The Role of Ammonia in Progressive Renal Injury

2015 ◽  
pp. 78-82 ◽  
Author(s):  
Karl A. Nath ◽  
Margaret K. Hostetter ◽  
Thomas H. Hostetter
Keyword(s):  
Renal Injury

scholarly journals Comparative Proteomics Analysis of Mouse Habu Nephritis Models with and without Unilateral Nephrectomy

2016 ◽  
Vol 39 (5) ◽  
pp. 1761-1776 ◽  
Author(s):  
Lei Chen ◽  
Yang Lu ◽  
Jun Wen ◽  
Xu Wang ◽  
Lingling Wu ◽  
...  
Keyword(s):  
Renal Injury ◽  
Quantitative Proteomics ◽  
Mesangial Cells ◽  
Unilateral Nephrectomy ◽  
Label Free ◽  
Proteomics Analysis ◽  
Single Kidney ◽  
Regulation Of Actin Cytoskeleton ◽  
Insight Into

Background/Aims: Individuals possessing a single kidney are at greater risk of renal injury upon exposure to harmful stimuli. This study aimed to explore the pathogenesis of renal injury in glomerulonephritis with versus without unilateral nephrectomy (UNX). Methods: Histological analysis and label-free quantitative proteomics were performed on two models—the Habu snake venom-induced glomerulonephritis model with versus without UNX (HabuU and Habu models, respectively). The role of villin 1, a differentially expressed protein (DEP) in mouse mesangial cells, was investigated. Results: Persistent mesangiolysis and focal hypercellularity together with reduced activation of cell proliferation in the HabuU model induced more serious renal injury compared with that in the Habu model. The DEPs between the two models were identified by label-free liquid chromatography-mass spectrometry. The KEGG pathway results indicated that regulation of actin cytoskeleton and focal adhesion were specifically enriched in the HabuU model. The cytoskeleton regulation protein villin 1 was downregulated in the HabuU model, but unchanged in the Habu model. Knockdown of villin 1 promoted apoptosis and inhibited the proliferation of mouse mesangial cells, suggesting villin 1 to be involved in qlomerular lesion self-repair insufficiency. Conclusion: By assessing the proteomic profiles of the two models, this study identified several important differences, particularly villin 1 expression, in regulatory mechanisms between the two models. Our findings provide novel insight into the mechanism of serious renal injury in glomerulonephritis with UNX.

scholarly journals Role of Prostaglandin E Receptor EP 1 Subtype in the Development of Renal Injury in Genetically Hypertensive Rats

Hypertension ◽  
2003 ◽  
Vol 42 (6) ◽  
pp. 1183-1190 ◽  
Author(s):  
Takayoshi Suganami ◽  
Kiyoshi Mori ◽  
Issei Tanaka ◽  
Masashi Mukoyama ◽  
Akira Sugawara ◽  
...  
Keyword(s):  
Renal Injury ◽  
Prostaglandin E ◽  
Hypertensive Rats ◽  
Genetically Hypertensive Rats ◽  
Genetically Hypertensive

scholarly journals The Role of β-Adrenergic Overstimulation in the Early Stages of Renal Injury

2017 ◽  
Vol 42 (6) ◽  
pp. 1277-1289 ◽  
Author(s):  
Mariana Charleaux de Ponte ◽  
Fernando Augusto Malavazzi Casare ◽  
Juliana Martins Costa-Pessoa ◽  
Vanessa Gerolde Cardoso ◽  
Gerhard Malnic ◽  
...  
Keyword(s):  
Renal Injury ◽  
Early Stages

scholarly journals Renalase and Biomarkers of Contrast-Induced Acute Kidney Injury

2015 ◽  
Vol 6 (1) ◽  
pp. 25-36 ◽  
Author(s):  
Maciej T. Wybraniec ◽  
Katarzyna Mizia-Stec
Keyword(s):  
Acute Kidney Injury ◽  
Renal Injury ◽  
Amine Oxidase ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Creatinine Concentration ◽  
Invasive Cardiology ◽  
Proximal Tubular ◽  
Novel Biomarkers

