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PubMed1991

Decreased anionic sites in different portions of the basement membrane in aminonucleoside nephrosis.

We induced aminonucleoside (AN) nephrosis in male Sprague-Dawley rats and evaluated the decreases in negative charge in the peripheral and proximal portions of the loop basement membrane and the basement membrane in the paramesangial area. Following intravenous injection of polyethyleneimine (PEI), the number of PEI granules per 0.1 micron 2 of the basement membrane, and those per 1 micron length of the lamina rara externa (LRE) and lamina rara interna (LRI) were counted in each portion under an electron microscope and compared with those in the control group. In the rats with AN nephrosis, the number of PEI granules per 0.1 micron 2 was significantly decreased in each portion of the basement membrane. However, the degree of decrease was similar among the 3 portions. The ratio of the numbers of granules in the proximal and paramesangial portions to that in the peripheral portion (peripheral:proximal:paramesangial) was 1:0.89:0.64 in the control group and 1:0.88:0.62 in the AN nephrosis group. Similar results were obtained for the numbers of PEI granules per 1 micron length of the LRE and LRI. These findings suggest that the negative charge is decreased in the loop basement membrane and paramesangial basement membrane in AN nephrosis, but the degree of decrease appears to be uniform.

Animals↗
PubMed1984

Typing of HLA antigens in a child population with nephrosis syndrome.

Using the microlymphocytotoxicity test of Terasaki, HLA--A, B, Cw antigen typing was done for 37 antigens in 28 children with steroid-sensitive nephrosis and five children with steroid-resistant nephrosis. Evaluation was made by the chi 2 test as corrected by the method of Yeates. In steroid-sensitive nephrosis the frequency of HLA--B 8 antigen was 33.3% and in the resistant cases 40% as against 18.5% in the controls. The difference, however, was not significant, the B 12 and B 13 antigens were more frequent in both steroid-sensitive and resistant nephrosis, though not significantly.

Child↗
PubMed1992

Cyclosporin reduces proteinuria in rats with aminonucleoside nephrosis.

The effect of cyclosporin (CS) was assessed in Sprague-Dawley rats with puromycin aminonucleoside (PA) nephrosis induced by a single intraperitoneal injection of PA. Three groups of rats were injected intraperitoneally with CS (10 mg/kg body weight) daily, beginning 1 day before PA administration, or 5 or 10 days after PA administration, for 10 days. CS significantly reduced proteinuria in rats with PA nephrosis in comparison with untreated nephrotic controls. After discontinuation of the CS treatment, proteinuria gradually increased, reaching values similar to those in control nephrotic rats. CS pretreatment did not prevent the induction of PA-induced nephrotic syndrome. Light microscopy and assessment of anionic sites in the glomerular basement membrane revealed no differences between normal rats, nephrotic controls, and CS-treated rats. These results show that CS can reduce proteinuria in PA nephrosis, but cannot ameliorate the glomerular changes.

Animals↗
PubMed2001

Prenatal diagnosis of congenital nephrosis by in utero kidney biopsy.

The diagnosis of congenital nephrosis is difficult during the antepartum period. The combination of an elevated amniotic fluid alpha-fetoprotein, a negative acetylcholinesterase, and a negative ultrasound examination is highly indicative of congenital nephrosis; however, these findings can also be associated with a normal gestation. This is the first report of pathologic confirmation of congenital nephrosis from an in utero fetal kidney biopsy.

Acetylcholinesterase↗
PubMed2006

Bacterial superantigen TSST-1 attenuates suppressive efficacy of glucocorticoids and calcineurin inhibitors against blastogenesis of peripheral blood mononuclear cells from patients with antineutrophil cytoplasmic antibody-associated vasculitis and nephrosis.

