scholarly journals Podocyte Injury and Albuminuria in Experimental Hyperuricemic Model Rats

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Shinichiro Asakawa ◽  
Shigeru Shibata ◽  
Chikayuki Morimoto ◽  
Takeshi Shiraishi ◽  
Takashi Nakamura ◽  
...  
Keyword(s):  
Uric Acid ◽  
Vascular Remodeling ◽  
Antioxidant Properties ◽  
Kidney Injury ◽  
Wall Thickening ◽  
Vascular Changes ◽  
Podocyte Injury ◽  
Transmission Electron ◽  
Afferent Arterioles ◽  
Oxonic Acid

Although hyperuricemia is shown to accelerate chronic kidney disease, the mechanisms remain unclear. Accumulating studies also indicate that uric acid has both pro- and antioxidant properties. We postulated that hyperuricemia impairs the function of glomerular podocytes, resulting in albuminuria. Hyperuricemic model was induced by oral administration of 2% oxonic acid, a uricase inhibitor. Oxonic acid caused a twofold increase in serum uric acid levels at 8 weeks when compared to control animals. Hyperuricemia in this model was associated with the increase in blood pressure and the wall-thickening of afferent arterioles as well as arcuate arteries. Notably, hyperuricemic rats showed significant albuminuria, and the podocyte injury marker, desmin, was upregulated in the glomeruli. Conversely, podocin, the key component of podocyte slit diaphragm, was downregulated. Structural analysis using transmission electron microscopy confirmed podocyte injury in this model. We found that urinary 8-hydroxy-2′-deoxyguanosine levels were significantly increased and correlated with albuminuria and podocytopathy. Interestingly, although the superoxide dismutase mimetic, tempol, ameliorated the vascular changes and the hypertension, it failed to reduce albuminuria, suggesting that vascular remodeling and podocyte injury in this model are mediated through different mechanisms. In conclusion, vasculopathy and podocytopathy may distinctly contribute to the kidney injury in a hyperuricemic state.

scholarly journals The Protective Effect of Shen Qi Wan on Adenine-Induced Podocyte Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Yiyou Lin ◽  
Jieying Zhang ◽  
Yunbo Fu ◽  
Liting Ji ◽  
Luning Lin ◽  
...  
Keyword(s):  
Metabolic Disorders ◽  
Kidney Injury ◽  
Glomerular Filtration Barrier ◽  
Podocyte Injury ◽  
Nitrogen Levels ◽  
Filtration Barrier ◽  
Transmission Electron ◽  
High Level ◽  
Food Processes

Podocytes are a special type of differentiated epithelial cells that maintain the glomerular filtration barrier in the kidney. Injury or damages in podocytes can cause kidney-related disorders, like CKD. The injury or dysfunction of podocytes can occur by different metabolic disorders. Due to the severity and complexity of podocyte injuries, this state is considered as a serious health issue worldwide. Here, we examined and addressed the efficacy of an alternative Chinese medicine, Shen Qi Wan (SQW), on podocyte-related kidney injury. We evaluated the role and mechanism of action of SQW in podocyte injury. We observed that SQW significantly reduced 24-hour urinary protein and blood urea nitrogen levels and alleviated the pathological damage caused by adenine. Moreover, SQW significantly decreased the expression of nephrin and increased the expression of WT1 and AQP1 in the kidney of mice treated with adenine. We observed that SQW did not effectively reduce the high level of proteinuria in AQP1−/− mice indicating the prominent role of AQP1 in the SQW-ameliorating pathway. Transmission electron microscopy (TEM) images indicated the food processes effacement in AQP1−/− mice were not lessened by SQW. In conclusion, podocyte injury could alter the pathological nature of the kidney, and SQW administration relieves the nature of pathogenesis by activating AQP1.

