Pathophysiology最新文献

{"title":"Low Serum Methylglyoxal Levels Correlate with Psoriasis Severity and Inflammatory Response Indices.","authors":"Aleksandra Damasiewicz-Bodzek, Agnieszka Nowak, Maciej Maciejczyk, Sławomir Waligóra, Brygida Przywara-Chowaniec","doi":"10.3390/pathophysiology32010008","DOIUrl":"10.3390/pathophysiology32010008","url":null,"abstract":"<p><p>Psoriasis is a multifactorial inflammatory disease. Methylglyoxal (MG) is a highly reactive dicarbonyl compound responsible for dicarbonyl stress in some inflammatory conditions, and it may play a role in the etiopathogenesis of psoriasis. <b>Methods:</b> A total of 50 patients with psoriasis and 35 healthy individuals participated in this study. The following indices were assessed in patients: Body Surface Area (BSA), Psoriasis Area and Severity Index (PASI), and Dermatology Life Quality Index (DLQI). MG concentration was evaluated in blood samples. The following inflammatory response indices were calculated: Systemic Inflammation Response Index (SIRI), Systemic Immuno-inflammation Index (SII), and Aggregate Index of Systemic Inflammation (AISI). <b>Results:</b> An analysis of the obtained data showed a statistically significant decrease in the mean serum MG concentration in patients with psoriasis when compared to the healthy individuals (1.19 ± 0.4 μg/mL vs. 1.75 ± 0.6 μg/mL; <i>p</i> = 0.000002). In the patients, MG concentration correlated negatively with psoriasis disease severity indicators (BSA and PASI), C-reactive protein (CRP) concentration, and inflammatory response indicators (SII and AISI). <b>Conclusions:</b> The decreased concentration of MG may be attributed to an increased accumulation of its derivatives (advanced glycation end-products) in the inflamed skin and/or scavenging by polyamines.</p>","PeriodicalId":19852,"journal":{"name":"Pathophysiology","volume":"32 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overweight-Related Hypertension in Middle-Aged Men Is Linked to Elevated Leptin, TNF-α, IL-6, Cholesterol, and Reduced Testosterone.","authors":"Shalan Alaamri, Abdulhalim S Serafi, Zahir Hussain, Shouq K Bafail, Mohammed A Bafail, Lusine Demirkhanyan, Christopher S Gondi, Sumera Sohail","doi":"10.3390/pathophysiology32010007","DOIUrl":"10.3390/pathophysiology32010007","url":null,"abstract":"<p><strong>Background/objectives: </strong>One of the major causes of hypertension (HT) is the transition of normal weight (NW) status to overweight (OW) status and obesity in a population, which leads to cardiovascular disease (CVD) and other disorders. A variety of factors/variables are involved in the development of HT and OW-related hypertension (OHT). However, we planned to investigate the pathophysiological role of serum leptin (Lep), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), total cholesterol (TC) and serum testosterone (ST) in OHT in middle-aged men.</p><p><strong>Methods: </strong>We consulted three groups of middle-aged men (age: 51-60 years)-an HT group (n: 97, high normal weight (HNW), body mass index (BMI): 23-24.9 kg/m²); an OHT group (n: 97, high overweight (HOW), BMI: 28-29.9 kg/m²) and a normal control group (NC, n: 98, HNW)-to investigate the variations in and correlations of Lep, IL-6, TNF-α, ST, TC and other variables.</p><p><strong>Results: </strong>Significant variations were obtained for the comparisons of TNF-α, Lep, ST and TC for the patient groups. OHT vs. NC showed a significant difference for ST. OHT vs. NC and OHT vs. HT had significant variations for IL-6. Significant changes were obtained for the serum levels of TNF-α, Lep, IL-6, ST and TC among groups. Significant and positive linear associations were obtained for TNF-α, Lep, TC and IL-6. Significant and negative linear associations were found for ST plotted against Lep, TNF-α and IL-6.</p><p><strong>Conclusions: </strong>The current report provides pathophysiological evidence of the interactive role of serum Lep, TNF-α, ST, TC and IL-6 in middle-aged men with HT and OHT. We suggest that the changes we noted in the present study would be helpful for further BMI-based studies in various subcategories of NW, OW and obese subjects with/without HT.</p>","PeriodicalId":19852,"journal":{"name":"Pathophysiology","volume":"32 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843874/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Vitamin D Receptor BsmI Polymorphism and Low Bone Mineral Density in Postmenopausal Women in the MENA Region.","authors":"Tara Al-Barazenji, Asma Allouch, Nedhal Al Husaini, Sondos Yousef, Wisam Nabeel Ibrahim, Amal Al-Haidose, Hatem Zayed, Atiyeh M Abdallah","doi":"10.3390/pathophysiology32010006","DOIUrl":"10.3390/pathophysiology32010006","url":null,"abstract":"<p><strong>Background/objectives: </strong>Low bone mineral density increases the risk of bone fractures, and this condition is especially common in postmenopausal women. Genetic factors significantly influence bone mineral density. This meta-analysis examined the relationship between vitamin D receptor (VDR) gene polymorphisms (BsmI, ApaI, and TaqI) and bone mineral density in postmenopausal women in the Middle East and North Africa (MENA) region.