scholarly journals Mycotoxic porcine nephropathy and spontaneous occurrence of ochratoxin A residues in kidneys of slaughtered swine

2009 ◽  
pp. 81-90 ◽  
Author(s):  
Dragan Milicevic ◽  
Verica Juric ◽  
Aleksandra Dakovic ◽  
Miljan Jovanovic ◽  
Srdjan Stefanovic ◽  
...  
Keyword(s):  
Ochratoxin A ◽  
Histopathological Examination ◽  
Kidney Injury ◽  
Kidney Tubules ◽  
Cell Vacuolization ◽  
Spontaneous Occurrence ◽  
Slaughtered Pigs

In order to find information on the occurrence of mycotoxic porcine nephropathy in Serbia, during a six month period (2006/2007) samples of kidney from individual healthy slaughtered pigs were collected (n=90) and analyzed by HPLC for ochratoxin A. In addition, histological examinations were carried out. The incidence of OTA in kidney was 33,3% and varied between 0.17-52.5 ng/g. Histopathological examination of kidneys confirmed tubulopathies with oedema and cell vacuolization. In addition, hemorrhages and necrosis of proximal kidney tubules cells were found. These findings indicate that it is likely that most of the kidney injury is related to ochratoxin A and other nephrotoxic compounds which enhance the toxicity of OTA.

Occurrence of ochratoxin A and heavy metals in tissues associated with porcine nephropathy in Serbia

2009 ◽  
Vol 2 (3) ◽  
pp. 347-356
Author(s):  
D. Milićević ◽  
V. Jurić ◽  
S. Stefanović ◽  
M. Jovanović ◽  
Z. Petrović ◽  
...  
Keyword(s):  
Heavy Metals ◽  
Ochratoxin A ◽  
Histopathological Examination ◽  
Kidney Injury ◽  
Kidney Tubules ◽  
Cadmium Lead ◽  
Slaughtered Pigs

In order to find information on the occurrence of mycotoxic porcine nephropathy in Serbia, during a six month period (2006/2007) samples of blood, kidney and liver from individual animals were collected from healthy slaughtered pigs (n=90) and analysed by HPLC for ochratoxin A (OTA). In addition, the presence of nephrotoxic heavy metals such as cadmium, lead, mercury and arsenic were measured and the kidneys pathohistologically examined. Of the 90 liver samples, 26.6% contained OTA in the range of 0.22-14.5 ng/g. The incidence of OTA in serum and kidney were very similar (30 and 31.1%), but varied between 0.24-220.8 ng/ml and 0.17-52.5 ng/g, respectively. The presence of mercury was confirmed in 33.3% of kidney samples and concentrations ranged between 0.005-0.055 mg/kg, while cadmium was found less frequently (27.7% positive samples) but at higher levels (0.05-1.23 mg/kg). The presence of arsenic was found in only one sample, while lead was not detected in any sample. Histopathological examination of kidneys confirmed tubulopathies with oedema and cell vacuolisation. In addition, haemorrhages and necrosis of proximal kidney tubules' cells were found. These findings indicate that it is likely that most of the kidney injury is related to OTA and other nephrotoxic compounds which enhance the toxicity of OTA.

scholarly journals Cytokine signatures of end organ injury in COVID-19

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Luis G. Gómez-Escobar ◽  
Katherine L. Hoffman ◽  
Justin J. Choi ◽  
Alain Borczuk ◽  
Steven Salvatore ◽  
...  
Keyword(s):  
T Cell ◽  
Inflammatory Cytokines ◽  
Histopathological Examination ◽  
Diffuse Alveolar Damage ◽  
Treatment Strategies ◽  
Kidney Injury ◽  
Hospitalized Patients ◽  
Organ Injury ◽  
Glomerular Sclerosis ◽  
Cell Immunity

