Kinetic changes in serum procalcitonin predict persistent acute kidney injury in critical patients

Nephrology ◽  
2021 ◽  
Author(s):  
Kan Shen ◽  
Wei Qu ◽  
Guang‐Kuo Zhao ◽  
Zhi‐Hui Cheng ◽  
Jun Li ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Critical Patients

scholarly journals Factors Determining Nephrotoxicity and Mortality in Critical Care Patients Receiving Colistin

2018 ◽  
Vol 11 (12) ◽  
pp. 912-917 ◽  
Author(s):  
Ali Ciftci ◽  
Seval Izdes ◽  
Neriman Defne Altintas
Keyword(s):  
Risk Factors ◽  
Acute Kidney Injury ◽  
Demographic Data ◽  
Kidney Injury ◽  
Apache Ii ◽  
Factors Affecting ◽  
Acute Kidney Injury Group ◽  
Injury Group ◽  
Independent Risk Factors ◽  
Critical Patients

Introduction: We aimed to determine risk factors for nephrotoxicity and factors affecting mortality in patients who received colistin. Methodology: Critical patients who received colistin were enrolled. Pregnancy, age < 18 years, basal creatinine level > 2 mg/dL, colistin use for < 48 hours, and previous renal replacement therapy were exclusion criteria. KDIGO stages were determined according to creatinine levels. Patients were grouped as those with no acute kidney injury (Group N0) and those with acute kidney injury (Group N). Their demographic data, APACHE II and SOFA scores, treatments, and laboratory results were recorded. Results: A total of 91 patients were included: 27 in Group N0 and 64 in Group N. Demographic data were similar between groups; however, higher admission APACHE-II scores (OR:1.179, 95% CI:1.033-1.346, p = 0.015) and need for vasopressors (OR:5.486, 95% CI:1.522–19.769, p = 0.009) were found to be independent risk factors for nephrotoxicity. Higher APACHE II scores (OR:1.253, %95 CI:1.093-1.437, p = 0.001), presence of coronary artery disease (OR:7.720, % 95 CI: 1.613-36.956, p = 0.011), need for vasopressors (OR: 4.587, % 95 CI: 1.224 – 17.241, p = 0.024), hypoalbuminemia (OR: 4.721, % 95 CI: 1.088 – 20.469, p = 0.038), and higher direct bilirubin levels (OR: 1.806, % 95 CI: 1.055 – 3.092, p = 0.031) were independent risk factors for mortality. Conclusion: When use of colistin is considered in ICU patients, presence of modifiable risk factors for nephrotoxicity such as hypoalbuminemia, nephrotoxic drug administration, and presence of shock should be determined and managed to prevent nephrotoxicity.

Renal support therapy

2021 ◽  
pp. 338-350
Author(s):  
Claudio Ronco ◽  
Stefano Romagnoli ◽  
Zaccaria Ricci
Keyword(s):  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Multiple Organ Failure ◽  
Replacement Therapy ◽  
Kidney Injury ◽  
Multiple Organ ◽  
Acute Illness ◽  
Renal Support Therapy ◽  
Critical Patients ◽  
Renal Support

Renal dysfunction is known to be frequently a component of multiple organ failure, a complex syndrome affecting the most severely ill critical patients. Bidirectional interaction between the kidneys and other organs has always been suspected; evidence suggests that severe kidney injury is an important protagonist in acute illness, even when managed by dialysis. In fact, if it seems that increasing the dose of renal replacement therapy does not reduce mortality, it could be inferred that acute kidney injury influences mortality through means that are not reversed by conventional renal support, either because the putative culprit toxins are not removed by renal replacement therapy or because renal replacement therapy is started too late to prevent these effects. It is known that the kidneys exert effects on other organs, such as the lung, liver, heart, and brain, in a process called 'crosstalk'. This effect means that the kidney is not only a victim, but also a culprit regarding the malfunction of other organs. This chapter will detail some traditional aspects of different renal replacement therapy modalities and prescription schedules, but it will also describe the most recent evidence on the management and support of the kidney during failure of other organs.

