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PubMed2002

Cadherin and catenin staining in podocytes in development and puromycin aminonucleoside nephrosis.

Podocytes have been shown to express classical cadherins in the early stage of glomerulogenesis, but it remains unclear whether podocytes in normal and pathological conditions express cadherins in the adult stage. To address this question, rat podocytes in the neonate, the adult and in puromycin aminonucleoside (PAN) nephrosis were examined by immunofluorescence microscopy using antibodies against alpha- and beta-catenins and anti-pan-cadherin antibody, and by immunoelectron microscopy using anti-alpha-catenin antibody. In the neonate, all the antibodies reacted with the junctional complex of podocytes in the S-shaped body stage. The staining disappeared during the capillary loop stage, when foot processes and slit diaphragms are formed. In the adult, podocytes were not stained with any of the antibodies, whereas distinct staining with the antibodies was detected in endothelial cells and mesangial cells in the glomerulus. These findings were identical in kidneys of PAN nephrosis; podocytes did not show any significant staining. These results indicate that the composition of intercellular junction molecules of podocytes in the adult is different from that of immature podocytes even under the pathological condition.

Animals↗

PubMed2003

MAP-LC3, a promising autophagosomal marker, is processed during the differentiation and recovery of podocytes from PAN nephrosis.

Microtubule-associated protein 1 light chain 3 (LC3) is a unique modifier protein. LC3-I, the cytosolic form, is modified to LC3-II, the membrane-bound form, by a mechanism similar to ubiquitylation by E1- and E2-like enzymes, Apg7p and Apg3p, respectively. In the present study, we found that LC3-I is processed to LC3-II during the differentiation and recovery from puromycin aminonucleoside-induced nephrosis of podocytes. LC3 is especially expressed in the podocytes of rat kidney as the membrane-bound form LC3-II. Biochemical analysis using a conditionally immortalized mouse podocyte clone (MPC) revealed that LC3-I is processed to LC3-II during the differentiation of cells into mature podocytes and accumulates in the membrane-rich fraction of the cell lysate. LC3-II-localized vesicles, which differ from lysosomes and endosomes, in differentiated MPC cells are morphologically similar to autophagic vacuoles during starvation-induced autophagy. During starvation-induced autophagy, autophagosomes fuses with lysosome and LC3-II on autophagosomes is finally degraded by lysosomal proteases. However, in differentiated MPC cells, little LC3-II on the vesicles is degraded by lysosomal proteases, suggesting that little LC3-II-localized vesicles in differentiated MPC cells fuse with lysosome. Furthermore, the LC3-II level in differentiated MPC cells increases with recovery from damage caused by experimental puromycin aminonucleoside-induced nephrosis. These results suggest that LC3-II-localized vesicles play an important role in the physiological function of podocytes.

Animals↗

PubMed1994

Synergistic effects of fish oil diet and dimethylthiourea in acute adriamycin nephrosis.

The synergistic effects of combining fish oil (FO) diet, which reduces thromboxane A production, with the free radical scavenger, dimethylthiourea (DMTU), were evaluated in acute adriamycin nephrosis, because proteinuria in adriamycin nephrosis is mediated by increased renal thromboxane A and free radical production. The effects of combined evening primrose oil (EPO) and DMTU were compared with the DMTU + FO combination because EPO increases prostaglandin E but not thromboxane A. After 7, 14, and 21 days, proteinuria was significantly (p < 0.05) reduced in rats receiving either DMTU + corn oil (CO) or DMTU + FO compared with untreated control rats. However, after 21 days, rats receiving DMTU + FO had significantly reduced urine protein excretion compared with those receiving DMTU + CO (103.9 +/- 20 mg daily vs 351.8 +/- 29.8 mg daily; P < 0.05). In contrast to FO, rats receiving EPO + DMTU had similar urine protein excretion to rats receiving DMTU + CO after 21 days (170.2 +/- 20.34 mg daily vs 179.45 +/- 26.38 mg daily). The mean serum cholesterol concentration was significantly (P < 0.01) reduced in rats receiving DMTU + FO (195.2 +/- 23.8 mg/dL) compared with DMTU + CO (377.9 +/- 28.5 mg/dL). Serum triglyceride levels also were significantly (P < 0.01) reduced in rats receiving DMTU + FO (52.5 +/- 26.4 mg/dL) compared with DMTU + CO (100.5 +/- 36.9 mg/dL). No significant differences in serum cholesterol concentrations or triglycerides occurred between rats receiving DMTU + CO and DMTU + EPO. Renal glutathione content was significantly (P < 0.05) increased by 23% in normal rats receiving FO diet and by 34% in rats receiving combined DMTU + FO compared with CO alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Is house dust allergen a possible causal factor for relapses in lipoid nephrosis?

