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PubMed1985

Increased glomerular thromboxane synthesis as a possible cause of proteinuria in experimental nephrosis.

Altered glomerular metabolism of arachidonic acid (AA) has already been demonstrated in experimental nephrotoxic nephritis. The enhanced synthesis of thromboxane A2 (TxA2) in isolated glomeruli that has been found may mediate changes in renal hemodynamics. The objectives of this investigation were: to check whether glomerular AA metabolism is also altered in a model of glomerulopathy in which no leukocyte infiltration or platelet deposition could be demonstrated; to establish a correlation between the altered AA metabolism and proteinuria; and to explore whether the alteration of the prostaglandin (PG) pathway found in isolated glomeruli is an in vitro artifact or reflects a modification in vivo. We used a model of glomerular damage characterized by heavy and persistent proteinuria, which was induced in the rat by a single intravenous injection of adriamycin. At light microscopy, minimal glomerular abnormalities were found in this model. Electron microscopy showed profound alterations of glomerular epithelial cells with extensive fusion of foot processes and signs of epithelial cell activation. Electron microscopy of numerous glomeruli showed no platelet deposition or macrophage and leukocyte infiltration in this model. Isolated glomeruli from nephrotic rats studied 14 or 30 d after a single intravenous injection of adriamycin (7.5 mg/kg) when animals were heavily proteinuric generated significantly more TxB2, the stable breakdown product of TxA2, than normal glomeruli. No significant changes were found in the other major AA metabolites formed through cyclooxygenase. Urinary excretion of immunoreactive TxB2 was also significantly higher in nephrotic than in normal animals. Administration of a selective Tx synthetase inhibitor, UK-38,485, from day 14 to day 18 after adriamycin resulted in a significant reduction of proteinuria compared with pretreatment values. Glomerular synthesis and urinary excretion of TxB2 were normal during the UK-38,485 treatment. Additional experiments showed that elevated glomerular synthesis and urinary excretion of TxB2 were not a consequence of increased substrate availability. Maximal stimulation of the renin-angiotensin axis with furosemide increased glomerular TxB2 synthesis in normal rats, which was significantly lower than in nephrotic animals. Finally, experiments using a unilateral model of adriamycin nephrosis indicated that the enhancement of glomerular TxB2 synthesis is not simply a consequence of the nephrotic syndrome. We conclude that: there is an abnormality of glomerular AA metabolism in nephritic syndrome, which leads to increased TxA2 production; the increased Tx generation correlates with protein excretion and might be responsible for altering the glomerular basement membrane permeability to protein; and the alteration found in isolated glomeruli probably reflects a modification in vivo, in that urinary excretion of immunoreactive TxB2 is also consistently increased in adriamycin nephrosis.

Animals↗
PubMedDate not supplied

Growth failure due to uremia and congenital nephrosis: growth enhancement by aggressive nutritional therapy.

The metabolic and nutritional effects of long-term parenteral and enteral nutrition were studied in two infants and one child with severe growth failure due to chronic renal failure (two patients) and congenital nephrosis (one patient). Six periods of treatment were analyzed. Both the parenteral nutrition and continuous enteral nutrition were found efficient in enhancing growth and correcting the metabolic abnormalities of uremia. The beneficial effects of this intensive nutrition were smaller in congenital nephrosis, although growth accelerated. Nitrogen balance studies confirmed effective nutrient utilization. The serum levels of calcium and phosphate were normalized as anabolism was achieved in the uremia. In fact, the rapid development of severe hypophosphatemia in one of the patients proved that the "fatal hyperalimentation syndrome" appears to be a specific threat in parenteral nutrition applied in uremia.

Body Height↗
PubMed1987

Hyalin droplet nephrosis in male Fischer-344 rats following inhalation of diisobutyl ketone.