AbstractIncreasing evidence has shown that Coronavirus disease 19 (COVID-19) severity is driven by a dysregulated immunologic response. We aimed to assess the differences in inflammatory cytokines in COVID-19 patients compared to contemporaneously hospitalized controls and then analyze the relationship between these cytokines and the development of Acute Respiratory Distress Syndrome (ARDS), Acute Kidney Injury (AKI) and mortality. In this cohort study of hospitalized patients, done between March third, 2020 and April first, 2020 at a quaternary referral center in New York City we included adult hospitalized patients with COVID-19 and negative controls. Serum specimens were obtained on the first, second, and third hospital day and cytokines were measured by Luminex. Autopsies of nine cohort patients were examined. We identified 90 COVID-19 patients and 51 controls. Analysis of 48 inflammatory cytokines revealed upregulation of macrophage induced chemokines, T-cell related interleukines and stromal cell producing cytokines in COVID-19 patients compared to the controls. Moreover, distinctive cytokine signatures predicted the development of ARDS, AKI and mortality in COVID-19 patients. Specifically, macrophage-associated cytokines predicted ARDS, T cell immunity related cytokines predicted AKI and mortality was associated with cytokines of activated immune pathways, of which IL-13 was universally correlated with ARDS, AKI and mortality. Histopathological examination of the autopsies showed diffuse alveolar damage with significant mononuclear inflammatory cell infiltration. Additionally, the kidneys demonstrated glomerular sclerosis, tubulointerstitial lymphocyte infiltration and cortical and medullary atrophy. These patterns of cytokine expression offer insight into the pathogenesis of COVID-19 disease, its severity, and subsequent lung and kidney injury suggesting more targeted treatment strategies.

scholarly journals Dexmedetomidine Protects against Ischemia and Reperfusion-Induced Kidney Injury in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Naren Bao ◽  
Di Dai
Keyword(s):  
Renal Function ◽  
Kidney Injury ◽  
Serum Levels ◽  
Protective Role ◽  
Sudden Onset ◽  
Clinical Syndrome ◽  
Ischemia And Reperfusion ◽  
Oxygen Species ◽  
Kidney Tubules ◽  
Tubular Cells

Acute kidney injury (AKI), a clinical syndrome, is a sudden onset of kidney failure that severely affects the kidney tubules. One potential treatment is dexmedetomidine (DEX), a highly selective α2-adrenoreceptor agonist that is used as an anesthetic adjuvant. It also has anti-inflammatory, neuroprotective, and sympatholytic qualities. The aim of this study was to establish whether DEX also offers protection against ischemia and reperfusion- (I/R-) induced AKI in rats. An intraperitoneal injection of DEX (25 μg/kg) was administered 30 min prior to the induction of I/R. The results indicate that in the I/R rats, DEX played a protective role by reducing the damage to the tubules and maintaining renal function. Furthermore, in response to I/R, the DEX treatment reduced the mRNA expression of TNF-α, IL-1β, IL-6, and MCP-1 in the kidney tissues and the serum levels of TNF-α, IL-1β, IL-6, and MCP-1. DEX also reduced the levels of oxidative stress and apoptosis in the tubular cells. These results indicate that in response to I/R kidney injury, DEX plays a protective role by inhibiting inflammation and tubular cell apoptosis, reducing the production of reactive oxygen species, and promoting renal function.

scholarly journals Effects of Chronic Exposure to Microcystin-LR on Kidney in Mice

2019 ◽  
Vol 16 (24) ◽  
pp. 5030 ◽  
Author(s):  
Xiping Yi ◽  
Shuaishuai Xu ◽  
Feiyu Huang ◽  
Cong Wen ◽  
Shuilin Zheng ◽  
...  
Keyword(s):  
Chronic Exposure ◽  
Kidney Injury ◽  
Oral Exposure ◽  
Control Group ◽  
Interstitial Tissue ◽  
Kidney Tubules ◽  
Potential Influence ◽  
First Time ◽  
Histopathological Investigation

Microcystin-LR (MC-LR) is a potent hepatotoxin, but a few studies suggested that it might also induce nephrotoxicity. However, nephrotoxicity induced by prolonged oral exposure to MC-LR is unknown. The aim of this study was to evaluate the potential influence of MC-LR on the kidney in mice following chronic exposure to MC-LR. In this study, we evaluated the nephrotoxicity of MC-LR in mice drinking water at different concentrations (1, 30, 60, 90, and 120 μg/L) for 6 months for the first time. The results showed that the kidney weights and the kidney indexes of mice were not altered in the MC-LR treated mice, compared with the control group. In addition, the renal function indicators revealed that the serum creatinine (SCr) levels were not significant changes after exposure to MC-LR. The blood urea nitrogen (BUN) levels were markedly decreased after exposure to 90 and 120 μg/L MC-LR for 3 months. The BUN levels were lower than that of the control group after exposure to 120 μg/L MC-LR for 6 months. The histopathological investigation revealed enlarged renal corpuscles, widened of kidney tubules, and lymphocyte infiltration in the interstitial tissue and the renal pelvis after exposure to 60, 90, and 120 μg/L MC-LR. Consequently, our results suggested that long-term exposure to MC-LR might be one important risk of kidney injury, which will provide important clues for the prevention of renal impairment.

