scholarly journals Editorial: Hypertension and Chronic Kidney Injury or Failure, Volume II

2022 ◽  
Vol 12 ◽  
Author(s):  
Zhengrong Guan ◽  
Suttira Intapad ◽  
Oleg Palygin ◽  
Jennifer C. Sullivan
Keyword(s):  
Kidney Injury ◽  
Chronic Kidney Injury

scholarly journals The Macrophage Phagocytic Receptor CD36 Promotes Fibrogenic Pathways on Removal of Apoptotic Cells during Chronic Kidney Injury

2015 ◽  
Vol 185 (8) ◽  
pp. 2232-2245 ◽  
Author(s):  
Subramaniam Pennathur ◽  
Katie Pasichnyk ◽  
Nadia M. Bahrami ◽  
Lixia Zeng ◽  
Maria Febbraio ◽  
...  
Keyword(s):  
Kidney Injury ◽  
Apoptotic Cells ◽  
Chronic Kidney Injury

Metastatische pulmonale calcificaties als zeldzame oorzaak van matglasopaciteiten op een CT-scan

2021 ◽  
Author(s):  
I. CARPENTIER ◽  
E. PEETERS ◽  
B. VANZIELEGHEM
Keyword(s):  
Correct Diagnosis ◽  
Kidney Injury ◽  
Lung Damage ◽  
Ground Glass ◽  
Literature Overview ◽  
Chronic Kidney Injury ◽  
Patient’S History ◽  
Pulmonary Calcifications ◽  
Metastatic Pulmonary Calcification

Metastatic pulmonary calcification: a case report and literature overview Ground-glass opacities have a broad differential diagnosis, including infectious, metabolic, inflammatory and malignant causes. This case presents an underdiagnosed entity of dense ground-glass opacities, namely metastatic pulmonary calcifications (MPC). This is a benign metabolic disease characterised by the deposition of calcium in the lungs, mostly described in patients with chronic kidney injury and secondary hyperparathyroidism. The majority of the patients require no treatment, but in some cases it may lead to irreversible lung damage. Clinical and radiological features, as well as the patient’s history, are crucial to make a correct diagnosis since MPC has a relatively specific appearance on imaging. This case study discusses the medical history and imaging appearance of a 44-year-old woman with MPC, followed by a literature overview.

scholarly journals Urinary angiotensinogen as a biomarker for acute to chronic kidney injury transition – prognostic and mechanistic implications

2018 ◽  
Vol 132 (21) ◽  
pp. 2383-2385 ◽  
Author(s):  
Katie L. Connor ◽  
Laura Denby
Keyword(s):  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Ischaemia Reperfusion Injury ◽  
Angiotensin System ◽  
Urinary Angiotensinogen ◽  
Tubular Necrosis ◽  
Ischaemia Reperfusion ◽  
Structural Recovery ◽  
Chronic Kidney Injury ◽  
Injury Model

Accurate biomarkers that both predict the progression to, and detect the early stages of chronic kidney disease (CKD) are lacking, resulting in difficulty in identifying individuals who could potentially benefit from targeted intervention. In a recent issue [Clinical Science (2018) 132, 2121–2133], Cui et al. examine the ability of urinary angiotensinogen (uAGT) to predict the progression of acute kidney injury (AKI) to CKD. They principally employ a murine ischaemia reperfusion injury model to study this and provide data from a small prospective study of patients with biopsy proven acute tubular necrosis. The authors suggest that uAGT is a dynamic marker of renal injury that could be used to predict the likelihood of structural recovery following AKI. Here we comment on their findings, exploring the clinical utility of uAGT as a biomarker to predict AKI to CKD transition and perhaps more controversially, to discuss whether the early renin–angiotensin system blockade following AKI represents a therapeutic target.

Activation of hypoxia-sensing pathways promotes renal ischemic preconditioning following myocardial infarction

2021 ◽  
Author(s):  
Andrew S Terker ◽  
Kensuke Sasaki ◽  
Juan Pablo Arroyo ◽  
Aolei Niu ◽  
Suwan Wang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ischemic Preconditioning ◽  
Renal Injury ◽  
Cardiac Injury ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Experimental Myocardial Infarction ◽  
Common Mechanism ◽  
Cardiac Damage ◽  
Chronic Kidney Injury

