This study revealed some useful and characteristic features for distinguishing IgG4-related from non-IgG4-related TIN on the basis of light-microscopic observation.
rum ferritin levels increased from 25.6 ± 24.3 ng/ml at baseline to 55.8 ± 33.5 ng/ml at 12 weeks with FCH administration. Serum intact FGF23 and C-term FGF23 levels significantly decreased at 12 weeks compared with baseline (2,000 (1,300.0-3,471.4) to 1,771.4 (1,142.9-2,342.9) pg/ml, p = 0.01, and 1,608.7 (634.8-2,308.7) to 1,165.2 (626.1-1,547.8) RU/ml, p = 0.007, respectively); serum intact PTH levels significantly increased (96 (65-125) to 173 (114-283) pg/ml, p < 0.001). Conclusions: Oral FCH administration decreased serum intact FGF23 and C-term FGF23 levels and increased intact PTH levels; phosphate and 1,25(OH) 2 D levels were unchanged. Oral FCH administration to treat iron deficiency is a possible strategy for reducing serum FGF23 levels independent of phosphate and VDRA.
Hypermagnesemia is generally considered an exceptional iatrogenic condition usually caused by magnesium-containing cathartics. In particular, this condition often develops when magnesium-containing cathartics are administered to elderly patients with renal insufficiency or bowel movement dysfunction. Although magnesium oxide (MgO) is widely prescribed as a laxative, serum magnesium concentration has not been examined in most cases. In this report, we present the cases of four elderly patients with constipation and symptomatic hypermagnesemia caused by MgO ingestion, one of which had a lethal course. All of the patients were older than 65 years and with renal dysfunction. In addition, they had difficulties in expressing their symptoms because of cerebrovascular events or dementia. These cases suggest that hypermagnesemia caused by magnesium-containing cathartics is more likely to develop than previously recognized and that physicians should be aware that patients with chronic kidney disease and the elderly are at risk of hypermagnesemia on magnesium administration. We recommend serum magnesium monitoring for high-risk patients after initial prescription or dose increase.
Narita I. Pentraxin-3 expression in acute renal allograft rejection.Abstract: Pentraxin-3 (PTX3) is an acute phase reactant produced by a variety of cell types at sites of local inflammation. We examined by immunohistochemistry renal biopsies from patients with acute rejection (n = 10), protocol biopsies without rejection (n = 37), and peri-operative donor biopsies of the same transplant patients (n = 94) for intra-renal expression of PTX3, and its correlation with clinical, laboratory, and histopathologic parameters. PTX3 was mainly expressed in the interstitium of renal allograft. In the non-rejection biopsies (pre-and post-reperfusion and protocol biopsies), PTX3 expression area (PTX3%) was equally maintained at a low level, whereas in the rejection biopsies, PTX3% was significantly higher (p < 0.0001). Treatment of acute rejection resulted in a significant reduction of PTX3% (p < 0.0001). PTX3% positively correlated with the degree of allograft dysfunction and acute rejection scores of Banff classification (2009). This study suggests that PTX3% may be an available histological marker of acute renal allograft rejection.
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