scholarly journals Biological Variation of Plasma and Urinary Markers of Acute Kidney Injury in Patients with Chronic Kidney Disease

2016 ◽  
Vol 62 (6) ◽  
pp. 876-883 ◽  
Author(s):  
Joanne L Carter ◽  
Christopher T Parker ◽  
Paul E Stevens ◽  
Gillian Eaglestone ◽  
Sarah Knight ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Kidney Function ◽  
Objective Assessment ◽  
Kidney Injury ◽  
High Signal ◽  
Urinary Biomarker ◽  
Reference Change Value ◽  
Concentration Changes

Abstract BACKGROUND Identification of acute kidney injury (AKI) is predominantly based on changes in plasma creatinine concentration, an insensitive marker. Alternative biomarkers have been proposed. The reference change value (RCV), the point at which biomarker change can be inferred to have occurred with statistical certainty, provides an objective assessment of change in serial tests results in an individual. METHODS In 80 patients with chronic kidney disease, weekly measurements of blood and urinary biomarker concentrations were undertaken over 6 weeks. Variability was determined and compared before and after adjustment for urinary creatinine and across subgroups stratified by level of kidney function, proteinuria, and presence or absence of diabetes. RESULTS RCVs were determined for whole blood, plasma, and urinary neutrophil gelatinase-associated lipocalin (111%, 59%, and 693%, respectively), plasma cystatin C (14%), creatinine (17%), and urinary kidney injury molecule 1 (497%), tissue inhibitor of metalloproteinases 2 (454%), N-acetyl-β-d-glucosaminidase (361%), interleukin-18 (819%), albumin (430%), and α1-microglobulin (216%). Blood biomarkers exhibited lower variability than urinary biomarkers. Generally, adjusting urinary biomarker concentrations for creatinine reduced (P < 0.05) within-subject biological variability (CVI). For some markers, variation differed (P < 0.05) between subgroups. CONCLUSIONS These data can form a basis for application of these tests in clinical practice and research studies and are applicable across different levels of kidney function and proteinuria and in the presence or absence of diabetes. Most of the studied biomarkers have relatively high CVI (noise) but also have reported large concentration changes in response to renal insult (signal); thus progressive change should be detectable (high signal-to-noise ratio) when baseline data are available.

scholarly journals Timing of AKI after urgent percutaneous coronary intervention and clinical outcomes: a high-dimensional propensity score analysis

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Alan S. Go ◽  
Thida C. Tan ◽  
Rishi V. Parikh ◽  
Andrew P. Ambrosy ◽  
Leonid V. Pravoverov ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Percutaneous Coronary Intervention ◽  
Kidney Disease ◽  
Propensity Score ◽  
Kidney Function ◽  
Kidney Injury ◽  
Coronary Intervention ◽  
High Dimensional ◽  
Percutaneous Coronary

Abstract Introduction Acute kidney injury is a common complication of percutaneous coronary intervention and has been associated with an increased risk of death and progressive chronic kidney disease. However, whether the timing of acute kidney injury after urgent percutaneous coronary intervention could be used to improve patient risk stratification is not known. Methods We conducted a retrospective cohort study in adults surviving an urgent percutaneous coronary intervention between 2008 and 2013 within Kaiser Permanente Northern California, a large integrated healthcare delivery system, to evaluate the impact of acute kidney injury during hospitalization at 12 (±6), 24 (±6) and 48 (±6) hours after urgent percutaneous coronary intervention and subsequent risks of adverse outcomes within the first year after discharge. We used multivariable Cox proportional hazards models with adjustment for a high-dimensional propensity score for developing acute kidney injury after percutaneous coronary intervention to examine the associations between acute kidney injury timing and all-cause death and worsening chronic kidney disease. Results Among 7250 eligible adults undergoing urgent percutaneous coronary intervention, 306 (4.2%) had acute kidney injury at one or more of the examined time periods after percutaneous coronary intervention. After adjustment, acute kidney injury at 12 (±6) hours was independently associated with higher risks of death (adjusted hazard ratio [aHR] 3.55, 95% confidence interval [CI] 2.19–5.75) and worsening kidney function (aHR 2.40, 95% CI:1.24–4.63). Similar results were observed for acute kidney injury at 24 (±6) hours and death (aHR 3.90, 95% CI:2.29–6.66) and worsening chronic kidney disease (aHR 4.77, 95% CI:2.46–9.23). Acute kidney injury at 48 (±6) hours was associated with excess mortality (aHR 1.97, 95% CI:1.19–3.26) but was not significantly associated with worsening kidney function (aHR 0.91, 95% CI:0.42–1.98). Conclusions Timing of acute kidney injury after urgent percutaneous coronary intervention may be differentially associated with subsequent risk of worsening kidney function but not death.

