On renal biopsy, CD68 staining was positive for tissue macrophages in all 8 patients who had tubulointerstitial nephritis (with or without typical granulomas), while Von Kossa staining showed calcification of tubules near or inside granulomas in 6 of these 8 patients.
Inhibition of the IL-1R signal transducer kinase IRAK4 <i>in vivo</i> or inhibition of MYC <i>in vivo</i> as well as in human kidney organoids <i>in vitro</i> abrogated fibrosis and reduced tubular injury.<b>Conclusions</b> Our findings define a connection between IL-1<i>β</i> and metabolic switch in fibrosis initiation and progression and highlight IL-1<i>β</i> and MYC as potential therapeutic targets in tubulointerstitial diseases.
Findings from this study revealed that (1) hydrophobic packing contributes significantly to binding free energy, (2) Ile136 and Leu60 exhibited high hydrogen-bond occupancy in XY018-ROR-γ and HC9-ROR-γ, respectively, (3) XY018-ROR-γ displayed a relatively high loop region residue fluctuation compared to HC9-ROR-γ, (4) electrostatic interactions are a potential binding force in XY018-ROR-γ complex compared to HC9-ROR-γ, (5) XY018-ROR-γ assumes a rigid conformation which is highlighted by a decrease in residual fluctuation, (6) XY018 could potentially induce pseudoporphyria, nephritis and interstitial nephritis but potentially safe in renal failure.
This is the first reported case of rapidly progressive renal failure caused by perivascular tubulointerstitial nephritis with the direct invasion of PTCL-NOS.
DNAJB11-associated disease is a phenotypic hybrid of ADPKD and ADTKD, characterized by normal-sized cystic kidneys and progressive interstitial fibrosis resulting in late-onset ESRD.
This is the first reported case of rapidly progressive renal failure caused by perivascular tubulointerstitial nephritis with the direct invasion of PTCL-NOS.
MiR-25 plays an important role in the pathogenesis of acute myocardial infarction, left ventricular hypertrophy, heart failure, diabetes mellitus, diabetic nephropathy, tubulointerstitial nephropathy, asthma bronchiale, cerebral ischemia/reperfusion injury, neurodegenerative diseases, schizophrenia, multiple sclerosis, etc.
In an analysis of the FAERS database, there were significantly fewer reports of tubulointerstitial nephritis for patients treated with FXa inhibitors than for patients not treated with inhibitors.
Inhibition of the IL-1R signal transducer kinase IRAK4 <i>in vivo</i> or inhibition of MYC <i>in vivo</i> as well as in human kidney organoids <i>in vitro</i> abrogated fibrosis and reduced tubular injury.<b>Conclusions</b> Our findings define a connection between IL-1<i>β</i> and metabolic switch in fibrosis initiation and progression and highlight IL-1<i>β</i> and MYC as potential therapeutic targets in tubulointerstitial diseases.
Here, we report a rare case of kidney injury with concurrent typical IgG4-related tubulointerstitial nephritis and IgG4 subclass of myeloperoxidase (MPO) ANCA-positive necrotizing crescentic glomerulonephritis.
Indeed, it has been thought that CD138-positive mature plasma cells secrete mainly IgG, and the occurrence of tubulointerstitial nephritis with CD138-positive plasma cells secreting IgM has rarely been reported.
Leptospira-specific IgM and IgG were detected at 15 days postinfection, and isotyping of the Ig subclass showed that the total IgG response switched from an IgG1 response to an IgG3 response after infection with <i>L. interrogans</i> Histological periodic acid-Schiff D staining of infected kidney showed interstitial nephritis, mononuclear cell infiltrates, and reduced size of glomeruli.
Our results showed that Egr-1 expression was upregulated in the kidney with TIN, and the tubular epithelial cell is the primary site for Egr-1 upregulation and nuclear translocation.
These findings support involvement of multiple cell types in subnephrotic forms of APOL1-associated nephropathy, particularly renal tubule cells with resultant tubulointerstitial disease.
This study found no association between rs7903146 polymorphism in the TCF7L2 gene and the increased risk for development of CKD caused by primary glomerulopathy and analysed tubulointerstitial nephropathy.