Successful immunosuppressive therapy is critical for the treatment of patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis and nephrosis. However, a considerable number of patients have shown clinical resistance to therapy. Bacterial infection might influence the clinical response of patients to immunosuppressive drugs, but few studies have been carried out to investigate the effect of bacterial superantigens on the efficacy of the drugs in these patients. We evaluated the suppressive efficacy of prednisolone, methylprednisolone, cyclosporine, and tacrolimus on the blastogenesis of PBMCs obtained from 12 ANCA-associated vasculitis patients (ANCA patients), eight patients with nephrotic syndrome, and eight healthy subjects. PBMC-stimulation index was calculated from the formula: [3H]thymidine incorporated in the presence of stimulant (dpm)/[3H]thymidine incorporated in the absence of stimulant (dpm). In vitro drug concentrations giving 50% inhibition (IC50s) of PBMC blastogenesis stimulated with concanavalin A (con A) or toxic shock syndrome toxin 1 (TSST-1) derived from Staphylococcus aureus (S. aureus) were calculated. The IC50 values for the four drugs evaluated in TSST-1-stimulated PBMCs were significantly higher than those evaluated in con A-stimulated PBMCs in both ANCA patients and nephrosis patients (p<0.012-0.044). Whereas, the IC50 values for these immunosuppressive drugs, except methylprednisolone, were not significantly different between con A- and TSST-1-stimulated PBMCs in healthy subjects. The stimulation index was not significantly different between the con A- and TSST-1-stimulated PBMCs in either of the subject groups. These observations raise the possibility that TSST-1 induced by S. aureus infection attenuates the clinical efficacy of glucocorticoids and calcineurin inhibitors in ANCA patients and nephrosis patients.

Adult↗
PubMed1992

Congenital nephrosis: detection of index cases through maternal serum alpha-fetoprotein screening.

Congenital nephrosis is an autosomal recessive disorder with an incidence of 1 in 8000 in Finland, but it is quite rare in non-Finnish populations. In families known to be at risk, prenatal detection is possible by means of maternal serum and/or amniotic fluid alpha-fetoprotein levels. We report the antenatal diagnosis of four cases of congenital nephrosis, three of which were index cases, through maternal serum alpha-fetoprotein screening. The diagnosis was confirmed at birth in two infants. Two patients elected to terminate their pregnancies, and the diagnoses were confirmed pathologically (obliteration of foot processes on electron microscopy of fetal glomeruli) in both. In cases of elevated maternal serum alpha-fetoprotein, with unexplained and marked elevations of amniotic fluid alpha-fetoprotein and normal acetylcholinesterase levels, the diagnosis of congenital nephrosis must be considered regardless of ethnic origin.

Adult↗
PubMed1991

Nasal administration of salmon calcitonin for prevention of glucocorticoid-induced osteoporosis in children with nephrosis.

To determine the effect of intranasal administration of salmon calcitonin on glucocorticoid-induced osteoporosis in children with nephrosis, we gave 100 U of calcitonin intranasally on alternate days with 1 alpha-hydroxyvitamin D3 to five children, 8 to 12 years of age, with frequently relapsing nephrosis. Four patients with osteoporosis, 10 to 14 years of age, were treated only with 1 alpha-hydroxyvitamin D3 and served as control subjects. Both groups were treated with an almost equal amount of glucocorticoids previously and during this study period. Bone mineral content of the spine was measured by a quantitative computed tomographic technique. The bone mineral content was preserved in both cortical and spongeous areas of the vertebrae during the 16-month period in the calcitonin-treated group but was decreased significantly in the control group. Urinary hydroxyproline and calcium excretion decreased significantly in the calcitonin-treated group. The serum calcium and phosphorus concentrations and the parathyroid function did not change significantly in either group. We conclude that calcitonin suppressed bone resorption and might be useful for the long-term treatment of osteoporosis, in combination with 1 alpha-hydroxyvitamin D3, in children with nephrosis requiring long-term glucocorticoid therapy.

Administration, Intranasal↗
PubMed1979

Renal failure owing to oxalate nephrosis after jejunoileal bypass.

