Deduction of the UTR-2/4 haplotypes to specific SNPs revealed that the +3003C variant (unique for UTR-4) in donors as well as in recipients is responsible for BKPyV/PyVAN and also provides protection against AMR; whereas the +3196G variant (unique for UTR-2) promotes allograft rejection.
We report here the involvement of two MT-ND5 pathogenic variants encoding for ND5 subunit of respiratory chain complex I, the m.13513G > A and the m.13514A > G, in adult-onset kidney disease in three unrelated patients.
The EMPA-REG, CANVAS, and DECLARE-TIMI 58 studies revealed that SGLT2 inhibitors reduce the risk of cardiovascular events and concomitantly suggested that these drugs slow the progression of kidney disease in type 2 diabetes.
Furthermore, ssbp1 suppression in zebrafish induced signs of nephropathy and reduced optic nerve size, the latter phenotype complemented by WT mRNA but not by SSBP1 mutant transcripts.
Patient's basic data included such as sex, age, height, and weight and RDT-related factors such as kidney disease that led to RDT, age at start of RDT, RDT history, medical history (past and present), and history of surgery.
Mitogen-activated protein kinases (MAP kinases) are functionally connected kinases that regulate key cellular process involved in kidney disease such as all survival, death, differentiation and proliferation.
The exosome/miR-19b-3p/SOCS1 axis played a critical pathologic role in tubulointerstitial inflammation, representing a new therapeutic target for kidney disease.
Thus, Twist1 in the distal nephron rather than in infiltrating macrophages propagates chronic inflammation and fibrogenesis during aristolochic acid-induced nephropathy.
Albuminuria is the currently accepted marker for detection of DN.This study aims to evaluate the urinary level of two novel renal tubular proteins (cyclophilin A and periostin) in patients with T2DM and among different nephropathy stages and also to validate the diagnostic accuracy of both cyclophilin A and periostin as potential markers for early prediction of DN relative to albuminuria.This cross-sectional study recruited 137 patients with T2DM, and they were divided based on their urinary albumin:creatinine ratio into T2DM with normoalbuminuria (<i>group II</i>), incipient T2DN with microalbuminuria (<i>group III</i>) and overt T2DN with macroalbuminuria (<i>group</i><i>IV</i>) beside 41 healthy subjects as <i>group I</i> Cyclophilin A and periostin were measured in the urine using ELISA.
USP36 is a deubiquitination enzyme involved in a variety of cellular biological processes, but its involvement in renal cell apoptosis and kidney disease is largely unknown.
Hazard ratios and 95% confidence intervals were estimated for the associations of variability in SBP with risk of diabetes nephropathy by using Cox proportional hazards regression models.
In this study, we established Adriamycin-induced NRK-52E cells, the normal rat kidney epithelial cell line, injury, and Sprague-Dawley rats with Adriamycin-induced nephropathy to evaluate the role and mechanisms of total extracts of <i>A. manihot</i> flower (TEA) both <i>in vitro</i> and <i>in vivo</i>.
We observed negative and significant correlations with the GDS score for the following components: PCS (r=-0.370, <i>P</i><0.001), MCS (r=-0.412, <i>P</i><0.001), burden of kidney disease (r=-0.403, <i>P</i><0.001), symptoms and problems of kidney disease (r=-0.360, <i>P</i><0.001) and effects of kidney disease (r=-0.355, <i>P</i><0.001).
Plasma sVE-cadherin levels by quartile were significantly higher in severe sepsis patients with acute kidney injury stage 3 (p = 0.044) as defined by Kidney Disease Improving Global Outcomes (KDIGO) criteria.
However, knowing the complexity of properdin's role in renal pathologies in vivo, further research is required to clarify the exact potential of properdin-targeted therapy in complement-mediated renal diseases.
The relative expression of miR-375 was increased in T2D patients with poor glycaemic control, while a decrease was seen in T2D patients with nephropathy and diabetic foot.
Hypertensive nephropathy (HN) is one of the most common secondary nephropathies that often progresses to severe renal fibrosis with limited treatment options beyond hypertension control.
By knocking down expression of K-Ras using antisense oligonucleotides in a mouse model of chronic folic acid nephropathy we can reduce fibrosis by 50% and prevent the loss of renal function over 3 months.
βOHB attenuates cisplatin-induced apoptosis by activation of HDAC5 in HRCE cells, suggesting that βOHB may be a new therapeutic agent for cisplatin nephropathy.