scholarly journals Genetic Susceptibility to Acute Kidney Injury

2021 ◽  
Vol 10 (14) ◽  
pp. 3039
Author(s):  
Christian Ortega-Loubon ◽  
Pedro Martínez-Paz ◽  
Emilio García-Morán ◽  
Álvaro Tamayo-Velasco ◽  
Francisco J. López-Hernández ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Effective Treatment ◽  
Genetic Factors ◽  
Kidney Injury ◽  
Prevention And Treatment ◽  
Novel Approaches ◽  
Key Genes ◽  
Shed Light

Acute kidney injury (AKI) is a widely held concern related to a substantial burden of morbidity, mortality and expenditure in the healthcare system. AKI is not a simple illness but a complex conglomeration of syndromes that often occurs as part of other syndromes in its wide clinical spectrum of the disease. Genetic factors have been suggested as potentially responsible for its susceptibility and severity. As there is no current cure nor an effective treatment other than generally accepted supportive measures and renal replacement therapy, updated knowledge of the genetic implications may serve as a strategic tactic to counteract its dire consequences. Further understanding of the genetics that predispose AKI may shed light on novel approaches for the prevention and treatment of this condition. This review attempts to address the role of key genes in the appearance and development of AKI, providing not only a comprehensive update of the intertwined process involved but also identifying specific markers that could serve as precise targets for further AKI therapies.

scholarly journals Eculizumab, a novel potential treatment for acute kidney injury associated with preeclampsia/HELLP syndrome

2019 ◽  
Vol 12 (9) ◽  
pp. e228709 ◽  
Author(s):  
Hatem Elabd ◽  
Mennallah Elkholi ◽  
Lewis Steinberg ◽  
Anjali Acharya
Keyword(s):  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Complement Activation ◽  
Hellp Syndrome ◽  
Kidney Injury ◽  
Complement Protein ◽  
Igg Antibody ◽  
Elevated Liver Enzymes

The kidney is one of the major organs affected in preeclampsia. There is evidence suggesting a role for excessive complement activation in the pathogenesis of preeclampsia. We describe a case of preeclampsia with severe features, including HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) and acute kidney injury (AKI) that developed following caesarian section. The patient required renal replacement therapy. A trial of daily plasma exchange was not effective. The patient received a single dose of eculizumab, a humanised monoclonal IgG antibody that binds to complement protein C5. One week post administration of eculizumab, there was significant improvement in haematologic, hepatic and renal function. Blood pressure had normalised and renal replacement therapy was discontinued. The use of eculizumab may have contributed to recovery of kidney function further supporting the role of complement activation in the pathogenesis of preeclampsia and associated AKI.

scholarly journals The Role of Exposed Phosphatidylserine on Microparticles and Blood Cells in Coagulant Activity in Acute Kidney Injury Patients on Continuous Renal Replacement Therapy

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 1219-1219
Author(s):  
Hui Liang ◽  
Li Hou ◽  
Tao Li ◽  
Yan Zhang ◽  
Baorong LI ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Continuous Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Blood Cells ◽  
Kidney Injury ◽  
Healthy Controls ◽  
Coagulation Time ◽  
Baseline Group

Abstract Introduction: Serving as the preferred treatment for patients with acute kidney injury (AKI), continuous renal replacement therapy (CRRT) is mostly interrupted by clotting caused by procoagulant state despite of persistent improvements in anticoagulant technology, reducing therapy time, enhancing cost and resulting in blood lost. Due to hemodynamics disorders and foreign material circuit, blood cells undergo definite activation. However, considered as markers of cell activation, the role of phosphatidylserine (PS) and microparticles (MPs) in the hypercoagulability remains largely unexplored. The aim of this study is to measure PS exposure on blood cells and MPs at baseline and after different therapy duration in AKI patients. Methods: Fifty AKI patients admitted to the First Affiliated Hospital of Harbin Medical University between March 2017 and May 2018 and forty healthy controls were enrolled in this study. Plasma samples were collected at baseline from patients were diagnosed with AKI and after receiving CRRT (Mode: CVVH; dose: 25mL/kg/h; Citrate which has relative little influence on PS exposure and MPs count was used as regional anticoagulant.) for 6hours, 12hours, 18hours, as well as from healthy controls. After being isolated, MPs were measured by flow cytometry (FCM) while procoagulant activity (PCA) of erythrocytes, platelets and MPs was assessed through coagulation time and purified coagulation complex. Lactadherin was applied as a probe and inhibitor of PS. Results: Between AKI baseline group and healthy controls, there was no obvious difference in lactadherin+ MPs, exposure on platelets and erythrocytes (Table 1,2), coagulation time and protein production (Fig. 1). While with therapy time prolonged to 6h, 12h and 18h, lactadherin+ MPs and blood cells showed a significant increase compared with baseline group (Table 1,2). Additionally, coagulation time shortened significantly (Fig. 1A) and purified coagulation complex increased visibly in parallel with total therapy time (Fig. 1B-D). Based on previous analysis, we used lactadherin to suppress PS exposure at time point 18h. Compared with the baseline, lactadherin+ MPs count declined by 75.5% (P < 0.001), coagulation time for MPs, platelets and erythrocytes was shortened by 74.6%, 77.2% and 71.9% (all p < 0.01) and procoagulant enzyme complexes were also reduced by 73.8, 78.7% and 72.9% (all p < 0.01). (Figure. 1) Conclusions: Our results first reveal that upon AKI patients on CRRT, a procoagulant role of PS-driven PCA and an immediate time-dependent elevation in PS+ MPs and blood cells is observed. What's more, suppression of PS obviously inhibits the PCA. Accordingly, PS shows potential to be a new predictor and new strategies focusing on blockade of PS may provide a novel way of anticoagulants in CRRT process. Disclosures No relevant conflicts of interest to declare.