Oxalate nephrosis resulted in progressive renal failure in 4 patients after jejunoileal bypass for morbid obesity. In general, increased levels of oxalates in the blood and urine of such patients result from enhanced absorption of exogenous oxalates. Urinary calculous formation is determined further by concomitant deficiency of inhibitor substances, whereas oxalate nephrosis probably occurs as a result of oxalate deposition in renal interstitium via the blood stream. Clinical manifestations of oxalate nephrosis include pain, infection, hematuria and renal failure. Routine postoperative renal function studies and early renal biopsy in suspicious cases are urged to establish early diagnosis. Continued deterioration of renal function, despite therapy with oxalate restruction and oxalate binding agents, indicates a reversal of the bypass to preserve unaffected renal substance.

Adult↗
PubMed1995

Volume regulation in children with early relapse of minimal-change nephrosis with or without hypovolaemic symptoms.

The cause of sodium retention in nephrotic syndrome is unclear. Hypovolaemia has traditionally been labelled as the cause but there is evidence in adults of a renal disturbance as the main cause. We aimed to find out whether children with early nephrosis can be classified as hypovolaemic by objective measures. We measured blood volume, kidney function, and hormone concentrations in children with early relapse of minimal-change nephrosis. Three presentations could be defined. The first was patients with incipient proteinuria and normal plasma protein, characterised by sodium retention, increased renal plasma flow, and slightly increased aldosterone, but normal noradrenaline. The second was patients with severe proteinuria, hypoproteinaemia, and hypovolaemic symptoms, who had oedema, sodium retention, and high concentrations of plasma renin, aldosterone, and noradrenaline, low atrial natriuretic peptide, and low glomerular filtration rate. The third was patients with equally severe proteinuria and hypoproteinaemia, but without hypovolaemic symptoms; they had oedema, but no active sodium retention, and normal plasma hormones and glomerular filtration. Neither blood pressure nor blood volume discriminated patients with or without hypovolaemic symptoms. These findings show that children with early full-blown nephrosis can present both with and without hypovolaemic symptoms and laboratory signs, despite equally severe hypoproteinaemia, and also that sodium retention precedes the reduction in serum protein.

Adolescent↗
PubMed1999

Effect of the in vivo catalase inhibition on aminonucleoside nephrosis.

Reactive oxygen species have been involved in the pathophysiology of puromycin aminonucleoside (PAN)-nephrosis. The role of H2O2 in these rats may be studied modulating the amount or activity of catalase, which breakdowns H2O2 to water and oxygen. To explore the role of H2O2 in this experimental model, we studied the effect of the in vivo catalase inhibiton with 3-amino-1,2,4-triazole (ATZ) on the course of PAN-nephrosis. Four groups of rats were studied: control rats (CT group), PAN-injected rats (PAN group), ATZ-injected rats (ATZ group), and ATZ- and PAN-injected rats (ATZPAN group). Rats were placed in metabolic cages to collect 24 h urine along the study, ATZ (1 g/kg) was given 24 h before PAN injection (75 mg/kg), and the proteinuria was measured on days 0, 2, 4, 6, 8, and 10. Proteinuria started before (day 4) and was significantly higher on days 6, 8, and 10 in the ATZPAN group than in the PAN group. On day 10, hypercholesterolemia was significantly higher in the ATZPAN group than in the PAN group. These data indicate that the in vivo catalase inhibition magnifies PAN-nephrosis, suggesting that H2O2 is produced in vivo and involved in the renal damage in this experimental disease.

Amitrole↗
PubMed1984

Unaltered anionic sites of glomerular basement membrane in aminonucleoside nephrosis.

Quantitative electron microscopic autoradiography was employed to determine the changes in the binding of 125I-cationic ferritin (CFI, pI approximately 7.2 to 7.4) to the anionic sites of the glomerular basement membrane (GBM) of rats following the induction of nephrosis. Animals were rendered nephrotic by a single intravenous injection of puromycin aminonucleoside (PAN) and sacrificed 0, 7, 14, and 21 days after its administration. CFI (10 mg/mCi/100 g body weight) was given intravenously. The kidneys were subsequently fixed by perfusion and processed for electron microscopic autoradiography. The mean grain densities over the GBMs on 0, 7, 14, and 21 days of PAN nephrosis were 1.50 +/- 0.04, 1.49 +/- 0.05, 1.50 +/- 0.05, and 1.51 +/- 0.04, respectively. These results indicate that there are no significant alterations in the anionic sites rich in heparan sulfate proteoglycan during the entire course of PAN nephrosis.

