title: Laboratory and imaging features of kidney involvement in autoimmune pancreatitis: incidence, correlation, and steroid therapy response.
abstract: OBJECTIVE
  Autoimmune pancreatitis (AIP) is a rare subtype of chronic pancreatitis. AIP has been suggested to be complicated by tubulointerstitial nephritis or glomerulonephritis, implying that the kidney is involved as a phenotype of IgG4-positive multi-organ lymphoproliferative syndrome; however, the clinical significance of this novel entity is not well-defined.
  
  
  METHODS
  We conducted a retrospective cohort analysis of 47 (male, 39; female, 8) AIP patients.
  
  
  RESULTS
  The patients (mean age, 70.3 +/- 9.5 years) had a mean observation period of 4.1 years. Before treatment, renal dysfunction with an eGFR of 30 and 15 ml/min/1.73 m2 developed only in 10.6% (5/47) and 2.1% (1/47) of the patients, respectively. Nevertheless, urinary N-acetyl-beta-D-glucosaminidase and alpha1-microglobulin levels were elevated in 78.6% (11/14) and 30.8% (4/13) of the patients, respectively. Renal involvement in contrast-enhanced CT imaging was present in 18.2% (8/44) of the patients and was associated with proteinuria (p = 0.04) and a decrease in eGFR (p < 0.01). Furthermore, a follow-up CT study (mean, 545 days) revealed improved kidney lesions in 80.0% (4/5) of the patients after oral corticosteroid administration. In contrast, first-time kidney involvements appeared newly in 3.6% (1/28) of the patients after steroid therapy for nonrenal AIP symptoms, and in 14.3% (1/7) of the patients under no specific therapy (p = 0.02).
  
  
  CONCLUSIONS
  Although severe renal failure develops rarely in AIP patients, renal abnormalities have been significantly detected by biochemical and radiological tests. Oral corticosteroid administration, even when not targeting symptomatic nephropathy, can treat and prevent kidney involvements in AIP.
authors.affiliation: Division of Nephrology and Endocrinology, University of Tokyo School of Medicine, Tokyo, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Nishi
authors.forename: Y
authors.initials: Y
authors.lastname: Shibagaki
authors.forename: K
authors.initials: K
authors.lastname: Hirano
authors.forename: M
authors.initials: M
authors.lastname: Akahane
authors.forename: R
authors.initials: R
authors.lastname: Kido
authors.forename: M
authors.initials: M
authors.lastname: Nangaku
authors.forename: S
authors.initials: S
authors.lastname: Kaname
authors.forename: N
authors.initials: N
authors.lastname: Sasahira
authors.forename: H
authors.initials: H
authors.lastname: Isayama
authors.forename: M
authors.initials: M
authors.lastname: Tada
authors.forename: R
authors.initials: R
authors.lastname: Tsukamoto
authors.forename: K
authors.initials: K
authors.lastname: Ohtomo
authors.forename: M
authors.initials: M
authors.lastname: Omata
authors.forename: T
authors.initials: T
authors.lastname: Fujita
mesh_terms: D001327:Autoimmune Diseases / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000473:pathology*; D015331:Cohort Studies; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D007668:Kidney / Q000000981:diagnostic imaging / Q000473:pathology*; D007674:Kidney Diseases / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000473:pathology*; D008297:Male; D050500:Pancreatitis, Chronic / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000473:pathology*; D011241:Prednisone / Q000627:therapeutic use; D011859:Radiography; D012044:Regression Analysis; D012189:Retrospective Studies; D016896:Treatment Outcome
chemical_list: D005938:Glucocorticoids; D011241:Prednisone