scholarly journals MO371TIME AND THE ETIOLOGY OF ACUTE KIDNEY INJURY DEFINE PROGNOSIS IN THE COURSE OF COVID-19

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Ahmet Murt ◽  
Mevlut Tamer Dincer ◽  
Cebrail Karaca ◽  
Sinan Trabulus ◽  
Nurhan Seyahi ◽  
...  

Abstract Background and Aims Kidneys are among the affected organs in COVID-19 and there may be different etiologies resulting in acute kidney injury (AKI) in different stages of the disease. There have been previous studies focusing on incidence and mortality of AKI in COVID-19 but none has made in depth analysis in relation to the background pathophysiology. Based on previous observations, we hypothesized that all AKIs seen in COVID-19 are not uniform and we aimed to analyze the etiologies and prognosis of AKI among hospitalized COVID-19 patients in relation to the time of AKI during different phases of the disease. Method A total of 1056 patients were admitted to the designated COVID-19 clinics from March to July in 2020. 77 Patients who were younger than 18 years old and 7 kidney transplant patients were excluded from the study. 427 of the remaining patients were confirmed by real time polymerase chain reaction (RT-PCR) test.). As eGFR below 60 mL/min/1,73 m2 was already shown to be related to mortality, these patients (44) were also excluded. As immunologic response is generally accepted to start with the second week of COVID-19 course, patients were classified into three groups, those who had AKI on admission, those who developed AKI in the first week and those who developed AKI starting from 7th day. Initial lymphocyte counts, creatinine levels, electrolytes, acid-base status and changes in the inflammatory markers were compared between the groups. A comparison between patients who survived and who died was also performed. Results 89 of the 383 included COVID-19 patients developed AKI. 24% of those who developed AKI died. Patients who developed AKI later had higher peak CRP and D-dimer levels with lower nadir lymphocyte counts (p=0,000, 0,004 and 0,003 respectively). Additionally, patients who died had higher initial inflammatory marker levels and lower lymphocyte counts than those who survived. Mortality of patients who had AKI on hospital admission (13%) was similar to the overall COVID-19 mortality for inpatients, however it was as high as 44% for those who developed AKI after 7th day. Early AKI was related to pre-renal causes and had a milder course. However, later AKIs were more related to immunologic response and had significantly higher mortality. Patients who died had significantly higher ferritin and d-dimer levels upon their hospital admissions (p=0,000). Electrolyte disturbances, metabolic acidosis and mortality were also higher in patients who developed AKI later. Hypernatremia (OR: 6,5, 95% CI: 3 – 13,9) and phosphorus disturbances (both hyperphosphatemia (OR: 3,3; 95%CI: 1,6 – 6,9) and hypophosphatemia (OR: 3,9; 95% CI: 2,0-7,9)) were related to mortality. Conclusion Findings of this study suggest that AKI in COVID-19 is not of one kind. When developed, AKI should be evaluated in conjunction with the disease stage and possible etiologies

2020 ◽  
Author(s):  
Ahmet Murt ◽  
Mevlut Tamer Dincer ◽  
Cebrail Karaca ◽  
Sinan Trabulus ◽  
Ridvan Karaali ◽  
...  

Abstract Introduction Kidneys are among the affected organs in COVID-19 and there may be different etiologies resulting in acute kidney injury (AKI) in different stages of the disease. This study aimed to analyze AKI among hospitalized COVID-19 patients in relation to the time and etiologies of AKI.Materials & Methods 1056 patients who were hospitalized with COVID-19 diagnosis in our institution were retrospectively evaluated and 383 of them met the inclusion criteria. Eighty-nine patients who developed AKI were involved in the final analysis. As immunologic response is generally accepted to start with the second week of COVID-19 course, patients were classified into three groups, those who had AKI on admission, those who developed AKI in the first week and those who developed AKI starting from 7th day. Initial lymphocyte counts, creatinine levels and inflammatory markers as well as changes in these parameters were compared between the groups.Results AKI was seen in 23% of the patients and 23% of those who developed AKI died. Patients who developed AKI later had higher peak CRP and D-dimer levels with lower nadir lymphocyte counts (p=0,000, 0,004 and 0,003 respectively). Additionally, patients who died had higher initial inflammatory marker levels and lower lymphocyte counts than those who survived. Mortality of patients who had AKI on hospital admission (13%) was similar to the overall COVID-19 mortality for inpatients, however it was as high as 44% for those who developed AKI after 7th day.Conclusion Early AKI was more related to pre-renal causes and had a milder course. However, later AKIs were more related to immunologic response and had significantly higher mortality. Findings of this study suggest that AKI in COVID-19 is not of one kind. When developed, AKI should be evaluated in conjunction with the disease stage and possible etiologies.


