Kidney Week

Abstract: SA-PO522

Outcome and Possible Mechanism of Acute Tubulointerstitial Nephritis

Session Information

• AKI: Clinical, Outcomes, Trials - II
  October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Yun, Dong hwan, Seoul National University College of Medicine, Seoul, Korea (the Republic of)

Dong hwan Yun,

• Kang, Min woo, Seoul National University College of Medicine, Seoul, Korea (the Republic of)

Min woo Kang,

• Kang, Minjung, Seoul National University College of Medicine, Seoul, Korea (the Republic of)

Minjung Kang,

• Kwon, Soie, Seoul National University College of Medicine, Seoul, Korea (the Republic of)

Soie Kwon,

• An, Jung Nam, Seoul National University Boramae Medical Center, Seoul, SEOUL, Korea (the Republic of)

Jung Nam An,

• Kim, Dong Ki, Seoul National University Hospital, Seoul, Korea (the Republic of)

Dong Ki Kim,

• Kim, Yon Su, Seoul National University College of Medicine, Seoul, Korea (the Republic of)

Yon Su Kim,

• Lee, Jung Pyo, Seoul National University Boramae Medical Center, Seoul, SEOUL, Korea (the Republic of)

Jung Pyo Lee,

• Chin, Ho Jun, Seoul National University Bundang Hospital, Seong nam, Korea (the Republic of)

Ho Jun Chin,

• Han, Seung Seok, Seoul National University College of Medicine, Seoul, Korea (the Republic of)

Seung Seok Han,

Background

Acute tubulointerstitial nephritis (ATIN) is an important cause of acute kidney injury (AKI) and often described as a potentially reversible disease. Some previous guidelines or studies recommended corticosteroid usage, but the role of steroids remains controversial and underlying mechanisms remain unresolved. The study purpose was to evaluate the steroid effect and the possible mechanism of ATIN.

Methods

A total of 82 adult patients with biopsy-proven ATIN except combined glomerulonephritis, pyelonephritis, and vasculopathy from three tertiary referral centers were recruited between 2001 and 2017. Renal recovery was defined as improvement in Cr level to 1.3 mg/dL or ≥ 50% decrease of the peak Cr. The effect of corticosteroid therapy was determined using multivariate logistic model. . Plasma and urine inflammatory cytokines at the time of biopsy were analyzed using a multi-analyte flow assay kit (n=33).

Results

Causes of ATIN included unknown (74.4%), drugs (17.1%), autoimmune (6.1%), and obstructive disease (2.4%). In drug-induced ATIN, herbal medication was the most common cause (35.7%), and followed by NSAID (28.6%), antibiotics (28.6%). Overall, 76.8% of ATIN patients experienced renal recovery once or more. 59.8% of patients encountered renal recovery status at 6 months post-biopsy. 23.2% of the patients were dependent on dialysis at final follow-up. Among a total of 82 patients with unknown and drug-induced ATIN, 24 patients (82.9%) were treated with corticosteroid. There were no significant difference in renal recovery, ESRD progression, and mortality between steroid-treated and non-treated groups. In both Cox regression for renal recovery and logistic regression for renal recovery at 6 months post-biopsy, steroid use was not significant factor. Among several inflammatory cytokines, monocyte chemotactic protein 1 and interleukin-8 levels were markedly elevated in both plasma and urine; and interleukin-18 levels were high in plasma alone

Conclusion

Steroid use may not determine the overall outcome of ATIN. Therefore, targeting therapy based on the pathophysiology of ATIN should be investigated to improve overall outcomes. The present cytokine results will be helpful to develop a novel targeting therapy for ATIN.