In three cases of minimal change nephrotic syndrome (lipoid nephrosis), an allergen sensitivity to house dust, cat hair and grass pollen was demonstrated by clinical and biological data. An increase in proteinuria after specific allergen contact and a decrease after withdrawal of the allergens, suggested that the cause was allergenic. Such cases demonstrate the necessity of an etiological investigation of particularly the atopic features in lipoid nephrosis. Results of these investigations can lead to specific therapy in selected cases.

Adolescent↗

PubMed1994

Lysosomal iron accumulation and tubular damage in rat puromycin nephrosis and ageing.

1. Energy dispersive X-ray spectrometry was used to examine the relationship between proteinuria and increased urinary iron excretion, and structural and functional damage in puromycin nephrosis. 2. After 11-12 days rats treated with puromycin (10 mg/100 g, i.v.i.) had greater proteinuria (211.6 +/- 35.7 mg/day, mean +/- s.e.m.) and urinary iron excretion (15.4 +/- 2.2 micrograms/day) than saline-treated controls (14.5 +/- 1.4 mg/day and 1.1 +/- 0.2 micrograms/day, respectively, both P < 0.001). 3. On day 13, mean lysosomal iron concentration of proximal tubular cells (306.6 +/- 64.5 vs 11.9 +/- 8.6 mg%, P < 0.001), and proximal tubular cell damage assessed semi-quantitatively (1.17 +/- 0.10 vs 0.62 +/- 0.10, P < 0.001) were higher and creatinine clearance (0.15 +/- 0.01 vs 0.29 +/- 0.02 mL/min per g kidney weight, P < 0.001) lower than in control rats. 4. At days 35, 60 and 360 there were no differences in any of the measured parameters between rats treated with puromycin or saline, and in both groups proteinuria, tissue damage and lysosomal iron concentration increased with time. 5. Lysosomal iron accumulation was the only independent predictor of both functional and structural damage. 6. In conclusion, the apparent association between proteinuria and tubulo-interstitial damage in puromycin nephrosis, and with ageing, is best explained by factors associated with accumulation of iron within lysosomes of proximal tubule cells.

Aging↗

PubMed1981

Renal pathology of fetal congenital nephrosis.

In 15 fetuses with congenital nephrosis, distinct colloid-filled cystic tubular dilations were seen scattered in the renal cortex. Similar structures were not present in the controls. It is suggested that these structures are pathognomonic of congenital nephrosis in the fetus and make diagnosis possible even without electron microscopy.

Female↗

PubMed1983

Relationship between microtubules and Golgi apparatus in hepatocytes: a quantitative study during experimental nephrosis.