2021 ◽  
Author(s):  
Ahmet Murt ◽  
Mevlut Tamer Dincer ◽  
Cebrail Karaca ◽  
Sinan Trabulus ◽  
Ridvan Karaali ◽  
...  

Abstract Aim Kidneys are among the affected organs in COVID-19 and there may be different etiologies resulting in acute kidney injury (AKI) in different stages of the disease. This study aimed to analyze AKI among hospitalized COVID-19 patients in relation to the time and etiologies of AKI. Methods 1056 patients who were hospitalized with COVID-19 diagnosis in our institution were retrospectively evaluated and 383 of them met the inclusion criteria. Eighty-nine patients who developed AKI were involved in the final analysis. Patients were classified into three groups, those who had AKI on admission, those who developed AKI in the first week and those who developed AKI starting from 7th day. Initial lymphocyte counts, creatinine levels, electrolytes, acid-base status and changes in the inflammatory markers were compared between the groups. A comparison between patients who survived and who died was also performed.Results AKI had 24% mortality in COVID-19 patients who had eGFRs of over 60 ml/min/1,73 m2. Patients who developed AKI later had higher peak CRP and D-dimer levels with lower nadir lymphocyte counts (p=0,000, 0,004 and 0,003 respectively). Mortality of patients who had AKI on hospital admission (13%) was similar to the overall COVID-19 mortality for inpatients, however it was 44% for those who developed AKI after 7th day. Early AKI was related to pre-renal causes and had a milder course. However, later AKIs were more related to immunologic response and had significantly higher mortality. Conclusions AKI in COVID-19 is not of one kind. When developed, AKI should be evaluated in conjunction with the disease stage and possible etiologies. AKI that develops later has a worse prognosis.


2018 ◽  
Vol 7 (11) ◽  
pp. 431 ◽  
Author(s):  
Diamantina Marouli ◽  
Kostas Stylianou ◽  
Eleftherios Papadakis ◽  
Nikolaos Kroustalakis ◽  
Stavroula Kolyvaki ◽  
...  

Background: Postoperative Acute Kidney Injury (AKI) is a common and serious complication associated with significant morbidity and mortality. While several pre- and intra-operative risk factors for AKI have been recognized in cardiac surgery patients, relatively few data are available regarding the incidence and risk factors for perioperative AKI in other surgical operations. The aim of the present study was to determine the risk factors for perioperative AKI in patients undergoing major abdominal surgery. Methods: This was a prospective, observational study of patients undergoing major abdominal surgery in a tertiary care center. Postoperative AKI was diagnosed according to the Acute Kidney Injury Network criteria within 48 h after surgery. Patients with chronic kidney disease stage IV or V were excluded. Logistic regression analysis was used to evaluate the association between perioperative factors and the risk of developing postoperative AKI. Results: Eleven out of 61 patients developed postoperative AKI. Four intra-operative variables were identified as predictors of AKI: intra-operative blood loss (p = 0.002), transfusion of fresh frozen plasma (p = 0.004) and red blood cells (p = 0.038), as well as high chloride load (p = 0.033, cut-off value > 500 mEq). Multivariate analysis demonstrated an independent association between AKI development and preoperative albuminuria, defined as a urinary Albumin to Creatinine ratio ≥ 30 mg·g−1 (OR = 6.88, 95% CI: 1.43–33.04, p = 0.016) as well as perioperative chloride load > 500 mEq (OR = 6.87, 95% CI: 1.46–32.4, p = 0.015). Conclusion: Preoperative albuminuria, as well as a high intraoperative chloride load, were identified as predictors of postoperative AKI in patients undergoing major abdominal surgery.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Shigeru Matsui ◽  
Junichi Ishii ◽  
Ryuunosuke Okuyama ◽  
Hiroshi Takahashi ◽  
Hideki Kawai ◽  
...  

