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Introduction The fractional excretion of sodium (FE.sub.Na) has been used as an index for the differential diagnosis of acute tubular necrosis (ATN) and prerenal acute kidney injury (AKI). The reliability of this index, however, decreases with the use of the diuretic agent furosemide. The fractional excretion of urea nitrogen (FE.sub.UN) has been shown to be useful in such settings in adults. The objective of this study was to examine whether FE.sub.UN is also useful in these settings in children. Methods We assessed 102 episodes of AKI in 74 children, classifying these into three groups based on history, physical examination, urine examination and subsequent clinical course: (1) prerenal AKI without furosemide (N = 37), (2) prerenal AKI with furosemide (N = 32) and (3) ATN (N = 33). Results Of the 37 prerenal AKI episodes without furosemide, 35 showed low FE.sub.Na of Conclusions FE.sub.UN is useful in detecting prerenal AKI in children administered furosemide., Author(s): Hisayo Fujita[sup.1] , Masayoshi Shinjoh[sup.2] , Tomohiro Ishii[sup.2] , Midori Awazu[sup.2] Author Affiliations: (1) Department of Pediatrics, Hiratsuka Kyosai Hospital, KanagawaJapan (2) Department of Pediatrics, Keio University School of [...]

We previously reported that p38 mitogen-activated protein kinase (p38) and phosphorylated ERK are upregulated in cyst epithelium of human renal dysplasia and obstructive uropathy in fetal lambs (Omori S, Fukuzawa R, Hida M, Awazu M. Kidney Int 61: 899-906, 2002; Omori S, Kitagawa H, Koike J, Fujita H, Hida M, Pringle KC, Awazu M. Kidney Int 73: 1031-1037, 2008). Dysplastic epithelium is characterized by proliferation, apoptosis, and upregulation of Pax2 and transforming growth factor (TGF)-[beta]1. In the present study, we investigated whether cyclic mechanical stretching of ureteric bud cells, a mimic of the hydrodynamic derangement after fetal urinary tract obstruction, reproduces events seen in vivo. Cyclic stretch activated p38 and ERK and upregulated Pax2 expression in a time-dependent manner in ureteric bud cells. Stretch-stimulated Pax2 expression was suppressed by a p38 inhibitor, SB203580, or a MEK inhibitor, PD98059.5-Deoxyuridine incorporation was increased by stretch at 24 h, which was also abolished by SB203580 or PD98059. On the other hand, apoptosis was not induced at 24 h by stretch but was significantly increased at 48 h. TGF-[beta]1 secretion was increased by stretch at 24 h, which was inhibited by SB203580 or PD98059. Inhibition of p38 or ERK as well as anti-TGF-[beta] antibody abolished the stretch-induced apoptosis. Finally, exogenous TGF-[beta]1 induced apoptosis of ureteric bud cells, which was inhibited by SB203580 and PD98059. In conclusion, cyclic stretch induces Pax2 upregulation, proliferation, and TGF-[beta]1-mediated apoptosis, features characteristic of dysplastic epithelium, via p38 and ERK in ureteric bud cells. dysplastic kidney; obstructive uropathy; kidney development; cell signaling doi: 10.1152/ajprenal.00402.2009.

Macrophage activation syndrome, a life-threatening complication of rheumatic disorders, is accompanied by the overproduction of cytokines. We describe a girl with macrophage activation syndrome complicating systemic-onset juvenile arthritis who developed hyponatremia, hypophosphatemia, and hypouricemia associated with a high level of serum tumor necrosis factor [alpha]. Renal proximal tubule dysfunction was considered to be the cause, which may be attributable to tumor necrosis factor [alpha]. Key Words: hemophagocytic lymphohistiocytosis, renal impairment, hypophosphatemia, sodium, MACROPHAGE ACTIVATION SYNDROME (MAS), a complication of rheumatic disorders (especially systemic-onset juvenile arthritis [SOJA]), is characterized by persistent fever, pancytopenia, lymphadenopathy, hepatosplenomegaly, elevated serum liver enzyme levels, and coagulation disorder. [...]

We investigated the expression of ERK, p38 mitogen-activated protein kinase (p38), and JNK in renal tubules of diabetic rats following 3 wk after streptozotocin injection (DM). Although the expression of ERK was not different between controls and DM, phosphorylated ERK was expressed more intensely in DM. p38 And phosphorylated p38 were detected only in the diabetic kidney and were localized in all tubular segments. JNK and phosphorylated JNK were expressed similarly in controls and DM. Transforming growth factor (TGF)-[beta] was expressed in all tubular segments of DM, coinciding with the localization of p38. In LLC-P[K.sub.1] cells, phosphorylation of ERK and p38 increased after 24- to 72-h exposure to high glucose (HG). Coincubation with a p38 inhibitor SB-203580 or a MEK inhibitor, PD-98059, suppressed the HG-induced increases in protein content, [[sup.3]H]leucine incorporation, and the protein-to-DNA ratio. SB-203580 or PD-98059 also abolished the HG-stimulated expression of TGF-[beta] protein. These results demonstrate that ERK and p38 are activated in renal tubular cells of DM and may mediate HG-induced cellular hypertrophy and TGF-[beta] expression. mitogen-activated protein kinase; diabetes; kidney