Excess production or absorption of oxalate can lead to hyperoxaluria and subsequent kidney injury. While many etiologies of hyperoxaluria have been well studied, diet-induced secondary oxalate nephropathy is a rare cause of renal damage that is still poorly understood. In this report, we present a 71-year-old man who lacked any known risk factors for secondary oxalate nephropathy other than a diet that was unusually high in peanut butter and coffee. The patient developed severe acute kidney injury, which resulted in end-stage renal disease and dependence on hemodialysis. Renal biopsy showed oxalate crystal buildup to be the culprit. It is likely that these cases of diet-induced secondary oxalate nephropathy have a strong genetic component that is yet to be fully understood. As the general public is likely unaware of the significance of dietary oxalate, we believe it is important to quickly identify and educate patients that have relevant risk factors to prevent development of acute or chronic kidney disease.

Background Microglia, the resident macrophages of the central nervous system, play an important role in immune defense by removing damaged neurons and cellular plaques. When activated microglia release pro‐inflammatory mediators (i.e. reactive oxygen intermediates, eicosanoids, cytokines, and metalloproteinases) which may contribute to the pathophysiology of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, and HIV encephalopathy. Although rodent microglia have been used for immunological and pharmacological research, extrapolation of observations from rat microglia to human microglia has become challenging. Methods In 2017, a research collaboration was established between Neurosurgery at Cook County Hospital and the Pharmacology Department, College of Graduate Studies, Midwestern University. Several human brain biopsies were cultured in vitro and progressively developed into human brain tissue cultures. One of the human primary cultures (culture # 464) generated from a de‐identified human WHO grade I meningioma contained several cell types as determined by immunohistochemistry and described in 2019 (1). To further characterize microglia in brain culture # 464 three antibodies were used, namely against: A) cell surface integrin CD11b; B) the ionized calcium binding adaptor molecule 1 (Iba1), and C) the transmembrane proteinTMEM119. Results Immuno‐histochemistry observations appear to confirm the presence of microglia in de‐identified human WHO grade I meningioma brain culture # 464. Further studies will be required to confirm our current observations and determine a method to isolate viable microglia from culture # 464. Conclusions Microglia are present in de‐identified human brain culture # 464. Isolation of microglia would enable pharmacological and toxicological research with marine‐derived natural products and toxins in future studies (2). (1) T. Moazezi, et al. Characterization of de‐identified human brain culture by immunofluorescence. Chicago Chapter of the Society for Neuroscience, 4/19/2019, abstract F7, page 69. (2) Mayer, A.M.S., et al. Toxicological Sciences 149(2):484‐95, 2016. PMID: 26609141.