scholarly journals Survey of Slaughtered Pigs for Occurrence of Ochratoxin A and Porcine Nephropathy in Serbia

2008 ◽  
Vol 9 (11) ◽  
pp. 2169-2183 ◽  
Author(s):  
Dragan Milićević ◽  
Verica Jurić ◽  
Srđan Stefanović ◽  
Milijan Jovanović ◽  
Saša Janković
Keyword(s):  
Ochratoxin A ◽  
Slaughtered Pigs

MK-886 attenuates kidney injury induced after trauma/shock by preventing flap and 5-lo interactions in kidney tubules

2013 ◽  
Vol 217 (3) ◽  
pp. S29
Author(s):  
John R. Stringham ◽  
Ernest E. Moore ◽  
Fabia Gamboni ◽  
Miguel Fragoso ◽  
Theresa L. Chin ◽  
...  
Keyword(s):  
Kidney Injury ◽  
Kidney Tubules

scholarly journals Villin and actin in the mouse kidney brush-border membrane bind to and are degraded by meprins, an interaction that contributes to injury in ischemia-reperfusion

2011 ◽  
Vol 301 (4) ◽  
pp. F871-F882 ◽  
Author(s):  
Elimelda Moige Ongeri ◽  
Odinaka Anyanwu ◽  
W. Brian Reeves ◽  
Judith S. Bond
Keyword(s):  
Brush Border ◽  
Knockout Mice ◽  
Brush Border Membrane ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Mouse Kidney ◽  
Cytoskeletal Proteins ◽  
Kidney Tubules ◽  
Wild Type

Meprins, metalloproteinases abundantly expressed in the brush-border membranes (BBMs) of rodent proximal kidney tubules, have been implicated in the pathology of renal injury induced by ischemia-reperfusion (IR). Disruption of the meprin β gene and actinonin, a meprin inhibitor, both decrease kidney injury resulting from IR. To date, the in vivo kidney substrates for meprins are unknown. The studies herein implicate villin and actin as meprin substrates. Villin and actin bind to the cytoplasmic tail of meprin β, and both meprin A and B are capable of degrading villin and actin present in kidney proteins as well as purified recombinant forms of these proteins. The products resulting from degradation of villin and actin were unique to each meprin isoform. The meprin B cleavage site in villin was Glu744-Val745. Recombinant forms of rat meprin B and homomeric mouse meprin A had Km values for villin and actin of ∼1 μM (0.6–1.2 μM). The kcat values varied substantially (0.6–128 s−1), resulting in different efficiencies for cleavage, with meprin B having the highest kcat/ Km values (128 M−1·s−1 × 106). Following IR, meprins and villin redistributed from the BBM to the cytosol. A 37-kDa actin fragment was detected in protein fractions from wild-type, but not in comparable preparations from meprin knockout mice. The levels of the 37-kDa actin fragment were significantly higher in kidneys subjected to IR. The data establish that meprins interact with and cleave villin and actin, and these cytoskeletal proteins are substrates for meprins.

Spontaneous occurrence of ochratoxin A residues in porcine kidneys in Belgium

1989 ◽  
Vol 42 (2) ◽  
pp. 181-186 ◽  
Author(s):  
Dominique M. Rousseau ◽  
Carlos H. Van Peteghem
Keyword(s):  
Ochratoxin A ◽  
Spontaneous Occurrence

Ameliorative, Antioxidant and Immunomodulatory Potential of Vitamin D on Aminoglycoside Induced Acute Kidney Injury in Wistar Rats

2021 ◽  
Author(s):  
Neeraj Thakur ◽  
S.K. Shukla ◽  
A.H. Ahmad ◽  
N.S. Jadon ◽  
J.L. Singh ◽  
...  
Keyword(s):  
Vitamin D ◽  
Acute Kidney Injury ◽  
Histopathological Examination ◽  
Kidney Injury ◽  
Serum Biochemistry ◽  
Mean Value ◽  
Tnf Α ◽  
The Mean ◽  
Group B ◽  
Immunomodulatory Potential