P0624INCREASED URINARY BIOMARKERS OF KIDNEY INJURY IN PATIENTS AFTER ALLOGENETICHEMATOPOETIC STEM CELL TRANSPLANTATION REFLECT KIDNEY DAMAGE EVEN IN NORMALN KIDNEY FUNCTION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Malgorzata Kepska ◽  
Inga Chomicka ◽  
Ewa Karakulska-Prystypiuk ◽  
Agnieszka Tomaszewska ◽  
Grzegorz Basak ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Stem Cell ◽  
Kidney Disease ◽  
Healthy Volunteers ◽  
Kidney Function ◽  
Kidney Injury ◽  
Allogeneic Hsct ◽  
Ckd Stage ◽  
Nephrotoxic Drugs

Abstract Background and Aims Chronic kidney disease (CKD) and acute kidney injury (AKI) are common complications of hematopoietic stem cell transplantation (HSCT) associated with increased morbidity and mortality. On the other hand, presence of CKD is often used as an exclusion criterion when selecting patients who undergo HSCT, especially when fludarabine in conditioning or GVHD prophylaxis with a calcineurin inhibitor is contemplated. There is also no threshold (CKD stage, level of serum creatinine etc) below which patients should not undergo allogeneic HSCT. Kidney function in patients undergoing HSCT is frequently worsened by previous chemotherapy and exposure to a variety of nephrotoxic drugs. Several biomarkers were widely investigated for early diagnosis of acute kidney injury, including neutrophil gelatinase associated lipocalin (NGAL), urinary liver-type fatty acid-binding protein (uL-FABP) and others, however, in patients undergoing HSCT, the published literature is exceptionally scarce. A few studies with inconclusive results stress the knowledge gap and need for further research. The aim of the study was to assess biomarkers of kidney injury in patients at least 3 months after HSCT (to avoid the effect of calcineurin inhibitors) under ambulatory care of Hematology, Oncology and Internal Medicine Department, University Teaching Hospital. Method We studied 80 prevalent patients after allogeneic HSCT and 32 healthy volunteers to obtained normal ranges for biomarkers. In this cross-sectional study following biomarkers of kidney injury in urine were evaluated: IGFBP-7/TIMP2 (insulin growth factor binding protein-7/, tissue inhibitor of metalloproteinases-2), netrin-1, semaphorin A2 using commercially available assays. Results All the biomarkers studied were significantly higher in patients after HSCT when compared to healthy volunteers (all p<0.001). When we divided patients according to kidney function (below and over 60 ml./min/1.72m2), we found that only concentration of IGFBP-7 was significantly higher in 23 patients with CKD stage 3 (i.e. eGFR below 60ml.min/1.72m2) relative to patients with eGFR over 60 ml.min.1.72m2. All biomarkers in both subgroups of patients with eGFR below and over 60 ml./min/1.72m2 were significantly higher relative to healthy volunteers. In univariate correlations sempahorinA2 was related to netrin 1 (r=0.47, p<0.001), IGFBP7 (r=0.35, p<0.01), TIMP2 (r=0.32, p<0.01), whereas IGFBP7 was positively related to serum creatinine (r=0.38, p<0.001) and inversely to eGFR (r=-0.36, p<0.001). Conclusion Concluding, patients after allogeneic HSCT despite normal or near normal kidney function show evidence of kidney injury, which might be due to comorbidities, previous chemotherapy, conditioning regimen,complement activation, calcineurin therapy after HSCT, other possible nephrotoxic drugs etc. Nephroprotective strategies are to be considered as chronic kidney disease is a risk factor for increased morbidity and mortality in this vulnerable population.

scholarly journals Acute kidney injury in 3182 patients admitted with COVID-19: a single center retrospective case-control study

2021 ◽  
Author(s):  
Fabio L Procaccini ◽  
Roberto Alcázar Arroyo ◽  
Marta Albalate Ramón ◽  
Esther Torres Aguilera ◽  
Juan Martín Navarro ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Respiratory Distress ◽  
Kidney Function ◽  
Case Control Study ◽  
Kidney Injury ◽  
Case Control ◽  
Retrospective Case ◽  
Control Study

Abstract Background Acute kidney injury (AKI) may develop in COVID-19 patients and may be associated with a worse outcome. The aim of this study is to describe AKI incidence during the first 45 days of the SARS-CoV2 pandemic in Spain, its reversibility and the association with mortality. Methods Observational retrospective case-control study based on patients hospitalized between March 1 and April 15, 2020 with SARS-CoV2 infection and AKI. Confirmed AKI cases were compared with stable kidney function patients for baseline characteristics, analytical data, treatment and renal outcome. Patients with end-stage kidney disease were excluded. Results AKI incidence was 17.22% among 3182 admitted COVID-19 patients and acute kidney disease (AKD) incidence was 6.82%. The most frequent causes of AKI were prerenal (68.8%) and sepsis (21.9%). Odds ratio for AKI was increased in patients with pre-existent hypertension (OR 2.58, 95% CI 1.71-3.89) and chronic kidney disease (OR 2.14, 95% CI 1.33-3.42) and in those with respiratory distress (OR 2.37, 95% CI 1.52-3.70). Low arterial pressure at admission increased the risk for stage 3 AKI (OR 1.65, 95% CI 1.09-2.50). Baseline kidney function was not recovered in 45.73% of overall AKI cases and in 52.75% of AKI patients with prior chronic kidney disease. Mortality was 38.5% compared to 13.4% of the overall sample population. AKI increased mortality risk at any time of hospitalization (HR 1.45, 95% CI 1.09-1.93). Conclusions AKI is frequent in COVID-19 patients and is associated to mortality, independently from acute respiratory distress syndrome. AKD was also frequent and merits adequate follow-up.

