Urinary Endopeptidase 24.11 as a New Marker of Proximal Tubular Injury

2015 ◽  
pp. 169-176 ◽  
Author(s):  
J�elle Nortier ◽  
Daniel Abramowicz ◽  
Tome Najdovski ◽  
Paul Kinnaert ◽  
Jean-Louis Vanherweghem ◽  
...  
Keyword(s):  
Tubular Injury ◽  
Endopeptidase 24.11 ◽  
Proximal Tubular

scholarly journals Intracellular prostaglandin E2 contributes to hypoxia-induced proximal tubular cell death

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Coral García-Pastor ◽  
Selma Benito-Martínez ◽  
Ricardo J. Bosch ◽  
Ana B. Fernández-Martínez ◽  
Francisco J. Lucio-Cazaña
Keyword(s):  
Hypoxia Inducible Factor ◽  
Renal Diseases ◽  
Prostaglandin E ◽  
Relevant Factor ◽  
Tubular Injury ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Proximal Tubular ◽  
Cox 2 ◽  
Induced Apoptosis

AbstractProximal tubular cells (PTC) are particularly vulnerable to hypoxia-induced apoptosis, a relevant factor for kidney disease. We hypothesized here that PTC death under hypoxia is mediated by cyclo-oxygenase (COX-2)-dependent production of prostaglandin E2 (PGE2), which was confirmed in human proximal tubular HK-2 cells because hypoxia (1% O2)-induced apoptosis (i) was prevented by a COX-2 inhibitor and by antagonists of prostaglandin (EP) receptors and (ii) was associated to an increase in intracellular PGE2 (iPGE2) due to hypoxia-inducible factor-1α-dependent transcriptional up-regulation of COX-2. Apoptosis was also prevented by inhibitors of the prostaglandin uptake transporter PGT, which indicated that iPGE2 contributes to hypoxia-induced apoptosis (on the contrary, hypoxia/reoxygenation-induced PTC death was exclusively due to extracellular PGE2). Thus, iPGE2 is a new actor in the pathogenesis of hypoxia-induced tubular injury and PGT might be a new therapeutic target for the prevention of hypoxia-dependent lesions in renal diseases.

Protective Effects of Pistacia lentiscus L. fruit extract against calcium oxalate monohydrate induced proximal tubular injury

2017 ◽  
Vol 209 ◽  
pp. 248-254 ◽  
Author(s):  
Nassima Cheraft-Bahloul ◽  
Cécile Husson ◽  
Meriam Ourtioualous ◽  
Sébastien Sinaeve ◽  
Djebbar Atmani ◽  
...  
Keyword(s):  
Calcium Oxalate ◽  
Calcium Oxalate Monohydrate ◽  
Pistacia Lentiscus ◽  
Protective Effects ◽  
Tubular Injury ◽  
Fruit Extract ◽  
Proximal Tubular

scholarly journals Palmitate aggravates proteinuria-induced cell death and inflammation via CD36-inflammasome axis in the proximal tubular cells of obese mice

2018 ◽  
Vol 315 (6) ◽  
pp. F1720-F1731 ◽  
Author(s):  
Lung-Chih Li ◽  
Jenq-Lin Yang ◽  
Wen-Chin Lee ◽  
Jin-Bor Chen ◽  
Chien-Te Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Tubular Injury ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Caspase 1 ◽  
Proximal Tubular ◽  
Renal Tubular ◽  
Nlrp3 Inflammasomes

High levels of serum free fatty acids (FFAs) and proteinuria have been implicated in the pathogenesis of obesity-related nephropathy. CD36, a class B scavenger receptor, is highly expressed in the renal proximal tubules and mediates FFA uptake. It is not clear whether FFA- and proteinuria-mediated CD36 activation coordinates NLRP3 inflammasomes to induce renal tubular injury and inflammation. In this study, we investigated the roles of CD36 and NLRP3 inflammasomes in FFA-induced renal injury in high-fat diet (HFD)-induced obesity. HFD-fed C57BL/6 mice and palmitate-treated HK2 renal tubular cells were used as in vivo and in vitro models. Immunohistochemical staining showed that CD36, IL-1β, and IL-18 levels increased progressively in the kidneys of HFD-fed mice. Sulfo- N-succinimidyl oleate (SSO), a CD36 inhibitor, attenuated the HFD-induced upregulation of NLRP3, IL-1β, and IL-18 and suppressed the colocalization of NLRP3 and ASC in renal tubular cells. In vitro, SSO abolished the palmitate-induced activation of IL-1β, IL-18, and caspase-1 in HK2 proximal tubular cells. Furthermore, treatment with SSO and the knockdown of caspase-1 expression by siRNA both inhibited palmitate-induced cell death and apoptosis in HK2 cells. Collectively, palmitate causes renal tubular inflammation, cell death, and apoptosis via the CD36/NLRP3/caspase-1 axis, which may explain, at least in part, the mechanism underlying FFA-related renal tubular injury. The blockade of CD36-induced cellular processes is therefore a promising strategy for treating obesity-related nephropathy.

scholarly journals Tubular Injury and Dendritic Cell Activation Are Integral Components of Light Chain–Associated Acute Tubulointerstitial Nephritis

2019 ◽  
Vol 143 (10) ◽  
pp. 1212-1224 ◽  
Author(s):  
Mingyu Cheng ◽  
Xin Gu ◽  
Elba A. Turbat-Herrera ◽  
Guillermo A. Herrera
Keyword(s):  
Dendritic Cells ◽  
Light Chain ◽  
Tubulointerstitial Nephritis ◽  
Light Chains ◽  
Tubular Injury ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Interstitial Inflammation ◽  
Biopsy Specimens ◽  
Proximal Tubular

