Disease relevance of nph

• It has been reported that the albuminuria in ICGN mouse was controlled by at least a single autosomal recessive gene (nep) [1].
• Hodgkin's disease and lipoid nephrosis [2].
• Glomerular overproduction of oxygen radicals in Mpv17 gene-inactivated mice causes podocyte foot process flattening and proteinuria: A model of steroid-resistant nephrosis sensitive to radical scavenger therapy [3].
• Marked hyperglycemia in animals and man leads to "glycogen nephrosis," which affects the distal tubule at the level of the macula densa of the juxtaglomerular apparatus (JGA) [4].
• The evidence is reviewed suggesting that the lesions in membranous nephropathy are immunologically mediated by tumor or viral antigen-antibody complexes and in lipoid nephrosis perhaps by a defect in t-lymphocyte function [5].

High impact information on nph

• These data indicate that LMX1B directly regulates the coordinated expression of alpha 3(IV) and alpha 4(IV) collagen required for normal GBM morphogenesis and that its dysregulation in GBM contributes to the renal pathology and nephrosis in NPS [6].
• Nephrin-deficient proteinuric patients with Finnish-type congenital nephrosis and nephrin-knockout mice had only narrow filtration slits that lacked the slit diaphragm network and the 35-nm-long strands but contained shorter molecular structures [7].
• With nephrosis, there were comparable (greater than twofold) increases in both lines of HDL-C, h-apo A-I, and hepatic h-apo A-I mRNA, suggesting that cis-acting elements regulating induced apo A-I gene expression were within its core promoter [8].
• Lamb2 knockout mice were reported to exhibit congenital nephrosis in association with anomalies of retina and neuromuscular junctions [9].
• 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 [10].

Chemical compound and disease context of nph

• Ret, the GDNF receptor tyrosine kinase, was upregulated in podocytes in the passive Heymann nephritis and puromycin aminonucleoside (PA) nephrosis rat models of podocyte injury [11].
• PCGG kidneys exhibited tubular nephrosis and tubular cell degeneration, with no oxalate crystals, documenting renal toxicity at this oral dose in mice [12].
• Our findings in ICG and experimental nephrosis showed that M2000 enables a significant decrease in proteinuria, BUN, serum creatinine and cholesterol, as well as glomerular lesion in M2000-treated rats [13].

Biological context of nph

• The linkage analysis revealed that the nep locus was localized on the distal part of chromosome 15 [1].
• Each of the four test materials caused increased water consumption, distinct caecal and colonic enlargement, a slightly increased incidence of intratubular nephrosis and, with the exception of AC-starch, also slightly lower body weights [14].
• Hemoglobinuric nephrosis and splenic extramedullary hematopoiesis were also noted [15].

Anatomical context of nph

• The proximity of infiltrating glomerular macrophages to the contractile mesangial cells during acute puromycin aminonucleoside (PA) nephrosis suggests the possibility of a paracrine effect on mesangial cell growth [16].
• A mild nephrosis characterized by focal vacuolization of the renal tubular epithelium was observed in an increased incidence in treated mice [17].
• The nephrotoxicity was characterized by the formation of hyaline droplets in the cytoplasm of proximal convoluted tubule epithelial cells, by the presence of granular casts at the outer zone of the medulla, and by chronic nephrosis [18].
• Oral administration of PER (3 g kg-1 body wt. day-1) in sesame oil for 15 days caused a significant increase in liver weight, degeneration/necrosis of hepatocytes and increase in kidney weight, glomerular nephrosis and degeneration [19].
• Among the common diseases of small rodents are ascariasis, pyoderma, incisor malocclusion and overgrowth, neoplasia and abcessation, nephrosis and amyloidosis, respiratory infection, enteritis, and neurologic disorders [20].

Associations of nph with chemical compounds

• After treatment, urinary, serologic, and histopathologic indices of nephrosis showed reversal of CG in 8 of 12 CYC202-treated mice compared with progression of CG in 10 of 12 vehicle-treated mice, demonstrating a significant therapeutic benefit from CYC202 (P < 0.05) [21].
• BACKGROUND: The mouse, as opposed to the rat, is relatively resistant to the experimental nephrosis induced by puromycin aminonucleoside [22].
• Following treatment, histopathological, serological and urinary indices of nephrosis were normalized in flavopiridol-treated but not in vehicle-treated transgenics [23].
• Interstrain differences in murine daunomycin-induced nephrosis [24].
• However, dose-related toxic nephrosis was found in mice given 1.35-5.0% BHT in the diet [25].

Other interactions of nph

• IP-10 may participate in the modulation of renal damage in experimental nephrosis [10].
• A severe nephrosis in heartwater-infected Angora goats, treated after the first day of the febrile reaction, is described [26].
• Increase in kidney weight, glomerular nephrosis, degeneration/desquamation of tubular epithelium and characteristic amyloid deposition in glomeruli were observed only in the group of mice treated with 2000 mg/kg TCE [27].

Analytical, diagnostic and therapeutic context of nph

• Linkage mapping of the mouse nephrosis (nep) gene to chromosome 15 [1].
• A case of diffuse, well differentiated, lymphocytic lymphoma and lipoid nephrosis documented by light microscopy, electron microscopy and immunofluorescent studies is reported [5].
• CONCLUSIONS: We succeeded in developing a model of persistent nephrosis without severe glomerular abnormalities, nephrectomy or other manoeuvres known to induce disturbed haemodynamics, using an agent without tubulointerstitial toxicity, and considered it to be suitable for investigating the direct toxicity of proteinuria [28].

References