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AKI in the setting of HSCT is commonly investigated among adult patients. In the same way, malignancies requiring treatment with HSCT are not limited to the adult patient population, AKI following HSCT is frequently encountered within pediatric patient populations. However, inadequate information regarding epidemiology and pathophysiology specific to pediatric patients prevents development of appropriate and successful therapeutic strategies for those afflicted. Addressing AKI in the context of sinusoidal obstruction syndrome, chemotherapy, thrombotic microangiopathy and hypertension post chemotherapy, glomerulonephritis, and graft versus host disease provides greater insight into renal impairment associated with these HSCT-related ailments. To obtain a better understanding of AKI among pediatric patients receiving HSCT, we investigated the current literature specifically addressing these areas of concern.

Calciphylaxis also known as calcific uraemic arteriolopathy is a rare condition mostly seen in patients with end-stage kidney disease. We report a case of a simultaneous-kidney-pancreas transplant patient with functioning grafts developing biopsy-proven calciphylaxis in the setting of chronic inflammation. Despite several modalities of management, the patient developed progression of her disease leading to multiple amputations. This case illustrates chronic inflammation driven by persistent infection as a probable contributing factor to the development and progression of calciphylaxis in a simultaneous kidney-pancreas recipient. Calciphylaxis should be considered in the differential for a painful, non-healing ulcer even in the absence of common risk factors.

Renal lipidosis or lipid deposits on kidney biopsy has been associated with nephrotic syndrome. 1 Systemic disorders of abnormal lipid metabolism including some lysosomal storage disorders and Lecithin Cholesterol Acyltransferase (LCAT) deficiency 2 are known to cause lipid deposition and progressive proteinuric kidney disease. However, lipid deposition disorders that are limited to the kidney without systemic manifestations are rare. Lipoprotein Glomerulopathy (LPG) is one such extensively described disorder classically characterized by lipoprotein thrombi in glomeruli, proteinuria and progressive kidney disease due to abnormal variants of Apolipoprotein E (ApoE). 3,4 More commonly occurring ApoE variants such as homozygosity for ApoE2 have also been associated with kidney disease. 4,5 As these lipid disorders are rare and have varying presentations, their identification can often be missed,

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