Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glomerular diseases account for the majority of cases with chronic renal failure. Several genes have been identified with key relevance for glomerular function. Quite a few of these genes show a specific or preferential mRNA expression in the renal glomerulus. To identify additional candidate genes involved in glomerular function in humans we generated a human renal glomerulus-enriched gene expression dataset (REGGED) by comparing gene expression profiles from human glomeruli and tubulointerstitium obtained from six transplant living donors using Affymetrix HG-U133A arrays. This analysis resulted in 677 genes with prominent overrepresentation in the glomerulus. Genes with 'a priori' known prominent glomerular expression served for validation and were all found in the novel dataset (e.g. CDKN1, DAG1, DDN, EHD3, MYH9, NES, NPHS1, NPHS2, PDPN, PLA2R1, PLCE1, PODXL, PTPRO, SYNPO, TCF21, TJP1, WT1). The mRNA expression of several novel glomerulus-enriched genes in REGGED was validated by qRT-PCR. Gene ontology and pathway analysis identified biological processes previously not reported to be of relevance in glomeruli of healthy human adult kidneys including among others axon guidance. This finding was further validated by assessing the expression of the axon guidance molecules neuritin (NRN1) and roundabout receptor ROBO1 and -2. In diabetic nephropathy, a prevalent glomerulopathy, differential regulation of glomerular ROBO2 mRNA was found.In summary, novel transcripts with predominant expression in the human glomerulus could be identified using a comparative strategy on microdissected nephrons. A systematic analysis of this glomerulus-specific gene expression dataset allows the detection of target molecules and biological processes involved in glomerular biology and renal disease.
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PMID:Systematic analysis of a novel human renal glomerulus-enriched gene expression dataset. 2063 63

We report a case of idiopathic, PLA2R-negative membranous nephropathy (MN) transplanted via a deceased donor kidney. Changes in glomerular immune deposits were followed in serial biopsies. The allograft recipient had end-stage disease without significant proteinuria from ischemic nephropathy due to chronic heart failure, hypertension, atherosclerosis and presumed diabetic nephropathy. Combined cardiac and renal transplants were performed. Maintenance immunosuppression consisted of prednisone, a calcineurin inhibitor and mycophenolate mofetil. MN was identified in the pre-implantation biopsy of the donor kidney. The recipient never developed significant proteinuria and there was no identifiable impact on graft function. Serial biopsies performed at Days 0, 18, 150, 234 and 812 revealed mild effacement of podocyte foot processes, progressive change from Ehrenreich-Churg Stage III-IV lesions of MN to segmental resolution by electron microscopy, and progressive decrease of IgG staining by immunofluorescence. The findings provide a novel observation of the protracted process of glomerular immune deposit resolution in healing MN transplanted in a neutral host environment.
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PMID:Membranous nephropathy transplanted in the donor kidney: observations of resolving glomerulopathy in serial allograft biopsies. 2537 90