Four groups, each consisting of 10 male and 10 female Fischer-344 rats, were exposed 6 h/day, 5 days/week, for 9 days to diisobutyl ketone (DIBK) vapor at concentrations of 905, 300, 98, or 0 (control) ppm. An additional 10 rats/sex were assigned to the 905 and 0 ppm groups and allowed two weeks recovery prior to sacrifice. Rats exposed to 905 ppm had mild ocular irritation (lacrimation) and evidence of kidney toxicity, manifested as: 1) an increase in absolute and relative (as a percentage of body weight) kidney weights, 2) an increase in urine volume (and water intake) with a concomitant decrease in urine osmolality (males only), and 3) an increase in severity of hyalin droplet nephrosis in the proximal tubules (males only). Absolute and relative liver weights were also increased in both male and female rats of the 905 and 300 ppm groups. These effects either disappeared or lessened in severity following the 2-week recovery period. Male rats exposed to 300 ppm had similar renal alterations to the males of the 905 ppm group, although the alterations were fewer in number and smaller in magnitude. Kidney weights and renal histology of the males of the 98 ppm group were similar to the control male rats, although an increase in urine volume with a decrease in urine osmolality was observed. The kidney findings in this study were not surprising because of the chemical relationship of DIBK with other aliphatic ketones (e.g., methyl isobutyl ketone, methyl isoamyl ketone) which, after repeated inhalation exposure, cause hyalin droplet nephropathy in male rats. The significance of this male rat nephrosis with regard to human exposure is unknown.

Administration, Inhalation↗
PubMed2000

Chronic angiotensin II infusion but not bradykinin blockade abolishes the antiproteinuric response to angiotensin-converting enzyme inhibition in established adriamycin nephrosis.

Angiotensin-converting enzyme (ACE) inhibition reduces proteinuria in established adriamycin nephrosis. To investigate whether the reduction in proteinuria is due to decreased generation of angiotensin II (AngII) or to decreased degradation of bradykinin, four series of experiments in established adriamycin nephrosis were performed. In the first series, 2 mg/kg lisinopril reduced BP from 117 +/- 4 to 67 +/- 2 mmHg and proteinuria from 335 +/- 66 to 57 +/- 10 mg/24 h after 2 wk of treatment. Subsequent continuous intraperitoneal infusion of AngII (250 ng/kg per min) for 2 wk partially restored proteinuria to 180 +/- 42 mg/24 h, whereas BP increased to 97 +/- 3 mmHg. Subsequent withdrawal of AngII restored the antiproteinuric effects of lisinopril, whereas subsequent withdrawal of lisinopril restored proteinuria to pretreatment values. In the second series, AT1 receptor blockade induced a fall in BP and proteinuria similar to that by lisinopril. In the third series, lisinopril reduced BP from 121 +/- 5 to 68 +/- 2 mmHg and proteinuria from 355 +/- 90 to 101 +/- 10 mg/24 h. Subsequent intraperitoneal infusion of bradykinin antagonist (HOE 140; 1 mg/kg per 24 h) for 2 wk did not affect BP (72 +/- 2 mmHg) or proteinuria (92 +/- 15 mg/24 h). In the fourth series, bradykinin (3 mg/kg per 24 h) was infused for 2 wk to mimic decreased bradykinin breakdown. This did not affect proteinuria, but induced a fall in BP from 114 +/- 3 to 93 +/- 4 mmHg. The BP-lowering effect of exogenous bradykinin was completely reversed by 1 wk infusion of HOE 140 (93 +/- 4 to 113 +/- 4 mmHg), while proteinuria remained unchanged. In conclusion, the antiproteinuric effect of ACE inhibition appears to be independent of bradykinin in this model, supporting a main role for reduction of AngII in the antiproteinuric action of ACE inhibition.

Angiotensin II↗
PubMed1993

Production of an inhibitor of rat mesangial cell growth by the glomerulus and its alteration in puromycin nephrosis.

