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PubMed2005

Increased expression of apoptosis-associated proteins in puromycin aminonucleoside nephrosis.

Increased apoptosis has been reported in acute puromycin aminonucleoside nephrosis (PAN). The aim of this study was to investigate if increased apoptosis is related to increased expression of apoptosis-associated proteins (AAP) in this model of nephrosis. Sprague-Dawley rats were made nephrotic by intraperitoneal injection of one dose of puromycin aminonucleoside. Renal tissues were obtained at 1, 2 and 7 weeks after injection and apoptosis was investigated by TUNEL and by electron microscopy. Fas, Fas ligand, p53, Bax and Bcl-2 expressions were analyzed by the respective monoclonal and polyclonal antibodies, using indirect immunofluorescence. In the glomerulus of nephrotic animals, increased apoptosis was accompanied with increased expression of p53, Fas and Bax. In the interstitium, high expression of apoptosis, Fas, Fas-L and Bax were observed and in tubules increased apoptosis was accompanied with increased expression of p53, Fas and Fas-L. Bcl-2 was increased in interstitium and tubules during PAN. The incidence of apoptosis during PAN was correlated with the expression of AAP in glomerulus (p53), interstitium (Fas, Fas-L and Bax) and tubules (Fas, Fas-L, p53 and Bcl-2). There was correlation between Fas and Fas-L expression in interstitium and tubules. About 4% of glomerular and 25% of tubular p53 positive cells were apoptotic cells. The data suggest that increased local expression of AAP could contribute to renal apoptosis in the glomerular, interstitial and tubular compartments during this experimental model of nephrosis.

Animals↗
PubMed1991

Ultrasonographic findings in dogs and cats with oxalate nephrosis attributed to ethylene glycol intoxication: 15 cases (1984-1988).

Renal ultrasonographic findings in 12 dogs and 3 cats determined to have oxalate nephrosis presumed to be secondary to ethylene glycol intoxication were examined. Ultrasonographic changes varied from mild to marked increases in renal cortical echogenicity. A pattern of greater than normal cortical and medullary echogenicity with persistence of areas of lesser echo intensity at the corticomedullary junction and central medullary regions was observed. This pattern, termed the halo sign, was recognized in 7 dogs and 1 cat concurrent with the development of clinical anuria. Ultrasonographic patterns in these clinical cases were similar to those observed in a previous study of dogs with experimentally induced ethylene glycol nephrosis. Ultrasonographic findings were not considered pathognomonic of ethylene glycol nephrosis. Due to the high death rate reported in the cases surveyed, detection of ultrasonographic changes was considered to warrant a guarded to poor prognosis. Because of the association of the halo sign with anuria, its detection was considered to warrant a grave prognosis.

Animals↗
PubMed1989

Altered functional characteristics of rat macrophages during nephrosis. Synergistic effects of hypercholesterolemia.

The effects of alimentary hypercholesterolemia and nephrotic hyperlipidemia, alone and in combination, on rat peritoneal macrophage phagocytosis, basal eicosanoid production, and glomerular macrophage number during peak PA nephrosis were evaluated in rats fed four different diets: 1) normal/standard chow; 2) PA/standard chow; 3) normal/cholesterol-supplemented diet; and 4) PA/cholesterol-supplemented diet. Both PA/standard chow and normal/cholesterol-supplemented rodent groups manifested significantly greater peritoneal macrophage phagocytosis and glomerular macrophage number when compared with normal/standard chow animals. However, the combination of the nephrotic state with superimposed alimentary hypercholesterolemia (PA/cholesterol-supplemented group) produced the greatest rise in these parameters, a rise that was significantly greater than was produced in the three other groups. Regarding basal eicosanoid production by macrophages, there was a numerical trend toward increased production of thromboxane B2 in the PA/standard chow animals and normal/cholesterol-supplemented rats when compared with normal/standard chow. Again, the combination of nephrosis and alimentary hypercholesterolemia in the PA/cholesterol-supplemented group was associated with a significantly greater amount of thromboxane B2 generated when compared with the other three groups. Regarding PGE2 production, there were no significant differences among the groups, despite marked differences in fasting serum lipid levels. This data suggest that there is a synergistic effect between alimentary hypercholesterolemia and the secondary hyperlipidemia of nephrosis in producing these macrophage functional alterations. Because fasting triglyceride values between the two nephrotic groups were indifferent, one can further speculate that it is the elevation of the serum cholesterol value that predominantly evokes these changes in macrophage function.

