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1  two pathways of regulated necrosis in acute oxalosis.
2 phrocalcinosis, kidney failure, and systemic oxalosis.
3 te, progressive kidney disease, and systemic oxalosis.
4 nti-glomerular basement membrane disease, 2; oxalosis, 2; and miscellaneous, 2.
5                      Among the patients with oxalosis, 56 patients had a liver transplant followed by
6 kidney and many other tissues, with systemic oxalosis and ESRD being a common outcome.
7 nal failure early in life, advanced systemic oxalosis, and a formidable mortality rate.
8 mias, familial hypercholesterolemia, primary oxalosis, and factor IX deficiency, among others, might
9 nsplant recipients from 1988 to 1998 who had oxalosis as their primary diagnosis for their ESRD.
10                              Mice with acute oxalosis displayed calcium oxalate crystals inside dista
11                     Indications for LTx were oxalosis (four), congenital hepatic fibrosis (two), cyst
12                     Indications for KTx were oxalosis (four), drug-induced (four), polycystic kidney
13 ew outcome data from patients with infantile oxalosis, from transplanted patients with type 1 PH (PH1
14  although concern exists about recurrence of oxalosis in the transplanted kidney.
15 survival in renal transplant recipients with oxalosis is similar to other transplant recipients with
16                                              Oxalosis, or calcium oxalate deposition in the tissues,
17                                              Oxalosis patients receiving a KTA had a significantly wo
18  death-censored graft survival compared with oxalosis patients who receive a cadaveric or living-dono
19 indicating poor renal allograft survival for oxalosis patients who receive a renal transplant alone.
20 -censored graft survival (76%) compared with oxalosis patients who received a KTA (47.9%, P<0.001) an
21                                 In addition, oxalosis patients who received a living-donor KTA had si
22  death-censored graft survival compared with oxalosis patients who received a LKTx (22% vs. 64%, P<0.
23                                 In contrast, oxalosis patients who received a LKTx had a significantl
24 Unadjusted death-censored graft survival for oxalosis patients with a cadaveric or living-donor KTA o
25                                          For oxalosis patients with minor enzyme deficiencies, renal
26               In this study, a case of renal oxalosis probably secondary to excessive parenteral vita
27                         Patient survival for oxalosis recipients with a KTA or a LKTx was not signifi
28 bules in diagnostic human kidney biopsies of oxalosis-related AKI.
29                                    Secondary oxalosis represents a possible cause of delayed recovery
30 raft survival for transplant recipients with oxalosis to a reference group with ESRD secondary to glo
31                                Patients with oxalosis who receive a LKTx have superior death-censored
32 th-censored graft survival for patients with oxalosis who received a LKTx or a KTA.
33 leading to renal failure, followed by tissue oxalosis with life-threatening complications.