An electron microscopic study of the intra-myocardial lesions in cases of acute myocardial infarction

1978 ◽  
Vol 36 (2) ◽  
pp. 484-485
Author(s):  
Masahiro Ono ◽  
Kaoru Aihara ◽  
Gompachi Yajima
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Coronary Vessels ◽  
Vascular Wall ◽  
Vascular Changes ◽  
Electron Microscopic ◽  
Main Trunk ◽  
Mechanical Destruction ◽  
Transmission Electron ◽  
Myocardial Lesions

The pathogenesis of the arteriosclerosis in the acute myocardial infarction is the matter of the extensive survey with the transmission electron microscopy in experimental and clinical materials. In the previous communication,the authors have clarified that the two types of the coronary vascular changes could exist. The first category is the case in which we had failed to observe no occlusive changes of the coronary vessels which eventually form the myocardial infarction. The next category is the case in which occlusive -thrombotic changes are observed in which the myocardial infarction will be taken placed as the final event. The authors incline to designate the former category as the non-occlusive-non thrombotic lesions. The most important findings in both cases are the “mechanical destruction of the vascular wall and imbibition of the serous component” which are most frequently observed at the proximal portion of the coronary main trunk.

scholarly journals CD73 Overexpression in Podocytes: A Novel Marker of Podocyte Injury in Human Kidney Disease

2021 ◽  
Vol 22 (14) ◽  
pp. 7642
Author(s):  
Zoran V. Popovic ◽  
Felix Bestvater ◽  
Damir Krunic ◽  
Bernhard K. Krämer ◽  
Raoul Bergner ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Kidney Diseases ◽  
Kidney Injury ◽  
Membranous Glomerulonephritis ◽  
Human Kidney ◽  
Protective Role ◽  
Control Group ◽  
Podocyte Injury ◽  
Ccr2 Expression ◽  
Cd73 Expression

The CD73 pathway is an important anti-inflammatory mechanism in various disease settings. Observations in mouse models suggested that CD73 might have a protective role in kidney damage; however, no direct evidence of its role in human kidney disease has been described to date. Here, we hypothesized that podocyte injury in human kidney diseases alters CD73 expression that may facilitate the diagnosis of podocytopathies. We assessed the expression of CD73 and one of its functionally important targets, the C-C chemokine receptor type 2 (CCR2), in podocytes from kidney biopsies of 39 patients with podocytopathy (including focal segmental glomerulosclerosis (FSGS), minimal change disease (MCD), membranous glomerulonephritis (MGN) and amyloidosis) and a control group. Podocyte CD73 expression in each of the disease groups was significantly increased in comparison to controls (p < 0.001–p < 0.0001). Moreover, there was a marked negative correlation between CD73 and CCR2 expression, as confirmed by immunohistochemistry and immunofluorescence (Pearson r = −0.5068, p = 0.0031; Pearson r = −0.4705, p = 0.0313, respectively), thus suggesting a protective role of CD73 in kidney injury. Finally, we identify CD73 as a novel potential diagnostic marker of human podocytopathies, particularly of MCD that has been notorious for the lack of pathological features recognizable by light microscopy and immunohistochemistry.

Study on Nano- and Microcrystallites in Urines of Uric Acid Stone Patients

2013 ◽  
Vol 655-657 ◽  
pp. 1927-1930 ◽  
Author(s):  
Guang Na Zhang ◽  
Zhi Yue Xia ◽  
Jian Ming Ouyang ◽  
Li Kuan
Keyword(s):  
Electron Microscopy ◽  
Uric Acid ◽  
X Ray Diffraction ◽  
Uric Acid Stone ◽  
Urine Ph ◽  
Stone Formers ◽  
Transmission Electron ◽  
Close Relationship ◽  
Ft Ir ◽  
Ft Ir Spectroscopy

The presence of crystallites in urine is closely related to stones formation. In this article, the components, morphology of nano- and micro-crystallites in urines of 20 uric acid (UA) stone formers as well as their relationship with the formation of UAstones were comparatively studied using X-ray diffraction (XRD), Fourier transform infrared (FT-IR) spectroscopy, scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The main constituent of urinary crystallites was uric acid. Their particle size distribution was highly uneven, ranging from several nanometers to several tens of micrometers, and obvious aggregation was observed. These results showed that there was close relationship among stone components, urinary crystallites composition and urine pH.

scholarly journals Hyperuricemia: An Early Marker for Severity of Illness in Sepsis

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Sana R. Akbar ◽  
Dustin M. Long ◽  
Kashif Hussain ◽  
Ahmad Alhajhusain ◽  
Umair S. Ahmed ◽  
...  
Keyword(s):  
Uric Acid ◽  
Poor Prognosis ◽  
Multiorgan Failure ◽  
Kidney Injury ◽  
Severity Of Illness ◽  
Acid Value ◽  
Morbidity Rate ◽  
End Point ◽  
Increased Risk ◽  
Medical Intensive Care