In many cell types, microtubules are preferentially associated with the Golgi apparatus. However, the existence of a functional link between these two organelles is still hypothetical. To gain insight into this question, the relationships between microtubules and the Golgi apparatus were studied in rat hepatocytes during experimental nephrosis induced by the aminonucleoside of puromycin. This condition is known to cause prolonged stimulation of plasma protein production by the hepatocytes. Rats were studied 2, 4, 5, 10 and 20 days after aminonucleoside injection. The amount of albumin was measured in serum and hepatic microsomes by laser immunonephelometry. The volume densities of microtubules around the Golgi apparatus and in the remaining cytoplasm were measured by ultrastructural morphometry. Changes of the Golgi apparatus were analysed by measuring the volume density of the whole organelle and the respective proportion of saccules and vesicles. Proteinuria began 5 days after aminonucleoside injection and was accompanied by a decrease in serum albumin and a rise in microsomal albumin. These changes were still more striking after 10 days, but protein and albumin levels were almost back to normal after 20 days. Concomitantly, the volume density of the microtubules increased significantly around the Golgi apparatus (32% after 10 days), and not in the remaining cytoplasm. The Golgi apparatus was enlarged (80% after 10 days) with a higher ratio of secretory vesicle to saccule volume densities. These results show that additional microtubules are present around the Golgi apparatus during the enhanced production of plasma proteins which occurs in nephrosis. They suggest that in hepatocytes, microtubules play a part in the Golgi apparatus function of plasma protein processing.

Animals↗

PubMed1991

Sublethal X-irradiation during acute puromycin nephrosis prevents late renal injury: role of macrophages.

Acute puromycin aminonucleoside (PA) nephrosis is associated with a surge in the glomerular macrophage number. Whole body X-irradiation (XI) was used to assess whether bone marrow depression, which depletes normal rat glomeruli of macrophages, is efficacious in ameliorating progressive glomerular disease. A solitary, sublethal dose of XI (600 rad) was administered 3 days after PA delivery to rats (PA/XI) that were followed for 18 wk. In contrast to a sham-irradiated nephrotic cohort (PA/Sham), the PA/XI rats had a complete prevention of the recurrent albuminuria and manifested a significant reduction in the percent of glomeruli exhibiting glomerulosclerosis (GS) lesions at 18 wk after PA. XI significantly reduced the glomerular and interstitial macrophage number as well as the circulating white blood and monocyte counts during peak albuminuria. This protection was independent of the magnitude of the acute albuminuria and elevations in the circulating lipid levels. These data show that whole body XI delivered during acute nephrosis is capable of preventing progressive glomerular disease in association with a reduction in the glomerular and interstitial macrophage number. Additionally, this study suggests that this immune effector cell is important in mediating the propagation of initial glomerular injury to GS.

Albuminuria↗

PubMed1992

Macrophages mediate adverse effects of cholesterol feeding in experimental nephrosis.

We tested whether the deleterious effects of hypercholesterolemia, in a progressive glomerular disease model, may be mediated by infiltrating renal macrophages. A single sublethal dose of whole body X-irradiation (XI) delivered to rats with acute puromycin aminonucleoside (PA) nephrosis fed a high-cholesterol (HC) diet resulted in significantly greater inulin and p-aminohippurate (PAH) clearances at 11 days after PA without any alterations in circulating lipid levels, in contrast to nonirradiated HC-fed nephrotic controls. This functional protection was associated with significant declines in both glomerular and cortical interstitial macrophage number. Over the course of this 16-wk model, HC-fed PA rats had significantly less albuminuria as well as significantly fewer glomerulosclerosis (GS) lesions and less mesangial matrix expansion at the end of the study despite an equivalent degree of sustained hypercholesterolemia. This data suggests that reducing the infiltrating glomerular and cortical interstitial macrophage burden with XI during acute PA nephrosis, unaccompanied by any hypolipidemic effect, produces not only early salutary effects on renal function but also a significant amelioration of the progressive glomerulopathic features of this model. This is consistent with the hypothesis that the infiltrating renal macrophage, in large part, directly mediates the adverse effects of hypercholesterolemia in this model.

Acute Disease↗

PubMed1994

Metabolic responses to nephrosis: effect of a low-protein diet.