Animals↗
PubMed1991

Involvement of thromboxane A2, leukotrienes and free radicals in puromycin nephrosis in rats.

Thromboxane A2 (TXA2), leukotrienes (LTs) and free radicals are considered to be possible mediators in the induction of glomerular injury and proteinuria. In this study, we examined the involvement of these three mediators and the protective effect of simultaneous inhibition of all three in puromycin aminonucleoside (PAN) nephrosis in rats. A single intraperitoneal injection of PAN (100 mg/kg) induced massive proteinuria and enhanced production of TXA2 and LTs from arachidonic acid in renal cortical slices and renal glomeruli, and increased malondialdehyde levels in plasma, urine and renal cortex. Oral administration of CV-6504(HCl) (3 to 20 mg/kg/day, for 1 to 2 weeks), a novel treble inhibitor of TXA2 synthetase, 5-lipoxygenase and lipid peroxidation, dose-dependently attenuated PAN-induced proteinuria and the increases in these three mediators. Any single specific inhibitor (CV-4151, a TXA2 synthetase inhibitor; AA-861, a 5-lipoxygenase inhibitor; or CV-3611, a radical scavenger) or a combination of two inhibitors showed no or only a slight antiproteinuric effect, but the combination of all three inhibitors significantly reduced PAN-induced proteinuria. These results suggest that, these three mediators may be involved in the pathogenesis of PAN nephrosis and that CV-6504(HCl), which can simultaneously inhibit all three, may be a useful therapeutic agent for nephrosis.

Animals↗
PubMed1991

Pathogenesis of interstitial fibrosis in chronic purine aminonucleoside nephrosis.

A cellular and molecular approach was used to gain new insight into the pathogenesis of interstitial fibrosis in chronic purine aminonucleoside nephrosis (PAN) nephrosis. Thirty experimental rats (PAN rats) were given 15 mg/100 g body wt of i.p. PAN at time 0, followed by 4.3 mg/100 g body wt i.p. on days 20, 27 and 34; 25 control rats received i.p. saline at the same time intervals. All rats had a right unilateral nephrectomy within the first four days. Groups of control and PAN rats were killed at 21, 37, 52, 72 and 91 days. Renal sections were studied by immunofluorescence to quantitate interstitial macrophages, T lymphocytes and fibroblasts, and to characterize the deposition of the extracellular matrix (ECM) proteins (collagens I, III and IV, fibronectin and laminin) and the tissue inhibitor of the metalloproteinases (TIMP). Steady state concentrations of mRNA from the whole kidney for these ECM proteins, the metalloproteinases, TIMP, and transforming growth factor beta (TGF-beta 1) were quantitated by Northern blot analysis. Significant increases in the number of interstitial macrophages and T lymphocytes were found in the PAN rat groups compared to that in controls. All ECM proteins examined were quantitatively increased in the tubulo-interstitium of PAN rats. The pattern of distribution of some ECM proteins was also modified in experimental animals. TIMP was increased in the interstitium of PAN rats; at later times, TIMP was most prominent in sclerotic regions of the glomeruli and in tubular protein droplets. Northern blot analysis revealed increased steady-state mRNA levels for components of each of the ECM proteins, no change for the metalloproteinases--stromelysin or collagenase--and a marked increase for TIMP and TGF-beta 1 in PAN animals. The results of this study suggest that the diffuse interstitial fibrosis found in chronic PAN nephrosis results from both increased production of ECM proteins and decreased matrix degradation.

Albuminuria↗
PubMed2003

Retinoids as a potential treatment for experimental puromycin-induced nephrosis.