Animals↗
PubMed1987

Stable analogs of prostaglandins E1 and F2 alpha ameliorate the proteinuria of aminonucleoside-of-puromycin nephrosis in Lewis rats.

Prostaglandins have been implicated by previous investigators in the pathogenesis of the nephrotic syndrome. A single subcutaneous injection of 1 mg/kg of stable analogs of prostaglandins E1 or F2 alpha (15[S]-15-methyl -PGE1 [M-PGE1] and -PGF2 alpha [M-PGF2 alpha]) was found in the present study to dramatically decrease proteinuria on Day 10 of puromycin aminonucleoside (PAN) nephrosis in Lewis rats. The decrease in proteinuria was mediated at least in part by a decrease in glomerular filtration rate (GFR), as quantitated by inulin clearances in nephrotic control and prostaglandin-treated rats. M-PGE1, moderately, and M-PGF2 alpha, to a lesser degree, also decreased the GFR in normal rats. Interestingly, the GFR was dramatically decreased in nephrotic as compared with nonnephrotic control rats, which suggests that PAN nephrosis may not be an ideal experimental model for human minimal change nephrosis in which the GFR is usually not severely compromised. The prostaglandin-induced decrease in GFR in both nephrotic and normal rats was coincident with a drop in systemic blood pressure. Nephrotic rats, however, had a slightly higher baseline blood pressure than normals, and the hypotensive effects of both prostaglandins were much less in nephrotic than in normal rats. The decrease in proteinuria was not related to a cytoprotective effect, as indicated by the failure of daily doses of 5 micrograms/kg M-PGE1 to reduce proteinuria 6, 8, or 10 days after injection of puromycin aminonucleoside. The similar antiproteinuric effects of prostaglandin synthesis inhibitors and of pharmacologic doses of prostaglandins are somewhat paradoxical but are reminiscent of the similarly paradoxical mutual antiinflammatory effects of these agents. The high doses of prostaglandins required to reduce proteinuria as well as their reduction of blood pressure and GFR will limit their clinical usefulness in the nephrotic syndrome.

Alprostadil↗
PubMed1987

Ameliorative effects of dietary protein restriction in chronic aminonucleoside nephrosis.

Because many investigators have demonstrated the efficacy of dietary protein restriction in various experimental models of glomerular injury that progress to focal and segmental glomerulosclerosis (FSGS), we used this dietary maneuver in chronic aminonucleoside nephrosis. This model of glomerular disease, which uses a single intravenous injection of the puromycin aminonucleoside (PAN), slowly progresses over 18 weeks with mesangial cell proliferation and FSGS as the pathologic hallmarks. We performed renal functional and histopathologic studies in 21 rats with chronic aminonucleoside nephrosis. Group 1 rats (n = 10) were fed a standard rodent diet containing 23.4% protein, whereas group 2 animals (n = 11) were maintained with a 6% protein diet replete with electrolytes, minerals, and vitamins. In those animals subjected to dietary protein restriction, proteinuria was significantly reduced at 14, 28, 84, and 126 days after PAN administration. In rats maintained with the 6% protein diet at 126 days after PAN delivery, there was also a significant reduction in the percent of glomeruli with segmental areas of glomerulosclerosis or hyalinosis and mesangial cell proliferation. We conclude that the renal functional and histologic consequences of chronic aminonucleoside nephrosis can be blunted by dietary protein restriction.

Animals↗
PubMed1981

Experimental nephrosis: interassociation of proteinuria with impaired lymphocyte blastogenesis.

The drug puromycin aminonucleoside (PA), used to induce an experimental nephrosis in rats, inhibited the blastogenic response of normal rat spleen cells when cultured in vitro with autologous or heterologous serum. Only at final PA concentrations of less than 5 microgram/ml did PHA induce normal blastogenesis. When PA was unilaterally perfused through the rat kidney a nephrosis developed, characterized by massive proteinuria. Microscopically, the foot process fusion and mesangial cell increase were similar to that seen in human steroid-responsive nephrotic syndrome. Once proteinuria had developed, there was marked suppression of the lymphocyte blastogenic response of the nephrotic rat spleen cells when cultured in autologous sera. Neither proteinuria nor inhibited blastogenesis was found in animals perfused with a buffered salt solution. Animals which were perfused with PA, nephrectomized 2 days after perfusion, and did not show proteinuria, had suppressed lymphocyte blastogenesis after stimulation with PHA. However, the degree of stimulation by the spleen cells of these animals was similar to that from control perfused and nephrectomized animals. Therefore, the aberration in lymphocyte response was consistent with the development of the nephrosis and proteinuria.