</p><p><strong>Methods: </strong>The PubMed, Embase, Scopus, and Web of Science databases were searched from inception to March 2024 for case-control studies on VDR BsmI, ApaI, and TaqI polymorphisms and their relationship with low bone density. Associations with low bone mineral density were tested with respect to different genetic models (dominant, recessive, allelic) using RevMan v5.3.</p><p><strong>Results: </strong>The meta-analysis included seven studies for BsmI, six for ApaI, and seven for TaqI, representing 704/689 cases/controls for BsmI, 914/711 for ApaI, and 974/895 for TaqI. No significant association was found between VDR polymorphisms and low bone mineral density in postmenopausal women, except in the dominant model (CC + CG vs. GG) for the BsmI variant (OR = 1.27, 95% CI: 1.01-1.59, <i>p</i> = 0.04).</p><p><strong>Conclusions: </strong>We found a modest association between the BsmI polymorphism and increased risk of low bone mineral density (BMD) in postmenopausal women from the MENA region, suggesting its potential as a biomarker. No associations were observed for ApaI or TaqI. These findings highlight the complex genetic-environmental interactions influencing BMD.</p>","PeriodicalId":19852,"journal":{"name":"Pathophysiology","volume":"32 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evolocumab Reduces Oxidative Stress and Lipid Peroxidation in Obese Zucker Rats.","authors":"Martina Cebova, Radoslava Bulkova, Olga Pechanova","doi":"10.3390/pathophysiology32010005","DOIUrl":"10.3390/pathophysiology32010005","url":null,"abstract":"<p><p><b>Background/Objectives</b>: Evolocumab inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9) binding to low-density lipoprotein (LDL) receptors, thus allowing more LDL receptors to remove LDL cholesterol from the blood. We aimed to determine the effects of evolocumab on the plasma lipid profile, reactive oxygen species (ROS), and nitric oxide (NO) generation in the heart of adult male obese Zucker rats. <b>Methods</b>: The rats were divided into lean and obese controls and obese rats treated with evolocumab subcutaneously at a dose of 10 mg/kg every two weeks. After 6 weeks, the lipid profile was determined in the plasma, and NO synthase (NOS) activity, thiobarbituric acid reactive substance (TBARS), conjugated diene (CD) concentration, and protein expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, nuclear factor kappaB (NF-κB), endothelial NOS (eNOS), and phosphorylated eNOS (peNOS) were measured in the heart. <b>Results</b>: Evolocumab treatment did not reduce body weight, relative heart weight, or systolic blood pressure in obese Zucker rats. Evolocumab treatment, however, reduced plasma LDL levels, TBARS, and CD concentrations along with decreasing expression of NADPH oxidase and NF-kappaB proteins in the heart. On the other hand, evolocumab had no effect on NOS activity or eNOS and peNOS protein expression. <b>Conclusions</b>: Besides its lipid-lowering effect, evolocumab may exert antioxidant properties and protect cardiomyocytes from lipid peroxidation while not affecting NO production.</p>","PeriodicalId":19852,"journal":{"name":"Pathophysiology","volume":"32 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Yamarthi et al. <i>Sepia pharaonis</i> Ink Mitigates Dehydroepiandrosterone-Induced Insulin Resistance in Mouse Model of Polycystic Ovarian Syndrome. <i>Pathophysiology</i> 2024, <i>31</i>, 408-419.","authors":"Prathyusha Yamarthi, Rama Satyasri Kotipalli, Samatasai Patnaik, Kv Veena, Muralidharan Kathirvel, Rajkumar Vutukuri, Manjula Bhanoori","doi":"10.3390/pathophysiology32010004","DOIUrl":"10.3390/pathophysiology32010004","url":null,"abstract":"<p><p><b>Error in Figure</b> [...].</p>","PeriodicalId":19852,"journal":{"name":"Pathophysiology","volume":"32 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755596/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143024043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cause of Death Analysis in a 9½-Year-Old with COVID-19 and Dravet Syndrome.","authors":"Vedashree R Meher, Richard J Huntsman, Francis H Y Green, Jill C Wooff, Roland N Auer","doi":"10.3390/pathophysiology32010003","DOIUrl":"10.3390/pathophysiology32010003","url":null,"abstract":"<p><p><b>Background</b>: Cause of death analysis is fundamental to forensic pathology. We present the case of a 9½-year-old girl with a genetically confirmed diagnosis of Dravet syndrome who died in her sleep with no evidence of motor seizure. She also had a lifelong history of recurrent pneumonias and, along with her family, had tested positive for COVID-19 10 days before death. <b>Methods</b>: Long-term clinical history of Dravet Syndrome and respiratory infections were obtained from