Critically ill, tubular injury, delayed early recovery: characteristics of acute kidney disease with renal oxalosis.
Renal oxalosis
acute kidney disease
acute kidney injury
drug-induced
renal tubular injury
Journal
Renal failure
ISSN: 1525-6049
Titre abrégé: Ren Fail
Pays: England
ID NLM: 8701128
Informations de publication
Date de publication:
Dec 2021
Dec 2021
Historique:
entrez:
5
3
2021
pubmed:
6
3
2021
medline:
14
10
2021
Statut:
ppublish
Résumé
This study aimed to analyze the clinicopathological features of acute kidney disease (AKD) with renal oxalosis. Data for biopsy-proven AKD with oxalosis diagnosed from Jan 2011 to Oct 2018 was collected. The underlying diseases, dietary habits, clinical and pathological characteristics of newly emerging kidney disease were analyzed. The long-term renal prognosis was observed. A total of 23 patients were included, comprised of 18 men and 5 women with a mean age of 51.6 ± 15.9 years. The peak Scr was 669.9 ± 299.8 μmol/L, and 95.7% of patients had stage 3 acute kidney injury (AKI). Drug-induced tubulointerstitial nephritis (TIN) was the most common cause (65.2%) of AKD, followed by severe nephrotic syndrome (17.4%). All patients had pathological changes indicating TIN, and 11 patients were complicated with the newly emerging glomerular disease (GD). The risk of oxalosis caused by increased enterogenous oxalate absorption accounted for only 26.1%, and others came from new kidney diseases. The majority (75%) of abundant (medium to severe) oxalosis occurred in patients without GD. There were no significant differences in the score for tubular injury (T-IS) and interstitial inflammation with different severities of oxalosis. Rate of Scr decrease (ΔScr%) at 2 weeks was negatively correlated with the severity of oxalosis ( The present findings revealed that 95.7% of AKD with secondary renal oxalosis occurred in critically ill patients. AKD from tubular injury was the prominent cause. Severe oxalosis contributed to delayed early recovery of AKD.
Identifiants
pubmed: 33663319
doi: 10.1080/0886022X.2021.1885443
pmc: PMC7939555
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
425-432Références
Curr Opin Nephrol Hypertens. 2016 Jul;25(4):363-71
pubmed: 27191349
Curr Opin Nephrol Hypertens. 2019 Jul;28(4):316-320
pubmed: 31045662
Kidney Int Rep. 2018 Jul 29;3(6):1363-1372
pubmed: 30450463
Arh Hig Rada Toksikol. 2013 Dec;64(4):609-30
pubmed: 24384768
Am J Med. 2013 Sep;126(9):768-72
pubmed: 23830537
Clin Biochem. 2017 Dec;50(18):1014-1019
pubmed: 28764885
Nat Rev Nephrol. 2017 Apr;13(4):241-257
pubmed: 28239173
Eur J Clin Invest. 1985 Feb;15(1):45-9
pubmed: 3921382
JAMA Intern Med. 2019 Apr 1;179(4):542-551
pubmed: 30830167
PeerJ. 2018 Jul 3;6:e5192
pubmed: 30002986
J Urol. 2010 Jun;183(6):2244-8
pubmed: 20400141
Kidney Int. 1973 Jul;4(1):61-6
pubmed: 4723994
Transplant Rev (Orlando). 2014 Oct;28(4):182-7
pubmed: 24999029
Urolithiasis. 2016 Oct;44(5):389-97
pubmed: 27040948
Am J Transplant. 2008 Apr;8(4):753-60
pubmed: 18294345
Semin Arthritis Rheum. 2015 Dec;45(3):315-20
pubmed: 26239907
Kidney Int. 2018 May;93(5):1098-1107
pubmed: 29395336
Kidney Int. 1999 Feb;55(2):713-23
pubmed: 9987096
Nephron Clin Pract. 2012;120(4):c179-84
pubmed: 22890468
BMC Nephrol. 2017 Mar 29;18(1):106
pubmed: 28356078
Am J Physiol Renal Physiol. 2019 Jan 1;316(1):F128-F133
pubmed: 30427220
Annu Rev Physiol. 2007;69:361-75
pubmed: 17002596
Kidney Dis (Basel). 2018 Jun;4(2):49-57
pubmed: 29998119
Kidney Int Rep. 2020 Jul 02;5(9):1503-1509
pubmed: 32954074
Nat Genet. 2006 Apr;38(4):403-4
pubmed: 16570061
Case Rep Nephrol Dial. 2018 Aug 10;8(2):147-154
pubmed: 30197903