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PubMed1991

Factor XIII and its substrates, fibronectin, fibrinogen, and alpha 2-antiplasmin, in plasma and urine of patients with nephrosis.

Plasma and urine concentrations of factor XIII and its circulating substrates (fibronectin, fibrinogen, and alpha 2-antiplasmin) were measured in a group of 36 patients with nephrotic syndrome. The results were compared with those obtained in a group of 32 normal volunteers (control group) and 12 patients with end-stage renal disease (ESRD). A mild but significant reduction in plasma level and an abnormal urinary excretion of alpha 2-antiplasmin was found in the nephrotic group. Plasma concentrations of factor XIII, fibronectin, and fibrinogen were significantly elevated in patients with nephrosis. In contrast, patients with ESRD showed no significant difference in the plasma concentrations of either factor XIII, fibronectin, or alpha 2-antiplasmin and only a modest elevation of fibrinogen when compared with normal controls. No significant correlation was found between serum creatinine concentration and plasma levels of factor XIII and its circulating substrates in the nephrotic group. No measurable quantities of factor XIII and only small quantities of fibronectin were found in the urine of patients with nephrosis. Elevation of plasma factor XIII, fibronectin, and fibrinogen concentrations in the nephrotic group is considered to be the result of a combination of increased synthesis and possibly contracted intravascular distribution of these macromolecular proteins in the face of their negligible urinary losses. The presence of the observed abnormalities in the nephrotic group and their absence in the non-nephrotic ESRD group tends to exclude renal failure as a cause of these abnormalities. Although the clinical significance of these abnormalities is uncertain, they can potentially contribute to the thrombophilic diathesis and platelet hyperaggregability in nephrotic syndrome.

Adolescent↗

PubMed1991

[Changes in intra-renal scavenging enzymes activities of the reactive oxygen species in experimental glomerulonephritis and nephrosis in rats].

The purpose of this study was to investigate the changes in scavenging enzymes activities of reactive oxygen species (ROS) in experimental nephritis and nephrosis. Anti-GBM nephritis was induced in rat by injecting 0.75 ml of the anti-GBM serum. Intrarenal SOD-like activity in nephritic rats was significantly decreased from the 5th day after i.v. injection of antiserum to the 10th day. Although catalase and glutathione peroxidase activities in nephritic rat were increased on 3hr to 6hr after i.v. injection of antiserum, the both activities were gradually decreased on 24hr onward. The decrease in ROS scavenging enzymes activities paralleled with the urinary protein excretion and the elevation of plasma lipid peroxide. Moreover, catalase, administered (4,600 U/hr) by osmotic minipump prevented the urinary protein excretion by about 60%. In accelerated passive Heymann nephritis and puromycin aminonucleoside nephrosis in rats, the activities of scavenging enzymes decreased in the course of experimental periods. It was concluded that the scavenging enzymes activities of ROS increased at beginning of heterologous phase and decreased at the end of this phase in anti-GBM nephritis, and the activities in the other models of experimental nephritis also decreased during experimental periods.

Animals↗

PubMed1991

Impaired endothelium-dependent relaxation in isolated thoracic aorta of rats with daunomycin-induced nephrosis.

A single i.v. injection of daunomycin (10 mg/kg) into rats produced severe proteinuria and hypercholesterolemia without atherosclerosis on the 20th and 40th days after the treatment. However, these changes were not observed on the 5th day. No change in systolic blood pressure was seen through the 40-day experimental period. Relaxation to acetylcholine, A23187 and nitroprusside was examined in aortic rings precontracted with phenylephrine (3 x 10(-6) M). Acetylcholine-induced relaxation was significantly attenuated in the nephrotic rats on the 20th and 40th days, in comparison to the control animals. In aortic rings taken from control and nephrotic rats on the 40th day, removal of the endothelium or treatment with methylene blue (10(-5) M) completely abolished the relaxation induced by acetylcholine (10(-5) M). In addition, acetylcholine (10(-5) M) induced a transient increase in the aortic cyclic GMP and this increase was completely abolished by removal of the endothelium. In the preparations of nephrotic rats on the 20th and 40th days, the cyclic GMP levels stimulated by acetylcholine (10(-5) M) were decreased to about 50% in comparison to their respective control. A23187 also evoked diminished relaxation in nephrotic rats on the 20th and 40th days. However, on the 40th day after the treatment, the effects of nitroprusside in relaxing the aorta and in elevating the cyclic GMP level in the aorta were not altered by nephrosis. In addition, the nitroprusside-induced relaxation and cyclic GMP accumulation were not affected by removal of the endothelium. These results indicate that endothelium-dependent relaxation is attenuated with the development of nephrosis.

