Acute Kidney Injury with Hemolysis after Glycerin Enema-induced Rectal Injury in a Patient with Type 2 Diabetes.

A 66-year-old man with type 2 diabetes was admitted for glycemic control and weight loss. The rectal mucosa was unfortunately injured during glycerin enema administration in preparation for colonoscopy, after which dark red urine and renal dysfunction were observed. Considering the clinical diagnosis of glycerol-induced hemolysis and acute kidney injury, intravenous hydration and haptoglobin administration were started, which successfully treated the dark red urine and renal dysfunction. This case highlights the importance of appropriate glycerin enema administration and emphasizes the need to recognize glycerol-induced hemolysis and acute kidney injury as complications of glycerin enemas. This case also provides insight into glycerol-induced hemolysis and acute kidney injury as complications of glycerin enemas.

Effects of 3,3',5-triiodothyronine on microglial functions.

L-tri-iodothyronine (3, 3', 5-triiodothyronine; T3) is an active form of the thyroid hormone (TH) essential for the development and function of the CNS. Though nongenomic effect of TH, its plasma membrane-bound receptor, and its signaling has been identified, precise function in each cell type of the CNS remained to be investigated. Clearance of cell debris and apoptotic cells by microglia phagocytosis is a critical step for the restoration of damaged neuron-glia networks. Here we report nongenomic effects of T3 on microglial functions. Exposure to T3 increased migration, membrane ruffling and phagocytosis of primary cultured mouse microglia. Injection of T3 together with stab wound attracted more microglia to the lesion site in vivo. Blocking TH transporters and receptors (TRs) or TRα-knock-out (KO) suppressed T3-induced microglial migration and morphological change. The T3-induced microglial migration or membrane ruffling was attenuated by inhibiting Gi /o -protein as well as NO synthase, and subsequent signaling such as phosphoinositide 3-kinase (PI3K), mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK). Inhibitors for Na(+) /K(+) -ATPase, reverse mode of Na(+) /Ca(2+) exchanger (NCX), and small-conductance Ca(2+) -dependent K(+) (SK) channel also attenuated microglial migration or phagocytosis. Interestingly, T3-induced microglial migration, but not phagocytosis, was dependent on GABAA and GABAB receptors, though GABA itself did not affect migratory aptitude. Our results demonstrate that T3 modulates multiple functional responses of microglia via multiple complex mechanisms, which may contribute to physiological and/or pathophysiological functions of the CNS.