d (5.21 +/- 1.19 versus 0.39 +/- 0.08, P less than 0.002 ml/min/kg BW). In addition, CPAH fell to less than 10 ml/min/kg BW by day 7 in controls, but remained the same as normal in the EFAD. After administration of PAN to control rats, there was no increase in urinary thromboxane excretion or an increase in glomerular thromboxane production. Furthermore, the effect of EFAD could not be mimicked by the administration of a thromboxane synthase inhibitor. Irradiation-induced leukopenia in rats on a normal diet markedly improved glomerular filtration and renal blood flow in acutely nephrotic rats. EFAD prevents the interstitial cellular infiltrate and the renal ischemia associated with experimental nephrosis. The recruitment of mononuclear cells into the kidney following PAN directly contributes to the decline in renal function.

Topics: Acute Disease; Animals; Fatty Acids, Essential; Female; Kidney; Kidney Diseases; Leukopenia; Macrophages; Methacrylates; Nephrotic Syndrome; Puromycin Aminonucleoside; Rats; Rats, Inbred Lew; Thromboxane B2

Platelet aggregation, beta-thromboglobulin (beta-TG) and platelet factor 4 (PF 4) release and thromboxane B2 (TxB2) formation in stimulated platelet-rich plasma were investigated in 13 patients with nephrotic syndrome who had normal serum creatinine levels (creatinine clearance greater than 70 ml/min/1.73 m2). In contrast to 13 sex- and age-matched controls, spontaneous platelet aggregation only occurred in patients with nephrotic syndrome with correlation to serum albumin and plasma fibrinogen levels. The EC50 (estimated concentration of aggregating agent to cause half maximum velocity of primary aggregation) for ADP and collagen and threshold concentration of arachidonic acid (threshold AA) were decreased in patients with nephrotic syndrome, reflecting a hyperaggregable state. In patients with nephrotic syndrome EC50 ADP values were significantly correlated to serum albumin, serum cholesterol and plasma fibrinogen, however, EC50 collagen or threshold AA did not correlate to these parameters. Plasma beta-TG levels were increased in patients, whereas plasma PF 4 levels were not significantly changed in patients compared to controls. In vitro TxB2 formation was elevated in patients only after stimulation with AA. Nevertheless, after stimulation with collagen and ADP, TxB2 formation was unchanged in patients compared to controls. Platelet hyperaggregability in nephrotic patients was confirmed in our study. However, unchanged thromboxane B2 formation after collagen stimulus as well as missing correlations between EC50 collagen or threshold AA and serum albumin were contradictory to the hypothesis that enhanced AA availability due to hypoalbuminemia is responsible for platelet hyperaggregability. Platelet hyperaggregability in terms of EC50 ADP being associated with serum albumin levels as well as to serum cholesterol and plasma fibrinogen indicate a multifactorial genesis.

Topics: beta-Thromboglobulin; Female; Humans; Male; Middle Aged; Nephrotic Syndrome; Platelet Aggregation; Platelet Factor 4; Radioimmunoassay; Thromboxane B2

To determine if a selective thromboxane (TX)A2 synthetase inhibitor is clinically effective for the treatment of nephrotic syndrome, 11 patients with nephrotic syndrome were treated only with OKY-046, (E)-3-4-(1-imidazolylmethyl)phenyl-2-propenoic acid hydrochloride monohydrate, for at least 8 weeks. Urinary excretion of protein, TXB2, 2,3-dinor-TXB2, and beta-N-acetyl-D-glucosaminidase decreased with OKY-046. Creatinine clearance value, and urinary excretion of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), however, did not show any significant change, while serum albumin level increased. Two patients with minimal change nephrotic syndrome showed complete remission only with OKY-046. These results demonstrate that the selective TXA2 synthetase inhibitor is an effective drug for the treatment of chronic glomerulonephritis accompanied by nephrotic syndrome.

Topics: 6-Ketoprostaglandin F1 alpha; Acrylates; Adolescent; Adult; Aged; Female; Glomerulonephritis; Humans; Male; Methacrylates; Middle Aged; Nephrosis, Lipoid; Nephrotic Syndrome; Proteinuria; Thromboxane B2; Thromboxane-A Synthase

In 20 patients with nephrotic syndrome we confirm previous findings of in vitro platelet hyperaggregability to arachidonic acid, and describe similar hyperaggregability to ristocetin. As previously reported also, the addition of albumin to nephrotic platelet-rich plasmas corrected platelet hyperaggregability to arachidonic acid, but exerted little effect on ristocetin-induced aggregation, and there was no correlation between platelet aggregation thresholds to arachidonate and to ristocetin. Incubation with indomethacin abolished the generation of thromboxane B2 after stimulation with arachidonate, but had no effect on the stimulation with ristocetin, during which no TxB2 was produced. The nephrotic patients had elevated factor VIII-related antigen (Factor VIII R:Ag) concentrations in their plasma, but in addition both decreased serum IgG and platelet-associated IgG were found which were correlated. The hyperaggregability of nephrotic platelets to ristocetin may relate to the elevated factor VIII R:Ag levels, or to the low platelet-associated IgG, since platelet IgG Fc receptors and von Willebrand factor receptors are spatially close or identical.

