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At least 343 records · Page 19Linked to original sources
PubMed1976

Cyclodextrin nephrosis in the rat.

The renal toxicity of the Schardinger dextrins, alpha and beta-cyclodextrin, is manifested as a series of alterations in the vacuolar organelles of the proximal convoluted tubule. These changes begin as an increase of apical vacuoles and the appearance of giant lysosomes. The giant lysosomes characteristic of cyclodextrin nephrosis are notable because of the prominent acicular microcrystals embedded in the lysosomal matrix. Giant vacuoles devoid of acid phosphatase reaction product are found in advanced lesions. The vacuolar apparatus shows advanced changes prior to manifestation of lesions in mitochondria and other organelles. These observations indicate a role of the vacuologenic apparatus in the nephrotic process. Intracellular concentration of toxin via the lysosomal pathway represents a perversion of the physiologic function of the proximal tubule which ultimately leads to cell death.

Animals↗
PubMed1992

The altered glomerular filtration slits seen in puromycin aminonucleoside nephrosis and protamine sulfate-treated rats contain the tight junction protein ZO-1.

Nephrosis induced in rats by puromycin aminonucleoside treatment (PAN) results in the apical displacement of the glomerular filtration slit membrane by newly formed, intercellular occluding-type junctions. Similar changes can also be induced by acute kidney perfusion with protamine sulfate (PS). We have investigated the molecular nature of these altered junctions using an antibody to ZO-1, a protein found exclusively in tight junctions. Immunoblotting demonstrates ZO-1, a 225-kd band, in glomerular extracts of normal, PAN-, and PS-treated rats. By immunofluorescence, ZO-1 was localized at the base of podocytes outlining the capillary loops of glomeruli from all three experimental groups. At the electron microscope level, using immunoperoxidase or immunogold labeling, ZO-1 was concentrated along the cytoplasmic surfaces of the slit diaphragms of normal rats. In PAN or PS rats, it was concentrated along both the newly formed occluding-type junctions and the remaining slit diaphragms. When podocalyxin (the major membrane sialoprotein of the podocyte) was similarly localized, it was found exclusively apical to the displaced slit membrane. Based on morphology and the presence of ZO-1, the altered junctions seen in PAN and PS rats appear to represent bona fide tight junctions. Their rapid (15-minute) induction in PS-treated rats suggests that on neutralization of the cell surface charge by polycation perfusion, discontinuous tight junctions form from a preexisting pool of junctional proteins. These findings raise the possibility that glomerular hydraulic conductivity may be regulated in part by regulating the relative patency and width of the filtration slits through focal tight junction assembly.

Animals↗
PubMed2003

Treatment of glomerular endothelial dysfunction in steroid-resistant nephrosis with Ganoderma lucidum, vitamins C, E and vasodilators.

Glomerular endothelial dysfunction is believed to be responsible for the proteinuria and nephronal damage, namely tubulointerstitial fibrosis and glomerulosclerosis, observed in severe nephrosis such as focal segmental glomerulosclerosis. A dysfunctioning glomerular endothelium is likely to be induced by oxidative stress and oxidized LDL as well as altered immunocirculatory balance with a defective anti-inflammatory pathway. A defective release of vasodilator inconjunction with enhanced production of angiotensin II induces hemodynamic maladjustment by preferential constriction at the efferent arteriole. Such a hemodynamic maladjustment exerts two significant hemodynamic impacts. Close to the efferent constriction, it induces intraglomerular hypertension and glomerulosclerosis. Far from the efferent constriction, it reduces peritubular capillary flow, which eventually leads to tubulointerstitial fibrosis. Treatment with a vasodilator improves the hemodynamic maladjustment but does not completely suppress proteinuria. A successful suppression of proteinuria is accomplished by using Ganoderma lucidum and vitamins C and E. The beneficial effect of Ganoderma lucidum appears to be multifactorial, including the modulation of immunocirculatory balance, antilipid, vasodilator, antiplatelet and improved hemorheology. Together with vitamins C and E, this helps to neutralize oxidative stress and suppress the toxic effect to the glomerular endothelial function.

Adrenal Cortex Hormones↗
PubMed2003

Glomerular endothelial cytotoxicity and dysfunction in nephrosis with focal segmental glomerulosclerosis.