Mesangial cell proliferation is found in many forms of progressive renal disease. This proliferation may be due to dysregulation of mesangial cell growth. The studies presented here test the hypothesis that the normal glomerulus produces a regulator of mesangial cell growth. Conditioned media (CM) from primary glomerular cultures were able to inhibit rat mesangial cell growth in a dose- and time-dependent fashion, from 30.0 +/- 3.8 to 86.6 +/- 3.9% growth inhibition. The growth inhibitor in glomerular CM appears to have a molecular weight of less than 3,000. Glomerular CM caused significantly more growth inhibition than did 3T3 fibroblast CM, 77.9 +/- 2.8% growth inhibition by 10% glomerular CM versus 21.2 +/- 5.4% by 10% 3T3 CM (P < 0.001). The growth inhibition was completely reversible. Glomerular CM had no effect on the growth of 3T3 fibroblasts. Treatment of the glomerular CM with either trypsin or neutral protease had no effect on its growth inhibitory activity. Glomerular CM obtained from rats with puromycin aminonucleoside nephrosis caused significantly less growth inhibition than did control glomerular CM; at a concentration of 10% CM, control glomerular CM had 65.1 +/- 1.9% growth inhibition and puromycin had 45.4 +/- 2.1% (P < 0.001). Thus, the rat glomerulus produces a small, nonprotein inhibitor of rat mesangial cell growth and the activity of this inhibitor is reduced in puromycin nephrosis. Impairment of mesangial cell growth regulation may be important in the pathogenesis of progressive renal disease.

3T3 Cells↗
PubMed1979

Suppressive effect of dipyridamole on the proteinuria of aminonucleoside nephrosis in rat.

The suppressive effect of dipyridamole on the proteinuria of aminonucleoside nephrosis and protamine-induced proteinuria, was investigated. Male Wistar rats were given puromycin aminonucleoside (80 mg/kg s.c.) or protamine sulfate (20 mg/kg i.v.), and the urine was collected in metabolic cages. The content of proteins in the urine was determined by using a continuous gradient microgel electrophoresis procedure. Dipyridamole (20 mg/kg p.o.) suppressed the excretion of albumin and proteins larger than albumin (HMP) in aminonucleoside nephrosis. But the excertion of proteins smaller than albumin (LMP) was not affected by dipyridamole. Dipyridamole also suppressed the excertion of HMP in protamine-induced proteinuria, though the excretion of albumin and LMP was not affected. Puromycin aminonucleoside and protamine sulfate were known to cause renal glomerular epithelial changes referred to as "fusion" of foot processes. Since dipyridamole was effective in suppressing the both types of proteinuria, this drug was considered to improve the damaged renal glomerular barrier for plasma proteins.

Albuminuria↗
PubMed1996

Lipoprotein metabolism in experimental nephrosis.

In experimental nephrosis, a decrease in plasma albumin resulting from proteinuria causes a decreased in the plasma oncotic pressure. The existence of an osmoreceptor, which responds to the low oncotic pressure and produces a factor(s) that signals the liver to increase the secretion of plasma proteins, is postulated. The hyperlipidemia characteristic of the nephrotic syndrome results primarily from increased hepatic secretion of apolipoproteins and lipoproteins representing the entire density spectrum from VLDL, IDL, and LDL to HDL. Not all plasma proteins and apolipoproteins are affected to the same extent. Increased mRNA levels due to increased transcription have been shown for albumin and apolipoprotein A-1 (apoA-1). The increased secretion of VLDL, the major vehicle for triglyceride transport from the liver, appears to be due mainly to posttranscriptional events possibly related to increased lipogenesis. Once proteinuria begins, the demand for amino acids for albumin and apolipoprotein synthesis by the liver is increased. To meet this demand, protein catabolism in the peripheral tissues is increased. One manifestation of this process is a decrease in lipoprotein lipase which reduces VLDL catabolism, contributing to the sustained elevation of plasma VLDL. The spectacular overproduction of apoA-1 in nephrosis in the rat is accompanied by a decreased fractional catabolic rate (FCR), contributing to the maintenance of high levels of HDL. Urinary loss of HDL and its renal catabolism does not account for the decreased FCR. The reason for the decreased FCR is not known. Work with nephrotic rats overexpressing transgenic human apoA-1 has shown that human A-1 forms smaller HDL3-sized particles, rather than the larger HDL2 of the rat. This may contribute to the failure of HDL levels to increase in the human nephrotic syndrome. High plasma VLDL and LDL with normal or low HDL probably account for the increased incidence of coronary artery disease in the nephrotic syndrome.

Animals↗
PubMed2006

Protective effect of radical scavenger edaravone against puromycin nephrosis.

