Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may reduce the risk of end-stage renal disease and slow the progression of nephropathy, but they do not appear to decrease all-cause or cardiovascular mortality in people with Type 2 diabetes and proteinuria.
In the multivariate regression model, independent predictors of serum hepcidin levels in ESRD patients before maintenance dialysis were interleukin-6, ferritin, phosphate, iron, and aspartate transaminase.
This difference was more pronounced in patients who had glomerulonephritis (HR = 0.72) or hypertension (HR = 0.81) than in those with end-stage renal disease (ESRD) due to diabetes mellitus or other causes.<i>Conclusion:</i>Peritoneal dialysis is less likely to be the first dialysis modality in patients with low serum albumin requiring dialysis.
Serum FGF23 concentration begins to increase early in the progression of CKD and can be remarkably high in hemodialysis patients with end-stage renal disease.
Mean FGF-23 levels increased markedly as time before ESKD decreased, while PTH and phosphate levels increased modestly and calcium levels declined minimally.
We therefore determined vertebral fracture prevalence and incidence in ESRD patients and assessed associations of vertebral trabecular bone mineral density (BMD) and PTH with vertebral fracture.
Mean FGF-23 levels increased markedly as time before ESKD decreased, while PTH and phosphate levels increased modestly and calcium levels declined minimally.
Living donors appear to have a higher risk of end-stage renal disease and this is especially true for obese donors and probably also for black donors with an APOL1 high-risk genotype.
IgA nephropathy (IgAN) is one the most common primary glomerulonephritis in children and adolescents worldwide, with 20% of children developing end-stage kidney disease (ESKD) within 20 years of diagnosis.
Diabetic nephropathy (dNP), a leading cause of end-stage renal disease in industrialized countries, is mechanistically closely linked with ER stress and renal cell death.
We also sought to investigate the relation of resistin and CAP1 to carotid intima media thickness (CIMT), CD36 gene expression, and matrix metalloproteinase 9 (MMP-9) circulating levels in ESRD patients and healthy controls.
The effect of GLP-1 to increase insulin concentrations relative to placebo levels tended to be lower during euglycaemia in ESRD and was significantly reduced during hyperglycaemia (50 [8-72]%, P=0.03).
Traditional management of diabetes mellitus has focused on glycemic control, beginning with lifestyle changes, followed by metformin, and then other classes of antiglycemic agents.<sup>1</sup> Sodium glucose co-transporter 2 (SGLT2) inhibitors reduce cardiovascular (CV) events, including CV death, myocardial infarction (MI) and heart failure, and slow progression of renal dysfunction, including prevention of end-stage kidney disease (ESKD).<sup>2-3</sup> Because initial clinical trials included mostly patients with baseline HbA1c >7%, current guidelines have recommended this class as add-on therapy for patients whose HbA1c is not at goal, typically ≥7%.<sup>1</sup> We hypothesized that there would be similar benefits on CV and renal endpoints regardless of baseline HbA1c, including those with HbA1c <7%.
Similarly, the effect of GIP relative to placebo levels tended to be lower during euglycaemia in ESRD and was significantly reduced during hyperglycaemia (34 [13-50]%, P=0.005).
Long non-coding RNA MALAT1 and microRNA-499a expression profiles in diabetic ESRD patients undergoing dialysis: a preliminary cross-sectional analysis.
CAP1 correlated positively with CIMT (r = 0.464, p = 0.008) in ESRD, and with CD36 in healthy controls (r = 0.447, p = 0.022) and ESRD (r = 0.824, p < 0.001).
The largest effects occurred with CHF (Incidence Rate Ratio [IRR] range: 4.84-13.4 across age strata), ESRD (IRR range: 3.30-9.02), CAD (IRR range= 2.77-10.7), and COPD (IRR range: 5.89-8.78) and tapered with age.
This condition is a renal-hepatic ciliopathy with phenotypic characteristics that include hepatosplenomegaly, hepatic fibrosis with bile cholestasis, increased kidney echogenicity, and end-stage renal disease.Here, we report a 13-year-old African-Caribbean female with areas of absence of heterozygosity suggesting parental consanguinity or identity by decent due to the founder effect, harboring a novel homozygous pathogenic variant (c.383C>G, p.S128*) in exon 3 of DCDC2.