Diffusion-weighted imaging in assessing renal pathology of chronic kidney disease: A preliminary clinical study

2014 ◽  
Vol 83 (5) ◽  
pp. 756-762 ◽  
Author(s):  
Qinghai Li ◽  
Jinning Li ◽  
Lan Zhang ◽  
Ying Chen ◽  
Minming Zhang ◽  
...  
2018 ◽  
Vol 91 (1091) ◽  
pp. 20170952 ◽  
Author(s):  
Haitian Liu ◽  
Zhangjian Zhou ◽  
Xiang Li ◽  
Chenxia Li ◽  
Rong Wang ◽  
...  

2017 ◽  
Vol 43 (7) ◽  
pp. 1749-1755 ◽  
Author(s):  
Xueqin Xu ◽  
Suzanne L. Palmer ◽  
Xiaozhu Lin ◽  
Weixia Li ◽  
Kemin Chen ◽  
...  

2008 ◽  
Vol 108 (2) ◽  
pp. c163-c168 ◽  
Author(s):  
Ryota Ikee ◽  
Yoshifumi Hamasaki ◽  
Machiko Oka ◽  
Kyoko Maesato ◽  
Tsutomu Mano ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Roberto Gordillo ◽  
Marcela Del Rio ◽  
David B. Thomas ◽  
Joseph T. Flynn ◽  
Robert P. Woroniecki

We report a child with Hermansky-Pudlak Syndrome (HPS) and chronic kidney disease (stage II) with histological diagnosis of focal segmental glomerulosclerosis (FSGS). A 15-year-old male of Puerto Rico ancestry with history of HPS, hypertension (HTN), asthma, obesity, and chronic kidney disease (CKD) stage II presented with new-onset proteinuria without edema. His blood pressure had been controlled, serum creatinine had been 0.9–1.4 mg/dL, and first morning urine protein/creatinine ratio (UPC) ranged from 0.2 to 0.38. Due to persistent nonorthostatic proteinuria with CKD, renal biopsy was performed and FSGS (not otherwise specified) with chronic diffuse tubulopathy (tubular cytoplasmic droplets) and acute tubular injury was reported. Ceroid-like material is known to infiltrate tissues (i.e., lungs, colon, and kidney) in HPS, but the reason for the renal insufficiency is unknown. Nonspecific kidney disease and in one adult case IgA nephropathy with ANCA-positive glomerulonephritis have previously been reported in patients with Hermansky-Pudlak syndrome. To our knowledge, we report the first pediatric renal pathology case of HPS associated with CKD. This paper discusses presentation and management of renal disease in HPS.


2017 ◽  
Vol 312 (1) ◽  
pp. F230-F244 ◽  
Author(s):  
Victoria Yum ◽  
Rachel E. Carlisle ◽  
Chao Lu ◽  
Elise Brimble ◽  
Jasmine Chahal ◽  
...  

Proteinuria is one of the primary risk factors for the progression of chronic kidney disease (CKD) and has been implicated in the induction of endoplasmic reticulum (ER) stress. We hypothesized that the suppression of ER stress with a low molecular weight chemical chaperone, 4-phenylbutyric acid (4-PBA), would reduce the severity of CKD and proteinuria in the Dahl salt-sensitive (SS) hypertensive rat. To induce hypertension and CKD, 12-wk-old male rats were placed on a high-salt (HS) diet for 4 wk with or without 4-PBA treatment. We assessed blood pressure and markers of CKD, including proteinuria, albuminuria, and renal pathology. Furthermore, we determined if HS feeding resulted in an impaired myogenic response, subsequent to ER stress. 4-PBA treatment reduced salt-induced hypertension, proteinuria, and albuminuria and preserved myogenic constriction. Furthermore, renal pathology was reduced with 4-PBA treatment, as indicated by lowered expression of profibrotic markers and fewer intratubular protein casts. In addition, ER stress in the glomerulus was reduced, and the integrity of the glomerular filtration barrier was preserved. These results suggest that 4-PBA treatment protects against proteinuria in the SS rat by preserving the myogenic response and by preventing ER stress, which led to a breakdown in the glomerular filtration barrier. As such, alleviating ER stress serves as a viable therapeutic strategy to preserve kidney function and to delay the progression of CKD in the animal model under study.


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