Albuminuria↗
PubMed1995

Overexpression of human apolipoprotein A-I in transgenic rats and the hyperlipoproteinemia associated with experimental nephrosis.

Hyperlipoproteinemia contributes both to kidney disease progression and the development of atherosclerosis. Elevated high density lipoprotein cholesterol and apolipoprotein A-I (apoA-I) serum levels are independent factors protective against the atherosclerotic process. We examined the effects in a transgenic rat model of human apoA-I expression on the hyperlipoproteinemia and edema after puromycin aminonucleoside-induced nephrosis in three groups of animals: low line (TgR[hAI]low, human plasma apoA-I = 16.0 mg/dl); high line (TgR[hAI]high, 284 mg/dl); and non-transgenic litter mates (TgR[hAI]non). Nephrosis increased total plasma apoA-I levels 2-fold in TgR[hAI]non rats (75 vs. 162 mg/dl) and 4-fold in the TgR[hAI]low (97 vs. 458 mg/dl) and TgR[hAI]high rats (356 vs. 1,346 mg/dl). In both transgenic lines, this increase was due mainly to elevations of serum human apoA-I. The hepatic steady-state levels of rat apoA-I mRNA increased 5- to 7-fold in all three groups, while human apoA-I mRNA levels increased 21- and 65-fold in the low and high expressing groups, respectively, indicating a different degree of responsiveness of the rat and human genes. While nephrotic TgR[hAI]non and TgR[hAI]low rats showed severe hyperlipoproteinemia and edema, much lower levels of edema and of serum triglycerides, phospholipids, and cholesterol were seen in the TgR[hAI]high group. Urinary excretion of apoA-I, phospholipids, and cholesterol was significantly increased in the TgR[hAI]high group, indicating this as one possible mechanism for the relatively lower serum levels of these lipids. We conclude that the human apoA-I gene is responsive to nephrosis and that human apoA-I-transgenic rats with this syndrome provide an animal model for the study of human high density lipoprotein and apoA-I metabolism.

Animals↗
PubMedDate not supplied

Dose of doxorubicin determines severity of renal damage and responsiveness to ACE-inhibition in experimental nephrosis.

Nephrosis induced by doxorubicin (adriamycin) is an experimental model of glomerulosclerosis with relative stable proteinuria which is commonly used for pharmacological intervention studies. It is induced by a single or a double dose of doxorubicin, with doses that vary considerably among investigators from 2 to 7.5 mg/kg. Intervention studies with ACE-inhibitors in this model have provided conflicting results. We hypothesized that these discrepancies might be due to different properties of the doxorubicin model, related to the dose of doxorubicin used to induce proteinuria. We tested this hypothesis by inducing doxorubicin nephrosis with 1, 2 and 3 mg/kg, and evaluating the response to intervention with lisinopril. The 1-mg/kg doxorubicin dose did not induce significant proteinuria. The 2- and the 3-mg/ kg dose resulted in a proteinuria of 684+/-215 mg/24 h and 736+/-277 mg/24 h 6 weeks after induction, respectively (Mean+/-SD). Treatment with lisinopril 2 mg/kg/day reduced proteinuria to 160+/-170 mg/24 h(p<0.01) in the 2-mg/kg doxorubicin group, whereas in the 3-mg/kg doxorubicin group, proteinuria did not respond to lisinopril (529+/-264 mg/24 h). In time control rats, proteinuria remained stable. Renal damage developed in both time control groups, with a glomerulosclerosis score of 29+/-22 in the 2-mg/kg group and 84+/-41 in the 3-mg/kg doxorubicin group. Lisinopril resulted in a significantly lower glomerulosclerosis score in the 2-mg/kg doxorubicin group only (16+/-15, p<0.05), whereas the 3-mg/kg group showed no significant reduction (56+/-29, NS). In conclusion, the dose of doxorubicin used to induce nephrosis is an important determinant not only of the severity of the ensuring renal damage, but also of the response to intervention by ACE-inhibition. These findings have an impact on the interpretation of intervention studies in this model.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

The incidence of chronic progressive nephrosis in young Sprague-Dawley rats from two different breeders.