Ischemic heart disease is the leading cause of death worldwide and is frequently comorbid with chronic kidney disease. Physiological communication is known to occur between the heart and the kidney and primary dysfunction in either organ can induce dysfunction in the other, a clinical entity known as cardiorenal syndrome, but mechanistic details are lacking. Here, we used a model of experimental myocardial infarction (MI) to test effects of chronic cardiac ischemia on acute and chronic kidney injury. Surprisingly, chronic cardiac damage protected animals from subsequent acute ischemic renal injury, an effect that was accompanied by evidence of chronic kidney hypoxia. The protection observed post-MI was similar to protection observed in a separate group of healthy animals housed in ambient hypoxic conditions prior to kidney injury, suggesting a common mechanism. There was evidence that chronic cardiac injury activates renal hypoxia-sensing pathways. Increased renal abundance of several glycolytic enzymes following MI suggested a shift towards anaerobic glycolysis may confer renal ischemic preconditioning. In contrast, effects on chronic renal injury followed a different pattern with post-MI animals displaying worsened chronic renal injury and fibrosis. These data show that while chronic cardiac injury following MI protected against acute kidney injury via activation of hypoxia-sensing pathways, it worsened chronic kidney injury. The results further our understanding of cardiorenal signaling mechanisms and have implications for the treatment of heart failure patients with associated renal disease.

Abstract 188: Loss of Renal Prolyl Carboxypeptidase in Mice With Chronic Kidney Disease

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Orly Leiva ◽  
Khalid M Elased ◽  
Mariana Morris ◽  
Nadja Grobe
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Protein Expression ◽  
Western Blot ◽  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Left Renal Artery ◽  
Renal Tubules ◽  
Ang Ii ◽  
Chronic Kidney Injury

There are 26 million adults with chronic kidney disease (CKD) in the U.S. and the incidence continues to increase. It is well documented that the activation of the renin angiotensin system and the elevated formation of angiotensin (Ang) II both contribute to renal pathophysiology in CKD. Emerging evidence suggests that the Ang II degrading protease prolyl carboxypeptidase (PCP) is renoprotective. Thus, we investigated protein expression and activity of renal PCP using immunofluorescence, western blot and mass spectrometry in a mouse model of CKD. Renal injury in male C57Bl6 mice was caused by constriction of the left renal artery using silver clips (2K1C-method). Blood pressure measurements by radiotelemetry revealed a significant increase of 36.1 ± 3.9 mm Hg in 2K1C animals compared with control animals 1 week after clip placement (p<0.0001). Using immunofluorescence and confocal microscopy, PCP was localized in the Bowman’s capsule of the glomerulus and in proximal and distal renal tubules. Western blot analysis showed PCP was significantly reduced in clipped 2K1C kidneys compared to unclipped kidneys of the 2K1C mice or compared to control mice (clipped 0.04 ± 0.02 vs unclipped 0.58 ± 0.16 vs control 0.65 ± 0.18, p < 0.05). In addition, renal PCP enzyme activity was found to be markedly reduced in 2K1C kidneys as assessed by mass spectrometric based enzyme assays (clipped 37.1 ± 4.3 pmol Ang-(1-7)/h/μg vs unclipped 77.3 ± 12.3 pmol Ang-(1-7)/h/μg vs control 120.7 ± 14.7 pmol Ang-(1-7)/h/μg, p < 0.01). In contrast, protein expression of prolyl endopeptidase, another enzyme capable of converting Ang II into Ang-(1-7), was not affected. Notably, renal pathologies were exacerbated in the 2K1C model as revealed by a significant increase in mesangial expansion (clipped 34.6 ± 3.1 vs unclipped 52.1 ± 4.0 vs control 1.2 ± 2.1, p < 0.0001) and renal fibrosis (clipped 57.5 ± 0.9 vs unclipped 33.0 ± 0.7 vs control 3.3 ± 0.2, p < 0.0001). Results suggest that PCP is suppressed in chronic kidney injury and that this downregulation may attenuate renoprotective effects via impaired Ang II degradation by PCP. Therefore, Ang II processing by PCP may have clinical implications in patients with renal pathologies.

FP257GROWTH/DIFFERENTIATION FACTOR 15 DEFICIENCY AGGRAVATES ACUTE AND CHRONIC KIDNEY INJURY CAUSED BY ISCHEMIA/REPERFUSION

2019 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Moritz Krill ◽  
Vivian Würf ◽  
Mohsen Honarpisheh ◽  
Andrea Ribeiro ◽  
Lech Maciej
Keyword(s):  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Differentiation Factor ◽  
Chronic Kidney Injury

scholarly journals MP097L-ARGININE SUPPLEMENTATION IMPROVES CHRONIC KIDNEY INJURY IN EXPERIMENTAL ARISTOLOCHIC ACID NEPHROPATHY