AIM: Recent studies have indicated that reactive oxygen species (ROS) play a role in the pathogenesis of glomerular injury leading to proteinuria in nephrotic syndrome. In the present investigation, we examined the effects of the radical scavenger edaravone administered at various time points to rats with puromycin nephrosis. MATERIALS AND METHODS: 35 Wistar rats were divided into five groups: treatment with puromycin aminonucleoside (PAN) alone, treatment with PAN followed by edaravone in the early period, treatment with PAN followed by edaravone administration in the late period, treatment with PAN and administration of edaravone for the whole experimental period, and untreated controls. On Days 3, 6 and 9, urinary protein excretion was measured. The levels of glomerular thiobarbituric acid-reactive substance (TBArs) were determined in all animals on Day 10. RESULTS: On Day 9, rats that had been administered edaravone showed reduced urinary protein excretion and reduced glomerular TBArs. In particular, edaravone administration in the late period, during which proteinuria was most acute, had the effect of reducing the severity of proteinuria. Glomerular TBArs were suppressed to the control level. Our results indicate that edaravone exerts a protective effect in the acute phase of PAN nephrosis when administered as antioxidant therapy at the onset of proteinuria. CONCLUSIONS: Edaravone can ameliorate urinary protein excretion after the onset of proteinuria in nephrotic syndrome.

Animals↗
PubMed2002

[New insights about immunopathology of lipoid nephrosis].

Clinical and experimental observations suggest that Lipoid Nephrosis (Minimal change nephrotic syndrome) results from T cell dysfunction due to still unknown mechanisms. By subtractive screening library, we identified 84 transcripts, of which twelve match with proteins of yet unknown function and thirty are unknown clones. Among the 42 known transcripts, at least 18 are closely involved in the TCR-mediated complex signaling cascade. This includes genes encoding components of the T cell receptor and proteins associated with the cytoskeleton scaffold, as well as transcription factors such as NF-kappa B and c-maf. During the relapse phase, we have found significant alterations of the NF-kappa B/I kappa Ba regulatory pathway, whereas very low levels of IL12R beta 2 mRNA were detected suggesting that T cell activation evolves toward a Th2 phenotype. We have shown that c-maf is highly induced, shuttling between nuclear and cytoplasmic compartment during the relapse and the remission phases, respectively. Contrasting with the nuclear expression of c-maf, low IL4 levels were detected in relapse. This suggests that the downstream target gene of c-maf in Lipoid Nephrosis, is not IL4 and provides new directions in research leading to identify the target gene, possibly an unknown Th2 cytokine, which might play a critical role in the pathophysiology of this disease. Thus, the combination of subtractive cloning and differential screening constitutes an efficient approach to identify genes likely to be involved in the pathophysiology of MCNS.

Adolescent↗
PubMed1976

Alterations of the glomerular epithelium in acute aminonucleoside nephrosis. Evidence for formation of occluding junctions and epithelial cell detachment.

The visceral glomerular epithelium of rats made nephrotic by daily injections of puromycin aminonucleoside was examined from the time of onset of proteinuria (day 6) to the time when many animals die (day 15) in order to establish the chronology of the pathologic alterations which occur during the course of the disease. In addition, the structure of the residual epithelial slits was examined using special fixatives and freeze-fracture. Changes seen early in the disease (7 to 9 days) are: (1) a reduction in the number of foot processes and filtration slits; (2) occurrence of occluding junctions in many of the residual slits coupled with displacement of the slit diaphragms; (3) thinning of the dense central portion of the basement membrane (lamina densa) with a corresponding widening of the space (lamina rara externa) between it and the epithelium; (4) heightened epithelial pinocytosis with increased numbers of protein absorption droplets or lysosomes. In freeze-fracture preparations the occluding junctions were seen to be limited in extent and made up of only a few strands, indicating they are incomplete and represent occluding maculae or fasciae rather than zonulae. Later on in the disease (10 to 15 days) no further changes in the number or arrangement of slits is evident, but other alterations occur: (1) denuded regions of basement membrane are seen where there is initially partial and eventually complete detachment of the epithelium from the basement membrane; (2) increasing numbers of large vacuoles or phagosomes and decreasing numbers of fully condensed lysosomes are present; and (3) basement membrane-like material is seen in the spaces between the partially detached epithelium and basement membrane. The new findings in this study are: (1) the clarification of early (reversible) versus late (probably irreversible) changes in the glomerular epithelium in a acute aminonucleoside nephrosis; (2) delineation of the structure of the residual epithelial slits; (3) the description of progressive loosening of the attachment between the epithelium and the basement membrane leading to focal or complete epithelial cell detachment; (4) the presentation of evidence indicating that exhaustion of the lysosomal system of the glomerular epithelium (in protein absorption and concentration) occurs late in the disease. The available evidence is summarized and indicates that the glomerular basement membrane, the main glomerular filter, is defective in aminonucleoside nephrosis and allows increased protein leakage. However, it seems likely that the main site of action of aminonucleoside is on the epithelium leading to the production of defective basement membrane.