Renal Resistive Index and mortality in critical patients with acute kidney injury

2016 ◽  
Vol 46 (3) ◽  
pp. 242-251 ◽  
Author(s):  
Maria Boddi ◽  
Manuela Bonizzoli ◽  
Marco Chiostri ◽  
Dario Begliomini ◽  
Adele Molinaro ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Resistive Index ◽  
Kidney Injury ◽  
Renal Resistive Index ◽  
Critical Patients

Efficacy and Safety of Regional Anticoagulation with 4% Trisodium Citrate Versus Heparin in Extended Hemodialysis among Critical Patients with Cancer and Acute Kidney Injury

2020 ◽  
pp. 1-7
Author(s):  
Edwiges Ita De Miranda Moura ◽  
Germana Alves de Brito ◽  
Joubert Araujo Alves ◽  
Marina Harume  Imanishe ◽  
Aline Lourenço Baptista ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Trisodium Citrate ◽  
Efficacy And Safety ◽  
Patients With Cancer ◽  
Critical Patients ◽  
Regional Anticoagulation

scholarly journals COVID-19–induced acute kidney injury in critically ill patients: epidemiology, risk factors, and outcome

2021 ◽  
Vol 36 (4) ◽  
pp. 308-316
Author(s):  
Ahlem Trifi ◽  
Sami Abdellatif ◽  
Yosri Masseoudi ◽  
Asma Mehdi ◽  
Oussama Benjima ◽  
...  
Keyword(s):  
Risk Factors ◽  
Acute Kidney Injury ◽  
Tissue Injury ◽  
Kidney Injury ◽  
Hematological Disorders ◽  
Tertiary Teaching ◽  
Tertiary Teaching Hospital ◽  
Critical Patients ◽  
High Level ◽  
Stage 1

Background: The kidney represents a potential target for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Acute kidney injury (AKI) can occur through several mechanisms and includes intrinsic tissue injury by direct viral invasion. Clinical data about the clinical course of AKI are lacking. We aimed to investigate the proportion, risk factors, and prognosis of AKI in critical patients affected with coronavirus disease 2019 (COVID-19).Methods: A case/control study conducted in two intensive care units of a tertiary teaching hospital from September to December 2020.Results: Among 109 patients, 75 were male (69%), and the median age was 64 years (interquartile range [IQR], 57–71 years); 48 (44%) developed AKI within 4 days (IQR, 1–9). Of these 48 patients, 11 (23%), 9 (19%), and 28 (58%) were classified as stage 1, 2, and 3, respectively. Eight patients received renal replacement therapy. AKI patients were older and had more frequent sepsis, acute respiratory distress syndrome, and rhabdomyolysis; higher initial urea and creatinine; more marked inflammatory syndrome and hematological disorders; and required more frequent mechanical ventilation and vasopressors. An elevated level of D-dimers (odds ratio [OR], 12.83; 95% confidence interval [CI], 1.9–85) was an independent factor of AKI. Sepsis was near to significance (OR, 5.22; 95% CI, 0.94–28; P=0.058). Renal recovery was identified in three patients. AKI, hypoxemia with the ratio of the arterial partial pressure of oxygen and the inspiratory concentration of oxygen <70, and vasopressors were identified as mortality factors.Conclusions: AKI occurred in almost half the patients with critical COVID-19. A high level of D-dimers and sepsis contributed significantly to its development. AKI significantly worsened the prognosis in these patients.

