<b><i>Introduction:</i></b> Secondary oxalate nephropathy (OxN) is associated with a variety of causes and has not been well characterized in Chinese population. To investigate the etiology, clinicopathological features, and outcomes of secondary OxN, we report a case series from a single center in China. <b><i>Methods:</i></b> A retrospective analysis of 68 patients diagnosed with secondary OxN by renal biopsy from January 2013 to February 2019 in Jinling Hospital was performed. <b><i>Results:</i></b> Secondary OxN accounted for 0.23% of the renal biopsies and 2.31% of patients who received renal biopsies due to acute kidney injury (AKI). A total of 49 men and 19 women with an average age of 51.6 ± 11.8 years were enrolled. The most common cause was iatrogenic medication, followed by oxalate-rich diet and industry exposure. Stage 1, 2, and 3 AKI and AKI on chronic kidney disease (ACKD) were found in 4.4, 8.8, 69.1, and 17.6% of the patients, respectively. The peak serum creatinine during hospitalization was 8.62 ± 4.67 mg/dL. The median urinary oxalate excretion was 51.5 (23.2–147.1) mg/24 h. Kidney biopsy showed extensive calcium oxalate crystal deposits with acute tubulointerstitial nephritis. Thirty-four patients (50.0%) required renal replacement therapy. At the end of a follow-up that lasted 8.7 (0.1–72.1) months, 81.0% of patients achieved renal function recovery in 50 (14–432) days. Patients with renal function recovery had a lower rate of ACKD, a higher level of hemoglobin, a lower level of urine lysozyme, and a lower degree of interstitial fibrosis/tubular atrophy, interstitial inflammation, and global glomerulosclerosis than those in the nonrecovery group. <b><i>Conclusions:</i></b> In this case series of secondary OxN, the most common cause was iatrogenic medication, and it presented with AKI or ACKD. Half of the patients required renal replacement therapy, and in most of them, the renal function was reversible. Renal biopsy played an important role in diagnosis and prognosis evaluation.
Oxalate Nephropathy in an Oxalobacter formigenes–Negative Subject