POS-022 ACUTE TUBULO-INTERSTITIAL NEPHRITIS WITH EOSINOPHILS, SUSPECTED TO BE DRUG-INDUCED, AS SEEN ON NATIVE KIDNEY BIOPSIES: 10-YEAR EXPERIENCE FROM AN INDEPENDENT CENTRAL PATHOLOGY LABORATORY IN KENYA

Abstract

Drug-induced acute tubulointerstitial nephritis (ATIN) is a well-recognised cause of unexplained AKI that can lead to CKD. The presence of eosinophils in the tubulo-interstitial inflammation associated with ATI is considered a hallmark of the diagnosis. There is scarcity of data on biopsy-proven drug-induced ATIN in Africa. The author set out to establish the extent of biopsy-proven drug-induced ATIN in native kidney biopsies a 10-year period from his experience at a pathology central referral laboratory that handles the highest number of kidney biopsies in the region. Histopathology reports in text form were searched for key words “tubulo-interstitial nephritis” and respective cases identified were further examined to confirm those that were acute or active tubule-interstitial nephritis with eosinophils present, which were deemed to be in keeping with a diagnosis of drug-induced acute tubulo-interstitial nephritis. Associated pathological findings present in the biopsies were also recorded. The results were tabulated and tallied on Excel spreadsheet to obtain the summary statistics. A total of 34 cases of suspected drug-induced ATIN were identified representing 3.2% of all native kidney biopsies in the 10-year period. The cases were reported in each year except for 2014, with 2011-2013 having a case each, 2015 had 4 cases, 2016 had 5 cases, while 2017-2019 had 6 cases each and 2020 had 4 cases. An equal gender distribution was noted with ½ the cases being males and ½ being females. The youngest patient was 15 years old and the oldest 69 years old, the mean age at 39.2 years and median of 40 years. The degree of inflammation and acute kidney injury was mild in 14 cases (41%), similarly moderate in 14 cases (41%) and severe in 6 cases (18%), while concurrent chronic kidney damage was minimal in 16 cases (47%), mild in 5 cases (15%), moderate in 12 cases (35%) and severe in 1 case (3%). All but 4 cases (12%) had an associated pathological diagnostic finding, of which the commonest associated pathological finding was hypertensive changes of benign nephrosclerosis in 6 cases (18%), membranous glomerulopathy 6 cases (18%), diabetic nephropathy 4 cases (12%), lupus nephritis 4 cases (12%), two cases each of AL amyloidosis, HIVAN and IgA nephropathy, and a case each of AA amyloidosis, primary FSGS, ascending infection and malignancy. The majority of biopsy-proven cases of drug-induced ATIN seen at this independent central laboratory in Kenya are associated with other renal pathologies on the same respective biopsies, and only 12% had no related renal pathologies on the biopsies thus only a minority of cases were 'purely' drug-induced ATIN as the primary pathology. The exact medication linked to the drug-induced ATIN was not indicated in the clinical details. Interestingly, none of the cases was actually clinically suspected pre-biopsy to be drug-induced ATIN. Although rare, biopsy-proven drug-induced ATIN is a significant cause of AKI, and based on this analysis, it appears that most cases of drug-induced ATIN compound or exacerbate other underlying renal pathologies with underlying hypertensive kidney disease, membranous nephropathy and diabetic nephropathy as the commonest associated pathologies. ATIN needs to be born in mind by nephrologists when working up patients for AKI, and also born in mind by pathologists when examining kidney biopsies.