Acetylcholine↗

PubMed1990

Acute effects of captopril and ibuprofen on proteinuria in patients with nephrosis.

Captopril decreases protein excretion in patients with nephrosis. To evaluate whether captopril has an acute antiproteinuric effect and to evaluate the role of changes in renal hemodynamics or glomerular permselectivity on this effect, renal clearance studies were performed in patients without diabetes but with nephrosis. Protein excretion and renal hemodynamics were measured at baseline and after the administration of captopril. To measure the contribution of renal prostaglandins, patients were restudied on a separate day, after the combined administration of captopril and the prostaglandin synthetase inhibitor ibuprofen. Both treatments significantly reduced mean protein excretion, but the change was greater with combined therapy than with captopril alone (40.6% vs 20.0%). Mean glomerular filtration rate (GFR) decreased by 4.8% (not significant) and 16.5% (p less than 0.001), and filtration fraction (FF) decreased by 13.6% (p less than 0.001) and 14.9% (p less than 0.001) after captopril alone and combined therapy, respectively. No significant correlation was found between changes in proteinuria and changes in GFR or FF after treatment with captopril alone. In contrast, the decrease in proteinuria correlated with the change in GFR after combined drug administration (r = 0.68, p = 0.06). The ratio of immunoglobulin G to albumin clearance, an index of glomerular permselectivity, was unaffected by captopril but decreased significantly (by 43%) after combined drug administration. The results suggest that the acute antiproteinuric effect of captopril is not due to changes in FF, GFR, or glomerular perselectivity. The addition of ibuprofen enhances the antiproteinuric effect of captopril by decreasing the GFR as well as by enhancing the permselectivity of the glomerular capillary membrane.

Captopril↗

PubMed1989

Hyperlipidemia of nephrosis: pathophysiologic role in progressive glomerular disease.

During the past few years, the increasing speculation that the hyperlipidemia of nephrosis may be one of several pathogenic mechanisms involved in the progression of initial glomerular injury to glomerulosclerosis has generated many clinical and experimental investigations. This discussion reviews pertinent studies that address two major issues. First, the underlying pathophysiologic mechanisms involved in the development of the hyperlipidemia of nephrosis are explored. Second, this article examines recent studies that investigate how this secondary hyperlipidemia may further aggravate initial glomerular injury and contribute to a progressive glomerulopathy, primarily mediated through alterations in monocyte/macrophage function.

Animals↗

PubMed1989

Glomerular epithelial detachment, not reduced charge density, correlates with proteinuria in adriamycin and puromycin nephrosis.

To identify the structural change coincident with increased glomerular permeability in both adriamycin (ADR) and puromycin-aminonucleoside (PAN) nephrosis, we explored the temporal correlation between developing proteinuria, the reduction in glomerular polyanions, and the detachment of epithelium from glomerular basement membrane (GBM). Sprague-Dawley rats received a single tail-vein injection of PAN (150 mg/kg), ADR (7.5 mg/kg) or saline. Nephrotic-range proteinuria appeared between days 2 to 5 in the PAN-treated and days 5 to 10 in the ADR-treated rats. The GBM heparan sulfate charge density and epithelial membrane sialic acid (SA) content were determined before, during and after the rise in proteinuria. Polyethyleneimine was used to detect heparan sulfate and the number staining of renal cortical slices was used to detect heparin sulfate and the number of sites/microns GBM in the lamina rara externa were counted on electron micrographs (magnification x60,000). Controls had a regular distribution of polyethyleneimine 20.19 +/- 1.72 sites/microns (X + SD). In ADR rats, the polyethyleneimine density decreased by day 5, 18.61 +/- 1.79 sites/microns (p less than 0.05) which persisted to day 15, 17.38 +/- 1.27 sites/microns (p less than 0.02). PAN rats, by day 1, had significant reduction, 14.94 +/- 1.47 sites/microns (p less than 0.05), which persisted to day 20. The total membrane-bound SA content of isolated glomeruli was analyzed with a modified Warren's method. The SA content in control glomeruli was 46.8 +/- 8.0 nmol/mg glomerular protein (X +/- SD). In ADR rats, there was significant decrease in SA content to 84 +/- 3% of control (p less than 0.01) at day 15. In PAN rats, by day 2, the SA content was decreased to 73 +/- 18% of control (p less than 0.05). In both models, scanning and transmission electron microscopy revealed epithelial foot process fusion, loss of slit diaphragms, and vacuolization before increased proteinuria. Epithelial detachment from the GBM and rupture of vacuoles occurred coincidently with rapid development of nephrotic proteinuria in both models. In summary, reduced GBM heparan sulfate and epithelial SA content do not correlate with the onset of altered glomerular permeability, whereas epithelial detachment is coincident with the development of massive proteinuria in both ADR and PAN nephrosis.

