scholarly journals Acute kidney injury pathology and pathophysiology: a retrospective review

2020 ◽  
Author(s):  
Joseph P Gaut ◽  
Helen Liapis
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Renal Function ◽  
Kidney Disease ◽  
Renal Biopsy ◽  
Retrospective Review ◽  
Patient Management ◽  
Kidney Injury ◽  
High Morbidity ◽  
Underlying Pathology

Abstract Acute kidney injury (AKI) is the clinical term used for decline or loss of renal function. It is associated with chronic kidney disease (CKD) and high morbidity and mortality. However, not all causes of AKI lead to severe consequences and some are reversible. The underlying pathology can be a guide for treatment and assessment of prognosis. The Kidney Disease: Improving Global Outcomes guidelines recommend that the cause of AKI should be identified if possible. Renal biopsy can distinguish specific AKI entities and assist in patient management. This review aims to show the pathology of AKI, including glomerular and tubular diseases.

scholarly journals Lymphocytes: Versatile Participants in Acute Kidney Injury and Progression to Chronic Kidney Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Chujin Cao ◽  
Ying Yao ◽  
Rui Zeng
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Renal Injury ◽  
Renal Fibrosis ◽  
Kidney Injury ◽  
Renal Parenchyma ◽  
Health Concern ◽  
High Morbidity ◽  
Parenchyma Cells

Background: Acute kidney injury (AKI) remains a major global public health concern due to its high morbidity and mortality. The progression from AKI to chronic kidney disease (CKD) makes it a scientific problem to be solved. However, it is with lack of effective treatments.Summary: Both innate and adaptive immune systems participate in the inflammatory process during AKI, and excessive or dysregulated immune responses play a pathogenic role in renal fibrosis, which is an important hallmark of CKD. Studies on the pathogenesis of AKI and CKD have clarified that renal injury induces the production of various chemokines by renal parenchyma cells or resident immune cells, which recruits multiple-subtype lymphocytes in circulation. Some infiltrated lymphocytes exacerbate injury by proinflammatory cytokine production, cytotoxicity, and interaction with renal resident cells, which constructs the inflammatory environment and induces further injury, even death of renal parenchyma cells. Others promote tissue repair by producing protective cytokines. In this review, we outline the diversity of these lymphocytes and their mechanisms to regulate the whole pathogenic stages of AKI and CKD; discuss the chronological responses and the plasticity of lymphocytes related to AKI and CKD progression; and introduce the potential therapies targeting lymphocytes of AKI and CKD, including the interventions of chemokines, cytokines, and lymphocyte frequency regulation in vivo, adaptive transfer of ex-expanded lymphocytes, and the treatments of gut microbiota or metabolite regulations based on gut-kidney axis.Key Message: In the process of AKI and CKD, T helper (Th) cells, innate, and innate-like lymphocytes exert mainly pathogenic roles, while double-negative T (DNT) cells and regulatory T cells (Tregs) are confirmed to be protective. Understanding the mechanisms by which lymphocytes mediate renal injury and renal fibrosis is necessary to promote the development of specific therapeutic strategies to protect from AKI and prevent the progression of CKD.

scholarly journals Role of SIK1 in the transition of acute kidney injury into chronic kidney disease

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jinxiu Hu ◽  
Jiao Qiao ◽  
Qun Yu ◽  
Bing Liu ◽  
Junhui Zhen ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Transcription Factor ◽  
Kidney Disease ◽  
Kidney Injury ◽  
High Morbidity ◽  
Mesenchymal Transition ◽  
Immunohistochemistry Staining ◽  
Hk2 Cells

