scholarly journals Urinary Biomarkers of Mycotoxin Induced Nephrotoxicity—Current Status and Expected Future Trends

Toxins ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 848
Author(s):  
Zsolt Ráduly ◽  
Robert G. Price ◽  
Mark E. C. Dockrell ◽  
László Csernoch ◽  
István Pócsi
Keyword(s):  
Animal Feed ◽  
Wide Spectrum ◽  
Large Population ◽  
Kidney Injury ◽  
Population Based ◽  
Fungal Species ◽  
Current Status ◽  
Screening Programs ◽  
Toxicological Effects ◽  
Kidney Injury Molecule 1

The intensifying world-wide spread of mycotoxigenic fungal species has increased the possibility of mycotoxin contamination in animal feed and the human food chain. Growing evidence shows the deleterious toxicological effects of mycotoxins from infants to adults, while large population-based screening programs are often missing to identify affected individuals. The kidney functions as the major excretory system, which makes it particularly vulnerable to nephrotoxic injury. However, few studies have attempted to screen for kidney injury biomarkers in large, mycotoxin-exposed populations. As a result, there is an urgent need to screen them with sensitive biomarkers for potential nephrotoxicity. Although a plethora of biomarkers have been tested to estimate the harmful effects of a wide spectrum of toxicants, β2-microglobulin (β2-MG) and N-acetyl-β-D-glucosaminidase (NAG) are currently the dominant biomarkers employed routinely in environmental toxicology research. Nevertheless, kidney injury molecule 1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) are also emerging as useful and informative markers to reveal mycotoxin induced nephrotoxicity. In this opinion article we consider the nephrotoxic effects of mycotoxins, the biomarkers available to detect and quantify the kidney injuries caused by them, and to recommend biomarkers to screen mycotoxin-exposed populations for renal damage.

scholarly journals Recurrent acute kidney injury: predictors and impact in a large population-based cohort

2019 ◽  
Vol 35 (8) ◽  
pp. 1361-1369 ◽  
Author(s):  
Jennifer Holmes ◽  
John Geen ◽  
John D Williams ◽  
Aled O Phillips
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Patient Outcomes ◽  
Large Population ◽  
Kidney Injury ◽  
Population Based ◽  
First Episode ◽  
Single Episode ◽  
Subsequent Episode ◽  
The Impact

Abstract Background This study examined the impact of recurrent episodes of acute kidney injury (AKI) on patient outcomes. Methods The Welsh National electronic AKI reporting system was used to identify all cases of AKI in patients ≥18 years of age between April 2015 and September 2018. Patients were grouped according to the number of AKI episodes they experienced with each patient’s first episode described as their index episode. We compared the demography and patient outcomes of those patients with a single AKI episode with those patients with multiple AKI episodes. Analysis included 153 776 AKI episodes in 111 528 patients. Results Of those who experienced AKI and survived their index episode, 29.3% experienced a second episode, 9.9% a third episode and 4.0% experienced fourth or more episodes. Thirty-day mortality for those patients with multiple episodes of AKI was significantly higher than for those patients with a single episode (31.3% versus 24.9%, P < 0.001). Following a single episode, recovery to baseline renal function at 30 days was achieved in 83.6% of patients and was significantly higher than for patients who had repeated episodes (77.8%, P < 0.001). For surviving patients, non-recovery of renal function following any AKI episode was significantly associated with a higher probability of a further AKI episode (33.4% versus 41.0%, P < 0.001). Furthermore, with each episode of AKI the likelihood of a subsequent episode also increased (31.0% versus 43.2% versus 51.2% versus 51.7% following a first, second, third and fourth episode, P < 0.001 for all comparisons). Conclusions The results of this study provide an important contribution to the debate regarding the need for risk stratification for recurrent AKI. The data suggest that such a tool would be useful given the poor patient and renal outcomes associated with recurrent AKI episodes as highlighted by this study.

scholarly journals The Cerebral Palsy Research Registry

2011 ◽  
Vol 26 (12) ◽  
pp. 1534-1541 ◽  
Author(s):  
Donna S. Hurley ◽  
Theresa Sukal-Moulton ◽  
Michael E. Msall ◽  
Deborah Gaebler-Spira ◽  
Kristin J. Krosschell ◽  
...  
Keyword(s):  
United States ◽  
Cerebral Palsy ◽  
Life Span ◽  
Social Systems ◽  
Large Population ◽  
The United States ◽  
Population Based ◽  
Current Status ◽  
Motor Disability ◽  
Prospective Longitudinal

Cerebral palsy is the most common neurodevelopmental motor disability in children. The condition requires medical, educational, social, and rehabilitative resources throughout the life span. Several countries have developed population-based registries that serve the purpose of prospective longitudinal collection of etiologic, demographic, and functional severity. The United States has not created a comprehensive program to develop such a registry. Barriers have been large population size, poor interinstitution collaboration, and decentralized medical and social systems. The Cerebral Palsy Research Registry was created to fill the gap between population and clinical-based cerebral palsy registries and promote research in the field. This is accomplished by connecting persons with cerebral palsy, as well as their families, to a network of regional researchers. This article describes the development of an expandable cerebral palsy research registry, its current status, and the potential it has to affect families and persons with cerebral palsy in the United States and abroad.

