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PubMed2004

Oxidative stress in a rat model of nephrosis can be quantified by electron spin resonance.

The pathogenesis of nephrotic syndrome is not clear. In this study, we used electron spin resonance (ESR) to evaluate levels of reactive oxygen species in rats with puromycin aminonucleoside (PAN)-induced nephrosis. Twenty-six Wistar rats were divided into four groups: (1) PAN treated, (2) PAN treated and alpha-tocopherol supplemented, (3) supplemented with alpha-tocopherol only, (4) control. On day 9, urinary protein excretion was measured. On day 10, all animals were sacrificed with retrograde perfusion via the aorta to obtain renal venous perfusates. The signal intensities of ascorbate radicals in the perfusates were determined by ESR. After perfusion, the kidneys were isolated and sieved to obtain glomeruli for determination of glomerular thiobarbituric acid-reactive substance (TBArs) and alpha-tocopherol. Urinary protein excretion by PAN-treated rats increased significantly on day 9 and was reduced by alpha-tocopherol supplementation. The ascorbate radical intensity and glomerular TBArs level were higher in PAN-treated than in control rats and were both suppressed to control levels by alpha-tocopherol supplementation. There were positive correlations between ascorbate radical intensity and the daily urinary protein, as well as between ascorbate radical intensity and the glomerular TBArs level. Hence, it is possible to quantify oxidative stress due to PAN nephrosis by ESR. Our findings suggest that lipid peroxidation plays an important role in the pathogenesis of proteinuria in PAN-treated rats.

Animals↗
PubMed2005

Effect of a novel free radical scavenger, edaravone, on puromycin aminonucleoside induced nephrosis in rats.

Recent studies indicate that excessive production of oxidants plays a role in the pathogenesis of glomerular injury leading to proteinuria in patients with minimal-change nephrotic syndrome (MCNS). The novel free radical scavenger, edaravone (EDA), which was recently developed in Japan, is currently used in patients with stroke. We studied whether this new agent would be beneficial in patients with MCNS by its antioxidant activity and examined its effect on proteinuria in nephrosis induced by puromycin-aminonucleoside (PAN) in rats. Nineteen Wistar-Kyoto rats injected with PAN were assigned to four groups: group 1, without EDA (n=4); group 2, concomitant EDA injection from 1 day prior to PAN administration (n=5); group 3, concomitant EDA injection from 1 day after PAN administration (n=5); group 4, concomitant EDA injection from 3 days after PAN administration (n=5). Daily urinary excretions of protein and 8-hydroxy-2'-deoxyguanosine (8-OHdG), a new sensitive marker of oxidative DNA damage in vivo, were measured in each group from the 1st to the 30th day after PAN injection. In group 1 proteinuria developed from the 5th day and reached the peak level on the 9th day. In groups 2, 3, and 4 proteinuria did not appear until the 6th day. The excretions in urinary protein and 8-OHdG were significantly lower in groups 2, 3, and 4 than group 1 on days 5, 9, and 25. In conclusion, EDA could delay and ameliorate the urinary protein excretion in accordance with the urinary 8-OHdG excretion in PAN-induced nephrosis.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1979

Lipoproteins in experimental nephrosis: plasma levels and composition.

Experimental nephrosis was induced in rats by administration of puromycin aminonucleoside and the levels of plasma lipoproteins were examined 7 days later and compared to controls. As determined by density ultracentrifugation, VLDL, IDL, LDL, and HDL protein levels were increased by 8, 4, 5, and 5 times, respectively. These increases were accompanied by changes in lipid and apoprotein composition. The VLDL, IDL, and LDL fractions contained less triglyceride and more phospholipid and cholesterol, while HDL lipid composition was not altered. The apoprotein composition of VLDL and IDL were not measurably altered, but LDL contained less apoE. HDL had a markedly abnormal composition characterized by an almost complete absence of apoA-IV and apoE, increased apoA-1, and decreased apoC. While increased hepatic synthesis can account for much of the observed hyperlipoproteinemia in nephrosis, the changes in lipoprotein composition suggest impaired catabolism as a contributory factor.

Animals↗
PubMed1997

Immunosuppressant pharmacodynamics on lymphocytes from healthy subjects and patients with chronic renal failure, nephrosis, and psoriasis: possible implications for individual therapeutic efficacy.