scholarly journals Sepsis-associated acute kidney injury

2021 ◽  
Vol 17 (6) ◽  
pp. 44-50
Author(s):  
L.A. Maltseva ◽  
L.V. Novytska-Usenko ◽  
V.V. Nykonov ◽  
T.V. Kanchura
Keyword(s):  
Acute Kidney Injury ◽  
Intensive Care ◽  
Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Creatinine Level ◽  
Kidney Injury ◽  
Plasma Creatinine ◽  
Advantages And Disadvantages ◽  
Plasma Creatinine Level

Acute kidney injury (AKI) is a condition that develops as a result of a rapid decrease in the glomerular filtration rate, which leads to the accumulation of nitrogenous, including urea and creatinine, and non-nitrogenous metabolic products with electrolytic disorders, impairment of the acid-base balance, and the volume of fluid excreted by the kidneys. Objective: to provide a review of the literature concerning sepsis-associated acute kidney injury. We presented the problems of diagnosis, risk factors, the pathogenesis of sepsis-associated acute kidney injury, as well as to outline terminologically the clinical form of sepsis-associated acute kidney injury: the paradigm shifts from ischemia and vasoconstriction to hyperemia and vasodilation, from acute tubular necrosis to acute tubular apoptosis. Sepsis contributes significantly to the development of AKI: in sepsis, it occurs in 19 % of patients; nevertheless, it is much more frequent in septic shock (45 % of cases), the mortality of individuals with AKI is especially high in non-septic and septic conditions (45 and 73 %, respectively). To effectively diagnose the functional state of the kidneys and conduct nephroprotective therapy, stratification scales for assessing the severity of acute kidney damage are applied, which are based on the determination of plasma creatinine level and urine output: RIFLE (risk, injury, failure, loss of kidney function, and end-stage renal failure), AKIN (Acute Kidney Injury Network), KDIGO (Kidney Disease Improving Global Outcomes); the experts considered KDIGO scale more modern and perfect. It has been found that plasma creatinine is not an early biomarker of AKI that indicates the advisability of using other integral indicators. AKI biomarkers are substances that either participate in the pathological process or witness it allowing diagnose AKI even before an increase in plasma creatinine level. The characteristics of the structure, role of functions of such biomarkers as neutrophil gelatinase-associated lipocalin, cystatin C, interleukin-18, kidney injury molecule-1 and others are given. Intensive care for sepsis-associated acute kidney injury includes the standard therapy corresponding to 2016 Surviving Sepsis Campaign and KDIGO guidelines. Also, the paper focuses on renal replacement therapy (RRT): renal and extrarenal indications for the initiation, factors affecting the initiation of RRT, the timing of initiation, ways of optimization, the timing of RRT discontinuation, recommendations for the dose of RRT, the dose of renal replacement therapy in sepsis-associated AKI, choice of method, advantages and disadvantages of continuous RRT and intermittent hemodialysis, medication support for continuous therapy, the role of hemodialysis machine in the intensive care unit.

scholarly journals Role of acute kidney injury biomarkers to guide renal replacement therapy initiation, what we learn from EARLY-RRT trial and FST trial?

2018 ◽  
Vol 10 (12) ◽  
pp. E835-E838
Author(s):  
Nattachai Srisawat ◽  
Kamonwan Tangvoraphonkchai ◽  
Nuttha Lumlertgul ◽  
Kriang Tungsanga ◽  
Somchai Eiam-Ong
Keyword(s):  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Kidney Injury ◽  
Therapy Initiation ◽  
Renal Replacement Therapy Initiation
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