Glomerular endothelial cell dysfunction (GED) with defective release of vasodilator has been delineated in nephrosis (NS) in vivo and in vitro studies. In NS with focal segmental glomerulosclerosis (FSGS), an immunocirculatory balance may be impaired due to defective anti-inflammatory cytokine. This study aimed at simultaneous determination of both proinflammatory cytokine (tumor necrosis factor alpha) and an anti-inflammatory cytokine (interleukin-10) in NS with FSGS. An endothelial cell cytotoxicity (ECC) was also examined using nephrotic serum. It was shown that (1) the initial endothelial cell cytotoxicity was significantly different from the control, (2) ratio between tumor necrosis alpha and interleukin-10 was significantly elevated, and (3) intrarenal hemodynamics was changed significantly.

Endothelium, Vascular↗
PubMed2003

[Lipoid nephrosis in childhood].

Lipoid nephrosis or idiopathic nephrotic syndrome, the most frequent glomerular disease in childhood, is defined by the association of a nephrotic syndrome and minimal changes on renal biopsy or unspecific lesions such as focal and segmental glomerular sclerosis or diffuse mesangial proliferation. Several complications related to the nephrotic syndrome may occur: infections particularly bacterial infections, thrombo-embolic accidents, hypovolemia with shock. Other complications are secondary to the treatment: steroid therapy, immunosuppressants. The outcome is related to the response to steroid therapy. In case of steroid responsiveness, the risk is the relapse when the steroid dosage is tapered or stopped and the complications related to the treatment which is given to maintain remission. In case of steroid resistance, the risk is that of progression to renal failure which occurs in approximately 50% of patients after 5 years. Moreover, the nephrotic syndrome may recur after renal transplantation.

Adrenal Cortex Hormones↗
PubMed1991

Amelioration of glomerular injury in doxorubicin hydrochloride nephrosis by dimethylthiourea.

The hydroxyl radical scavengers dimethylthiourea (DMTU), sodium benzoate, and dimethylsulfoxide (DMSO) were administered to rats before doxorubicin hydrochloride (ADR) (5 mg/kg, IV) to probe the role of free radicals in mediating proteinuria in doxorubicin hydrochloride nephrosis (AN). Because ADR stimulates free radical production, the role of renal glutathione was also evaluated; glutathione metabolism is involved in tissue detoxification processes. DMTU administration to rats with AN caused a significant (p less than 0.01) reduction in their proteinuria after 7 days (52.84 +/- 13.21 mg/24 hours) when they were compared with ADR controls (155.81 +/- 20.16 mg/24 hours). In similar fashion, their urine albumin excretion was also significantly reduced when compared with that of ADR controls (11.13 +/- 2.75 mg/24 hours vs 32.08 +/- 4.14 mg/24 hours; p less than 0.01). DMTU-treated rats also had significantly (p less than 0.001) reduced urinary protein and albumin excretion at 14 days when compared with rats that received ADR alone. The urinary excretion of lysozyme and N-acetyl-glucosaminidase, markers of renal tubular injury, were significantly increased after 7 or 14 days in rats with AN, despite DMTU treatment. Creatinine clearance was significantly reduced (p less than 0.05) in rats receiving ADR alone (0.223 +/- 0.011 ml/min/100 gm) when compared with that in normal controls (0.331 +/- 0.027 ml/min/100 gm) or DMTU-treated rats (0.289 +/- 0.035 ml/min/100 gm). Unlike DMTU, neither sodium benzoate nor DMSO reduced proteinuria in rats with AN.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMed1991

Changes of negative charge on RBC and glomeruli and its relation to the proteinuria of adriamycin nephrosis in rats.

The depth and area-percentage of Alcian blue (AB) staining of glomeruli, the ability of RBC to bind AB and the onset of proteinuria in adriamycin nephrosis in rats were studied. The results showed that the negative charge (NC) on RBC and glomeruli decreased significantly after injection of adriamycin and there was a positive correlation between them (r = 0.77, P less than 0.01). There was a negative correlation between the amount of NC on the RBC and the amount of urinary protein (r = -0.5231, P less than 0.01), and also between the amount of NC on the glomeruli and the amount of urinary protein (r = -0.5140, P less than 0.05).

Animals↗
PubMed1991

Evaluation of the role of reactive oxygen species in doxorubicin hydrochloride nephrosis.