1 Puromycin aminonucleoside (PAN)-induced nephrosis is a model of human minimal change disease. In rats, PAN induces nephrotic-range proteinuria, renal epithelial cell (podocyte) damage, infiltration of mononuclear leukocytes, and apoptosis of several renal cell types. 2 Retinoic acid (RA) modulates a wide range of biological processes, such as inflammation and apoptosis. Since renal damage by PAN is characterized by inflammatory infiltration and epithelial cell death, the effect of treatment with all-trans RA (tRA) was examined in the PAN nephrosis model and in the cultured differentiated podocyte. 3 Treatment with tRA 4 days after PAN injection did not inhibit the proteinuria peak but reversed it significantly. However, treatment with tRA both before and 2 days after the injection of PAN protected the glomerular epithelial cells, diminishing the cellular edema and diffuseness of the foot process effacement. Preservation of the podocyte architecture correlated with the inhibition of proteinuria. The anti-inflammatory effect of tRA was evidenced by the inhibition of PAN-induced interstitial mononuclear cell infiltration and the decreased renal expression of two molecules involved in monocyte infiltration: fibronectin and monocyte chemoattractant protein-1. TUNEL assays showed that tRA inhibited the PAN-induced apoptosis of cultured differentiated mouse podocytes. 4 We conclude that tRA treatment may prevent proteinuria by protecting the podocytes from injury and diminishing the interstitial mononuclear infiltrate in the model of PAN nephrosis. Retinoids are a potential new treatment for kidney diseases characterized by proteinuria and mononuclear cell infiltration.

Administration, Oral↗
PubMed1993

Altered glomerular steady-state levels of tumour necrosis factor-alpha mRNA during nephrotic and sclerotic phases of puromycin aminonucleoside nephrosis in rats.

1. We determined glomerular and medullary tumour necrosis factor-alpha mRNA levels in acute puromycin aminonucleoside nephrosis on days 0, 8 and 20. 2. Tumour necrosis factor-alpha mRNA levels were increased fourfold in glomeruli and twofold in the medulla during the nephrotic stage of acute puromycin aminonucleoside nephrosis (day 8). 3. The high tumour necrosis factor-alpha mRNA levels in both glomeruli and the medulla were ameliorated significantly by methylprednisolone administration. 4. Focal glomerular sclerosis was induced in rats by injection of puromycin aminonucleoside on days 0, 27, 34 and 41 and by unilateral nephrectomy on day 22. 5. The percentage of sclerosing glomeruli was 16.6% on day 48 and had increased significantly to 72.8% on day 80. 6. During the sclerotic phase of puromycin amino-nucleoside nephrosis, glomerular tumour necrosis factor-alpha mRNA levels increased as glomerular sclerosis progressed. On day 80, glomerular tumour necrosis factor-alpha mRNA levels were 13-fold higher than levels in control rats. 7. These data suggest that glomerular tumour necrosis factor-alpha mRNA expression is associated with the development of puromycin aminonucleoside-induced glomerular sclerosis.

Acute Disease↗
PubMed2001

Increased expression of heparanase in puromycin aminonucleoside nephrosis.