scholarly journals Shroom3, a gene associated with chronic kidney disease, modulates epithelial recovery after acute kidney injury

Kidney360 ◽  
2021 ◽  
pp. 10.34067/KID.0003802021
Author(s):  
Aihua Li ◽  
Joanna Cunanan ◽  
Hadiseh Khalili ◽  
Timothy Plageman ◽  
Kjetil Ask ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Kidney Function ◽  
Genetic Variants ◽  
Association Studies ◽  
Kidney Injury ◽  
Tubular Damage ◽  
Genome Wide Association Studies ◽  
Cellular Mechanisms

Background: Ischemia induced acute kidney injury (AKI) resulting in tubular damage can often progress to chronic kidney disease (CKD) and is a common cause of nephrology consultation. Following renal tubular epithelial damage, molecular and cellular mechanisms are activated to repair and regenerate the damaged epithelium. If these mechanisms are impaired, AKI can progress to CKD. Even in patients whose kidney function returns to normal baseline are more likely to develop CKD. Genome-wide association studies have provided robust evidence that genetic variants in SHROOM3, which encodes an actin-associated protein, are associated with CKD and poor outcomes in transplanted kidneys. Here, we sought to further understand the associations of Shroom3 in CKD. Methods: Kidney ischemia was induced in wild-type and Shroom3 heterozygous null mice (Shroom3Gt/+) and the mechanisms of cellular recovery and repair were examined. Results: A 28-minute bilateral ischemia in Shroom3Gt/+ mice resulted in 100% mortality within 24 hours. After 22-minute ischemic injury, Shroom3Gt/+ mice had a 16% increased mortality, worsened kidney function, and significantly worse histopathology, apoptosis, proliferation, inflammation, and fibrosis after injury. The cortical tubular damage in Shroom3Gt/+ was associated with disrupted epithelial redifferentiation, disrupted Rho-kinase/myosin signaling, and disorganized apical F-actin. Analysis of Madin Darby Canine Kidney Cells showed the levels of Shroom3 are directly correlated to apical organization of actin and actomyosin regulators. Conclusion: These findings establish that Shroom3 is required for epithelial repair and redifferentiation through the organization of actomyosin regulators and could explain why genetic variants in Shroom3 are associated with CKD and allograft rejection.

The kidney

2013 ◽  
pp. 185-193
Author(s):  
Mark Little ◽  
Alan Salama
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Kidney Function ◽  
Medication Use ◽  
Kidney Injury ◽  
Excretory Function ◽  
Rheumatological Disease ◽  
Glomerular Involvement ◽  
Work Up

Kidney dysfunction is common in patients with rheumatological disease, be it secondary to renal (usually glomerular) involvement by a multisystem rheumatological disorder, renal impairment due to nephrotoxic medication use, or incidentally noted during a rheumatological work-up. It is therefore important for the rheumatologist to know how to assess kidney function biochemically and radiologically, to appreciate when an organ-threatening process is present, and to understand the basic steps to take in the event of acute kidney injury. This chapter reviews assessment of kidney function with respect to estimating excretory function, and the degree of proteinuria and haematuria. It provides an in-depth review of the causes, assessment, and management of acute kidney injury as encountered in rheumatological practice, and a summary of the causes and approach to chronic kidney disease.

scholarly journals Postoperative acute kidney injury in adult non-cardiac surgery: joint consensus report of the Acute Disease Quality Initiative and PeriOperative Quality Initiative

2021 ◽  
Author(s):  
John R. Prowle ◽  
Lui G. Forni ◽  
Max Bell ◽  
Michelle S. Chew ◽  
Mark Edwards ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Kidney Disease ◽  
Kidney Injury ◽  
Adverse Outcomes ◽  
Baseline Risk ◽  
Major Surgery ◽  
Increased Risk

AbstractPostoperative acute kidney injury (PO-AKI) is a common complication of major surgery that is strongly associated with short-term surgical complications and long-term adverse outcomes, including increased risk of chronic kidney disease, cardiovascular events and death. Risk factors for PO-AKI include older age and comorbid diseases such as chronic kidney disease and diabetes mellitus. PO-AKI is best defined as AKI occurring within 7 days of an operative intervention using the Kidney Disease Improving Global Outcomes (KDIGO) definition of AKI; however, additional prognostic information may be gained from detailed clinical assessment and other diagnostic investigations in the form of a focused kidney health assessment (KHA). Prevention of PO-AKI is largely based on identification of high baseline risk, monitoring and reduction of nephrotoxic insults, whereas treatment involves the application of a bundle of interventions to avoid secondary kidney injury and mitigate the severity of AKI. As PO-AKI is strongly associated with long-term adverse outcomes, some form of follow-up KHA is essential; however, the form and location of this will be dictated by the nature and severity of the AKI. In this Consensus Statement, we provide graded recommendations for AKI after non-cardiac surgery and highlight priorities for future research.

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