Context.— Light chain–associated acute tubulointerstitial nephritis (LC-ATIN) is a variant of light chain proximal tubulopathy (LCPT). It is characterized by interstitial inflammation with tubulitis and deposition of monoclonal light chains in the tubulointerstitium. LC-ATIN is a rather poorly recognized pattern of LCPT and not much is known about this entity. Objective.— To determine the clinicopathologic features of patients with LC-ATIN and investigate the proximal tubular injury and mechanism of interstitial inflammation in LC-ATIN. Design.— A total of 38 cases of LC-ATIN were identified from the archives of 5043 renal biopsy specimens. In all cases, routine light microscopic examination, immunofluorescence, and electron microscopic examination were performed. In selected cases, immunofluorescent staining of dendritic cells and immunohistochemical staining for 4 tubular injury markers—KIM-1, p53, bcl-2, and Ki-67—were performed. Results.— A characteristic finding in LC-ATIN cases was immunofluorescence staining of monoclonal light chains along tubular basement membranes in linear fashion and inside proximal tubular cells with a granular pattern. No monoclonal light chains were present in glomerular or vascular compartments confirmed with immunofluorescence, electron microscopy, and ultrastructural gold labeling. Ten of 15 LC-ATIN cases (67%) were concurrently positive for the 4 tubular injury markers. Dendritic cells were identified within the tubulointerstitium in the renal biopsy specimens, interacting with surrounding tubules with light-chain deposits and inflammatory cells. Conclusions.— Significant proximal tubular injury occurs associated with LC-ATIN, and the monoclonal light chains accumulated in proximal tubular cells contribute to the injury. Dendritic cells are involved in the pathogenesis of interstitial inflammation in LC-ATIN.

scholarly journals Hyponatremia with Persistent Elevated Urinary Fractional Uric Acid Excretion: Evidence for Proximal Tubular Injury?

2016 ◽  
Vol 41 (5) ◽  
pp. 535-544 ◽  
Author(s):  
S.-M.Kurt Lee ◽  
Miguel A. Lanaspa ◽  
Laura G. Sánchez-Lozada ◽  
Richard J. Johnson
Keyword(s):  
Uric Acid ◽  
Acid Excretion ◽  
Tubular Injury ◽  
Uric Acid Excretion ◽  
Proximal Tubular

Identification of urinary miRNA biomarkers for detecting cisplatin-induced proximal tubular injury in rats

Toxicology ◽  
2014 ◽  
Vol 324 ◽  
pp. 158-168 ◽  
Author(s):  
Masayuki Kanki ◽  
Akira Moriguchi ◽  
Daisuke Sasaki ◽  
Hikaru Mitori ◽  
Atsushi Yamada ◽  
...  
Keyword(s):  
Tubular Injury ◽  
Proximal Tubular

scholarly journals Evaluation of Novel Biomarkers of Nephrotoxicity in Two Strains of Rat Treated with Cisplatin

2010 ◽  
Vol 38 (6) ◽  
pp. 943-956 ◽  
Author(s):  
Jean-Charles Gautier ◽  
Björn Riefke ◽  
Jakob Walter ◽  
Petra Kurth ◽  
Lou Mylecraine ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Collecting Duct ◽  
Kidney Injury ◽  
Renal Proximal Tubule ◽  
Tubular Injury ◽  
Sprague Dawley ◽  
Glutathione S Transferase ◽  
Proximal Tubular ◽  
Novel Biomarkers ◽  
Noninvasive Biomarkers

Cisplatin is an anticancer agent that induces renal proximal tubule lesions in many species. Studies were conducted in Sprague-Dawley and Han-Wistar rats to evaluate the utility of novel preclinical biomarkers of nephrotoxicity for renal lesions caused by this compound. Groups of 10 males of each strain were given a single intraperitoneal injection of 0.3, 1, or 3 mg/kg cisplatin and were sacrificed on days 2, 3, and 5. The novel biomarkers α-glutathione-S-transferase (α-GST) (for proximal tubular injury), μ-glutathione-S-transferase (μ-GST) (for distal tubular injury), clusterin (for general kidney injury), and renal papillary antigen-1 (RPA-1) (for collecting duct injury) were measured in urine by enzyme immunoassay. Histologically, degeneration and necrosis of the S3 segment of the renal proximal tubule were observed on day 2 (Han-Wistar) and days 3 and 5 (both strains) at 1 and 3 mg/kg. Results showed that in both strains of rats, urinary α-GST and clusterin can be detected in urine soon after injury, are more sensitive than BUN and serum creatinine, and therefore are usable as noninvasive biomarkers of proximal tubule injury. Changes in both μ-GST or RPA-1 were considered to represent secondary minor effects of proximal tubular injury on distal segments of the nephron.

scholarly journals The role of cysteine proteases in hypoxia-induced rat renal proximal tubular injury.

1995 ◽  
Vol 92 (17) ◽  
pp. 7662-7666 ◽  
Author(s):  
C. L. Edelstein ◽  
E. D. Wieder ◽  
M. M. Yaqoob ◽  
P. E. Gengaro ◽  
T. J. Burke ◽  
...  
Keyword(s):  
Cysteine Proteases ◽  
Tubular Injury ◽  
Proximal Tubular ◽  
Renal Proximal Tubular
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