To determine whether dietary protein restriction (LPD) causes protein catabolism in adriamycin nephrosis, nephrotic and control rats were paired by weight and gavage fed an 8.5% protein diet for 3 days (protocol 1) or 12 days (protocol 2). Fasting whole body protein turnover was then measured using a constant infusion of L-[1-14C]leucine. After 3 days of LPD, proteinuria decreased slightly and body weight did not change in either group. In contrast, leucine oxidation and urinary urea nitrogen excretion in nephrotic rats decreased by 18% and 37%, respectively (P < or = 0.05). After 12 days of LPD, weight loss did not differ between groups. In contrast to protocol 1, proteinuria decreased by 45% in nephrotic rats fed LPD for 12 days, and leucine oxidation rats increased to the level of control rats. Rates of whole body protein synthesis (PS) and degradation (PD) did not differ between nephrotic and control rats receiving LPD for 3 or 12 days, but were significantly lower than rates measured in rats fed 22% protein. We conclude that 1) proteinuria stimulates protein conservation even when dietary protein intake is restricted; 2) the decrease in amino acid oxidation was dependent on moderate proteinuria, since prolonged LPD ameliorated nephrosis and leucine oxidation rates increased to control levels; and 3) since weight loss and rates of whole body PS and PD in nephrotic and control animals were indistinguishable, moderate proteinuria did not increase protein catabolism.

Animals↗

PubMed1999

Suppressed activities of cathepsins and metalloproteinases in the chronic model of puromycin aminonucleoside nephrosis.

Glomerulosclerosis and tubulointerstitial fibrosis are the hallmarks of chronic renal diseases. In the present study, we have investigated the potential involvement of various proteinases in these alterations in the model of puromycin aminonucleoside (PAN) nephrosis. Two groups of male Wistar rats were given either three or seven injections of PAN (2.0 mg/100 g body weight) over a 4- and 12-week period, respectively. The two control groups received saline injections. Activities of cathepsins (B, H and L) were determined in isolated glomeruli and proximal tubules. Moreover, collagenase-like and gelatinase-like activities were analyzed in isolated glomeruli. Three weeks after weekly PAN injection, the rats developed heavy proteinuria (140.8+/-22.0 vs. 13.5+/-3.29 mg/day; p<0.001), and at week 11 protein excretion reached 606.6+/-23.00 vs. 22.8+/-1.5 mg/day. Renal morphology revealed minimal glomerular mesangial changes at the 4th week after PAN administration. At the 12th week a marked mesangial matrix accumulation as well as severe tubulointerstitial infiltration and fibrosis associated with tubular dilation and atrophy were observed. Glomerular cathepsins B, H, and L and gelatinase-like activities decreased at the 4th week after the first PAN injection and remained at this low level throughout the entire study period. Glomerular collagenase-like activity decreased at the 4th week (p<0.05) and was still mildly lower than that of the control group at the 12th week, but without significance. In the isolated proximal tubules, the activities of cathepsins B, H, and L showed the same pattern of decreases as those found in the glomeruli over the whole experimental period. Taken together, our data in the model of chronic PAN nephrosis suggest that the suppressed activities of cathepsins as well as the decreased gelatinase- and collagenase-like activities participate in the accumulation of extracellular matrix and thereby may contribute to the development of glomerulosclerosis and tubulointerstitial fibrosis.

Animals↗

PubMed1999

Effects of human alpha-1-acid glycoprotein on aminonucleoside-induced minimal change nephrosis in rats.

A minimal change nephrosis was induced in rats by a single intraperitoneal injection of puromycin aminonucleoside (100 mg/kg). This resulted in increased urine protein output, plasma creatinine, blood urine nitrogen, and relative kidney weight. Electronoptically, there was a retraction of the glomerular podocytic foot processes. When human alpha1-acid glycoprotein was injected at 600 mg/kg intravenously on experimental days 6, 7, 8, and 9 into these animals, urine protein output decreased significantly, and the number of podocytic foot processes increased significantly. alpha1-Acid glycoprotein is rich in sialic acid and largely negatively charged. Its therapeutic role in nephrosis, which is characterized by a loss of sialic acid and a loss of negative charge, thereby leading to a loss of permselectivity, is discussed.

Animals↗

PubMedDate not supplied

Increased apoptosis in acute puromycin aminonucleoside nephrosis.