Chronic progressive nephrosis (CPN) in rats may not only become a problem in long-term toxicity studies but also in short-term studies, if the breeding stock is not carefully selected with respect to the kidney function. This paper presents differences in kidney function between young rats of the same strain, Sprague-Dawley, but from two different breeders ('set A' and 'set B' rats). In set A rats, protein in the urine was present in the males, which is a common finding. In set B rats, not only the males but also the females excreted protein in the urine. The method used to detect protein in the urine does not normally show a positive protein result in the young female rats. At the age of 3 months signs of chronic progressive nephrosis were observed in 55% of the males and in 15% of the females in set B. Two months later, the incidence had increased to about 70-80% in males and 50% in females. At 8 months, the incidence was similar, but the severity had increased. These values were compared with those obtained from the set A rats, none of which showed any signs of the disease at the age of 5 months and only 5% of the males and females at the age of 8 months. The results indicated that an increased excretion of protein in the urine may be used as an indicator for chronic progressive nephrosis in the rat and that not only the strain but also the source is important in selecting laboratory rats for toxicity studies.

Animals↗
PubMedDate not supplied

[Lipoid nephrosis in a child with advanced Hodgkin's lymphoma].

This is a case of an eight year old male, with Hodgkin's disease grade IV-B, with initial clinical presentation of nephrotic syndrome. The renal biopsy showed minimal change lesions. He had a complete remission of the nephrotic syndrome and Hodgkin's disease after been given prednisone and chemotherapy respectively. The remission of the nephrotic persisted 22 months and the Hodgkin's disease, 23 months. It has been established that cellular immunity is altered in Hodgkin's disease. The etiopathogenesis of lipoid nephrosis is unknown. There are clinical and experimental evidences showing cellular immunity in patients with lipoid nephrosis, suggesting a possible involvement of this mechanism in the etiopathogenesis of lipoid nephrosis. This could explain a relationship between the nephrotic syndrome (lipoid) and Hodgkin's disease. Our patient, besides Hodgkin's disease, showed clinical, biochemical and histologic changes, as well as clinical course compatible with nephrotic syndrome with minimal changes lesions.

Adolescent↗
PubMed1993

Inner ear damage due to lipoid nephrosis.

Inner ear pathology was studied in adult rats with lipoid nephrosis induced by puromycin aminonucleoside. Although no abnormality was observed in auditory brain-stem responses, significant changes were noted in the stria vascularis. The most striking observation was that intermediate cells were markedly swelled, there-by pressing adjacent marginal cells. Severely affected marginal cells have vacuoles and increased lysosomes and protruded toward the endolymphatic space. The organ of Corti remained virtually intact. Although the vestibular maculae were relatively normal, type I hair cells in the semicircular canal underwent a conspicuous vaculolization. These findings support a postulate that the inner ear is liable to damage in lipoid nephrosis.

Animals↗
PubMed1983

Pachygyria and congenital nephrosis disorder of migration and neuronal orientation.

A case of pachygyria with associated nephrosis has been studied. Several microscopic abnormalities have been identified: cytoarchitectonic disorders including neuronal ectopies in the molecular layer and in the meninges, improperly oriented neurons shown with Golgi stain, fetal aspect of inferior olives. The mechanism of the disorder of migration and neuronal and dendritic orientation are discussed. The significance of the association of microcephaly and nephrosis is also reviewed in light of recent literature.

Brain↗
PubMed1984

An ultrastructural study of the effect of the steroid in puromycin aminonucleoside nephrosis rats.

In order to investigate the significance of the histological change in glomerular epithelial cells in minimal change nephrotic syndrome in man (MCNS) and to help in clarifing the mechanism of action of a steroid in this disease, methylprednisolone was administered to rats with puromycin aminonucleoside nephrosis (PAN). This is an experimental nephrosis having a close resemblance morphologically and physiologically, to human MCNS. Morphological changes in the glomerulus were observed ultrastructurally. The administration of the steroid to PAN rats showed remarkable changes including, rapid disappearance of proteinuria in PAN rats in a manner similer to that seen in human MCNS, and significantly faster recovery of changes in glomerular epithelial cells when compared with spontaneous recovery. From the present study, it is clear that the steroid is effective in rapidly restoring the normal shape of glomerular epithelial cells in PAN rats. The filtration barrier in the glomerular capillary wall (GCW) is also thought to have recovered and proteinuria is cured. Based on these considerations, it may be suggested that proteinuria in human MCNS is caused by changes in glomerular epithelial cells, and that the clinical treatment of proteinuria in MCNS is effective when glomerular epithelial cells have functionally recovered.