BACKGROUND: In organ transplantation, patients with peripheral blood mononuclear cells (PBMCs) that exhibit resistance to cyclosporine (INN, ciclosporin) or glucocorticoids in vitro are refractory to therapy based on these drugs in vivo. However, detection or distribution of the resistant patients with immunologic disorders remains to be documented. METHODS: Drug sensitivity tests were performed with PBMCs from four subject groups: 69 healthy subjects, 100 patients with chronic renal failure, 38 patients with nephrosis, and 51 patients with psoriasis. The values for the concentration that produces 50% lymphocyte-mitosis inhibition (IC50) of the drugs on PBMC blastogenesis were estimated, and individual variations or group differences in the IC50 values were examined. RESULTS: The median cyclosporine IC50 values of the four subject groups were similar, but large individual deviations in the IC50 values were observed. Individual differences in prednisolone IC50 values were spread from 1 to 3500 ng/ml. When compared with healthy subjects, a significantly large number of the patients with chronic renal failure group exhibited low responses to prednisolone (p < 0.04). In contrast, no significant difference in the methylprednisolone IC50 was observed among the groups. Normal upper thresholds for IC50 values of these drugs were estimated from the mean + 2 standard deviations (SD) of the IC50 values of healthy PBMCs, and the patients with IC50 values above these levels were considered to be resistant. The incidence of resistant patients with nephrosis or psoriasis was similar to that of healthy subjects; however, the incidence of cyclosporine- or prednisolone-resistant subjects with chronic renal failure was significantly higher (p < 0.04). Significant correlations between PBMC sensitivity to cyclosporine in vitro and clinical efficacy of the drug in vivo were observed in renal transplant recipients and in patients with psoriasis. CONCLUSIONS: A large subset of patients with chronic renal failure showed PBMC resistance to cyclosporine and prednisolone. Hyperresistant patients have a high risk of being refractory to immunosuppressive therapy with one of these drugs. Alternative treatment should be considered according to the individual drug-sensitivity data.

Adult↗
PubMed1994

Treatment of childhood steroid-resistant idiopathic nephrosis with a combination of cyclosporine and prednisone. French Society of Pediatric Nephrology.

Sixty-five children with steroid-resistant idiopathic nephrosis were treated with cyclosporine, 150 to 200 mg/m2, in combination with prednisone, 30 mg/m2, daily for 1 month and on alternate days for 5 months. Renal biopsy had shown minimal change disease in 45 children and focal segmental glomerular sclerosis in 20. Twenty-seven patients achieved complete remission. At latest examination, 14 to 60 months after initiation of the treatment (mean, 38 months), 17 patients were in complete remission, 8 had had a relapse but had become steroid sensitive, and 2 had a nephrotic syndrome. Four children responded partially to the treatment. At latest examination, 28 to 58 months after initiation of the treatment, 1 was in complete remission, 1 was in partial remission, 1 had a nephrotic syndrome, and 1 had end-stage renal failure. Thirty-four children did not respond to the combined treatment. At latest examination, 12 to 63 months after initiation of the treatment (mean, 38 months), 5 of these patients were in complete remission, 2 were in partial remission, 15 had a persistent nephrotic syndrome (with moderate renal failure in 5), and 12 children had end-stage renal failure. Forty-eight percent of the patients with minimal change disease and 30% of those with focal segmental glomerular sclerosis achieved complete remission (p = 0.27). We conclude that cyclosporine in combination with prednisone can induce a complete remission in some children with steroid-resistant idiopathic nephrosis.

Adolescent↗
PubMed2002

Identification by an EPR technique of decreased mitochondrial reducing activity in puromycin aminonucleoside-induced nephrosis.

The temporal changes in the electron paramagnetic resonance (EPR) signal intensities of a nitroxide radical, 4-hydroxy 2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPOL), in the kidney in rat puromycin aminonucleoside (PAN) nephrosis were investigated in vivo and in vitro. The rats of the PAN nephrosis group received intraperitoneal injections of PAN at 75 mg/kg body weight while those of control group received saline. The in vivo renal half-lives of TEMPOL were calculated from the decay curve of EPR signal intensities after the intravenous injection of the TEMPOL solution. The mitochondrial half-lives were obtained from the decay curve of the EPR signals after mixing the mitochondrial fraction of the kidney and TEMPOL solution. The in vivo half-lives of TEMPOL of the kidney from 7 to 14 d after PAN administration were significantly longer than those of the controls. The mitochondrial half-lives of TEMPOL on the 9th day after the PAN administration prolonged remarkably compared to the controls (378 +/- 69 vs. 676 +/- 183 s, p <.01). These findings indicate that the in vivo and mitochondrial reducing activity in PAN treated rats decreased markedly, because the half-life of TEMPOL in the kidney reflects the renal reducing activity.