In subcellular systems, doxorubicin hydrochloride (ADR) leads to the generation of reactive oxygen species such as superoxide anion. Because reactive oxygen species have been shown to be important mediators of glomerular injury in several animal models, we sought to determine whether reactive oxygen species play a significant role in the pathogenesis of ADR-induced nephrotic syndrome in the rat. Rats pretreated with a variety of free radical scavengers (superoxide dismutase conjugated to polyethylene glycol [PEGSOD], catalase, catalase plus PEGSOD, dimethylsulfoxide, desferoxamine, or n-acetyl cysteine) had no significant reduction in proteinuria at 3 weeks after ADR administration when compared with rats receiving ADR in the absence of scavengers. No evidence was seen of increased lipid peroxidation or depletion of reduced glutathione in renal cortex tissue obtained up to 24 hours after administration of ADR. No changes were seen in the renal cortical levels of either enzyme activity or immunoreactive protein for the endogenous antioxidant enzymes superoxide dismutase (either the Mn or CuZn forms) or catalase after ADR. Total and MnSOD activities in glomeruli isolated from rats after ADR administration fell significantly, though CuZnSOD activity was increased. The effect of ADR on cultured rat mesangial or epithelial cells was also evaluated. ADR inhibited growth of both cell types at concentrations of approximately 5 to 10 mumol/L, an order of magnitude below the reported Michaelis-Menten constant for ADR-induced superoxide production. The growth inhibitory effect could not be prevented in either cell type by treatment with PEGSOD, catalase, or PEGSOD plus catalase. This combination of results from in vivo and in vitro studies provides no evidence for an important role of reactive oxygen species in ADR nephrosis and suggests that other known mechanisms of ADR cytotoxicity, such as interference with DNA metabolism, mediate the glomerular injury.

Animals↗
PubMed1991

Altered renal fibronectin excretion in early adriamycin nephrosis of rats.

The anticancer drug adriamycin (ADR) induces severe nonselective glomerular proteinuria in rats. The proliferation of the glomerular mesangium in chronic ADR nephrosis suggests a disturbed metabolism of extracellular matrix proteins. In the present study the structural protein fibronectin was analyzed by immunological methods in urine and plasma in two rat strains after a single injection of 5 mg of ADR/kg b.wt. After ADR administration the excretion of 220 kd-plasma fibronectin, identified by its electrophoretic mobility and Western blotting, increased. This was confirmed by quantitative measurement (ELISA) of total urinary fibronectin (ADR-treated Munich Wistar Frömter rats: 85.4 +/- 49.5 ng/hr, N = 31; controls: 1.7 +/- 0.7 ng/hr, N = 26; day 7 after ADR injection). Control urines contained distinct fragments of fibronectin with a molecular weight range of 40 to 60 kd. It is suggested that these fragments did not originate from plasma inasmuch as only little correspondence between the fibronectin patterns of urine and plasma was found, and also because in ADR-treated rats the excretion of the fibronectin fragments decreased from day 4 of ADR administration. The data suggest that the urinary fibronectin fragments are released from cellular fibronectin during the normal catabolism of the glomerular extracellular matrices, and that ADR interferes in the metabolism of matrix components. Only as a consequence of an enhanced glomerular permeability is plasma fibronectin excreted in ADR-treated rats.

Animals↗
PubMedDate not supplied

[Lipoid nephrosis in children. Development and anatomo-clinical correlation].

Lipoid nephrosis was identified by light, immunofluorescence and electron microscopy in 34 children aged 1 month to 10 years (23 males). These patients were followed up for a mean of 6.8 years (range 2.2 to 14 years). Treatment included oral prednisone (2 mg.kg.day for 4 weeks and then four days a week for 2 months). In steroid dependent or resistant patients oral cyclophosphamide 2.5 mg.kg.day was given for 2 months. Satisfactory responses to steroid therapy were recorded in 73.5% steroid dependence in 23.5% and steroid resistance in 3% of cases respectively. As a whole, 97% of patients responded before 8 week to steroids, cyclophosphamide or both. No morphologic differences were recorded from kidney biopsies among corticoid responders, dependents or resistants, neither between first and second biopsies which were done in four steroid dependent and one steroid resistant children. Slight morphologic differences were observed depending on the time elapsed from initial symptoms to renal biopsy: 39 days (means) when total disappearance of foot processes was seen (5 cases); 11 month (means) in 14 cases with partial pedicular absence and 20 months (means) in 15 children with segmental pedicular absence alternating with zones of normal foot process morphology. The total number of nephrotic episodes was 149, with a mean of 4.3 recurrences per patient, including three children (all girls) whose disease never recurred. Serious infections were detected in 4.7% of recurring episodes. At 5 years follow up 94% of patients were in remission. No deaths occurred among these patients.

Child↗
PubMed1990

Role of oxygen radicals in adriamycin-induced nephrosis.