Animals↗

PubMed1987

Decrease in the sialoglycoprotein content of the glomerular basement membrane in experimental nephrosis.

Phosphotungstic acid at low pH on glycolmethacrylate sections allows the detection of sialic acid groups in the lamina rara externa of the glomerular basement membrane. This staining procedure was used to study the alterations in puromycin aminonucleoside nephrosis and adriamycin nephrosis. In both model systems defects were detected in the sialic acid content of the lamina rara externa and the epithelial cell coat was also affected. The possible role of sialic acid in glomerular filtration is discussed.

Animals↗

PubMed1983

Analysis of mortality from nephritis and nephrosis among nickel-cadmium battery workers.

Mortality from nephritis and nephrosis (and other diseases of the genitourinary system) experienced by a study cohort of 3,025 nickel-cadmium battery workers was investigated. Observed (O) numbers of deaths from these diseases for the period 1946 through 1981 were compared with those that might be expected (E) to occur on the basis of rates of mortality for the general population of England and Wales (nephritis and nephrosis, International Classification of Diseases, eighth revision [ICD 8th] Code No. 580-584; E = 5.49, O = 10: all disease of the genitourinary system (noncancers), ICD 8th 580-629; E = 11.50, O = 17). These differences were not statistically significant at the 5% level. When the estimated cadmium exposures of those who died from these causes were compared with those of all matching survivors using the method of regression models in life-tables, no statistically significant association was found between occupational exposure to cadmium and mortality from these diseases. A separate analysis was made of the mortality experience of 39 workers with cadmium nephropathy.

Adolescent↗

PubMed1984

Inhibition of glomerular visceral epithelial cell endocytosis during nephrosis induced by puromycin aminonucleoside.

Puromycin aminonucleoside (PA), injected intravenously into rats in a single dose, causes proteinuria and ultrastructural pathology reminiscent of human lipoid nephrosis (puromycin aminonucleoside nephrosis (PAN]. Glomerular epithelial cell (GEC) endocytosis was studied in this model and in rats with protein-overload proteinuria using ultrastructural morphometry. Disappearance curves were constructed for protamine-heparin aggregates (PHA), which localized in the subepithelial region of the glomerular basal lamina following intravenous injection of protamine followed by heparin. Five groups were studied: (a) preproteinuric PAN, 4 days after PA (mean 4.5 +/- 1.5 mg of urinary protein/24 hours); (b) proteinuric PAN, 10 days after PA (mean 128 +/- 9.6 mg/24 hours); (c) recovery from PAN (mean 12.5 +/- 1.5 mg/24 hours); (d) protein-overload proteinuria, induced by injecting albumin intraperitoneally (mean 211 +/- 15.9 mg/24 hours); and (e) saline-injected controls (mean 1.2 +/- 0.2 mg/24 hours). Only the proteinuric PAN animals (group 2) had altered GEC endocytosis with a PHA half-disappearance time different from the group 5 saline controls (143.2 versus 72.6 minutes, p less than 0.05). The half-disappearance times in groups 1, 3, and 4 were 74.6, 80.7 and 86.5 minutes, respectively. Altered GEC function was further characterized by comparing PHA disappearance with the abundance of albumin-filled vacuoles in the GEC. Prolongation of PHA disappearance in group 2 correlated with the virtual absence of vacuoles; they were abundant in nonproteinuric phases of PAN and in animals with overload proteinuria. We conclude (a) GEC endocytosis is reduced only during the proteinuric phase of PAN, (b) GEC endocytosis is active during the preproteinuric phase of PAN and is a factor that may account for the absence of protein in the urine despite abnormal GBM permeability, (c) decreased GEC endocytosis during proteinuric PAN reflects abnormal cell metabolism due to PA and is not simply a consequence of albuminuria, as overload proteinuria did not produce diminished PHA or albumin uptake.

Animals↗

PubMed1983

Adverse effect of indomethacin in experimental chronic nephrosis.