Animals↗
PubMed1975

An ultrastructural study of the mechanisms of proteinuria in aminonucleoside nephrosis.

Sprague-Dawley rats injected i.v. with a single dose of puromycin aminonucleoside (PAN) developed massive proteinuria five days later. Electron microscopic studies of perfusion-fixed glomeruli showed that loss of epithelial foot processes and their replacement by flattened expanses of epithelial cytoplasm began at two days and was extensive by four days after the injection of PAN. At and after five days (correlating with the onset and persistence of massive proteinuria), areas of focal loss of the epithelial covering on the outside of the glomerular basement membrane (GBM) were observed in 30% of glomeruli. Intravenously administered ferritin was distributed normally in most sections of the GBM of nephrotic animals, but abnormally deep penetration of particles was observed in GBM segments that lacked an external covering of epithelium. The same changes were found following in situ fixation of superficially placed glomeruli of Munich-Wistar rats with PAN nephrosis. We propose that the massive, early proteinuria in PAN nephrosis may be primarily due to a glomerular epithelial lesion, leading to scattered focal defects in the external covering of the GBM. Increased bulk flow of glomerular filtrate across the GBM in such areas may explain the highly selective proteinuria found in this form of the nephrotic syndrome.

Animals↗
PubMed1987

Status of glomerular proteoglycans in aminonucleoside nephrosis.

Status of glomerular proteoglycans (PGs) in puromycin aminonucleoside nephrosis was investigated. Rats were made nephrotic and sacrificed 0, 7, 14, and 21 days later. Maximal proteinuric response was observed between 7 and 14 days. Prior to sacrifice, they received injections of conjugated or unconjugated anti-heparan-sulfate-proteoglycan antibody, directed against its core protein (Mr = 18,000). Their kidneys were processed for direct and indirect immunofluorescence, immunoperoxidase, tannic-acid staining, and tissue autoradiography (ARG). By tannic-acid staining, antibody binding sites identical to the anionic sites described previously were discovered. No qualitative differences were observed by these immunohistochemical techniques. Quantitative tissue ARG did not reveal any statistical differences in the binding of antibody between the control and nephrotic groups. For de novo biosynthetic studies, rats were sacrificed on day 10. Their kidneys were utilized for labeling of basement membrane PGs by employing [35S]-sulfate as the precursor product. Tissue ARG, as well as biochemical studies, were performed on the radiolabeled glomeruli. PGs were extracted with 4 M GuCl and characterized by Sepharose CL-6B and DEAE-Sephacel chromatography. There was an overall increase in the total incorporated radioactivities in the glomerular and media fractions. No differences were observed in the macromolecular size characteristics of intact PGs and glycosaminoglycan chains of either glomerular or media fractions. However, an increase in the charge-density characteristics was observed in PGs of the nephrotic group. By tissue ARG, an increase in the grain densities over the basement membrane and mesangial matrices of the glomerulus was noted. These data indicate that the intact PGs, their chains and core protein do not undergo significant biochemical alterations; however, de novo synthesized PGs have higher charge-density characteristics which may be related to a higher degree of sulfation that occurs during the course of aminonucleoside nephrosis.

Animals↗
PubMed1987

Cathepsin B and L in nephron segments of rats with puromycin aminonucleoside nephrosis.

