American Journal of Kidney Diseases / 2016-11-17 23:55
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RECENT ARTICLES FROM THE MEDICAL LITERATURE IN KIDNEY TRANSPLANT. Shared by Dr. Alberto Reino Buelvas
American Journal of Kidney Diseases / 2016-11-17 23:55
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Transplantation - Most Popular Articles / 2016-11-20 11:07
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American Journal of Kidney Diseases / 2016-11-14 18:08
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American Journal of Transplantation / 2016-11-09 20:25
The aim of this study (NCT01744470) was to determine the efficacy and safety of two different doses of extended-release tacrolimus (TacER) in kidney transplant recipients (KTR) between 4 and 12 months post-transplantation. Stable steroid-free KTR were randomized (1:1) after 4 months: Group A 50%-reduction in TacER dose with targeted TacERC0>3μg/L; Group B no change in TacER dose (TacERC0=7-12μg/L). The primary outcome was eGFR at 1 year. Of 300 patients, intent-to-treat analysis included 186 patients (Group A 87, Group B 99). TacERC0 were lower in Group A than in Group B at 6 (4.1±2.7 vs 6.7±3.9μg/L, p<0.0001) and 12 months (5.6±2.0 vs 7.4±2.1μg/L, p<0.0001). eGFR was similar in both groups at 12 months (Group A 56.0±17.5ml/min/1.73m², Group B 56.0±22.1ml/min/1.73m²). More rejection episodes occurred in Group A (Group A 11, Group B 3; p=0.016). At one year, sub-clinical inflammation was more frequent in Group A than in Group B (i>0: 21.4% vs. 8.8%, p=0.047; t>0: 19.6% vs. 8.7%, p=0.076, i+t: 1.14±1.21 vs 0.72±1.01, p=0.038). DSA appeared only in Group A (6 patients vs. 0, p=0.008). TacERC0 should be maintained above 7μg/L during the first year post-transplantation in low immunological risk steroid-free KTR receiving moderate dose of MPA.
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Transplantation Direct - Current Issue / 2016-11-03 02:09
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The New England Journal of Medicine: Search Results in Nephrology / 2016-11-03 03:12
A 72-year-old woman with poorly controlled hyperlipidemia and diabetes presented to the emergency department with a 5-day history of lower abdominal pain. She also had fever and reported nausea and vomiting. Physical examination revealed lower abdominal tenderness. Blood tests revealed leukocytosis associated with a left shift (neutrophil count of 11,800 per cubic millimeter) and elevation of the levels of C-reactive protein (24.0 mg per deciliter) and glucose (735 mg per deciliter [41 mmol per liter]). A plain radiograph of the kidneys, ureters, and bladder showed air surrounding the bladder (Panel A, arrows). An abdominal computed tomographic scan revealed an area of gas dissecting the bladder wall, bilateral hydronephrosis, and intramural gas with a cobblestone or beaded-necklace appearance (Panel B, arrows), findings consistent with emphysematous cystitis. The patient was treated with broad-spectrum antimicrobial agents and placement of a Foley catheter. Subsequently, a urine culture was positive for Escherichia coli; the patient was treated with antibiotics and recovered uneventfully. Emphysematous cystitis is a urinary tract infection that is associated with gas formation and is commonly caused by E. coli and Klebsiella pneumoniae.
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Nephrology Dialysis Transplantation - current issue / 2016-11-02 02:56
Inflammation plays an important role in polycystic kidney disease (PKD). The current study aimed to examine the efficacy of the anti-inflammatory compound resveratrol in PKD and to investigate its underlying mechanism of action.
MethodsMale Han:SPRD (Cy/+) rats with PKD were treated with 200 mg/kg/day resveratrol or vehicle by gavage for 5 weeks. Human autosomal dominant (AD) PKD cells, three-dimensional (3D) Madin-Darby canine kidney cells and zebrafish were treated with various concentrations of resveratrol or the nuclear factor B (NF-B) inhibitor QNZ.
ResultsResveratrol treatment reduced blood urea nitrogen levels and creatinine levels by 20 and 24%, respectively, and decreased two-kidney/total body weight ratio by 15% and cyst volume density by 24% in Cy/+ rats. The proliferation index and the macrophage infiltration index were reduced by 40 and 43%, respectively, in resveratrol-treated cystic kidneys. Resveratrol reduced the levels of the pro-inflammatory factors monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α) and complement factor B (CFB) in Cy/+ rat kidneys in parallel with the decreased activity of NF-B (p50/p65). The activation of NF-B and its correlation with pro-inflammatory factor expression were confirmed in human ADPKD cells and kidney tissues. Resveratrol and QNZ inhibited the expression of MCP-1, TNF-α and CFB and reduced NF-B activity in ADPKD cells. Moreover, NF-B blockage minimized the inhibition of inflammatory factor production by resveratrol treatment. Furthermore, resveratrol or QNZ inhibited cyst formation in the 3D cyst and zebrafish models.
ConclusionsThe NF-B signaling pathway is activated and partly responsible for inflammation in polycystic kidney tissues. Targeting inflammation through resveratrol could be a new strategy for PKD treatment in the future.
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