Animals↗
PubMed1988

Clinical efficacy of levamisole in the treatment of primary nephrosis in children.

The purpose of the study was to evaluate the efficacy and the toxicity of levamisole given for 1 year to 16 children suffering from minimal change primary nephrosis who were relapsing frequently. The overall results showed that under levamisole the relapse rate decreased by 55% and the steroid requirements by 50%. After cessation of levamisole administration, most children (11/16) relapsed again. A second course of levamisole treatment reduced the relapse rate significantly once again. At the dosage of 2.5 mg/kg given every other day for 1 year or more, no side effects of levamisole does not cure nephrosis but reduces the incidence of relapses for the period it is administered. It also reduces the steroid requirements without any important side effects.

Adolescent↗
PubMed1993

Ultrastructural changes in glomerular epithelial cells in acute puromycin aminonucleoside nephrosis: a study by high-resolution scanning electron microscopy.

Ultrastructural changes in the podocytes were studied during the development of, and recovery from, acute puromycin aminonucleoside (PAN) nephrosis using high-resolution scanning electron microscopy (hrSEM) and transmission electron microscopy (TEM). In the process of development of PAN nephrosis, four types of early structural changes were observed before total loss of foot processes: formation of cytoplasmic blebs, masking of filtration clefts, flattening of foot processes, and retraction of foot processes. The masking of filtration clefts visualized by hrSEM corresponded to the multiplication of slit diaphragms and adhesion of foot processes in the TEM findings, and preceded retraction of the foot processes. Changes of podocyte configuration were produced. Recovery from this change of podocyte configuration began as islands of podocyte interdigitation, and was proceeded by expansion of the islands. During recovery, the primary processes were re-established either by retraction or perforation of the thin cytoplasm after the formation of foot processes. We conclude that loss of foot processes begins with the masking of filtration clefts. Recovery from the change in podocyte configuration begins with the formation of new foot processes.

Acute Disease↗
PubMed1990

Nephrosis in two siblings with infantile sialic acid storage disease.

The diagnosis of infantile sialic acid storage disease (ISSD) was established in two siblings on the basis of typical clinical signs and the biochemical findings of hyperexcretion and intracellular storage of free sialic acid. A severe, steroid resistant nephrosis occurred in both siblings. The activities of lysosomal enzymes, including sialidase, were normal. A combined detection method for sialic acids with Limax flavus agglutinin labelling and phosphotungstic acid staining showed severely alterated sialic acid components in epithelial kidney cells and indicate a causal relationship between the nephrosis and the underlying biochemical defect. Further observations of ISSD patients with renal involvement will prove if a separate nephropathic phenotype exists.

Carbohydrate Metabolism, Inborn Errors↗
PubMed2003

Effect of grape seed extract on puromycin-aminonucleoside-induced nephrosis in rats.

Recent studies indicate that an excessive production of oxidants plays an important role in the pathogenesis of glomerular disease. Grape seed extract (GSE) is a potent antioxidant, and the aim of this pilot study was to evaluate its effect on puromycin-aminonucleoside (PAN)-induced nephrosis in rats. Fifty Sprague-Dawley rats were divided into five groups. Groups 1 and 2 rats received water from day 0 to day 30. Rats in groups 3, 4, and 5 received GSE at 10 mg/100g of body weight (BW), which was started on day 0, 6, and 3 of the experiment, respectively. In group 5 animals the GSE dose was increased (40 mg/100g BW) on day 9. Intraperitoneal dextrose (group 1) or PAN 15 mg/100g BW (groups 2-5) was administered on day 3. Urine and blood specimens were collected at regular intervals, and the comparison between the various groups was made by analysis of variance (ANOVA). Rats in all study groups (groups 3-5) showed a decrease in urine protein and serum cholesterol and triglyceride levels, which was statistically significant in group 3 animals. No significant changes were noted in serum albumin and creatinine levels. In conclusion, GSE administration decreases urine protein excretion and serum cholesterol and triglyceride levels in rats with PAN-induced nephrosis.

Animals↗