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The macrophage is a key factor in renal injuries caused by glomerular hyperfiltration.
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2011
Year
Glomerular DiseaseRenal PathologyImmunologyRenal InflammationPathologyGlomerular HyperfiltrationInflammationGlomerulonephritisRenal FunctionAcute Kidney InjuryChronic Kidney DiseaseMacrophage BiologyRemnant KidneysAutoimmune DiseaseGene Expression ProfileKey FactorVascular BiologyRenal PathophysiologyUrologyRenal DiseaseDiabetic Kidney DiseaseGlomerulopathyMedicineNephrologyKidney ResearchRenal Injuries
Glomerular hyperfiltration is a common pathway leading to glomerulosclerosis in various kinds of kidney diseases. The 5/6 renal ablation is an established experimental animal model for glomerular hyperfiltration. On the other hand, low-grade inflammation is also a common mechanism for the progression of kidney diseases including diabetic nephropathy and atherosclerosis. Here we analyzed the gene expression profile in the remnant kidney tissues of 5/6 nephrectomized mice using a DNA microarray system and compared it with that of sham-operated control mice. The 5/6 nephrectomized mice showed glomerular hypertrophy and an increase in the extracellular matrix in the glomeruli. DNA microarray analysis indicated the up-regulated expression of various kinds of genes related to the inflammatory process in remnant kidneys. We confirmed the up-regulated expression of platelet factor-4, and monocyte chemoattractant protein-1, 2, and 5 in remnant kidneys by RT-PCR. The current results suggest that the inflammatory process is involved in the progression of glomerulosclerosis and is a common pathway of the pathogenesis of kidney disease.