BACKGROUND: The beta-D-endoglycosidase heparanase has been proposed as an important contributor to loss of glomerular charge in proteinuria. Expression of heparanase was, therefore, determined in acute puromycin aminonucleoside (PAN) nephrosis. METHODS: A rabbit polyclonal antibody was produced against a 17-amino acid peptide derived from the predicted amino acid sequence of heparanase. The antibody was validated by Western blot. Immunohistochemical staining and Western blotting were used to localize heparanase protein in normal kidneys and kidneys from rats with PAN nephrosis. Northern blot analysis was used to determine mRNA expression. RESULTS: Immunohistochemical staining showed that heparanase protein was localized to tubular cells in the distal convoluted tubules, thick ascending limb of the loop of Henle, and transitional cell epithelium in normal kidney. Minimal expression was noted in normal glomeruli. Western blot analysis of protein from isolated normal glomeruli showed minimal expression of the 65 kD proheparanase protein. A marked increase in the staining for heparanase was found at day 5 of the PAN nephrosis model, at approximately the time of onset of proteinuria, and at day 14. Expression was predominantly seen in podocytes. At day 5, only the 65 kD proheparanase species was identified, but at day 14, mature 58 kD heparanase also was present. Northern blot analysis of sieved glomeruli at day 14 confirmed an increase in heparanase mRNA. The human podocyte cell line 56/10A1 also produced both proheparanase and mature heparanase, suggesting that podocytes can activate heparanase without other cell types. CONCLUSION: The previously mentioned data confirm that the novel beta-D-endoglycosidase heparanase is up-regulated and activated in glomeruli from rats with proteinuria. Heparanase may be involved, therefore, in the loss of glomerular charge seen in proteinuria. Moreover, the presence of heparanase in normal tubules suggests that it may also be involved in cell migration or turnover.

Animals↗
PubMed1957

An electron microscope study of the glomerulus in nephrosis, glomerulonephritis, and lupus erythematosus.

Renal biopsies from 16 patients with nephrosis, 7 patients with glomerulonephritis, and 3 patients with disseminated lupus erythematosus were studied with the electron microscope. The observations presented indicate that early in the course of each of these diseases alterations occur in the fine structure of the glomeruli which serve to distinguish one disease process from another. In nephrosis, some distortion of the organization of the epithelial foot processes was seen in all patients. These epithelial changes constituted the early, consistent lesion of the disease. There was frequently also a swelling of the endothelium. In glomerulonephritis, pronounced proliferative changes involving the endothelium and to a lesser extent the epithelium, together with the laying down of a basement membrane-like material, represented the predominate pathologic processes. There was also a swelling of both endothelial and epithelial cytoplasm. The epithelial foot processes generally appeared normal. In patients with a clinically "mixed" picture of nephrosis and nephritis, the glomerular changes were likewise "mixed," for various combinations of epithelial, endothelial, and basement membrane abnormalities were present. In disseminated lupus erythematosus, a more or less generalized thickening of the basement membrane proper associated with a variable degree of endothelial proliferation was seen. It is suggested that an accentuation of the process of basement membrane thickening results in the "wire loop" appearance sometimes seen by light microscopy. Although the earliest alterations in glomerular fine structure were characteristic for each of the disease processes, at later stages the changes were not always distinctive. The resulting scarred or "hyalinized" glomeruli, composed of relatively homogeneous, basement membrane-like material, and a few atrophic cells, appeared quite similar. Although the functional implications of the structural changes observed remain obscure at this time, it is believed that insight into mechanisms may stem from such observations.

Basement Membrane↗
PubMed1975

Zinc metabolism in aminonucleoside-induced nephrosis.

Nephrosis was induced in Sprague-Dawley rats in two separate studies by injections of aminonucleoside with sacrifice of animals on days 20 and 54, respectively. Experimental animals in both studies showed the typical findings of nephrosis, i.e., hypoalbuminemia, hypercholesterolemia, and proteinuria. Biochemical findings included hypozincemia and hyperzincuria. A significant correlation between hypozincemia and hypoalbuminemia was noted in the short-term study. Proteinuria occurred on the 10th day in the short-term study and the 15th day in the long-term study and increased quantitatively over the remaining days. The hyperzincuria and proteinuria correlated significantly in the long-term study. Measurements of tissue zinc revealed no change in testes and kidney in the short-term study. Kidney and muscle zinc were increased, testicular zinc was unchanged and femur zinc was decreased in the long-term study. Our conclusions are that in the aminonucleoside induced nephrosis of the rat: 1) hypozincemia occurs probably as a result of hypoalbuminemia, 2) the hyperzincuria is likely due to proteinuria and 3) zinc deficiency is not observed in nephrotic rats who receive ample zinc in their diet and who are observed up to 6 weeks.

Animals↗