Vancomycin- and piperacillin-induced acute interstitial nephritis in a patient with lupus: A case report showcasing rapid decline in renal function.

Drug-induced acute interstitial nephritis (AIN) presents as acute kidney injury (AKI) with the use of certain offending drugs. Antibiotics, such as ß-lactams, trimethoprim-sulfamethoxazole, fluoroquinolones, and rifampin, account for up to 50% of drug-induced AIN cases. The onset of drug-induced AIN following drug exposure usually ranges from few days to several weeks or months. We present a patient with lupus who had rapid decline in renal function with a single dose of vancomycin and piperacillin-tazobactam (VPT) administration, termed as the "workhorse" regimen at many institutions. In addition, she did not exhibit many clinical and laboratory signs of AIN, making diagnosis challenging. Prompt kidney biopsy and early steroid therapy had a critical role in recovery of the patient's renal function. The median duration for renal impairment in vancomycin-induced AIN is 26 days. Onset of AKI is usually rapid from VPT, within 3 - 5 days of drug exposure. However, the severity of AKI is often low, in contrast to this patient whose AKI reached a stage 3 (AKIN/KDIGO) within 2 days from drug exposure. This study highlights the nephrotoxic potential of piperacillin, especially when used along with vancomycin, concurrent with recent evidence. Within rising antibiotic usage rates, is important to consider AIN in the differential diagnosis of rapidly declining AKI, especially with the combined use of VPT.

The expression of YAP1 is increased in high-grade prostatic adenocarcinoma but is reduced in neuroendocrine prostate cancer.

BACKGROUND: After long-term androgen deprivation therapy, 25-30% prostate cancer (PCa) acquires an aggressive neuroendocrine (NE) phenotype. Dysregulation of YAP1, a key transcription coactivator of the Hippo pathway, has been related to cancer progression. However, its role in neuroendocrine prostate cancer (NEPC) has not been assessed. METHODS: Immunohistochemistry and bioinformatics analysis were conducted to evaluate YAP1 expression levels during PCa initiation and progression. RESULTS: YAP1 expression was present in the basal epithelial cells in benign prostatic tissues, lost in low-grade PCa, but elevated in high-grade prostate adenocarcinomas. Interestingly, the expression of YAP1 was reduced/lost in both human and mouse NEPC. CONCLUSIONS: The expression of YAP1 is elevated in high-grade prostate adenocarcinomas but lost in NEPC.