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Kidney Week

Abstract: SA-PO077

Parenchymal and Nontraditional Etiologies of AKI in Patients with End-Stage Liver Disease

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

  • Varghese, Vipin, Ochsner Health, New Orleans, Louisiana, United States
  • Ramanand, Akanksh, Ochsner Health, New Orleans, Louisiana, United States
  • Cohen, Lauren, Ochsner Health, New Orleans, Louisiana, United States
  • Chalmers, Dustin R., Ochsner Health, New Orleans, Louisiana, United States
  • Velez, Juan Carlos Q., Ochsner Health, New Orleans, Louisiana, United States
Background

In the context of acute kidney injury (AKI) and end-stage liver disease (ESLD), AKI is frequently attributed to either hepatorenal syndrome type 1 (HRS-1), ischemic acute tubular injury (ATI), or pre-renal azotemia (PRA). We hypothesized that other parenchymal causes of AKI including toxic ATI, acute glomerulonephritis (AGN) and acute interstitial nephritis (AIN) may account for a small but not negligible proportion of cases of AKI in patients with ESLD.

Methods

We established prospective data collection in patients with ESLD with AKI stage ≥ 2 (AKIN) over 5-years who were seen by the nephrology consultation service. Demographic and clinical data were collected. Etiology of AKI was adjudicated based on history, clinical assessment, laboratory results, urine microscopy findings, and kidney biopsy data.

Results

We included 234 patients with AKI and ESLD. The median age was 57 (20-88), 37% were female, 76% were white, and 15% were black. CKD was a pre-existing comorbidity in 26%. PRA was the cause of AKI in 12 (5%) (low rate likely explained by resolution without consultation to nephrology), HRS-1 in 76 (32%), cardiorenal syndrome type 1 (CRS-1) in 6 (3%) abdominal compartment syndrome (ACS) in 2 (1%) and obstructive uropathy (OU) in 3 (1%). Parenchymal etiologies of AKI were noted in 137 (59%) of patients. Among parenchymal etiologies of AKI, ischemic ATI was the primary diagnosis in 78 (58%), toxic ATI in 26 (19%), ischemic/toxic ATI in 22 (16%), AIN in 2 (1%), and AGN in 7 (5%). Among those with toxic ATI, 3 were due to vancomycin, 2 to ciprofloxacin, 1 to uric acid, 1 to contrast, 15 to cholemic tubulopathy, and 4 due to other drugs. Both cases of AIN were associated with ciprofloxacin use. Among those with AGN, 4 were biopsy-proven (3 IgA nephropathy, 1 immune complex-GN) and 3 were clinical diagnoses (2 IgA nephropathy, 1 SLE-GN).

Conclusion

Combining toxic ATI (drug-induced, endogenous toxins), AIN, and AGN, non-traditional parenchymal causes of AKI accounted for 15% of the cases in these cohort of patients with ESLD and AKI. When added to CRS-1, ACS and OU, a total of 19% of the cases were not within the traditional 3-way split (PRA, HRS-1, ischemic ATI). Comprehensive diagnostic assessment is recommended in this clinical setting.