Abstract Background Acute kidney injury (AKI), with a high morbidity and mortality, is recognized as a risk factor for chronic kidney disease (CKD). AKI-CKD transition has been regarded as one of the most pressing unmet needs in renal diseases. Recently, studies have showed that salt inducible kinase 1 (SIK1) plays a role in epithelial-mesenchymal transition (EMT) and inflammation, which are the hallmarks of AKI-CKD transition. However, whether SIK1 is involved in AKI-CKD transition and by what mechanism it regulates AKI-CKD transition remains unknown. Methods We firstly detected the expression of SIK1 in kidney tissues of AKI patients and AKI mice by immunohistochemistry staining, and then we established Aristolochic acid (AA)-induced AKI-CKD transition model in C57BL/6 mice and HK2 cells. Subsequently, we performed immunohistochemistry staining, ELISA, real-time PCR, Western blot, immunofluorescence staining and Transwell assay to explore the role and underlying mechanism of SIK1 on AKI-CKD transition. Results The expression of SIK1 was down-regulated in AKI patients, AKI mice, AA-induced AKI-CKD transition mice, and HK2 cells. Functional analysis revealed that overexpression of SIK1 alleviated AA-induced AKI-CKD transition and HK2 cells injury in vivo and in vitro. Mechanistically, we demonstrated that SIK1 mediated AA-induced AKI-CKD transition by regulating WNT/β-catenin signaling, the canonical pathway involved in EMT, inflammation and renal fibrosis. In addition, we discovered that inhibition of WNT/β-catenin pathway and its downstream transcription factor Twist1 ameliorated HK2 cells injury, delaying the progression of AKI-CKD transition. Conclusions Our study demonstrated, for the first time, a protective role of SIK1 in AKI-CKD transition by regulating WNT/β-catenin signaling pathway and its downstream transcription factor Twist1, which will provide novel insights into the prevention and treatment AKI-CKD transition in the future.

scholarly journals Epigenetic Modification Drives Acute Kidney Injury-to-Chronic Kidney Disease Progression

Nephron ◽  
2021 ◽  
pp. 1-11
Author(s):  
Zhenzhen Li ◽  
Ningning Li
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Structural Damage ◽  
Epigenetic Modification ◽  
Kidney Injury ◽  
Epigenetic Modifications ◽  
High Morbidity ◽  
Inflammatory Factor

Acute kidney injury (AKI) is a common clinical critical disease. Due to its high morbidity, increasing risk of complications, high mortality rate, and high medical costs, it has become a global concern for human health problems. Initially, researchers believed that kidneys have a strong ability to regenerate and repair, but studies over the past 20 years have found that kidneys damaged by AKI are often incomplete or even unable to repair. Even when serum creatinine returns to baseline levels, renal structural damage persists for a long time, leading to the development of chronic kidney disease (CKD). The mechanism of AKI-to-CKD transition has not been fully elucidated. As an important regulator of gene expression, epigenetic modifications, such as histone modification, DNA methylation, and noncoding RNAs, may play an important role in this process. Alterations in epigenetic modification are induced by hypoxia, thus promoting the expression of inflammatory factor-related genes and collagen secretion. This review elaborated the role of epigenetic modifications in AKI-to-CKD progression, the diagnostic value of epigenetic modifications biomarkers in AKI chronic outcome, and the potential role of targeting epigenetic modifications in the prevention and treatment of AKI to CKD, in order to provide ideas for the subsequent establishment of targeted therapeutic strategies to prevent the progression of renal tubular-interstitial fibrosis.

scholarly journals Star fruit intoxication leading to acute kidney injury

2016 ◽  
Vol 48 (1-2) ◽  
pp. 37-39 ◽  
Author(s):  
Md Arshad Ul Azim ◽  
Abdus Salam
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Renal Function ◽  
Kidney Disease ◽  
Normal Renal Function ◽  
Case Reports ◽  
Kidney Injury ◽  
Young Male ◽  
Star Fruit ◽  
Oxalate Nephropathy

There are few case reports regarding star fruit's nephrotoxicity and neurotoxicity in chronic kidney disease patients. Recently cases are found in people with normal renal function Star fruit nephrotoxicity is believed to be due to its high oxalate content which causes acute obstructive oxalate nephropathy. A neurotoxin (caramboxin) present in the fruit is responsible for neurotoxic features. Here we present a young male who developed acute kidney injury following star fruit ingestion in empty stomach. After admission, patient was treated conservatively and recovered completely.Bang Med J (Khulna) 2015; 48 : 37-39

scholarly journals Impact on Outcomes across KDIGO-2012 AKI Criteria According to Baseline Renal Function