Sepsis and acute kidney injury as two-way street: values of biomarkers

2019 ◽  
Vol 1 (4) ◽  
pp. 27-36
Author(s):  
V. V. Velkov
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Acute Injury ◽  
Renal Tubules ◽  
Early Diagnostics ◽  
Critical Care Units ◽  
Renal Markers ◽  
Critical Patients ◽  
Degree Of Severity ◽  
Proinflammatory Factors

The brief review, dedicated to Septic Acute Injury (S-AKI) - the syndrome simultaneously corresponding to criteria of sepsis and acute kidney Injury. Sepsis or AKI are diagnosed 30-50 % of critical patients. Sepsis is promoting the developing of AKI and AKI is promoting the development of sepsis. Morbidity and lethality in S-AKI is higher than that is sepsis and in AKI separately. The main mechanisms of the development of: a) AKI in sepsis - the toxic septic blood containing huge amounts of proinflammatory factors damage the renal tubules resulting tubular disfunction; b) sepsis in AKI - uremia is damaging distal organs and functions of immune systems which provoke sepsis development. For early diagnostics of S-AKI in patients admitting in critical care units the simultaneous measurements and monitoring of sepsis and kidney biomarkers are to be made. The problems of such measurements is that AKI decreases the clearance of septic markers and their levels are increasing in noninfectious conditions. From the other hand in septic conditions inflammation can increase the levels of renal markers independently of renal pathologies. In general in sepsis, AKI and in S-AKI the increased levels of sepsis markers reflect simultaneously severity of infectious inflammation and of renal disfunction, and kidney markers reflect simultaneously severity of renal disfunction and of infectious inflammation. The correction of cut-off values of septic markers used for S-AKI diagnostics must be based on the degree of severity of renal disfunction in critical patients.

Renal support therapy

2016 ◽  
Author(s):  
Claudio Ronco ◽  
Zaccaria Ricci
Keyword(s):  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Multiple Organ Failure ◽  
Replacement Therapy ◽  
Kidney Injury ◽  
Multiple Organ ◽  
Acute Illness ◽  
Renal Support Therapy ◽  
Critical Patients ◽  
Renal Support

Renal dysfunction is known to be frequently a component of multiple organ failure, a complex syndrome affecting the most severely ill critical patients. Bidirectional interaction between the kidneys and other organs has always been suspected; evidence suggests that severe kidney injury is an important protagonist in acute illness, even when managed by dialysis. In fact, if it seems that increasing the dose of renal replacement therapy does not reduce mortality, it could be inferred that acute kidney injury influences mortality through means that are not reversed by conventional renal support, either because the putative culprit toxins are not removed by renal replacement therapy or because renal replacement therapy is started too late to prevent these effects. It is known that the kidneys exert effects on other organs, such as the lung, liver, heart, and brain, in a process called ‘crosstalk’. This effect means that the kidney is not only a victim, but also a culprit regarding the malfunction of other organs. This chapter will detail some traditional aspects of different renal replacement therapy modalities and prescription schedules, but it will also describe the most recent evidence on the management and support of the kidney during failure of other organs.

Renal support therapy

2015 ◽  
Author(s):  
Claudio Ronco ◽  
Zaccaria Ricci
Keyword(s):  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Multiple Organ Failure ◽  
Replacement Therapy ◽  
Kidney Injury ◽  
Multiple Organ ◽  
Acute Illness ◽  
Renal Support Therapy ◽  
Critical Patients ◽  
Renal Support

Renal dysfunction is known to be frequently a component of multiple organ failure, a complex syndrome affecting the most severely ill critical patients. Bidirectional interaction between the kidneys and other organs has always been suspected; evidence suggests that severe kidney injury is an important protagonist in acute illness, even when managed by dialysis. In fact, if it seems that increasing the dose of renal replacement therapy does not reduce mortality, it could be inferred that acute kidney injury influences mortality through means that are not reversed by conventional renal support, either because the putative culprit toxins are not removed by renal replacement therapy or because renal replacement therapy is started too late to prevent these effects. It is known that the kidneys exert effects on other organs, such as the lung, liver, heart, and brain, in a process called ‘crosstalk’. This effect means that the kidney is not only a victim, but also a culprit regarding the malfunction of other organs. This chapter will detail some traditional aspects of different renal replacement therapy modalities and prescription schedules, but it will also describe the most recent evidence on the management and support of the kidney during failure of other organs.

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