The effects of long-term indomethacin therapy were studied in rats with chronic nephrosis induced by puromycin of aminonucleoside (PAN). Fifteen PAN rats received indomethacin (2 mg/kg/d) administered by daily gavages, and fifteen received glucose. A control group received indomethacin but no PAN. Three to five animals per group were sacrificed monthly. Proteinuria was similar in both PAN rat groups. Renal function and histology were normal in the control rats. In the PAN animals, renal failure developed earlier in the treated rats than in the others. Histological examination revealed in all PAN rats early tubulo-interstitial lesions and progressive glomerular damage. The pattern of the lesions was identical in both PAN rats, but the glomerular changes developed earlier, were more diffuse and more severe in the indomethacin treated rats. Thus, indomethacin resulted in an accelerated destruction of the glomeruli in experimental nephrosis. Such a deleterious effect remains unexplained, and its relevance to human disease is not demonstrated.

Animals↗

PubMed1983

Hemolytic uremic syndrome and crescentic glomerulonephritis complicating childhood nephrosis.

Three children with nephrotic syndrome and focal segmental glomerulosclerosis and/or mesangial proliferation on renal biopsy developed the sudden onset of renal failure, microangiopathic hemolytic anemia, and thrombocytopenia. Two of the three children developed crescentic glomerulonephritis and never regained renal function while the third showed no change from his original histologic pattern and also developed chronic renal failure. These cases suggest an association between the lipoid nephrosis-focal segmental glomerulosclerosis group of glomerular diseases and crescentic glomerulonephritis, and may represent an unusual pathway in the evolution of childhood nephrosis.

Child↗

PubMed1982

A breeding study to control chronic progressive nephrosis in rats.

Breeder male Sprague-Dawley rats were categorized as potential low and high protein excretors at 4 months of age. The average selection values of these two groups were 0.59 and 1.75 mg/ml, respectively. Paris of females were mated to these males in two breeding cycles in the fashion of a diallele cross. The heritability index based on protein excretion values of 263 male offspring at 6 months of age from both cycles of high and low excretor males was 0.526 with approximate variance of 0.0668. Significantly different (p less than 0.01) survival distributions were shown. The mean and median survival times of the high excretor offspring were 611.1 and 652 days, respectively, compared to 651.4 and 680.5 days, respectively, in low excretor offspring. The proportion of offspring with marked chronic progressive nephrosis was significantly greater (p less than 0.01) in the high excretor group, both prior to and after 700 days of age, than that of offspring in the low excretor group. The selection of low excretor males for breeding stock appears to offer a practical basis for minimizing the total expression of chronic progressive nephrosis in this strain of rat.

Animals↗

PubMed1982

Current estimates of the incidence of steroid responsive idiopathic nephrosis in Kentucky children 1-9 years of age.

A review of the medical literature relating to childhood nephrosis revealed no surveys conducted since 1968 which either substantiated or refuted the range in incidence rates reported in earlier studies. Those rates ranged from 1.3 to 2.5 new cases per year among 100,000 white and non-white children under 10 years of age. The present report documents the incidence of steroid responsive idiopathic nephrosis in the eastern part of Kentucky during the years 1970 through 1979. The overall rate of 1.8 new cases per year was similar to that described in previous reports. A suggestion of an increased rural vs urban incidence was noted.

Adrenal Cortex Hormones↗

PubMed1981

Depression of endostreptosin, streptolysin O and streptozyme antibodies in patients with idiopathic nephrosis with and without a nephrotic syndrome.

We determined antibody titers to Endostreptosin (ESS), a recently described protein antigen in the cytoplasm and the plasma membrane of Group A streptococci in 286 normals of different age groups and in 34 children and 19 adults who had or had had at one time a nephrotic syndrome due to idiopathic nephrosis. Antistreptolysin O titers were also determined in 33 of the idiopathic nephrotics. Similarly, antibody titers to Streptozyme were determined in 21 patients with idiopathic nephrosis and 61 normals with a similar age distribution. Severe depression of these antibody titers was found in almost all patients with this disease not only during the presence of a nephrotic syndrome but for long periods up to 20 years following an episode of a nephrotic syndrome when the patients were in complete remission. Patients with a nephrotic syndrome due to chronic glomerulonephritis (5), S.L.E. (4), membranous nephropathy (5), diabetes mellitus (1) or amyloidosis (1) did not show abnormally low values for antibodies to Endostreptosin, Streptolysin O or Streptozyme. High-dose steroid medication as such for prolonged periods of time does not depress Endostreptosin or Streptolysin O antibody titers below the expected mean, as demonstrated in 15 patients with S.L.E.

Adolescent↗

PubMed1981

Glomerular mesangium. Analysis of the increased activity observed in experimental acute aminonucleoside nephrosis in the rat.

