SLE phenotypes were stratified according to the MEX-SLEDAI scores into two subgroups (<or=10 and >10), and then according to renal disorder and neurological disorder, aiming to minimize any loss of power associated with disease heterogeneity.
We also evaluated the intron 8 Apa-1 alleles in patients with (P=0.480) and without nephropathy (P=0.543) and determined there were no differences between these groups.
In conclusion, the results of the present study indicated that GLP‑1 may be a promising target for the development of novel therapeutic strategies for HG‑induced nephropathy, and may function through the activation of SIRT1.
Both GLP1-RA (HR, 0.82; 95% CI, 0.75-0.89; P<0.001) and SGLT2i (HR, 0.62; 95% CI, 0.58-0.67; P<0.001) reduced the risk of progression of kidney disease including macroalbuminuria, but only SGLT2i reduced the risk of worsening estimated glomerular filtration rate, end-stage kidney disease, or renal death (HR, 0.55; 95% CI, 0.48-0.64; P<0.001).
GLP-1 agonists did not affect the risk of MI (RR: 0.917; CI: 0.830-1.014; p = 0.092) as well as the risk of stroke (RR: 0.882; CI: 0.759-1.023; p = 0.097), HF (RR: 0.967; CI: 0.803-1.165; p = 0.725), retinopathy (RR: 1.000; CI: 0.807-1.238; p = 0.997) and nephropathy (RR: 0.866; CI: 0.625-1.199; p = 0.385).
These benefits may be consistent with the known effects of GLP-1 RA on traditional risk factors for progressive kidney disease including glucose lowering, blood pressure lowering, reduced insulin levels and weight reduction.
GLP1-RA appear to reduce the incidence and/or progression of nephropathy and to have no specific effect on retinopathy-with the notable exception of semaglutide, which could have a negative impact on the retina.
GLP-1 plasma levels were determined in 3 different patient cohorts: 1) critically ill patients admitted to our intensive care unit (n = 215); 2) patients with chronic kidney disease on hemodialysis (n = 173); and 3) a control group (no kidney disease, no acute inflammation, n = 105).
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).
The specificity and sensitivity of anti-phospholipase A2 receptor-IgG4 in the diagnosis of IMN were further assessed in patients with different kidney diseases.
This study explored Wilms' tumor 1 (<i>WT1</i>) mutations in children with, or suspected of having, steroid-resistant nephrotic syndrome (SRNS), referred to or treated in our hospital in the past 6 years as well as the correlation between genotype and phenotype in <i>WT1</i> mutation-associated nephropathy in Chinese patients.
We describe here a novel WT1 gene mutation, i.e. a point mutation at intron 7 (+2) in both the tumor and the germline cells of a patient with Wilms' tumor and congenital male genitourinary malformation, but without renal disorder.
We report a novel sequence variant (c.1012A>T) of the WT1 gene in exon 6 (p.R338X) in a 18-year-old girl with a history of Wilms' tumour, minor gonadal changes and relatively late-onset nephropathy.