The intralysosomal proteinases, cathepsins B and L, were measured in microdissected segments of rat nephrons following a single injection of puromycin aminonucleoside (PAN). Z-Phenylalanyl-arginine-7-amido-4-methylcoumarin served as substrate. Enzyme activities, proteinuria, creatinine clearance and renal morphology were determined at specific time intervals following induction of PAN nephrosis. During the first three days following PAN injection, enzyme activities in S2 and S3 segments, protein excretion, creatinine clearance and appearance of the renal parenchyma resembled control animals. The enzyme activity in S1 segments was slightly decreased, but returned to control levels at day six after injection. Days four through eight post-PAN injection were characterized by a dramatic increase in protein excretion and an increase in cathepsin B and L activity in S2 and S3 segments of the proximal tubule. During days 9 through 15 enzyme activity decreased significantly in S2 segments despite continued proteinuria. Overt necrosis and cell injury were seen in the proximal tubule and probably account for the decrease in proteolytic activity. After day 15 following PAN injection, the level of proteinuria decreased, restoration of cathepsin activities occurred and a histopathologic picture of healing was present. The data suggest a positive relationship exists between stimulation of cathepsin B and L activity in S2 and S3 segments of the proximal tubule and increased protein filtration in PAN nephrosis. The increased enzyme activity reflects enhancement of the proteolytic capacity of the lysosomal system that is necessary for increased protein catabolism.

Animals↗
PubMed1988

Differences in puromycin aminonucleoside nephrosis in two rat strains.

Administration of puromycin aminonucleoside (PAN) to Wistar rats induces proteinuria and enhanced mesangial deposition of circulating macromolecules. After proteinuria of longer duration focal and segmental glomerular hyalinosis and sclerosis (FSGHS) develops. The present report analyzes these aspects of PAN nephrosis in PVG/c rats, a strain previously shown to be remarkably resistant to proteinuria and FSGHS with aging or after uninephrectomy. In Wistar rats multiple injections of PAN during five months resulted in sustained severe proteinuria and FSGHS lesions in 8.1 +/- 1.0% (mean +/- 1 SEM) of their glomeruli (N = 6). In PVG/c rats a 1.3-fold higher dose of PAN was needed to induce chronic proteinuria similar to the Wistar rats. After five months 3.3 +/- 0.9% of their glomeruli showed FSGHS (N = 6, P less than 0.01) and the glomerular lesions were considerably less advanced. In acute PAN nephrosis induced by a single intravenous injection of PAN the mesangium of Wistar rats contained large amounts of lipid in contrast to a few small mesangial lipid droplets in nephrotic PVG/c rats. After injection of colloidal carbon in nephrotic PVG/c rats no enhanced carbon accumulation was found in the mesangium when compared to nonproteinuric controls. This result clearly differs from the increased mesangial sequestration of circulating material in nephrotic Wistar, and most other rat strains. The unchanged mesangial traficking of macromolecules in nephrotic PVG/c rats and the low incidence of FSGHS lesions in the presence of sustained glomerular proteinuria may reflect a relative resistance to PAN-induced glomerular damage in this particular rat strain.

Acute Disease↗
PubMed1993

Post-transplantation nephrosis in congenital nephrotic syndrome of the Finnish type.

Congenital nephrotic syndrome of the Finnish type (CNF) is an autosomal recessively inherited disease manifesting as massive proteinuria, edema and ascites in the neonatal period. The disease is believed to be limited to the kidneys and recurrences after renal transplantation have not been reported. At our center 29 transplantations have been performed on 28 CNF patients. One to 33 months after transplantation, seven grafts (24%) of six patients have developed a steroid-resistant nephrotic syndrome. The clinical data and renal histology of these patients were analyzed in order to elucidate the cause of the proteinuria. At the onset of six of the seven episodes of nephrosis, the patient had evidence of a preceding CMV- or EBV-infection and the remaining patient had sinusitis. Upon light and electron microscopy examination, endothelial swelling of the glomerular capillaries resembling transplant glomerulopathy (TG) was seen, but unlike TG, the glomerular basement membranes were normal. The response of proteinuria to steroid or cyclophosphamide therapy was poor, with total remission in only two patients and partial remission in one patient, all treated with methylprednisolone and cyclophosphamide immediately after the diagnosis. Four grafts have been lost. Our data show that CNF patients have an increased tendency for post-transplantation nephrosis.

Biopsy↗
PubMed1996

Re-evaluation of foot process effacement in acute puromycin aminonucleoside nephrosis.