Animals↗
PubMed1992

Renal extracellular matrix accumulation in acute puromycin aminonucleoside nephrosis in rats.

Progressive renal fibrosis is considered to be the final common pathway leading to chronic renal insufficiency. In this study, the authors examined some of the cellular and molecular mechanisms regulating the renal accumulation of extracellular matrix (ECM) proteins using rats with puromycin amino-nucleoside (PAN) nephrosis as an acute model system. Puromycin aminonucleoside rats developed reversible nephrotic syndrome accompanied by an interstitial infiltrate of monocytes. The number of interstitial fibroblasts expressing ST4 antigen did not increase. During the first 4 days, steady-state mRNA levels for all genes examined remained at or below control levels. At 1 week, nephrotic syndrome and interstitial inflammation were established, and a period of renal cell proliferation occurred, identified by increased histone mRNA levels and localized by tritiated thymine autoradiography to tubular epithelial cells and occasional interstitial cells. Transforming growth factor-beta (TGF-beta) steady-state mRNA levels were increased eightfold, but returned to control levels by 3 weeks. At week 1, there was a 10- to 20-fold increase in kidney steady-state mRNA levels for genes encoding interstitial matrix proteins collagen I and fibronectin and basement membrane collagen IV. By in situ hybridization, alpha 1(I) procollagen mRNA was localized to interstitial cells. Immunofluorescence microscopy demonstrated focal accumulation of ECM proteins in the tubulointerstitial compartment at 2 and 3 weeks, but by 6 weeks, kidney immunohistology was normal again. Steady-state mRNA levels for the matrix degrading metalloproteinase stromelysin remained at control values, whereas the levels for interstitial collagenase were normal at week 1 and increased twofold to threefold at 2 and 3 weeks. Steady-state mRNA levels for the tissue inhibitor of metalloproteinases (TIMP) increased fivefold at 1 week and returned to baseline values over the next 2 weeks. The results of this study suggest that tubulointerstitial ECM accumulation occurs in rats with acute PAN nephrosis because of the activation of genes encoding several matrix proteins and inhibition of matrix degradation mediated by TIMP. These events are reversed during the phase of recovery from nephrotic syndrome. Increased mRNA levels for TGF-beta, possibly originating from inflammatory interstitial monocytes, are likely to be one of the mediators of the molecular events observed.

Animals↗
PubMed1956

Management of nephrosis; the use of long continued hormone therapy.

The course of nephrosis in 36 children was evaluated. Twelve of 24 who received no treatment or short-term courses of steroids died. Eleven of the 24 had been well for six months to five years at the time of this report. Twelve patients received steroids by schedule over extended periods. One died and eleven had been free of signs and symptoms of nephrosis for four to eighteen months at the time of report. In only two cases was therapy discontinued. It seems evident that these patients are experiencing a better state of well-being. Whether or not the prognosis is being altered for any single patient cannot be determined.

Adrenocorticotropic Hormone↗
PubMed1992

[Neurectodermal malignant tumor of the soft tissues after treatment with immunosuppressive agents of lipoid nephrosis].