Kinetic studies have revealed increased mesangial macromolecular uptake in acute aminonucleoside of puromycin (PAN) nephrosis in the rat. The mechanisms leading to this increased activity, however, are poorly understood. Therefore, we studied mesangial function and ultrastructure in rats 8 days after intravenous injection of 6 mg. of PAN per 100 gm. of body weight. One hour after intravenous injection of 20 mg. of colloidal carbon per 100 gm., no differences in mesangial carbon could be detected between PAN rats and controls. After 24 hours, the amount of mesangial carbon was significantly higher in PAN rats; rates of disappearance did not differ. Ultrastructural examination revealed no differences in localization of mesangial carbon at the 1-hour interval. After 24 hours, mesangial cells of PAN rats showed an increased number of lysosomes filled with carbon; the number of carbon particles in the mesangial matrix was not increased. Using an ultrastructural immunoperoxidase technique, we found increased amounts of endogenous IgG in the extracellular space of segmental mesangial lobules of PAN rats. IgG was mainly present in matrix substance of electron-lucent aspect, and quantitative morphometric analysis revealed an increase in volume of this loose permeable matrix component (mesangial channels). No increased staining of IgG was found in the lacis area indicating that there was no increased mesangial egress of macromolecules in PAN nephrosis. The increased volume of the permeable mesangial channels in segmental mesangial lobules of PAN rats may lead to a pooling of tracer material with consequent increased phagocytosis by mesangial cells.

Acute Disease↗

PubMedDate not supplied

[Must renal biopsy be still performed in "lipoid nephrosis"? (author's transl)].

In 52 out of 272 children with one of the following diseases: nephrotic or nephritic syndrome, persistent humaturia and/or proteinuria, renal biopsy was performed on the basis of commonly accepted indications. 18 biopsies were from patients with a clinical picture of lipoid nephrosis and clinical course of "non responders" or "frequent relapsers" types. All of them showed the histologic pattern of minimal changes and had a value of Y index according to ISKCD greater than 0,85. Moreover all patients with minimal changes nephrotic syndrome had a Y index greater than 0.85. If these observations will be confirmed renal biopsy would not later be indicated in children with "lipoid nephrosis".

Biopsy↗

PubMed1996

Interferon-inducible protein-10 is highly expressed in rats with experimental nephrosis.

Interferon-inducible protein (IP)-10 is a small glycoprotein member of a family of chemotactic cytokines structurally related to interleukin-8. We have recently described the induction of IP-10 mRNA in mouse mesangial cells stimulated with lipopolysacharide, interferon-gamma, and tumor necrosis factor-alpha. To further evaluate a possible role for this chemokine in renal injury, we have studied IP-10 in an experimental model of nephrosis induced in rats by adriamycin. High levels of glomerular IP-10 mRNA expression and glomerular and tubulointerstitial IP-10 protein were seen on day 21, coinciding with maximal proteinuria, glomerular tumor necrosis factor mRNA expression, and interstitial cellular infiltrates. Maintenance on a low protein diet not only delayed the appearance of proteinuria and interstitial cellular infiltrate but also decreased glomerular IP-10 mRNA expression. Isolated normal glomeruli and cultured glomerular epithelial and mesangial cells from normal rats expressed IP-10 mRNA upon stimulation with 100 U/ml interferon or 1 microgram/ml lipopolysaccharide for 3 hours. IP-10 mRNA expression was also inducible by lipopolysaccharide and cytokines in NRK 49F renal interstitial fibroblasts and, to a lesser extent, in NRK 52E tubular epithelial cells. Furthermore, IP-10 protein was inducible in murine mesangial cells. We conclude that IP-10 is highly inducible in vitro and in vivo in resident glomerular and tubulointerstitial cells. IP-10 may participate in the modulation of renal damage in experimental nephrosis.

Animals↗

PubMedDate not supplied

Hemoglobinuric nephrosis in a rhea (Rhea americana).

An eighteen-month-old female rhea (Rhea americana) was presented dead for necropsy. The owner reported having observed blood in the droppings. Gross examination revealed a rhea in good body condition with a copious amount of frank blood in the cloaca. Large masses of matted fescue grass (Festuca spp.) distended the ventriculus and jejunum. No hemorrhage was evident in the digestive tract, which was otherwise void of ingesta. The kidneys were dark brown in color. Renal histopathology revealed a severe accumulation of eosinophilic pigment in the tubular epithelial cells of the proximal convoluted tubules, with tubular nephrosis and eosinophilic casts in the collecting tubules. It was concluded that the renal pigment was hemoglobin and not myoglobin, based on lack of evidence of muscle injury and the severe erythrophagocytosis evident in hepatic macrophages. The renal pigment also stained positive with the hemoglobin-specific Okajima stain. Hemoglobinuric nephrosis has not previously been reported in an avian species.

Animals↗