Etiologies, Clinical Features, and Outcome of Oxalate Nephropathy.
chronic pancreatitis
fat malabsorption
gastric bypass
hyperoxaluria
steatorrhea
Journal
Kidney international reports
ISSN: 2468-0249
Titre abrégé: Kidney Int Rep
Pays: United States
ID NLM: 101684752
Informations de publication
Date de publication:
Sep 2020
Sep 2020
Historique:
received:
17
04
2020
revised:
17
06
2020
accepted:
23
06
2020
entrez:
21
9
2020
pubmed:
22
9
2020
medline:
22
9
2020
Statut:
epublish
Résumé
Oxalate nephropathy is a potentially underestimated cause of kidney failure characterized by massive deposition of calcium oxalate crystals in the renal parenchyma. The prevalence and modes of presentation of this entity are ill-defined. Here we report on the largest consecutive series of cases of adult oxalate nephropathy diagnosed on native kidney biopsies from January 2010 to December 2018 in the UCLouvain Kidney Disease Network. We screened 2265 native kidney biopsies and identified 22 cases (1%) of oxalate nephropathy. Patients had a mean age at diagnosis of 61 years (±20) and presented either with acute on chronic kidney disease (CKD) (62%) or with acute kidney injury (AKI) (38%). Mean serum creatinine at biopsy was 8.0 ± 4.5 mg/dl. Kidney biopsies showed abundant calcium oxalate crystal deposits, associated with acute interstitial nephritis and tubular necrosis, and variable degrees of interstitial fibrosis and tubular atrophy. Chronic pancreatitis and gastric bypass were the most common causes of oxalate nephropathy (48%). During a mean follow-up of 29 months, half of the patients (52%) progressed to kidney failure, all within the month following diagnosis. Higher serum creatinine level at presentation and interstitial fibrosis and tubular atrophy score were associated with progression to kidney failure. Oxalate nephropathy is the cause of kidney disease in 1% of consecutive native kidney biopsies and typically presents as acute on CKD or AKI. The prognosis of the disease is poor, with a high rate of kidney failure within the first month after the diagnosis.
Sections du résumé
BACKGROUND
BACKGROUND
Oxalate nephropathy is a potentially underestimated cause of kidney failure characterized by massive deposition of calcium oxalate crystals in the renal parenchyma. The prevalence and modes of presentation of this entity are ill-defined.
METHODS
METHODS
Here we report on the largest consecutive series of cases of adult oxalate nephropathy diagnosed on native kidney biopsies from January 2010 to December 2018 in the UCLouvain Kidney Disease Network.
RESULTS
RESULTS
We screened 2265 native kidney biopsies and identified 22 cases (1%) of oxalate nephropathy. Patients had a mean age at diagnosis of 61 years (±20) and presented either with acute on chronic kidney disease (CKD) (62%) or with acute kidney injury (AKI) (38%). Mean serum creatinine at biopsy was 8.0 ± 4.5 mg/dl. Kidney biopsies showed abundant calcium oxalate crystal deposits, associated with acute interstitial nephritis and tubular necrosis, and variable degrees of interstitial fibrosis and tubular atrophy. Chronic pancreatitis and gastric bypass were the most common causes of oxalate nephropathy (48%). During a mean follow-up of 29 months, half of the patients (52%) progressed to kidney failure, all within the month following diagnosis. Higher serum creatinine level at presentation and interstitial fibrosis and tubular atrophy score were associated with progression to kidney failure.
CONCLUSION
CONCLUSIONS
Oxalate nephropathy is the cause of kidney disease in 1% of consecutive native kidney biopsies and typically presents as acute on CKD or AKI. The prognosis of the disease is poor, with a high rate of kidney failure within the first month after the diagnosis.
Identifiants
pubmed: 32954074
doi: 10.1016/j.ekir.2020.06.021
pii: S2468-0249(20)31344-9
pmc: PMC7486173
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1503-1509Informations de copyright
© 2020 International Society of Nephrology. Published by Elsevier Inc.
Références
Nephrol Dial Transplant. 2016 Mar;31(3):375-82
pubmed: 25701816
N Engl J Med. 2013 Aug 15;369(7):649-58
pubmed: 23944302
Gut. 1977 Jul;18(7):561-6
pubmed: 873337
Kidney Int. 2011 Dec;80(12):1278-91
pubmed: 21956187
Am J Gastroenterol. 1997 Dec;92(12):2280-4
pubmed: 9399770
Blood. 2014 Oct 9;124(15):2467-8
pubmed: 25301337
Nephrol Dial Transplant. 2012 Oct;27(10):3855-62
pubmed: 22844106
Clin Nephrol. 2008 Aug;70(2):176-7
pubmed: 18793536
Diabet Med. 2012 Aug;29(8):1047-54
pubmed: 22273174
Am J Gastroenterol. 2004 Jul;99(7):1350-4
pubmed: 15233677
QJM. 2001 Feb;94(2):69-77
pubmed: 11181982
Kidney Int. 2020 Jan;97(1):219-220
pubmed: 31901348
Kidney Int Rep. 2018 Jul 29;3(6):1363-1372
pubmed: 30450463
Clin J Am Soc Nephrol. 2011 Aug;6(8):1895-902
pubmed: 21737848
BMC Gastroenterol. 2009 Dec 14;9:93
pubmed: 20003450
Acta Paediatr. 2001 Aug;90(8):873-5
pubmed: 11529533
Ann Intern Med. 2009 May 5;150(9):604-12
pubmed: 19414839
Clin J Am Soc Nephrol. 2008 Nov;3(6):1676-83
pubmed: 18701613
Diabetes Metab. 2016 Feb;42(1):62-4
pubmed: 26454353
Am J Dig Dis. 1977 Oct;22(10):921-8
pubmed: 920694
Am J Kidney Dis. 2002 Jul;40(1):E3
pubmed: 12087589
Exp Diabetes Res. 2011;2011:761950
pubmed: 21822421
Kidney Int. 2020 Aug;98(2):294-309
pubmed: 32709292
Nat Rev Nephrol. 2017 Apr;13(4):226-240
pubmed: 28218266
Medicine (Baltimore). 2017 May;96(19):e6758
pubmed: 28489752