Background: Acute kidney injury causes an abrupt decline in renal filtration and affects animals in a similar way to humans. Diagnosis can be made based on urinalysis, serum biochemistry and various biomarkers. The present study was conducted to evaluate the ameliorative, antioxidant and immunomodulatory potential of vitamin D in rats induced with acute kidney injury. Methods: In the present study, group A rats were taken as healthy control, group B rats were given gentamicin @ 100 mg/kg BW intraperitoneally for 8 days and were considered as disease control and group C rats were treated with Vitamin D @ 0.4 µg/kg/day subcutaneously for 8 days along with intraperitoneal gentamicin injection. Reduced glutathione (GSH), lipid peroxide (LPO), catalase and superoxide dismutase (SOD) were estimated in erythrocytes on day 0, 4 and 8. Tumor necrosis factor alpha (TNF α) and interleukin 10 (IL 10) were also estimated along with urine and serum biochemistry on day 0, 4 and 8. Kidney tissue samples were collected on day 8 for histopathological examination. Result: The mean values of GSH, catalase and SOD were significantly (P less than 0.05) higher whereas the mean value of LPO was significantly (P less than 0.05) lower in group C compared to group B on day 4 and 8. On day 4 and 8, the mean value of TNF α was significantly (P less than 0.05) lower, while the mean value of IL-10 was significantly (P less than 0.05) higher in rats treated with vitamin D as compared to disease control. Histopathological examination along with urine and serum biochemistry revealed protective efficacy of vitamin D in acute kidney injury. Based on the findings of the present study, it is concluded that vitamin D is having ameliorative efficacy along with antioxidant and immunomodulatory potential in case of gentamicin induced acute kidney injury in Wistar rats. However, detailed studies are required to explore the therapeutic potential of vitamin D in clinical cases of kidney diseases.

scholarly journals Pre-Treatment with Curcumin Ameliorates Cisplatin-Induced Kidney Damage by Suppressing Kidney Inflammation and Apoptosis in Rats

Drug Research ◽  
2018 ◽  
Vol 69 (02) ◽  
pp. 75-82 ◽  
Author(s):  
Vivian Soetikno ◽  
Shinta Sari ◽  
Lulu Ul Maknun ◽  
Nielda Sumbung ◽  
Deliana Rahmi ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Molecular Mechanisms ◽  
Histopathological Examination ◽  
Kidney Injury ◽  
Kidney Damage ◽  
Protective Effects ◽  
Protection Effect ◽  
Tnf Α ◽  
Pre Treatment ◽  
Damage Protection

Abstract Objective In addition to oxidative stress, inflammation and apoptosis have an important role in the pathogenesis of cisplatin-induced kidney damage. This study aimed to investigate the molecular mechanisms of protective effects of curcumin against cisplatin-induced kidney inflammation and apoptosis in rats. Materials and Methods Eighteen rats were equally divided into three groups; normal (0.5% CMC-Na), cisplatin (CDPP) (7 mg/kg i.p.), and cisplatin+curcumin (CMN100) groups. Curcumin was given at a dose of 100 mg/kg orally for nine days, starts one week before giving a single dose of cisplatin. Kidney and plasma were taken for analysis. Results Cisplatin challenged rats demonstrated kidney injury as shown by reduced creatinine clearance, increased of plasma BUN, plasma creatinine, and kidney MDA, decreased of kidney GSH levels, and kidney histopathology alterations. Also, cisplatin increased ERK1/2 phosphorylation and NF-κB expression, which subsequently increased mRNA expression of TNF-α, IL-6, KIM-1, NGAL, and Bax/Bcl-2 ratio as well as decreased mRNA expression of IL-10 in kidney tissues. Pre-treatment with curcumin significantly ameliorated inflammation and apoptosis induced by cisplatin. In addition, curcumin downregulated Ctr1 and OCT2 drug transporters as compared to cisplatin group. Histopathological examination furthers confirmed the kidney damage protection effect of curcumin. Conclusions These data indicate that curcumin has nephroprotective properties against cisplatin-induced kidney damage in rats and this effect is associated with its anti-inflammatory and anti-apoptosis profiles, in addition to its antioxidant. Hence, curcumin may be useful for preventing kidney damage against cisplatin administration.

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