Topics: Adult; Antigens; Arachidonic Acid; Arachidonic Acids; Blood Platelets; Factor VIII; Humans; Immunoglobulin G; In Vitro Techniques; Indomethacin; Male; Middle Aged; Nephrotic Syndrome; Platelet Aggregation; Ristocetin; Serum Albumin; Thromboxane B2; von Willebrand Factor

Topics: 6-Ketoprostaglandin F1 alpha; Female; Glomerulonephritis; Humans; Hypertension; Kidney Diseases; Liver Cirrhosis; Male; Nephrotic Syndrome; Radioimmunoassay; Thromboxane B2; Uremia

The production of malondialdehyde (MDA) and thromboxane B2 (TxB2) by platelets following an arachidonic acid (AA) challenge was greater in nephrotic platelet rich plasma (PRP) than in normal PRP. The uptake of 14C-AA, and its subsequent conversion to 14C-TxB2 following a thrombin stimulus, was also greater in nephrotic than normal PRP. Normal plasma diminished the MDA production by nephrotic platelets. The addition of albumin to nephrotic PRP, or, the intravenous infusion of albumin in quantities sufficient to correct hypoalbuminemia also diminished the excessive production of prostaglandin metabolites by nephrotic platelets. The platelet aggregate ratio (PAR), which measures circulating platelet aggregates, was abnormal during the acute phase of nephrotic syndrome but reverted to normal following remission. These data indicate that hypoalbuminemia is associated with increased AA metabolism by platelets and suggest that platelet "hyperactivity" may contribute to the proclivity toward thrombosis observed in nephrotic syndrome.

Topics: Albumins; Arachidonic Acid; Arachidonic Acids; Blood Platelets; Humans; Infusions, Parenteral; Malondialdehyde; Nephrotic Syndrome; Platelet Aggregation; Thromboxane B2

Glomerular arachidonate cyclooxygenation by isolated rat glomeruli was assessed in vitro in antiglomerular basement membrane (anti-GBM) antibody-induced glomerulonephritis by radioimmunoassay for prostaglandins (PG) and thromboxane. After a single intravenous injection of rabbit anti-rat GBM serum, we observed enhancement of glomerular thromboxane B2 (TxB2) synthesis as early as 2 to 3 h with smaller increments in PGF2 alpha, PGE2 and 6-keto-PGF1 alpha synthetic rates. On day 2 of the disease, the glomerular synthesis of TxB2 and, to a lesser extent, PGF2 alpha and PGE2 remained enhanced, whereas on days 8, 11, and 14, TxB2 was the only prostanoid synthesized at increased rates. Glomerular TxB2 synthesis correlated with the presacrifice 24-h protein excretion. 60 min after intravenous infusion of anti-GMB serum, glomerular filtration rate (GFR) decreased (0.66 +/- 0.04 to 0.44 +/- 0.03 ml/min per 100 g, P less than 0.05), without a significant change in renal plasma flow (RPF): 1.97 +/- 0.23 to 1.80 +/- 0.23 ml/min per 100 g) and without a change in glomerular PG synthetic rates. At 2 h, GFR and RPF reached a nadir (0.25 +/- 0.04 and 1.3 +/- 0.1 ml/min per 100 g, respectively) coinciding with a fivefold increment in glomerular TxB2. By 3 h GFR and RPF partially recovered to 0.43 +/- 0.07 and 1.77 +/- 0.20 ml/min per 100 g, respectively, P less than 0.05, despite further increments in TxB2 synthesis. This recovery of GFR and RPF coincided with increments in vasodilatory PG, (PGE2 and PGI2). The thromboxane synthetase inhibitor OKY-1581 markedly inhibited platelet and glomerular TxB2 synthesis and preserved GFR at 1, 2, and 3 h. Another thromboxane synthetase inhibitor, UK-38485, also completely inhibited platelet and glomerular TxB2 synthesis and prevented decrements of GFR at 2 and 3 h. A cyclooxygenase inhibitor, ibuprofen, inhibited platelet TxB2 and PGE2 synthesis and significantly reduced glomerular PGE2 but not TxB2 synthesis. In the ibuprofen-treated rats, the partial recoveries of GFR and RPF at 3 h were attenuated. The in vitro glomerular TxB2 synthesis correlated inversely with the presacrifice GFR and filtration fraction. These observations indicate that in anti-GBM nephritis there is enhanced synthesis of TxA2 and PG in the glomerulus that mediate changes in renal hemodynamics.

Topics: Animals; Blood Physiological Phenomena; Glomerular Filtration Rate; Glomerulonephritis; Ibuprofen; Kidney Glomerulus; Male; Methacrylates; Nephrotic Syndrome; Prostaglandin Antagonists; Prostaglandins; Rabbits; Rats; Rats, Inbred Strains; Renal Circulation; Thromboxane B2; Thromboxane-A Synthase; Thromboxanes

Increased platelet aggregability on stimulation with sodium arachidonate (NaAA), collagen and ADP was found in a group of 14 patients with nephrotic syndrome when compared with age and sex matched controls. Five of the group also exhibited spontaneous platelet aggregation (SPA), associated with synthesis of thromboxane B2 (TxB2), and which appeared to correlate with a markedly increased serum triglyceride concentration. Thromboxane B2 generation in response to NaAA was increased and reflected both the low serum albumin concentration and the platelet aggregation response to this agent. Addition of albumin in vitro decreased the amount of TxB2 generated for a given dose of NaAA and increased NaAA and collagen-induced platelet aggregation thresholds. However, albumin had no significant effect on collagen-induced TxB2 production. The results suggest that the hypoalbuminaemia and associated reduced binding of arachidonic acid and increased synthesis of TxA2 account in part for the increased platelet aggregability seen in the nephrotic syndrome but that other mechanisms are also involved.

Topics: Adenosine Diphosphate; Adolescent; Adult; Aged; Arachidonic Acid; Arachidonic Acids; Blood Platelets; Cholesterol; Collagen; Female; Humans; Male; Middle Aged; Nephrotic Syndrome; Platelet Aggregation; Serum Albumin; Thromboxane B2; Thromboxanes; Triglycerides