patient's medical charts and radiology reports. A Rapid-Antigen Test was used to confirm SARS-CoV2 infection days prior to death. At autopsy, brain, heart and lung tissues were obtained. Paraffin-embedded tissues were double-stained with H&E, and immunohistochemically stained using various antibodies. <b>Results</b>: Autopsy revealed evidence of previous seizure activity in the brain and cellular interstitial thickening in the lung. The brain showed edema and fibrillary gliosis without neuronal loss in neocortex and hippocampus. The lung showed inflammatory interstitial thickening with histiocytes, megakaryocytes, B-lymphocytes, and T-lymphocytes, including helper/suppressor cells and cytotoxic T-lymphocytes. Diffuse alveolar damage was observed as alveolar flooding with proteinaceous fluid. <b>Conclusions</b>: The cause of death may be attributed to Sudden Unexpected Death in Epilepsy (SUDEP) in Dravet syndrome, sudden death in viral pneumonia, or some combination of the two. When two independent risk factors for sudden unexpected death are identified due to co-pathology, it may not be possible to determine a single cause of death beyond a reasonable doubt.</p>","PeriodicalId":19852,"journal":{"name":"Pathophysiology","volume":"32 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of Creatine Monohydrate Supplementation on the Gastrocnemius Muscle of Mice with Muscular Dystrophy: A Preliminary Study.","authors":"Victor Augusto Ramos Fernandes, Gabriela Pereira Dos Santos, Amilton Iatecola, Daniela Vieira Buchaim, Ionaly Judith Faria Garcia, Carlos Henrique Bertoni Reis, Lívia Maluf Menegazzo Bueno, Bruna Trazzi Pagani, Rogerio Leone Buchaim, Marcelo Rodrigues da Cunha","doi":"10.3390/pathophysiology32010002","DOIUrl":"10.3390/pathophysiology32010002","url":null,"abstract":"<p><p><b>Background/Objectives:</b> Duchenne muscular dystrophy (DMD) is a genetic disease characterized by a lack of dystrophin caused by mutations in the DMD gene, and some minor cases are due to decreased levels of dystrophin, leading to muscle weakness and motor impairment. Creatine supplementation has demonstrated several benefits for the muscle, such as increased strength, enhanced tissue repair, and improved ATP resynthesis. This preliminary study aimed to investigate the effects of creatine on the gastrocnemius muscle in dystrophy muscle (MDX) and healthy C57BL/10 mice. <b>Methods:</b> Twenty MDX and C57Bl/10 mice were organized into groups and supplemented or not with creatine in a dosage of 0.3 mg for 8 weeks. Gastrocnemius tissue was analyzed using histomorphology and histomorphometric techniques. <b>Results:</b> The results demonstrated potential anti-inflammatory effects of creatine, with less observation of inflammatory infiltrates, the preservation of intramuscular glycogen, and reduction in tissue fibrosis in supplemented animals. <b>Conclusions:</b> These findings suggest that creatine may enhance tissue function and slow the progression of DMD. However, further research, with more analysis, is needed to elucidate molecular mechanisms underlying creatine's effects on reducing mononuclear leukocytes and its role in mitigating tissue fibrosis.</p>","PeriodicalId":19852,"journal":{"name":"Pathophysiology","volume":"32 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143024046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatic Estrogen Receptor Alpha Overexpression Protects Against Hepatic Insulin Resistance and MASLD.","authors":"Ester S Alves, Jessica D M Santos, Alessandra G Cruz, Felipe N Camargo, Carlos H Z Talarico, Anne R M Santos, Carlos A A Silva, Henrique J N Morgan, Sandro L Matos, Layanne C C Araujo, João Paulo Camporez","doi":"10.3390/pathophysiology32010001","DOIUrl":"10.3390/pathophysiology32010001","url":null,"abstract":"<p><p><b>Background/Objectives:</b> Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with cardiometabolic risk. Although studies have shown that estradiol positively contributes to energy metabolism via estrogen receptor alpha (ERα), its role specifically in the liver is not defined. Therefore, this study aimed to evaluate the effects of ERα overexpression, specifically in the liver in mice fed a high-fat diet (HFD). <b>Methods:</b> Male C57BL/6J mice were divided into four groups, vehicle fed with regular chow (RC) (RC-Vehicle); vehicle fed an HFD (HFD-Vehicle); AAV-treated fed with RC (RC-AAV); and AAV-treated fed an HFD (HFD-AAV), for 6 weeks (8-10 mice per group). AAV was administered intravenously to induce ERα overexpression. <b>Results:</b> We demonstrate that overexpression of ERα in RC-fed mice reduces body fat (28%). These mice show increased oxygen consumption in cultured primary hepatocytes, both in basal (19%) and maximal respiration (34%). In HFD-fed mice, we showed a decrease in hepatic TAG content (43%) associated with improved hepatic insulin sensitivity (145%). <b>Conclusions:</b> From this perspective, our results prove that hepatic ERα signaling is responsible for some of the metabolic protective effects of estrogen in mice. Overexpression of ERα improves hepatocyte mitochondrial function, consequently reducing hepatic lipid accumulation and protecting animals from hepatic steatosis and hepatic insulin resistance. Further investigations will be needed to determine the exact molecular mechanism by which ERα improves hepatic metabolic health.