Background.Uric acid can acutely activate various inflammatory transcription factors. Since high levels of oxyradicals and lower antioxidant levels in septic patients are believed to result in multiorgan failure, uric acid levels could be used as a marker of oxidative stress and poor prognosis in patients with sepsis.Design.We conducted a prospective cohort study on Medical Intensive Care Unit (MICU) patients and hypothesized that elevated uric acid in patients with sepsis is predictive of greater morbidity. The primary end point was the correlation between hyperuricemia and the morbidity rate. Secondary end points were Acute Kidney Injury (AKI), mortality, Acute Respiratory Distress Syndrome (ARDS), and duration of stay.Results.We enrolled 144 patients. 54 (37.5%) had the primary end point of hyperuricemia. The overall morbidity rate was 85.2%. The probability of having hyperuricemia along with AKI was 68.5% and without AKI was 31.5%. Meanwhile the probability of having a uric acid value <7 mg/dL along with AKI was 18.9% and without AKI was 81.1% (pvalue < 0.0001).Conclusion.We report that elevated uric acid levels on arrival to the MICU in patients with sepsis are associated with poor prognosis. These patients are at an increased risk for AKI and ARDS.

scholarly journals Calcitriol Treatment Attenuates Uric Acid-Induced Kidney Injury via Super Oxide Dismutase-1 (SOD-1) Upregulation and Fibrosis Reduction

2021 ◽  
Vol 25 (6) ◽  
pp. 417-425
Author(s):  
Muhammad Mansyur Romi ◽  
Nur Arfian ◽  
Wiwit Ananda Wahyu Setyaningsih ◽  
Rachma Greta Perdana Putri ◽  
Mohammad Juffrie ◽  
...  
Keyword(s):  
Uric Acid ◽  
Kidney Injury ◽  
Super Oxide Dismutase

scholarly journals Preoperative hemoglobin and uric acid levels as risk factors for acute kidney injury in cardiac surgery patients

2020 ◽  
Vol 73 (1-2) ◽  
pp. 5-12
Author(s):  
Miodrag Golubovic ◽  
Andrej Preveden ◽  
Ranko Zdravkovic ◽  
Jelena Vidovic ◽  
Bojan Mihajlovic ◽  
...  
Keyword(s):  
Risk Factors ◽  
Acute Kidney Injury ◽  
Uric Acid ◽  
Cardiac Surgery ◽  
Kidney Injury ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Preoperative Hemoglobin ◽  
Significant Difference ◽  
Acute Kidney Injury Development

Introduction. Acute kidney injury associated with cardiac surgery is a common and significant postoperative complication. With a frequency of 9 - 39% according to different studies, it is the second most common cause of acute kidney injury in intensive care units, and an independent predictor of mortality. This study aimed to investigate the importance of preoperative hemoglobin and uric acid levels as risk factors for acute kidney injury in the postoperative period in cardiac surgery patients. Material and Methods. The study included a total of 118 patients who were divided into two groups. Each group included 59 patients; the fist group included patients who developed acute kidney injury and required renal replacement therapy, and the second included patients without acute kidney injury. Types of cardiac surgery included coronary, valvular, combined, aortic dissection, and others. All necessary data were collected from patient medical records and the electronic database. Results. A statistically significant difference was found between the groups in preoperative hemoglobin levels (108.0 vs. 143.0 g/l, p = 0.0005); postoperative urea (26.4 vs. 5.8 mmol/l, p = 0.0005) and creatinine (371.0 vs. 95.0 ?mol/l, p = 0.0005), acute phase inflammatory reactants C-reactive protein (119.4 vs. 78.9 mg/l, p = 0.002) and procalcitonin (7.0 vs. 0.2 ng/ml, p = 0.0005), creatine kinase myocardial band isoenzyme (1045.0 vs. 647.0 mg/l, p = 0.014); duration of extracorporeal circulation (103.5 vs. 76.0 min, p = 0.0005) and ascending aortic clamp during cardiac surgery (89.0 vs. 67.0 min, p = 0.0005). The exception was the preoperative uric acid level, where there was no statistically significant difference (382.0 vs. 364.0 ?mol/l, p = 0.068). There was a statistically significant correlation between the use of inotropic agents and acute kidney injury development. Conclusion. There is a correlation between the preoperative low hemoglobin levels and postoperative acute kidney injury. There is no statistically significant correlation between the preoperative levels of uric acid and postoperative acute kidney injury.

scholarly journals Role of oxidative stress in the renal abnormalities induced by experimental hyperuricemia