Immunosuppressive drugs are known to increase the risk of inducing neoplasia, especially acute leukaemia when high doses are used. A case of nephrosis in a 10 year-old boy treated with chlormethine (cumulative dose: 0.8 mg/kg) and chlorambucil (cumulative dose: 10 mg/kg) is reported. Four years after the beginning of the treatment an extraskeletal Ewing's sarcoma occurred. Since the review of literature failed to find any malignancy induced by such an immunosuppressive treatment for nephrosis, the question whether or not this extraskeletal Ewing's sarcoma was attributable to this treatment remains unanswered.

Adrenal Cortex Hormones↗
PubMedDate not supplied

[Histocompatibility antigens (HLA) in children with lipoid nephrosis].

Actual knowledge on the HLA relationship with the primary glomerulopathies, with particular reference to steroid - sensitive nephrosis of childhood, is surveyed. Occurrence of HLA B-8 and B-35 in this nephropathy has been investigated. The studies involved 47 patients aged between 3 and 15 years and 117 healthy children from Lower Silesian region. It has been showed, that HLA B-8 is present more frequently in sick children, than in healthy controls. The situation is reverse in case of HLA B-35 antigen. However, the difference is statistically insignificant. A probability of the lipid nephrosis sensitivity to corticosteroids can not be predicted on the base of the presence of these HLA antigens.

Adolescent↗
PubMed2004

[Relativity of nuclear factor-kappaB (P65/Rel-A) and angiotensin II type 1 receptor expression in early stage of lesions of adriamycin nephrosis in young rats and the effects of intervention].

OBJECTIVE: To investigate the trend and potential pathogenic role of nuclear factor (NF)-kappaB P(65)/Rel-A mRNA and angiotensin-II (AngII) receptor type 1 (AT(1)) proteins expression, and the relativity between them in early stage of renal tubulointerstitial lesions in young rats with adriamycin nephrosis and the interfering effects of treatment with angiotensin converting enzyme inhibitor (ACEI) benazepril and ACEI combined with AngII type 1 receptor antagonist (AT(1)RA) Losartan. METHODS: Male young Wistar rats with adriamycin nephrosis were used as experimental models. At different time points (weeks 1, 2, and 3 in early nephritic phase, the urinary protein and blood biochemical parameters were measured, and P(65)/Rel-A mRNA was detected; AT(1) protein expression was determined by in situ hybridization and immunohistochemical methods. The relativity between them was evaluated. RESULTS: In the early phase of tubulointerstitial lesions, following adriamycin injection and proteinuria aggravated progressively, at week 3, the proteinuria level had reached heavy proteinuria (123.2 +/- 7.7 mg/24 h). The serum parameters reflecting renal function were elevated. The inflammatory cells infiltrated into renal tissues, especially in tubulointerstitial regions, were increased markedly. Swelling of tubular epithelial cells, broadened tubulointerstitial areas, and protein casts in tubule were observed. In situ hybridization and immunochemical staining showed that AT(1) protein was expressed in tubular epithelial cell cytoplasm and on nuclear membranes (AT(1): 1st week 19.8 +/- 1.1%, 2nd week 25.0 +/- 2.6%, 3rd week 37.1 +/- 1.0% (control: 10.3 +/- 0.8%, 10.4 +/- 1.6%, 10.2 +/- 1.5%); and P(65)/Rel-A mRNA expression in the same locations was upregulated. P(65)/Rel-A translocation from cytoplasm into nucleus increased markedly simultaneously. The positive signal of hybridization dominated in cytoplasm gradually became dominant in the nuclei as the pathological changes progressed. The semiquantitative expression of P(65)/Rel-A was 24.0 +/- 3.3% at week 1, 34.2 +/- 2.4% at week 2, 39.9 +/- 6.4% at week 3, while the values of controls were 8.5 +/- 0.4%, 8.7 +/- 1.0%, and 8.4 +/- 0.9%, respectively. There was a positive correlation between AT(1) and P(65)/Rel-A expression in localization and time phase (r = 0.857, P < 0.01). However, the tendency of those factor's expression was all decreased in each treated group, the semiquantitative results were AT(1): 14.6 +/- 2.1%, 13.7 +/- 2.3%, 11.4 +/- 1.1%; P(65)/Rel-A: 18.5 +/- 3.4%, 22.8 +/- 1.6%, 26.7 +/- 4.9% at 1, 2, 3 weeks in ACEI treated group; AT(1): 12.4 +/- 1.5%, 11.1 +/- 1.0%, 10.3 +/- 0.8%; P(65)/Rel-A: 17.9 +/- 5.0%, 21.3 +/- 6.0%, 22.5 +/- 2.5% in AT(1)RA (Losartan) group, respectively. The significant difference were observed between all groups in different time points (P < 0.05). CONCLUSIONS: The present study suggested that NF-kappaB (P(65)/Rel-A) mRNA expression and its activity was enhanced significantly that synchronized with aggravating injures in tubulointerstitial lesions initial period induced by proteinuria-loading in nephrotic young rats. This tendency was related with AngII and its receptors system that may accelerate lesions progressing in many renal diseases.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