The mechanism of cellular processes responsible for proteinuria induced by adriamycin (ADR) remains unclear. In this study, we examined whether oxygen radicals contribute to the development of proteinuria in ADR-induced nephrosis. The peak concentration of malondialdehyde (MDA) of kidney was found on 8th day after ADR treatment in rats. ADR-treated rats received either superoxide dismutase (SOD, scavenger of O2-, catalase (CAT, scavenger of . H2O2) or dimethyl sulfoxide (DMSO, scavenger of OH). The SOD, CAT or DMSO treated groups had a significant suppression of urinary protein excretion, serum and renal MDA compared to ADR control group. There were also less severe renal morphologic changes in the former three groups vs the ADR controls. These data provide indirect evidence that oxygen radicals generated by ADR are important mediators of ADR-induced proteinuria.

Animals↗
PubMed1990

[The status of negative charge of the RBC and glomeruli and its relation to proteinuria in adriamycin nephrosis in rats].

The status of negative charge on RBC and glomeruli and its relation to proteinuria of adriamycin nephrosis in rats were studied by electron computerized picture analysis. The results showed that the negative charge (NC) on glomeruli decreased significantly at 48 hrs and 14 days after ADR injection although there was no proteinuria simultaneously. There was a positive relation between the changes of NC on glomeruli and those on RBC (r = 0.77, p less than 0.01), and there was negative relation between either of them and proteinuria respectively (r = -0.5140, p less than 0.05; r = -0.5231, p less than 0.01). The focal fusions of foot processes occurred prior to the onset of proteinuria.

Animals↗
PubMed1990

[Effects of human Cu, Zn-superoxide dismutase in aminonucleoside nephrosis--evaluation of the morphology and glomerular basement membrane anionic charge sites].

It was examined whether superoxide dismutase (SOD) had protective effects in puromycin aminonucleoside nephrosis (PAN). Nephrotic rats were induced by a single intraperitoneal injection of puromycin aminonucleoside (PA, 60 mg/kg). Subcutaneous administration of SOD (30 mg/kg) was started the day before PA injection and continued every 24 hours. Animals were sacrificed 10 days later to assess the morphology and glomerular basement membrane anionic charge sites (CSs). GBM CSs were stained in vitro with polyethyleneimine (PEI) and studied by electron microscopic examination. The SOD-injected group had a significant reduction of urinary protein excretion compared to the PA-treated group. Light microscopy revealed that vast majority of glomeruli in PA-treated group had segmental mesangial expansion and epithelial cell adhesions of the glomerular tuft to Bowman's capsule. Contrasted to these changes in the PA group, glomeruli from SOD-treated group showed less severe morphologic changes. On electron microscopy, the PA-treated rats exhibited marked glomerular epithelial loss of foot processes, epithelial attenuation, cytoplasmic vacuolization and protein reabsorption droplets. The SOD-treated animals demonstrated a lesser degree of epithelial loss of foot processes with a few protein reabsorption droplets. There was also a significant decrease in GBM lamina rara externa CSc stained with PEI in PAN compared to the control. The SOD-treated rats had a significant increase in GBM CSs compared to those of the PAN rats. SOD has protective effects in urinary protein excretion, the morphology and GBM CSc in PAN, which indicate indirect evidence that superoxide and/or its metabolites are responsible for glomerular injury.

Animals↗
PubMed1987

Changes in glomerular heparan sulfate in puromycin aminonucleoside nephrosis.

Changes in glomerular anionic sites in puromycin aminonucleoside nephrosis (PAN) in the rat are controversial. The authors examined glomerular anionic sites in PAN by in vivo staining with polyethyleneimine (PEI). They also quantitated and characterized glomerular heparan sulfate (HS), which is known to be a major glomerular polyanion in PAN, using in vivo incorporation of 35S-sulfate. PAN rats had a mean protein excretion of 96 +/- 23 mg per 24 hours. Staining of anionic sites with PEI showed 15.3 +/- 2.8 sites per 1000-nm length of glomerular basement membrane in controls, 13.7 +/- 1.9 sites in PAN rats (P greater than 0.05), and 50% of rats with early PAN had absent staining. Total 35S-sulfate incorporation was similar in both the controls and established PAN rats (2900 +/- 150 dpm/mg dry wt of glomeruli versus 3005 +/- 260, P greater than 0.05) but decreased in early PAN rats (2025 +/- 148). The percentage of 35S-sulfate incorporated into chondroitin sulfate was similar in all three groups of animals. HS uronic acid was also similar (1.8 +/- 0.2 g/mg dry wt of glomeruli versus 1.7 +/- 0.3, P greater than 0.05) but decreased in early PAN (1.1 +/- 0.2). The distribution of 35S-sulfate activity within the HS subfractions was examined by ion-exchange chromatography and showed a shift in percent present from 1.0 M to 1.25 M fraction in established and early PAN animals (control 1.0 M 37% +/- 3.2% versus PAN 19% +/- 3.4%, P less than 0.01, and 1.25 M 36% +/- 2.9% versus 53% +/- 2.9%, P less than 0.01). These results demonstrate that glomerular heparan sulfate is unchanged in established PAN but decreased in early PAN. SO4 incorporation is unchanged in established PAN and diminished in early PAN. Thus, early in PAN HS synthesis is impaired, but in established PAN the HS is normal, and changes in glomerular HS cannot explain the increased permeability.