Acute puromycin aminonucleoside nephrosis (PAN) in rats is characterized by heavy proteinuria associated with renal hypercellularity. The role of apoptosis in the resolution of renal hypercellularity was investigated in PAN. To study the participation of apoptosis in PAN, renal tissues were collected from nephrotic and control rats on weeks 1, 2 and 7 after a single puromycin aminonucleoside injection. Apoptosis was evaluated by light and electron microscopy. Apoptotic DNA fragmentation was detected by TUNEL staining. Renal tissues were also evaluated by the presence of leukocyte common antigen (LCA), ED1 (macrophages) and proliferating cell nuclear antigen (PCNA) with corresponding monoclonal antibodies. An increased number of apoptotic (TUNEL+) cells was observed in the glomerulus at week 1. Electron microscopy analysis showed glomerular apoptosis mainly in endothelial cells. In the interstitium and tubules, increased apoptosis was observed at weeks 1 and 2. Increased apoptosis was accompanied with increased LCA+, ED1+ and PCNA+ cells in the interstitium and with increased PCNA+ cells in tubules. There was a high significant correlation between the number of apoptotic cells and the number of interstitial LCA+, ED1+ and PCNA+ cells. Tubular PCNA expression was correlated with tubular apoptosis. We also observed significant correlation between glomerular, interstitial and tubular apoptosis with proteinuria during the nephrosis. Double staining analysis showed that about 13% of interstitial or tubular apoptotic cells were positive for PCNA. All these values returned to normal by week 7. These results indicate that apoptosis is involved in the repairing process of this disease model.

Acute Disease↗

PubMed1995

Unreliability of the abdominal fat pad biopsy in the evaluation of nephrosis: report of 3 consecutive cases.

In the workup of unexplained nephrotic syndrome in the elderly patient, renal biopsy has shown amyloidosis to be the cause in 15-30% of the cases. Most of the cases of amyloidosis are primary and are, therefore, treatable with alkylating agents, albeit at a high level of toxicity. Abdominal fad pad biopsy has been suggested as a minimally invasive, low-cost method for diagnosing amyloidosis that is 100% specific. We report our experience with 3 consecutive cases of fat pad biopsy in the workup of unexplained nephrosis in the elderly patient: including the first false positive reported with respect to nephrotic renal disease, a false negative, and a true positive. We feel that in an elderly patient with unexplained nephrosis though the abdominal fat pad biopsy may be helpful, the patient should not be committed to a regimen with potentially very high toxicity on the basis of a positive fat pad biopsy alone. We recommend that the more invasive renal biopsy be performed should therapy with alkylating agents be contemplated.

Abdomen↗

PubMed1992

Modulation of proteinuria and renal xanthine oxidase activity by dietary proteins in acute adriamycin nephrosis in rats: lack of correlation with intra- and extracellular amino acids.

Protein restriction ameliorates proteinuria in acute adriamycin (ADR) nephrosis and decreases the renal levels of xanthine oxidase (XO), a putative mediator of ADR nephrotoxicity. Hypothetically, the effect of protein restriction on renal XO levels may be due to variations in plasma and tissue proteic amino acids (AA). To elucidate this point, the levels of AA in plasma and in renal homogenates were determined in rats with ADR nephrosis and fed diets with different protein contents: (a) high (35%) casein; (b) standard (21%) casein; (c) low (9%) casein; (d) low casein plus a synthetic mixture of Val, Leu and Ile. The protein content of the diet determined certain marked variations in plasma AA: high levels of Val, Leu and Ile were found in rats fed on a high protein diet, while the same AA were low, in rats on low protein regimen. Supplementation of the low protein diet with a synthetic mixture of branched-chain AA (Val, Leu and Ile) normalized the plasma levels of these AA. In spite of these changes, tissue AA were similar in all groups, regardless of the protein contents of the diets. Furthermore, the levels of renal XO and proteinuria were unrelated to variations in plasma AA, since both parameters were low in protein-restricted and protein-restricted AA-supplemented rats while high in rats fed a high or normoproteic diet. These data demonstrate that low protein diets induce marked alterations in plasma AA composition which are similar in may respects to those found in protein malnutrition.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMedDate not supplied

Macrophagelike vacuolated renal tubular cells in the urine of a male with osmotic nephrosis associated with intravenous immunoglobulin therapy. A case report.