The sequence of morphological changes during foot process effacement in acute puromycin aminonucleoside (PAN) nephrosis was examined by means of NaOH maceration and freeze cracking for scanning electron microscopy (SEM). The micrographs of SEM and those of transmission electron microscopy (TEM) were quantitatively analyzed by computerized morphometry, and were correlated with renal function. On day 2 after PAN injection, the slit length was moderately decreased by both shortening and degradation of the foot processes. On day 4, membrane-bounded vesicles were scattered in the lamina rara externa. During foot process effacement, the basal surface of podocytes developed palm-like domains that represented the cytoplasmic areas between interdigitation. The decrease in the length of podocyte cell borders paralleled the decrease of 24-hour creatinine clearance. The development of the palm-like domains on the basal aspects of podocytes estimated by distance class analysis was closely correlated with the sudden onset of proteinuria. We conclude that foot process effacement in PAN nephrosis caused by the retraction and degradation of foot processes leads to the development of palm-like domains, which is correlated with podocyte detachment as well as massive proteinuria.

Animals↗
PubMed1985

Effects of experimental nephrosis on basement-membrane components and enzymes of collagen biosynthesis in rat kidney.

The aim of the present study was to find out whether the basement-membrane proteins laminin and type IV collagen are involved in the development of aminonucleoside-induced nephrosis. These proteins were measured by specific radioimmunoassays in serum, urine and kidney-cortex samples, and they were localized in the glomeruli by indirect immunofluorescence. Nephrosis was induced in rats with a single intraperitoneal injection of puromycin aminonucleoside. Serum laminin concentrations, detected by a radioimmunoassay for the P2 domain of the protein, increased to reach a maximum at days 5-7, and they remained elevated until at least day 14. The increase preceded the development of proteinuria, suggesting a role for laminin in glomerular function. Concomitant with proteinuria, increasing amounts of laminin antigenicity were also found in the urine. The size of the laminin antigen in serum was estimated by gel filtration, and the serum forms were found to contain both the P1 and the P2 regions of the intact laminin molecule. On the other hand, there were no changes in the serum or urinary concentrations of type-IV-collagen-derived antigens, as detected by a radioimmunoassay for the 7S collagen domain of this protein. The total content of laminin in kidney cortex, measured after digestion of the tissue with trypsin and collagenase, was, at day 9, still comparable with normal values, and the distribution of both basement-membrane proteins in the glomeruli, studied by indirect immunofluorescence, was similar to that in the controls. The tissue damage induced by aminonucleoside, however, seems to stimulate collagen biosynthesis, as the activities of prolyl 4-hydroxylase, lysyl hydroxylase and galactosylhydroxylysyl glucosyltransferase in kidney tissue increased significantly, with maxima at days 8-10.

Animals↗
PubMed1996

Antiproteinuric effect predicts renal protection by angiotensin-converting enzyme inhibition in rats with established adriamycin nephrosis.

1. The mechanism of renal protection by angiotensin-converting enzyme inhibition is still the subject of debate. Inhibition of proteinuria might play a role. If so, a good antiproteinuric response to angiotensin-converting enzyme inhibition should predict subsequent protection against renal structural damage. This hypothesis has not been tested in models where treatment is started after the renal disease is well established, i.e. models that mimic the clinical situation. 2. We therefore investigated this hypothesis in 96 male Wistar rats with established adriamycin nephrosis. Reduction of proteinuria was achieved by lisinopril (0, 2, 5 and 10 mg day-1 kg-1) on two different sodium diets (0.3% and 0.05% NaCl). Therapy started 6 weeks after adriamycin (at stable proteinuria) and was continued for 6 weeks. 3. Lisinopril reduced blood pressure by 32 +/- 4% and proteinuria by an average of 72 +/- 7%, with stabilization after 2 weeks. Considerable interindividual differences in antiproteinuric response was found. Glomerulosclerosis score was reduced by 15 +/- 5%. All the effects of angiotensin-converting enzyme inhibitors were enhanced by sodium depletion, but sodium depletion in itself did not affect blood pressure (124 +/- 4 mmHg), proteinuria (664 +/- 68 mg/day) or glomerulosclerosis score (30 +/- 5%). Interestingly, the more proteinuria was reduced initially in an individual rat, the less sclerosis was found in the long term in that rat. 4. In conclusion, angiotensin-converting enzyme inhibition lowers proteinuria and prevents glomerulosclerosis in established adriamycin nephrosis. These effects are enhanced by sodium depletion. The individual short-term antiproteinuric effect predicts the protection against ultimate glomerular damage. This is consistent with the hypothesis that reduction of proteinuria is a mechanism by which angiotensin-converting enzyme inhibitors exert renoprotection.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