Background: Acute kidney injury (AKI) detected after admission to coronary care unit (CCU) is associated with very poor outcomes. We prospectively investigated the prognostic value of a combination of AKI and high plasma D-dimer levels for 1-year mortality in patients hospitalized to CCUs. Methods: D-dimer, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and high-sensitive C-reactive protein (hsCRP) levels were measured in 1228 patients on admission to CCUs, of whom 56% had decompensated heart failure and 38% had acute coronary syndrome. AKI was defined as an increase of >25% in creatinine from baseline or an absolute increase of ≥0.5 mg/dL within 48 h after admission. Left ventricular ejection fraction (LVEF) and E/e’ ratio were estimated using echocardiography with tissue Doppler imaging. Results: AKI was detected in 163 (13%) patients. During 1-year follow-up period, there were 149 (12%) deaths. The patients who died were older (median: 77 vs. 73 years; p < 0.0001) and exhibited higher D-dimer (2.7 vs. 1.3 μg/mL; p < 0.0001), NT-proBNP (5495 vs. 1525 pg/mL; p < 0.0001), and hsCRP levels (0.92 vs, 0.26 mg/L; p < 0.0001) and E/e’ ratio (15.0 vs. 13.2; p = 0.006). They also had a higher incidence of AKI (26% vs. 12%; p < 0.0001) and lower LVEF (39% vs. 49%; p < 0.0001) and estimated glomerular filtration rate (45 vs. 62 mL/min/1.73 m 2 ; p < 0.0001) than patients who survived. Multivariate Cox regression analysis, including 12 clinical, biochemical, and echocardiographic variables, identified AKI (relative risk: 1.79; p = 0.008) and increased D-dimer level (relative risk: 1.83 per 10-fold increment; p = 0.002) as independent predictors of 1-yeart mortality. The combined assessment of AKI and D-dimer quartiles was significantly associated with 1-year mortality rates (Figure). Conclusions: The combined assessment of AKI and high D-dimer levels may be useful for evaluating the risk of 1-year mortality in patients admitted to CCUs.


ESC CardioMed ◽  
2018 ◽  
pp. 2670-2673
Author(s):  
Susanna Price

Chronic kidney disease is a global health burden, with an estimated prevalence of 11–13%, with the majority of patients diagnosed as stage 3, and is an independent risk factor for cardiovascular disease. The incidence of acute kidney injury is increasing, and estimated to be present in one in five acute hospital admissions, and there is a bidirectional relationship between acute and chronic kidney disease. The relevance to the patient with cardiovascular disease relates to increased perioperative risk, as reduced kidney function is an independent risk factor for adverse postoperative cardiovascular outcomes including myocardial infarction, stroke, and progression of heart failure. Furthermore, patients undergoing cardiovascular investigations are at risk of developing acute kidney injury, in particular where iodinated contrast is administered. This chapter reviews the classification of renal disease and its impact on cardiovascular disease, as well as potential methods for reducing the development of contrast-induced acute kidney injury.


Author(s):  
Graham T. McMahon

Acute renal failure, now referred to as acute kidney injury (AKI), complicates 5–10% of general hospital admissions and is associated with increased morbidity and mortality and prolonged hospitalizations. The definition of AKI varies, but it is usually defined as an increase in serum creatinine concentration of 25–50% above the baseline, a decline in estimated glomerular filtration rate (eGFR) of 25–50%, or the need for renal replacement therapy. It is now recognized that changes in GFR are delayed manifestations of renal injury, and the development of urinary biomarkers may help to identify AKI earlier in the course of injury. The major causes of AKI in hospitalized patients include prerenal causes (~40%), postrenal causes (~5–10%), and intrinsic diseases affecting blood vessels, glomeruli, or tubules. Of the intrinsic causes, tubular disorders (acute tubular necrosis and acute interstitial nephritis) are the most common etiologies, accounting for 40–50% of all causes of AKI. Acute glomerulonephritis and vascular disorders are rare etiologies of AKI in hospitalized patients (〈5%).


Nephron ◽  
2020 ◽  
Vol 144 (10) ◽  
pp. 498-505
Author(s):  
Anna L. Barton ◽  
Sam B.M. Williams ◽  
Stephen J. Dickinson ◽  
Rob G. Parry ◽  
Adam Pollard

Author(s):  
Kianoush B. Kashani ◽  
Amy W. Williams

Renal failure is caused by acute kidney injury or chronic kidney disease. Acute kidney injury (AKI) is a common, devastating complication that increases mortality and morbidity among patients with various medical and surgical illnesses. Also known as acute renal failure, AKI is a rapid deterioration of kidney function that results in the accumulation of nitrogenous metabolites and medications and in electrolyte and acid-base imbalances. This chapter discusses the definition, epidemiology, pathophysiology, and etiology of AKI; the clinical approach to patients with AKI; and the management of AKI. Chronic kidney disease (CKD) has been categorized into 5 stages. When renal function decreases to stage 3, the complications of CKD become evident. These complications include hypertension, cardiovascular disease, lipid abnormalities, anemia, metabolic bone disease, and electrolyte disturbances. To prevent the progression of CKD, therapy must be directed toward preventing these complications and achieving adequate glucose control in diabetic patients with CKD.


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