4 research outputs found
La diffusion d'une innovation portant les germes de son plafonnement: la réutilisation des hémodialyseurs au Québec
PowerPoint Slides for: Pre-End-Stage Renal Disease Care and Early Survival among Incident Dialysis Patients in the US Military Health System
<p><b><i>Background:</i></b> Previous reports showed an increased early
mortality after chronic dialysis initiation among the end-stage renal
disease (ESRD) population. We hypothesized that ESRD patients in the
Military Health System (MHS) would have greater access to pre-ESRD care
and hence better survival rates during this early high-risk period. <b><i>Methods:</i></b>
In this retrospective cohort study, using the US Renal Data System
database, we identified 1,256,640 patients initiated on chronic dialysis
from January 2, 2004 through December 31, 2014, from which a bootstrap
sample of 3,984 non-MHS incident dialysis patients were compared with
996 MHS patients. We assessed care by a nephrologist and dietitian,
erythropoietin administration, and vascular access use at dialysis
initiation as well as all-cause mortality as outcome variables. <b><i>Results:</i></b>
MHS patients were significantly more likely to have had pre-ESRD
nephrology care (adjusted OR [aOR] 2.9; 95% CI 2.3-3.7) and
arteriovenous fistula used at dialysis initiation (aOR 2.2; 95% CI
1.7-2.7). Crude mortality rates peaked between the 4th and the 8th week
for both cohorts but were reduced among MHS patients. The baseline
adjusted Cox model showed significantly lower death rates among MHS vs.
non-MHS patients at 6, 9, and 12 months. This survival advantage among
MHS patients was attenuated after further adjustment for pre-ESRD
nephrology care and dialysis vascular access. <b><i>Conclusions:</i></b>
MHS patients had improved survival within the first 12 months compared
to the general ESRD population, which may be explained in part by
differences in pre-ESRD nephrology care and vascular access types.</p
Mast cells: the forgotten cells of renal fibrosis
Background/Aims—Mast cells, when activated, secrete a large number of fibrogenic factors and have been implicated in the development of fibrotic conditions of the liver, lung, and skin. There is evidence that renal fibrosis is closely linked with a chronic inflammatory cell infiltrate within the interstitium, but a potential role for mast cells in this process has yet to be defined. Therefore, the numbers of mast cells in normal and fibrotic kidneys with various pathologies were investigated. Methods—Mast cells were quantified in renal transplants showing acute and chronic rejection and cyclosporin toxicity, kidneys removed for chronic pyelonephritis, and renal biopsies from patients with IgA nephropathy, membranous nephropathy, and diabetic nephropathy. Mast cells were stained using two methods: acid toluidine blue detected less than 30% of the mast cells revealed by immunohistochemistry for mast cell tryptase. Results—Mast cells were scarce or absent in normal kidney (median, 1.6 mast cells/mm(2)) but numerous throughout the cortex and medulla in all specimens that showed fibrosis. They were almost entirely confined to the renal interstitium. Mast cells were present in large numbers in biopsies from patients with membranous nephropathy (median, 21.7 mast cells/mm(2)) and diabetic nephropathy (median, 29.2 mast cells/mm(2)), which were selected on the basis of showing chronic injury. In 24 unselected IgA nephropathy biopsies there was a close correlation between numbers of mast cells and the extent of interstitial fibrosis (r = 0.771; p < 0.0001). In renal transplant biopsies, mast cells were associated with allograft fibrosis in chronic rejection (median, 27.1 mast cells/mm(2)) and chronic cyclosporin toxicity (median, 10.6 mast cells/mm(2)) but not acute rejection (median, 2.7 mast cells/mm(2)) or acute cyclosporin toxicity (median, 2.0 mast cells/mm(2)). There was no detectable increase in mast cell numbers during acute rejection in those transplants that subsequently progressed to chronic rejection. In some biopsies the mast cells were largely intact, but in most cases some or all were degranulated. Conclusions—An increased number of mast cells is a consistent feature of renal fibrosis, whatever the underlying pathology, and the number of mast cells correlates with the extent of interstitial fibrosis. This suggests that mast cells might play a pathogenetic role in the fibrotic process. Key Words: mast cells • kidney • fibrosi