scholarly journals Plasma kidney injury molecule-1 (p-KIM-1) levels and deterioration of kidney function over 16 years

2019 ◽  
Vol 35 (2) ◽  
pp. 265-273 ◽  
Author(s):  
Christina-Alexandra Schulz ◽  
Gunnar Engström ◽  
Jan Nilsson ◽  
Peter Almgren ◽  
Marinka Petkovic ◽  
...  
Keyword(s):  
Kidney Function ◽  
Cystatin C ◽  
Risk Model ◽  
Kidney Injury ◽  
Predictive Marker ◽  
Population Based ◽  
Preventive Action ◽  
Net Reclassification Improvement ◽  
Kidney Injury Molecule 1

Abstract Background The kidney injury molecule-1 (KIM-1) has previously been associated with kidney function in rodents and humans. Yet its role as a predictive marker for future decline in kidney function has remained less clear. Methods At baseline (1991–1994), fasting plasma KIM-1 (p-KIM-1) was measured in 4739 participants of the population-based Malmö Diet and Cancer Study. Creatinine and cystatin C were used to calculate estimated glomerular filtration rate (eGFR) according to Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) Collaboration 2012 creatinine–cystatin C equation at baseline and follow-up examination (2007–2012). Incident CKD was defined as an eGFR <60 mL/min/1.73 m2 at follow-up. Results During a mean follow-up time of 16.6 years, high p-KIM-1 levels were associated with a greater decline in eGFR (quartile 1 −1.36 versus quartile 4 −1.54 mL/min/1.73 m2; P < 0.001). In multivariate analyses, the risk for incident CKD at the follow-up examination was higher among participants with baseline p-KIM-1 levels in the highest quartile {odds ratio [OR] 1.45 [95% confidence interval (CI) 1.10–1.92]} compared with those within the lowest quartile. The relative impact of baseline p-KIM-1 on incidence of CKD [OR 1.20 (95% CI 1.08–1.33) per 1 standard deviation (SD) increase in p-KIM-1] was comparable to those of age and systolic blood pressure (SBP) [OR 1.55 (95% CI 1.38–1.74) and OR 1.21 (95% CI 1.09–1.35) per 1 SD increase, respectively]. Adding p-KIM-1 to a conventional risk model resulted in significantly improved C-statistics (P = 0.04) and reclassified 9% of the individuals into the correct risk direction (continuous net reclassification improvement P = 0.02). Furthermore, the risk for hospitalization due to impaired renal function increased with increasing baseline p-KIM-1 [hazard ratio per 1 SD 1.43; (95% CI 1.18–1.74)] during a mean follow-up time of 19.2 years. Conclusion Our results show that p-KIM-1 predicts the future decline of eGFR and risk of CKD in healthy middle-aged participants. Whether p-KIM-1 can be used to prioritize preventive action that needs to be further investigated.

scholarly journals Risk Factors for Recurrent Acute Kidney Injury in a Large Population-Based Cohort

2019 ◽  
Vol 73 (2) ◽  
pp. 163-173 ◽  
Author(s):  
Kathleen D. Liu ◽  
Jingrong Yang ◽  
Thida C. Tan ◽  
David V. Glidden ◽  
Sijie Zheng ◽  
...  
Keyword(s):  
Risk Factors ◽  
Acute Kidney Injury ◽  
Large Population ◽  
Kidney Injury ◽  
Population Based

scholarly journals Intermediate and Long-term Outcomes of Survivors of Acute Kidney Injury Episodes: A Large Population-Based Cohort Study

2017 ◽  
Vol 69 (1) ◽  
pp. 18-28 ◽  
Author(s):  
Simon Sawhney ◽  
Angharad Marks ◽  
Nick Fluck ◽  
Adeera Levin ◽  
Gordon Prescott ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cohort Study ◽  
Large Population ◽  
Kidney Injury ◽  
Population Based ◽  
Long Term Outcomes

scholarly journals Role of New Biomarkers: Functional and Structural Damage

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Evdoxia Tsigou ◽  
Vasiliki Psallida ◽  
Christos Demponeras ◽  
Eleni Boutzouka ◽  
George Baltopoulos
Keyword(s):  
Structural Damage ◽  
Delayed Diagnosis ◽  
Kidney Injury ◽  
Current Status ◽  
Critically Ill Patient ◽  
Fatty Acid Binding ◽  
Prolonged Length ◽  
Genomics And Proteomics ◽  
New Biomarkers ◽  
Kidney Injury Molecule 1