Addition of AT1 blocker fails to overcome resistance to ACE inhibition in adriamycin nephrosis.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors provide renoprotection, but there is considerable interindividual variability in therapeutic efficacy, with residual proteinuria and progressive renal function loss in many individuals. This requires additional strategies to optimize therapy response, particularly for individuals with a poor response to ACE inhibition. We studied whether co-treatment with an angiotensin II subtype 1 (AT1) receptor antagonist (AII-A) improves the individual antiproteinuric response of maximal ACE inhibition in established adriamycin nephrosis. METHODS: Rats were instituted on lisinopril (75 mg/L) six weeks after disease induction. After two weeks rats were re-stratified for residual proteinuria to continue this regimen, to a higher dose of lisinopril (150 mg/L) or to co-treatment with the AII-A L 158,809 for another four weeks. Groups on monotherapy AII-A and vehicle served as controls (all groups N=15). RESULTS: Lisinopril lowered proteinuria by 63% from 741 to 246 g/day (range of percentage change -90 to +2%). Neither increasing the dose of the ACE inhibitor nor addition of AII-A to ACE inhibition improved the antiproteinuric efficacy on a group or individual level: non-responders remained non-responders. All drug categories reduced hard end-points of focal glomerulosclerosis to a similar degree. CONCLUSIONS: ACE inhibition has variable renal protective efficacy in the adriamycin model. Neither increasing the dose of the ACE inhibitor beyond the optimal level nor co-treatment with AII-A overcome the individual therapy resistance. Thus, in established adriamycin nephrosis, blockade of the renin-angiotensin system at two different levels offers no additional benefit over ACE inhibition alone, either on the group or individual level.

Angiotensin Receptor Antagonists↗
PubMed1962

Transfer of an autoimmune nephrosis in the rat by means of lymph node cells.

An autoimmune nephrosis produced in rats by repeated injections of kidney extract with Freund's adjuvant has been transferred by means of lymph node cells to recipient animals rendered tolerant by neonatal injection with spleen cells from prospective donors. Transfer of the disease was manifested in the recipients by the development of proteinuria, hypoalbuminemia, hypercholesterolemia,and histological changes. The latter consisted of glomerular epithelial swelling, increase in basement membrane material and the presence of protein droplets in the glomerular and tubular epithelium. Appropriate control experiments were negative. Attempts to transfer with serum were unsuccessful. The transfer described is believed to provide evidence for an immunological mechanism for kidney and adjuvant induced nephrosis in the rat.

Animals↗
PubMed1992

Mechanisms involved in the progression to glomerular sclerosis induced by systemic hypertension during mild puromycin aminonucleoside nephrosis.

To evaluate the contribution of systemic hypertension in the progression of nephropathies to glomerular sclerosis, a mild form of puromycin aminonucleoside (PAN) nephrosis was associated with Goldblatt hypertension and studied after 18 weeks. We studied four groups: Group I, controls; Group II, Goldblatt hypertension; Group III, PAN nephrosis; and Group IV, both conditions. Systolic blood pressure, 24-h proteinuria, serum cholesterol, triglycerides, glomerular hemodynamics, and histological studies were compared among the groups. Rats in groups II and IV developed systemic hypertension, but only group IV rats showed persistent proteinuria. No alterations in lipid metabolism were present in any of the groups. The most striking findings in the micropuncture studies were a significant increase of glomerular capillary pressure in group IV rats (63.15 +/- 1.34 mm Hg) as compared to controls (48.74 +/- 0.97 mm Hg) and to groups II and III (55.31 +/- 2.11 and 48.17 +/- 1.23 mm Hg, respectively), and a marked fall in Kf in groups III and IV. Only group IV showed significant histological alterations such as glomerular sclerosis, interstitial damage, and increased glomerular area. These results suggest that, in the presence of an underlying nephropathy, a greater fraction of systemic pressure is transmitted to the glomerular capillaries when systemic hypertension is present; the resulting elevation in glomerular pressure and proteinuria seems to be responsible for the progression to glomerular sclerosis.

Animals↗