2008 ◽  
Vol 295 (4) ◽  
pp. F1134-F1141 ◽  
Author(s):  
Laura G. Sánchez-Lozada ◽  
Virgilia Soto ◽  
Edilia Tapia ◽  
Carmen Avila-Casado ◽  
Yuri Y. Sautin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Uric Acid ◽  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Systemic Hypertension ◽  
Sprague Dawley ◽  
Renal Vasoconstriction ◽  
Renal Abnormalities ◽  
Oxonic Acid

Endothelial dysfunction is a characteristic feature during the renal damage induced by mild hyperuricemia. The mechanism by which uric acid reduces the bioavailability of intrarenal nitric oxide is not known. We tested the hypothesis that oxidative stress might contribute to the endothelial dysfunction and glomerular hemodynamic changes that occur with hyperuricemia. Hyperuricemia was induced in Sprague-Dawley rats by administration of the uricase inhibitor, oxonic acid (750 mg/kg per day). The superoxide scavenger, tempol (15 mg/kg per day), or placebo was administered simultaneously with the oxonic acid. All groups were evaluated throughout a 5-wk period. Kidneys were fixed by perfusion and afferent arteriole morphology, and tubulointerstitial 3-nitrotyrosine, 4-hydroxynonenal, NOX-4 subunit of renal NADPH-oxidase, and angiotensin II were quantified. Hyperuricemia induced intrarenal oxidative stress, increased expression of NOX-4 and angiotensin II, and decreased nitric oxide bioavailability, systemic hypertension, renal vasoconstriction, and afferent arteriolopathy. Tempol treatment reversed the systemic and renal alterations induced by hyperuricemia despite equivalent hyperuricemia. Moreover, because tempol prevented the development of preglomerular damage and decreased blood pressure, glomerular pressure was maintained at normal values as well. Mild hyperuricemia induced by uricase inhibition causes intrarenal oxidative stress, which contributes to the development of the systemic hypertension and the renal abnormalities induced by increased uric acid. Scavenging of the superoxide anion in this setting attenuates the adverse effects induced by hyperuricemia.

Activation of the Nitric Oxide Pathway and Acute Myocardial Infarction Complicated by Acute Kidney Injury

2020 ◽  
Vol 10 (2) ◽  
pp. 85-96 ◽  
Author(s):  
Jiri Parenica ◽  
Petr Kala ◽  
Alexandre Mebazaa ◽  
Simona Littnerova ◽  
Klara Benesova ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Infarction ◽  
Acute Kidney Injury ◽  
Uric Acid ◽  
Predictive Value ◽  
Kidney Injury ◽  
Cardiac Biomarkers ◽  
Receiver Operating Curve ◽  
Circulating Biomarkers ◽  
Clinical Model

Background/Aims: The pathophysiology of acute kidney injury (AKI) in ST-elevation myocardial infarction (STEMI) patients remains poorly explored. The involvement of the nitric oxide (NO) pathway has been demonstrated in experimental ischemic AKI. The aim of this study was to assess the predictive value of circulating biomarkers of the NO pathway for AKI in STEMI patients. Methods: Four hundred and twenty-seven STEMI patients treated with primary percutaneous coronary intervention were included. The primary end point was AKI. Biomarkers of the NO pathway (plasma superoxide dismutase [SOD], uric acid, nitrite/nitrate [NOx], neopterin) as well as cardiac biomarkers (B-type natriuretic peptide [BNP] and troponin) were sampled 12 h after admission. The predictive value of circulating biomarkers was evaluated in addition to the multivariate clinical model. Results: AKI developed in 8.9% of patients. The 3-month mortality was significantly higher in patients with AKI (34.2 vs. 4.1%; p < 0.001). SOD, uric acid, NOx, neopterin, BNP and troponin were significantly associated with the development of AKI (area under curve [AUC]-receiver operating curve [ROC] ranging between 0.70 and 0.81). In multivariate analysis cardiogenic shock, neopterin, NOx and troponin were independent predictors of AKI. AUC-ROC of the association of multibiomarkers and clinical model was 0.90 and outperformed the predictive value of the clinical model alone. OR of NOx ≥45 µmol/L was 8.0 (95% CI 3.1–20.6) for AKI. Conclusion: Biomarkers of the NO pathway are associated with the development of AKI in STEMI patients. These results provide insights into the pathophysiology of AKI and may serve at developing preventing strategies for AKI targeting this pathway.

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