BACKGROUND: Osmotic nephrosis is a form of renal tubular injury that has been found in patients treated with intravenous immunoglobulin (IVIG). CASE: A 46-year-old male who had two courses of chemotherapy for acute myelogenous leukemia was found to have refractory thrombocytopenia. After IVIG (Sandoglobulin 12%, Novartis) administration (1 g/kg) for five consecutive days, the patient became oliguric and eventually anuric on the fifth dose. Hemodialysis was initiated, and urine production was noted on day 2 of hospitalization. Routine cytologic examination of fresh, voided urine showed numerous macrophagelike, bland epithelial cells with abundant, multivacuolated cytoplasm. Cytokeratin immunostain revealed positivity, thus confirming the epithelial origin of these cells. CONCLUSION: To our knowledge, this is the first such case reported in the English-language cytology literature. Awareness of a patient's clinical history may be helpful in avoiding an incorrect diagnosis. Urine cytology may be useful in obtaining an early diagnosis of osmotic nephrosis in patients receiving high-dose IVIG therapy that may eliminate the need for a renal biopsy.

Acute Kidney Injury↗

PubMed1985

Nephrosis with varicocele: probable renal vein thrombosis.

A 3-year-old boy with relapsing nephrosis presented with a left sided varicocele. Echographic studies demonstrated enlargement of the left kidney, and there was delayed excretion on renal scintigraphy suggesting the presence of renal vein thrombosis. The varicocele resolved with remission of his nephrosis.

Child, Preschool↗

PubMed1984

Catabolism of very low density lipoproteins in experimental nephrosis.

The effects of experimental nephrosis in rats, produced by puromycin aminonucleoside, include an elevation of plasma levels of all lipoprotein density classes and the appearance of high density lipoprotein (HDL) rich in apoprotein (apo) A-I and deficient in apo A-IV and apo E. The hyperlipoproteinemia is associated with an increase in hepatic synthesis of lipoproteins. The possible role of decreased very low density lipoprotein (VLDL were obtained from nonfasting animals by ultracentrifugation at d 1.006 and included chylomicrons) catabolism and its relationship to the apolipoprotein composition of nephrotic high density lipoproteins (1.063 less than d less than 1.210, or 1.072 less than d less than 1.210 [HDL]) was explored. When 125I-VLDL was injected, the faster plasma clearance of lower molecular weight apolipoprotein B (apo BL) compared with that of higher molecular weight apo BH which is seen in normal rats was not observed in nephrotic rats. Less labeled phospholipid, apo C, and apo E were transferred from VLDL to higher lipoprotein density classes. Heparin-releasable plasma lipoprotein lipase and hepatic lipase activities were decreased by 50% in nephrotic rats compared with pair-fed controls. Perfusion of livers with medium that contained heparin released 50% less lipase activity in nephrotic rats than in controls. When heparin was injected intravenously, significant decreases in plasma levels of triglycerides and significant increases in levels of free fatty acids were observed in both groups of animals. In the nephrotic rats, 86% of the free fatty acids were in the lipoprotein fractions, as compared with 16% in the controls. Heparin treatment did not restore to normal the decreased apo BL clearance in nephrotic rats but it produced an increased amount of apo A-IV and apo E in the plasma HDL. In vitro addition of partially pure lipoprotein lipase to whole serum from nephrotic rats significantly increased the content of apo E in HDL. We conclude that the abnormal apoprotein composition of HDL in experimental nephrosis is the result of altered entry of apolipoproteins from triglyceride-rich lipoproteins, probably because of decreased lipolysis.

Animals↗