Traditional diagnosis of acute kidney injury (AKI) depends on detection of oliguria and rise of serum creatinine level, which is an unreliable and delayed marker of kidney damage. Delayed diagnosis of AKI in the critically ill patient is related to increased morbidity and mortality, prolonged length of stay, and cost escalation. The discovery of a reliable biomarker for early diagnosis of AKI would be very helpful in facilitating early intervention, evaluating the effectiveness of therapy, and eventually reducing cost and improving outcome. Innovative technologies such as genomics and proteomics have contributed to the discovery of new biomarkers, such as neutrophil gelatinase-associated lipocalin (NGAL), cystatin C (Cys C), kidney injury molecule-1 (KIM-1), interleukin-18 (IL-18), and liver-type fatty acid binding protein (L-FABP). The current status of the most promising of these novel AKI biomarkers, including NGAL, Cys C, KIM-1, L-FABP, and IL-18, is reviewed.

scholarly journals Toxicological effects of thimerosal on rat kidney: a histological and biochemical study

2023 ◽  
Vol 83 ◽  
Author(s):  
M. U. Ijaz ◽  
S. A. Majeed ◽  
A. Asharaf ◽  
T. Ali ◽  
K. A. Al-Ghanim ◽  
...  
Keyword(s):  
Biochemical Study ◽  
Rat Kidney ◽  
Kidney Injury ◽  
Thiobarbituric Acid ◽  
Male Rats ◽  
Control Group ◽  
Albino Rats ◽  
Toxicological Effects ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Kidney Injury Molecule 1

Abstract Thimerosal is an organomercurial compound, which is used in the preparation of intramuscular immunoglobulin, antivenoms, tattoo inks, skin test antigens, nasal products, ophthalmic drops, and vaccines as a preservative. In most of animal species and humans, the kidney is one of the main sites for mercurial compounds deposition and target organs for toxicity. So, the current research was intended to assess the thimerosal induced nephrotoxicity in male rats. Twenty-four adult male albino rats were categorized into four groups. The first group was a control group. Rats of Group-II, Group-III, and Group-IV were administered with 0.5µg/kg, 10µg/kg, and 50µg/kg of thimerosal once a day, respectively. Thimerosal administration significantly decreased the activities of catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), glutathione reductase (GR), glutathione (GSH), and protein content while increased the thiobarbituric acid reactive substances (TBARS) and hydrogen peroxide (H2O2) levels dose-dependently. Blood urea nitrogen (BUN), creatinine, urobilinogen, urinary proteins, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) levels were substantially increased. In contrast, urinary albumin and creatinine clearance was reduced dose-dependently in thimerosal treated groups. The results demonstrated that thimerosal significantly increased the inflammation indicators including nuclear factor kappaB (NF-κB), tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Interleukin-6 (IL-6) levels and cyclooxygenase-2 (COX-2) activities, DNA and histopathological damages dose-dependently. So, the present findings ascertained that thimerosal exerted nephrotoxicity in male albino rats.

High-potency statins increase the risk of acute kidney injury: Evidence from a large population-based study

2014 ◽  
Vol 234 (1) ◽  
pp. 224-229 ◽  
Author(s):  
Giovanni Corrao ◽  
Davide Soranna ◽  
Manuela Casula ◽  
Luca Merlino ◽  
Maria Gabriella Porcellini ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Large Population ◽  
Kidney Injury ◽  
Population Based ◽  
High Potency ◽  
Population Based Study

scholarly journals Genetic contributions to bipolar disorder: current status and future directions

2021 ◽  
pp. 1-12
Author(s):  
Kevin S. O'Connell ◽  
Brandon J. Coombes
Keyword(s):  
Bipolar Disorder ◽  
Large Population ◽  
Population Based ◽  
Therapeutic Interventions ◽  
Current Status ◽  
Genetic Risk Prediction ◽  
Genetic Overlap ◽  
Causal Variants ◽  
Genetic Contributions

Abstract Bipolar disorder (BD) is a highly heritable mental disorder and is estimated to affect about 50 million people worldwide. Our understanding of the genetic etiology of BD has greatly increased in recent years with advances in technology and methodology as well as the adoption of international consortiums and large population-based biobanks. It is clear that BD is also highly heterogeneous and polygenic and shows substantial genetic overlap with other psychiatric disorders. Genetic studies of BD suggest that the number of associated loci is expected to substantially increase in larger future studies and with it, improved genetic prediction of the disorder. Still, a number of challenges remain to fully characterize the genetic architecture of BD. First among these is the need to incorporate ancestrally-diverse samples to move research away from a Eurocentric bias that has the potential to exacerbate health disparities already seen in BD. Furthermore, incorporation of population biobanks, registry data, and electronic health records will be required to increase the sample size necessary for continued genetic discovery, while increased deep phenotyping is necessary to elucidate subtypes within BD. Lastly, the role of rare variation in BD remains to be determined. Meeting these challenges will enable improved identification of causal variants for the disorder and also allow for equitable future clinical applications of both genetic risk prediction and therapeutic interventions.

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