2019 ◽  
Vol 8 (9) ◽  
pp. 1323 ◽  
Author(s):  
Isabel Acosta-Ochoa ◽  
Juan Bustamante-Munguira ◽  
Alicia Mendiluce-Herrero ◽  
Jesús Bustamante-Bustamante ◽  
Armando Coca-Rojo
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Renal Function ◽  
Kidney Disease ◽  
Hospital Mortality ◽  
Kidney Injury ◽  
Clinical Syndrome ◽  
Increment Rate ◽  
Associated Risk Factors ◽  
Baseline Renal Function

Acute kidney injury (AKI) and Chronic Kidney Disease (CKD) are global health problems. The pathophysiology of acute-on-chronic kidney disease (AoCKD) is not well understood. We aimed to study clinical outcomes in patients with previous normal (pure acute kidney injury; P-AKI) or impaired kidney function (AoCKD) across the 2012 Kidney Disease Improving Global Outcomes (KDIGO) AKI classification. We performed a retrospective study of patients with AKI, divided into P-AKI and AoCKD groups, evaluating clinical and epidemiological features, distribution across KDIGO-2012 criteria, in-hospital mortality and need for dialysis. One thousand, two hundred and sixty-nine subjects were included. AoCKD individuals were older and had higher comorbidity. P-AKI individuals fulfilled more often the serum creatinine (SCr) ≥ 3.0× criterion in AKI-Stage3, AoCKD subjects reached SCr ≥ 4.0 mg/dL criterion more frequently. AKI severity was associated with in-hospital mortality independently of baseline renal function. AoCKD subjects presented higher mortality when fulfilling AKI-Stage1 criteria or SCr ≥ 3.0× criterion within AKI-Stage3. The relationship between mortality and associated risk factors, such as the net increase of SCr or AoCKD status, fluctuated depending on AKI stage and stage criteria sub-strata. AoCKD patients that fulfil SCr increment rate criteria may be exposed to more severe insults, possibly explaining the higher mortality. AoCKD may constitute a unique clinical syndrome. Adequate staging criteria may help prompt diagnosis and administration of appropriate therapy.

Increased progression to kidney fibrosis after erythropoietin is used as a treatment for acute kidney injury

2014 ◽  
Vol 306 (6) ◽  
pp. F681-F692 ◽  
Author(s):  
Glenda C. Gobe ◽  
Nigel C. Bennett ◽  
Malcolm West ◽  
Paul Colditz ◽  
Lindsay Brown ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Renal Function ◽  
Kidney Disease ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Acute Injury

Treatment of renal ischemia-reperfusion (IR) injury with recombinant human erythropoietin (rhEPO) reduces acute kidney injury and improves function. We aimed to investigate whether progression to chronic kidney disease associated with acute injury was also reduced by rhEPO treatment, using in vivo and in vitro models. Rats were subjected to bilateral 40-min renal ischemia, and kidneys were studied at 4, 7, and 28 days postreperfusion for renal function, tubular injury and repair, inflammation, and fibrosis. Acute injury was modulated using rhEPO (1,000 or 5,000 IU/kg, intraperitoneally) at the time of reperfusion. Renal tubular epithelial cells or fibroblasts in culture were subjected to hypoxia or oxidative stress, with or without rhEPO (200 IU/ml), and fibrogenesis was studied. The results of the in vivo model confirmed functional and structural improvement with rhEPO at 4 days post-IR ( P < 0.05). At 7 days post-IR, fibrosis and myofibroblast stimulation were increased with IR with and without rhEPO ( P < 0.01). However, at 28 days post-IR, renal fibrosis and myofibroblast numbers were significantly greater with IR plus rhEPO ( P < 0.01) compared with IR only. Mechanistically, rhEPO stimulated profibrotic transforming growth factor-β, oxidative stress (marker 8-hydroxy-deoxyguanosine), and phosphorylation of the signal transduction protein extracellular signal-regulated kinase. In vitro, rhEPO protected tubular epithelium from apoptosis but stimulated epithelial-to-mesenchymal transition and also protected and activated fibroblasts, particularly with oxidative stress. In summary, although rhEPO was protective of renal function and structure in acute kidney injury, the supraphysiological dose needed for renoprotection contributed to fibrogenesis and stimulated chronic kidney disease in the long term.