Animals↗
PubMed1989

[Lipoid nephrosis: changes in proteinemia and albuminemia after resolution of proteinuria].

Changes in serum protein and albumin levels following resolution of proteinuria were studied in 67 children with nephrosis. These two parameters returned to normal only after the 21st day, i.e. well after the natriuretic crisis and resolution of edema. Our results are consistent with recent studies showing that the fluid and electrolyte changes seen in the urine at resolution of the proteinuria (increased diuresis and natriuresis) are not due to a return to normal of serum protein and albumin levels. They probably reflect correction of an intrarenal abnormality whose mechanism is unclear.

Adolescent↗
PubMed1989

Decreased production of interleukin-1 by monocytes from patients with lipoid nephrosis.

In order to further characterize monocyte function in patients with lipoid nephrosis (LN), we studied the production of interleukin-1 (IL-1). In this study we examined the ability of peripheral blood monocytes (PBM) from LN patients to produce this monokine in vitro under the stimulus of bacterial lipopolysaccharide (LPS). The levels of IL-1 were decreased in patients with LN compared with those in normal controls and lower in LN patients with nephrotic syndrome (NS) than in those without NS. In contrast, the values in IgA nephropathy (IgAN) patients with or without NS did not differ from normal subjects. The addition of indomethacin, an inhibitor of prostaglandin synthesis, partially restored this defect. These results suggest that the impaired IL-1 production of LN PBM is probably attributable, at least in part, to increased prostaglandin production and possibly influences the immune status of LN patients.

Adolescent↗
PubMed1986

Effect of captopril on chronic puromycin aminonucleoside nephrosis in rats.

The effect of captopril, an angiotensin converting enzyme inhibitor, on the progression of chronic puromycin aminonucleoside (PAN) nephrosis was examined. Rats were injected with 15 mg/100 gm body weight PAN and 5 mg/100 gm body weight, on weeks - 1 and 5, respectively. A third group was injected with an equivalent volume of 0.9% saline, intraperitoneally (Group III) on week - 1 and 5. Beginning week 0, group I received 50 mg/kg captopril daily in the drinking water for 12 weeks. Group II received no treatment. Captopril failed to attenuate the peak level of proteinuria induced by the first injection of PAN or to alter the rate of decline of proteinuria when begun 1 week after the PAN injection. However, captopril did blunt the increase in urinary protein excretion following the second injection of PAN (p less than 0.05). Group II became hypertensive compared to Group I on week 8 and 12 and Group III on week 12 (p less than 0.05). Group I and II could not be distinguished on the basis of renal histologic rank (p = 0.80). We conclude that captopril affords some protection against the development of PAN-induced proteinuria, but it does not accelerate the recovery phase when glomerular permselectivity is being regained.

Animals↗
PubMed1985

Depression of local graft-versus-host reaction in patients with lipoid nephrosis.

The local graft-versus-host reaction (GVHR) following intradermal injection of peripheral blood lymphocytes (PBL) in Lewis rats was examined in order to test the cell-mediated immunity (CMI) in 31 patients with renal disease and in healthy controls. It was found that patients with lipoid nephrosis (LN) in the nephrotic stage and systemic lupus erythematosus (SLE) had less mean lesion of the local GVHR and a smaller proportion with positive reactions as compared to normal subjects. This abnormality in LN patients was correlated well with the degree of delayed hypersensitivity skin test responses to purified protein derivative (PPD) and improved with the onset of clinical remission. In contrast, the mean lesion in PBL from LN patients without nephrotic syndrome (NS) and from chronic mesangial proliferative glomerulonephritis (CGN) did not differ from the normal subjects. These findings raise the question of a selective defect in CMI in LN patients with NS. Our studies also indicate that the local GVHR represents a rapid, clinically useful test for assessing cellular immunocompetence in renal disease.

Adolescent↗