Malaria is a parasitic infection transmitted by mosquitos, resulting in significant morbidity and mortality. It affects 212 million worldwide, causing death in up to 303,000 children annually. In the USA, up to 1700 people are affected yearly. Although the prevalence in developed countries is less than in developing countries, travelers from low transmission areas, and those from endemic areas who later return, are very susceptible to malaria and its complications. Severe malaria can cause significant multiorgan dysfunction including acute kidney injury (AKI). The pathogenesis is not clearly understood but proposed mechanisms include acute tubular necrosis (ATN) due to impediments in renal microcirculation, infection-triggered proinflammatory reactions within the kidney, and metabolic disturbances. Providers must consider malarial infection in cases of AKI in someone with a travel history, as early recognition and treatment are crucial to improving outcomes. This article will review malariainduced AKI in order to provide a better understanding of this infection's effect on the kidneys.

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Radiation exposure through environmental, medical, and occupational settings is increasingly common. While radiation has harmful effects, it has utility in many applications such as radiotherapy for cancer. To increase the efficacy of radiation treatment and minimize its risks, a better understanding of the individual differences in radiosensitivity and the molecular basis of radiation response is needed. Here, we integrated human genetic and functional genomic approaches to study the response of human cells to radiation. We measured radiation-induced changes in gene expression and cell death in B cells from normal individuals. We found extensive individual variation in gene expression and cellular responses. To understand the genetic basis of this variation, we mapped the DNA sequence variants that influence expression response to radiation. We also identified radiation-responsive genes that regulate cell death; silencing of these genes by small interfering RNA led to an increase in radiation-induced cell death in human B cells, colorectal and prostate cancer cells. Together these results uncovered DNA variants that contribute to radiosensitivity and identified genes that can be targeted to increase the sensitivity of tumors to radiation. [Supplemental material is available for this article.]Radiation exposure is increasingly common. Medical diagnostic tools such as the X-ray and computed tomography imaging expose patients to ionizing radiation (IR), which can cause DNA damage and increase one's risk of malignancies. However, these radiation-based devices have greatly improved the diagnosis and treatment of many diseases. Thus, the solution is not to eliminate radiation exposure but to protect individuals who are the most sensitive to radiation and to minimize dose and exposure to all individuals (Barnett et al. 2009).Pharmacogenetics has made significant contributions in maximizing therapeutic gains while minimizing side effects; however, those studies have focused mainly on chemicals as therapeutics and have not included radiation. The exclusion of radiation in pharmacogenetics is not surprising since radiation presents a unique set of challenges. Most people are exposed to radiation in nonmedical settings in addition to medical exposures, thus complicating the monitoring of exposure. Safety trials of radiation are impossible given its known toxic effects. Third, most drugs are developed for one or a few diseases. In contrast, radiation is used in a wide range of treatment; over 50% of all cancer treatment protocols include the use of radiation. Target tissues range from skin to skeletal muscles and bone marrow; each tissue type has special cellular components that influence the absorbed radiation dose, and manifests side effects differently.In recent years, cell-based and genetic studies have improved our understanding of the molecular and genetic basis of radiosensitivity by identifying the genes and pathways that are involved in radiation response (Amundson et al. 2001(Amundson et al. , 2008Smirnov et al. ...

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FSGS is a potentially devastating form of nephrotic syndrome. Treatment of SRNS can be difficult, especially post‐transplantation. The current therapy of post‐transplant SRNS includes plasmapheresis, ACE‐I, CNI, and monoclonal antibodies (rituximab). Patients who are refractory to these interventions have limited therapeutic alternatives. We present a case of a patient with SRNS secondary to FSGS. He did not respond to immunosuppressive medications prior to transplant, progressed to ESRD, and was started on chronic hemodialysis. He received a DDKT which was complicated by post‐transplant FSGS recurrence. A course of plasmapheresis, rituximab, and CNI were administered with some response. Ofatumumab was then given to the patient. As a result, the patient achieved partial remission. Ofatumumab may be a safe and effective option for post‐transplant recurrence of FSGS.