Evaluation of renal function in primary care

2018 ◽  
Vol 8 (2) ◽  
pp. 202-205
Author(s):  
B. Musiałowska ◽  
M. Rudzińska ◽  
E. Koc-Żórawska ◽  
M. Żórawski
Keyword(s):  
Primary Care ◽  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Renal Function ◽  
Kidney Disease ◽  
Chronic Diseases ◽  
Kidney Injury ◽  
Treatment Monitoring ◽  
Primary Care Patients ◽  
Drug Doses

Evaluation of renal function is one of the primary tools used in treatment and monitoring kidney injury such as acute kidney injury (AKI) or chronic kidney disease (CKD) in Primary Care patients. Accompanying chronic diseases also have an impact on the assessment of renal function, treatment monitoring and adjustment of drug doses.

scholarly journals Using circulating O-sulfotyrosine in the differential diagnosis of acute kidney injury and chronic kidney disease

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Shuai Chen ◽  
Yong-Hua Liu ◽  
Dao-Peng Dai ◽  
Zheng-Bin Zhu ◽  
Yang Dai ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Renal Function ◽  
Differential Diagnosis ◽  
Kidney Disease ◽  
Linear Regression Analysis ◽  
Kidney Injury ◽  
Serum Levels ◽  
Multivariate Linear Regression Analysis ◽  
Post Translational Modification

Abstract Background Sulfation of tyrosine, yielding O-sulfotyrosine, is a common but fixed post-translational modification in eukaryotes. Patients with increased circulating O-sulfotyrosine levels experience a faster decline in renal function with progression to end-stage renal disease (ESRD). In the present study, we measured serum O-sulfotyrosine levels in individuals with chronic kidney disease (CKD) and acute kidney injury (AKI) to explore its ability to differentiate AKI from CKD. Methods A total of 135 patients (20 with AKI and 115 with CKD) were recruited prospectively for liquid chromatography-mass spectrometry assessment of circulating O-sulfotyrosine. We also studied C57BL/6 mice with CKD after 5/6 nephrectomy (Nx). Blood samples were drawn from the tail vein on Day 1, 3, 5, 7, 14, 30, 60, and 90 after CKD. Serum separation and characterization of creatinine, blood urea nitrogen (BUN), and O-sulfotyrosine was performed. Thus, the time-concentration curves of the O-sulfotyrosine level demonstrate the variation of kidney dysfunction. Results The serum levels of O-sulfotyrosine were markedly increased in patients with CKD compared with AKI. Median O-sulfotyrosine levels in CKD patients versus AKI, respectively, were as follows:243.61 ng/mL(interquartile range [IQR] = 171.90–553.86) versus 126.55 ng/mL (IQR = 48.19–185.03, P = 0.004). In patients with CKD, O-sulfotyrosine levels were positively correlated with creatinine, BUN, and Cystatin C (r = 0.63, P < 0.001; r = 0.49, P < 0.001; r = 0.61, P < 0.001, respectively) by the multivariate linear regression analysis (β = 0.71, P < 0.001; β = 0.40, P = 0.002; β = 0.73, P < 0.001, respectively). However, this association was not statistically significant in patients with AKI (r = − 0.17, P = 0.472; r = 0.11, P = 0.655; r = 0.09, P = 0.716, respectively). The receiver operating characteristic (ROC) analysis illustrated that the area under the curve was 0.80 (95% confidence interval [CI] 0.71–0.89; P < 0.001) and the optimal cut-off value of serum O-sulfotyrosine suggesting AKI was < 147.40 ng/mL with a sensitivity and specificity of 80.90 and 70.00% respectively. In animal experiments, serum levels of O-sulfotyrosine in mice were elevated on Day 7 after 5/6 nephrectomy (14.89 ± 1.05 vs. 8.88 ± 2.62 ng/mL, P < 0.001) until Day 90 (32.65 ± 5.59 vs. 8.88 ± 2.62 ng/mL, P < 0.001). Conclusion Serum O-sulfotyrosine levels were observed correlated with degrading renal function and in CKD patients substantially higher than those in AKI patients. Thus serum O-sulfotyrosine facilitated the differential diagnosis of AKI from CKD.

Sign in / Sign up

Export Citation Format

Share Document