</p>","PeriodicalId":19852,"journal":{"name":"Pathophysiology","volume":"32 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755535/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143023997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low Renalase Levels in Newly Diagnosed CML: Dysregulation Sensitive to Modulation by Tyrosine Kinase Inhibitors.","authors":"Jelena Milenkovic, Dijana Stojanovic, Sanja Velickovic, Branka Djordjevic, Goran Marjanovic, Maja Milojkovic","doi":"10.3390/pathophysiology31040053","DOIUrl":"10.3390/pathophysiology31040053","url":null,"abstract":"<p><p><b>Background:</b> A dysregulated proinflammatory microenvironment is considered one of the reasons why current therapies of chronic myeloid leukemia (CML) with tyrosine kinase inhibitors (TKI) do not secure disease control. Therefore, the development of BCR-ABL1-independent therapies is encouraged. Renalase (RNLS) is a multifunctional protein that exhibits both enzymatic and non-enzymatic cytokine-like properties, along with potent anti-inflammatory and anti-apoptotic effects. It is expressed in various tissues, including tumors. <b>Methods:</b> We investigated the levels of RNLS in the blood of CML patients in the chronic phase, treatment naïve patients, and those in remission under TKI treatment (either imatinib or nilotinib) and compared them to healthy individuals. <b>Results:</b> Renalase concentration was markedly decreased in treatment-naive CML patients compared to other groups (<i>p</i> = 0.000), while lower levels in the TKI group were not statistically significant compared to controls. The levels correlated negatively with the total leukocyte and neutrophil count (<i>p</i> < 0.05), while a positive correlation was present with CRP levels in treatment naïve patients. <b>Conclusions:</b> Dynamic regulation of RNLS expression and activity is coupled with transcription factors NF-κB and STAT3. Interpretation of our results might rely on differential requirements of activated STATs (STAT3/5) during CML clone development and maintenance, including the observation of RNLS rise upon TKI introduction. Overall, our research provides new insights into the field of hematological malignancies. Unlike other malignancies studied, RNLS plasma levels are significantly decreased in CML. In future perspectives, RNLS could potentially serve as a diagnostic, prognostic, or therapeutic option for these patients.</p>","PeriodicalId":19852,"journal":{"name":"Pathophysiology","volume":"31 4","pages":"787-796"},"PeriodicalIF":2.7,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11676128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic Kidney Disease of Unknown Etiology: A Global Health Threat in Rural Agricultural Communities-Prevalence, Suspected Causes, Mechanisms, and Prevention Strategies.","authors":"Zineb Ben Khadda, Haitam Lahmamsi, Yahya El Karmoudi, Said Ezrari, Laila El Hanafi, Tarik Sqalli Houssaini","doi":"10.3390/pathophysiology31040052","DOIUrl":"10.3390/pathophysiology31040052","url":null,"abstract":"<p><p>Chronic Kidney Disease of Unknown Etiology (CKDu) is a worldwide hidden health threat that is associated with progressive loss of kidney functions without showing any initial symptoms until reaching end-stage renal failure, eventually leading to death. It is a growing health problem in Asia, Central America, Africa, and the Middle East, with identified hotspots. CKDu disease mainly affects young men in rural farming communities, while its etiology is not related to hypertension, kidney stones, diabetes, or other known causes. The main suspected causal factors are heat-stress, dehydration, exposure to agrochemicals, heavy metals and use of hard water, infections, mycotoxins, nephrotoxic agents, altitude, and genetic factors. This review gives an overview of CKDu and sheds light on its medical history, geographic distribution, and worldwide prevalence. It also summarizes the suspected causal factors, their proposed mechanisms of action, as well as the main methods used in the CKDu prior detection and surveillance. In addition, mitigation measures to reduce the burden of CKDu are also discussed. Further investigation utilizing more robust study designs would provide a better understanding of the risk factors linked to CKDu and their comparison between affected regions.</p>","PeriodicalId":19852,"journal":{"name":"Pathophysiology","volume":"31 4","pages":"761-786"},"PeriodicalIF":2.7,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11677577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}