Background: Contrast-induced acute kidney injury (CI-AKI) remains one of the crucial issues related to the development of invasive cardiology. The massive use of contrast media exposes patients to a great risk of contrast-induced nephropathy and chronic kidney disease development, and increases morbidity and mortality rates. The serum creatinine concentration does not allow for a timely and accurate CI-AKI diagnosis; hence numerous other biomarkers of renal injury have been proposed. Renalase, a novel catecholamine-metabolizing amine oxidase, is synthesized mainly in proximal tubular cells and secreted into urine and blood. It is primarily engaged in the degradation of circulating catecholamines. Notwithstanding its key role in blood pressure regulation, renalase remains a potential CI-AKI biomarker, which was shown to be markedly downregulated in the aftermath of renal injury. In this sense, renalase appears to be the first CI-AKI marker revealing an actual loss of renal function and indicating disease severity. Summary: The purpose of this review is to summarize the contemporary knowledge about the application of novel biomarkers of CI-AKI and to highlight the potential role of renalase as a functional marker of contrast-induced renal injury. Key Messages: Renalase may constitute a missing biochemical link in the mutual interplay between kidney and cardiac pathology known as the cardiorenal syndrome.

scholarly journals The role of serum and urinary carbohydrate antigen 19-9 in predicting renal injury associated with ureteral stone

Renal Failure ◽  
2016 ◽  
Vol 38 (10) ◽  
pp. 1626-1632 ◽  
Author(s):  
Erfan Amini ◽  
Farhad Pishgar ◽  
Asal Hojjat ◽  
Mohammad Soleimani ◽  
Majid Ali Asgari ◽  
...  
Keyword(s):  
Renal Injury ◽  
Ureteral Stone ◽  
Carbohydrate Antigen

scholarly journals Dicer deficiency in proximal tubules exacerbates renal injury and tubulointerstitial fibrosis and upregulates Smad2/3

2018 ◽  
Vol 315 (6) ◽  
pp. F1822-F1832 ◽  
Author(s):  
Zhengwei Ma ◽  
Qingqing Wei ◽  
Ming Zhang ◽  
Jian-Kang Chen ◽  
Zheng Dong
Keyword(s):  
Kidney Disease ◽  
Renal Injury ◽  
Renal Fibrosis ◽  
Interstitial Fibrosis ◽  
Proximal Tubules ◽  
Tubulointerstitial Fibrosis ◽  
Obstructive Nephropathy ◽  
Pathological Feature ◽  
Tubular Injury

Renal fibrosis is a common pathological feature in chronic kidney disease (CKD), including diabetic kidney disease (DKD) and obstructive nephropathy. Multiple microRNAs have been implicated in the pathogenesis of both DKD and obstructive nephropathy, although the overall role of microRNAs in tubular injury and renal fibrosis in CKD is unclear. Dicer (a key RNase III enzyme for microRNA biogenesis) was specifically ablated from kidney proximal tubules in mice via the Cre-lox system to deplete micoRNAs. Proximal tubular Dicer knockout (PT- Dicer KO) mice and wild-type (WT) littermates were subjected to streptozotocin (STZ) treatment to induce DKD or unilateral ureteral obstruction (UUO) to induce obstructive nephropathy. Renal hypertrophy, renal tubular apoptosis, kidney inflammation, and tubulointerstitial fibrosis were examined. Compared with WT mice, PT- Dicer KO mice showed more severe tubular injury and renal inflammation following STZ treatment. These mice also developed higher levels of tubolointerstitial fibrosis. Meanwhile, PT- Dicer KO mice had a significantly higher Smad2/3 expression in kidneys than WT mice (at 6 mo of age) in both control and STZ-treated mice. Similarly, UUO induced more severe renal injury, inflammation, and interstitial fibrosis in PT- Dicer KO mice than WT. Although we did not detect obvious Smad2/3 expression in sham-operated mice (2–3 mo old), significantly more Smad2/3 was induced in obstructed PT- Dicer KO kidneys. These results supported a protective role of Dicer-dependent microRNA synthesis in renal injury and fibrosis development in CKD, specifically in DKD and obstructive nephropathy. Depletion of Dicer and microRNAs may upregulate Smad2/3-related signaling pathway to enhance the progression of CKD.

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