2016 ◽  
Vol 31 (suppl_1) ◽  
pp. i374-i374
Author(s):  
Inès Jadot ◽  
Vanessa Colombaro ◽  
Blanche Martin ◽  
Isabelle Habsch ◽  
Olivia Botton ◽  
...  
Keyword(s):  
Aristolochic Acid ◽  
Kidney Injury ◽  
Aristolochic Acid Nephropathy ◽  
Chronic Kidney Injury ◽  
Arginine Supplementation

New Criterion to Evaluate Acute-on-Chronic Kidney Injury Based on the Creatinine Reference Change

2020 ◽  
Vol 51 (6) ◽  
pp. 453-462
Author(s):  
Xin Xu ◽  
Long Wang ◽  
Mengqi Xiong ◽  
Sheng Nie ◽  
Zhangsuo Liu ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Hospital Mortality ◽  
Kidney Injury ◽  
Adverse Outcomes ◽  
Ckd Progression ◽  
Clinical Prognosis ◽  
Reference Change Value ◽  
Chronic Kidney Injury ◽  
Increased Risk ◽  
Ckd Stage

Background: The lack of consensus criteria of acute on chronic kidney injury (ACKI) affects the judgment for its clinical prognosis. Methods: In this study, we analyzed the data from 711,615 hospitalized adults who had at least 2 serum creatinine (SCr) tests within 30 days. We estimated the reference change value (RCV) of SCr given initial SCr level in adults without known risks of acute kidney injury other than chronic kidney disease (CKD). We proposed a criterion for ACKI based on the RCV of SCr (cROCK), which defined ACKI as a ≥25% increase in SCr in 7 days. We validated cROCK by its association with the risks of in-hospital mortality, death after discharge, and CKD progression in a large cohort of patients with CKD stage 3. Results: In 21,661 patients with CKD stage 3, a total of 3,145 (14.5%), 1,512 (7.0%), and 221 (1.0%) ACKI events were detected by both cROCK and Kidney Disease Improving Global Outcomes (KDIGO), cROCK only, and KDIGO only, respectively. cROCK detected 40% more ACKI events than KDIGO. Compared with patients without ACKI by both definitions, those with cROCK- but not KDIGO-defined ACKI had a significantly increased risk of in-hospital mortality (hazard ratio [HR] 5.53; 95% CI 3.75–8.16), death after discharge (HR 1.51; 95% CI 1.21–1.83), and CKD progression (OR 5.65; 95% CI 3.05–10.48). Conclusions: RCV-based criterion (cROCK) for ACKI is clinically valid in that it has a substantially improved sensitivity in identifying patients with high risk of adverse outcomes.

scholarly journals Exosomal CCL2 from Tubular Epithelial Cells Is Critical for Albumin-Induced Tubulointerstitial Inflammation

2018 ◽  
Vol 29 (3) ◽  
pp. 919-935 ◽  
Author(s):  
Lin-Li Lv ◽  
Ye Feng ◽  
Yi Wen ◽  
Wei-Jun Wu ◽  
Hai-Feng Ni ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Cell ◽  
Kidney Injury ◽  
Tubular Epithelial Cells ◽  
Tail Vein Injection ◽  
Chronic Kidney Injury ◽  
Ccl2 Mrna ◽  
Injury Models ◽  
Tubulointerstitial Inflammation

Albuminuria is a key instigator of tubulointerstitial inflammation associated with CKD, but the mechanism through which filtered albumin propagates renal injury remains unclear. In this study, we explored the role in this process of exosome mRNA released from tubular epithelial cells (TECs). Compared with control mice, acute and chronic kidney injury models had more exosomes containing inflammatory cytokine mRNA, particularly the chemokine CCL2, in kidneys and urine. In vitro stimulation of TECs with BSA recapitulated this finding. Notably, the internalization of purified TEC exosomes by cultured macrophages increased if TECs were exposed to BSA. Macrophage internalization of exosomes from BSA-treated TECs led to an enhanced inflammatory response and macrophage migration, but CCL2 silencing in TECs prevented these effects. Using a GFP-CCL2 fusion mRNA construct, we observed direct transfer of CCL2 mRNA from TEC exosomes to macrophages. Mice subjected to tail vein injection of purified BSA-treated TEC exosomes developed tubular injury with renal inflammatory cell infiltration. However, injection of exosomes from BSA-treated CCL2-deficient TECs induced less severe kidney inflammation. Finally, in patients with IgA nephropathy, the increase of proteinuria correlated with augmented urinary excretion of exosomes with exaggerated expression of CCL2 mRNA. Moreover, the level of CCL2 mRNA in urinary exosomes correlated closely with levels of renal interstitial macrophage infiltration in these patients. Our studies demonstrate that the increasing release of exosomes that transfer CCL2 mRNA from TECs to macrophages constitutes a critical mechanism of albumin-induced tubulointerstitial inflammation.

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