Disease relevance of Nephrosis

• Increased glomerular thromboxane synthesis as a possible cause of proteinuria in experimental nephrosis [1].
• Severe steroid-responsive nephrosis associated with hypersensitivity [2].
• Mapping a gene (SRN1) to chromosome 1q25-q31 in idiopathic nephrotic syndrome confirms a distinct entity of autosomal recessive nephrosis [3].
• These data provide evidence that MCP-1, and possibly IP-10, are important in the pathogenesis of monocyte/macrophage infiltration in the tubulointerstitial nephritis associated with PAN nephrosis [4].
• Puromycin aminonucleoside nephrosis (PAN) is a model for human minimal change nephropathy induced in rats by injection of puromycin [5].

High impact information on Nephrosis

• We conclude that congenital nephrosis results from failure of heparan sulfate--rich anionic sites to develop in the lamina rara externa of the glomerular basement membrane [6].
• Chlorambucil for childhood nephrosis: a word of caution [7].
• Finally, active targeted protease did not affect proteinuria in the nonimmune mediated nephrosis induced by puromycin aminonucleoside [8].
• Glomerular function and structure were assessed after reduction of nephron number and restriction of protein intake in rats with adriamycin nephrosis [9].
• Effect of aminonucleoside nephrosis on immune complex localization in autologous immune complex nephropathy in rats [10].

Chemical compound and disease context of 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 [11].
• Dynamics of renal histamine in normal rat kidney and in nephrosis induced by aminonucleoside of puromycin [12].
• Localization of sialic acid in kidney glomeruli: regionalization in the podocyte plasma membrane and loss in experimental nephrosis [13].
• Irreversible tubulointerstitial damage associated with chronic aminonucleoside nephrosis. Amelioration by angiotensin I converting enzyme inhibition [14].
• This study shows that maneuvers that modulate the glomerular macrophage number are also associated with corresponding changes in the number of proliferating cells within the mesangium, suggesting a paracrine growth stimulation by the infiltrating macrophage during acute PA nephrosis [15].

Biological context of Nephrosis

• Initial results with semiquantitative reverse transcriptase-polymerase chain reaction analysis showed a remarkable down-regulation of nephrin-specific mRNA in the puromycin nephrosis of the rat [16].
• After a long period of culture and during aminonucleoside nephrosis, situations when VECs lose differentiated phenotypes, most of the cells had no perinuclear plectin [17].
• Gene expression of hepatic cholesterol 7 alpha-hydroxylase in the course of puromycin-induced nephrosis [18].
• In this study, we examined the serum levels of vitamin D metabolites, and kinetics of renal 25(OH)D-1-hydroxylase activity in vitro, and nephrogenous cyclic AMP excretion in response to exogenous PTH administration in puromycin aminonucleoside-induced nephrosis in rats [19].
• Modulation of basement membrane component gene expression in glomeruli of aminonucleoside nephrosis [20].

Anatomical context of Nephrosis

• Podocytic cytoskeletal disaggregation and basement-membrane detachment in puromycin aminonucleoside nephrosis [21].
• Thus, the rat glomerulus produces a small, nonprotein inhibitor of rat mesangial cell growth and the activity of this inhibitor is reduced in puromycin nephrosis [22].
• CONCLUSIONS: Acute puromycin nephrosis does not cause a notable reduction in visceral epithelial cell number [23].
• We examined the effect of 1% L-arginine in the drinking water on the infiltration of the kidney by macrophages in rats with puromycin aminonucleoside-induced nephrosis (PAN) and in rats with bilateral ureteral obstruction (BUO) of 24 hours duration [24].
• Effects of methylprednisolone on glomerular and medullary mRNA levels for extracellular matrices in puromycin aminonucleoside nephrosis [25].

Gene context of Nephrosis

• Eight days after PAN injection, ET-1 levels in plasma and glomeruli were not significantly altered in rats with PAN-induced nephrosis (glomeruli, 104.68 +/- 16.46 pg/mg of protein versus 98.24 +/- 13.68 pg/mg of protein; plasma, 2.68 +/- 1.10 versus 2.52 +/- 0.98 pg/mL) [26].
• AIM: We aimed to examine the possible involvement of vascular endothelial growth factor (VEGF) in the pathogenesis of puromycin aminonucleoside nephrosis (PAN) [27].
• Short-term effects of renal transplantation on plasma lipids and lipoprotein lipase in children with congenital nephrosis [28].
• The purpose of this study was to investigate the effect of CGS 26303, an endothelin-converting enzyme (ECE) inhibitor, on puromycin aminonucleoside (PA)-induced nephrosis in rats [29].
• Changes in angiopoietin expression in glomeruli involved in glomerulosclerosis in rats with daunorubicin-induced nephrosis [30].

Analytical, diagnostic and therapeutic context of Nephrosis

• Alpha-fetoprotein in antenatal diagnosis of congenital nephrosis [31].
• Immunofluorescence studies of podocyte-associated proteins nephrin and podocin revealed diminished and discontinuous staining patterns in rats with PAN nephrosis, indicating severe podocyte injury [32].
• Nephrosis was induced in rats with a single intraperitoneal injection of puromycin aminonucleoside [33].
• Previous studies, using perfusion of isolated, intact kidneys, have shown that the excretion and metabolism of mevalonate are both impaired in nephrosis [34].
• 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 [35].

References