[Alteration of renal hemodynamic in adriamycin-induced nephrosis rats administrated with Wulingsan].

OBJECTIVE: To investigate the effect of traditional classical compound Wulingsan on renal hemodynamic in rats with adriamycin (ADR)-induced nephrosis. METHOD: After establishing a model of rats with adriamycin-induced nephrosis, we administrated wulin-san to the ADR rats via oral gavage for four weeks and measured mean arterial blood preasure (MABP) with manometer. Renal clearance of paraaminohippuric acid (PAH) and inulin were detected, then renal plasma flow (RPF) and glomerular filtration rate (GFR) were calculated. Renal vascular resistance (RVR) was calculated as the division of MABP by RPF. Renal endothelin (ET) and angiotensin II (Ang II) were detected with radioimmunity assay kits, and nitrous oxide (NO) was detected with biochemical kits. RESULT: There was no significant change of GFR in ARD rats, but RPF and NO were decreased, which accompanied by enhanced RVR, ET and Ang II. RPF was increased in the administrated rats, in company with RVR, ET and Ang II decreased, whereas NO was not influenced after the administration. CONCLUSION: Wulingsan can improve the renal hemodynamic in ADR rats, at least in part by modulating the levels of vasoactive factor.

Angiotensin II↗
PubMed1991

[Idiopathic nephrosis (minimal glomerular lesions, segmental and focal hyalinosis)].

Idiopathic nephrosis, the most common cause of nephrotic syndrome, is histologically defined by minimal glomerular changes, diffuse mesangial proliferation or focal and segmental glomerulosclerosis. The response to corticosteroids carries greater prognostic weight than the histological features seen on the initial renal biopsy. The severity of the condition lies in the risk of relapses which occurs in more than half of cases when steroid dosage is decreased (steroid dependency), then requiring, in case of steroid toxicity, the use of alkylating agents or, more recently, cyclosporine. In 10% of the cases, nephrosis is steroid resistant and the severity of the disease lies in the risk of developing end stage renal failure which occurs in nearly one half of those cases.

Glomerulosclerosis, Focal Segmental↗
PubMed1991

Pharmacological activities of a novel thienodiazepine derivative as a platelet-activating factor antagonist. Effects on microvascular permeability, hypotension and nephrosis.

The effects of a newly synthesized platelet-activating factor (PAF) antagonist, (S)-(+)-6-(2-chlorophenyl)-3-cyclopropanecarbonyl-8,11- dimethyl-2,3,4,5-tetrahydro-8H-pyrido[4',3':4,5]thieno[3,2-f] [1,2,4]triazolo[4,3-a][1,4]diazepine (E-6123, CAS 131614-02-3) on microvascular permeability, systemic hypotension and nephrosis were investigated. E-6123 inhibited PAF injection-induced microvascular permeability (edema) in guinea pigs after oral administration at 3 micrograms/kg. The inhibitory effects of E-6123 were very potent compared to those of other PAF antagonists. E-6123 reversed PAF and/or endotoxin injection-induced hypotension in rats after intravenous administration at 3 micrograms/kg. The increase in urinary protein excretion of rats in which nephrosis had been induced by intraperitoneal injection of aminonucleoside was not inhibited by oral administration of E-6123 at 10 mg/kg/d.

Animals↗