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Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
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Acute Kidney Injury I: Introduction01:22

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Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
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Acute Kidney Injury III: Clinical Manifestations01:29

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Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...
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Cardiac catheterization is an invasive diagnostic technique used to identify and evaluate structural and functional diseases of the heart and major blood vessels. This technique diagnoses congenital heart disease, coronary artery disease, valvular heart disease, and coronary spasms and assesses ventricular function. It helps guide treatment decisions, including the need for revascularization procedures like percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) and...
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Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
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Ischemia-reperfusion Model of Acute Kidney Injury and Post Injury Fibrosis in Mice
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Using Serum Cystatin C to Predict Acute Kidney Injury Following Infant Cardiac Surgery.

Maher Abadeer1, Michael F Swartz2, Susan D Martin1

  • 1Department of Pediatrics, Golisano Children's Hospital, University of Rochester Medical Center, 601 Elmwood Ave, Rochester, NY, 14642, USA.

Pediatric Cardiology
|January 13, 2023
PubMed
Summary

Serum Cystatin C showed a significant difference in infants 12 hours post-cardiopulmonary bypass (CPB) with acute kidney injury (AKI). However, only urine output independently predicted AKI, not Cystatin C levels.

Keywords:
BiomarkerCardiac surgeryKidney injuryPediatric

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Area of Science:

  • Pediatric Cardiology
  • Nephrology
  • Biomarker Research

Background:

  • Acute kidney injury (AKI) following cardiopulmonary bypass (CPB) in infants is a significant clinical concern, associated with poor outcomes.
  • Serum Cystatin C (CysC) is a potential early biomarker for AKI due to its synthesis by all nucleated cells.
  • Early identification of AKI in infants undergoing CPB is crucial for timely intervention and improved patient management.

Purpose of the Study:

  • To investigate the utility of serum Cystatin C (CysC) as an early biomarker for acute kidney injury (AKI) in infants undergoing cardiopulmonary bypass (CPB).
  • To compare CysC levels and changes over time between infants who develop AKI and those who do not following CPB.
  • To identify independent predictors of AKI in this vulnerable infant population.

Main Methods:

  • Prospective observational study involving infants under 1 year of age requiring CPB for cardiac surgery.
  • Serum CysC levels were measured at baseline and at 12, 24, 48, and 72 hours post-CPB.
  • AKI was classified using the Kidney Disease Improving Global Outcomes (KDIGO) criteria, with clinical variables, urine output (UOP), and serum creatinine (SCr) also monitored.

Main Results:

  • AKI developed in 41.9% of the 43 infants studied; baseline demographics and CysC levels were similar between AKI and non-AKI groups.
  • Serum CysC levels correlated directly with serum creatinine (R=0.71, p<0.0001).
  • While the percentage change in CysC at 12 hours post-CPB (%CysC12h) was significantly higher in the AKI group, multivariate analysis identified lower urine output (OR: 0.298) as the sole independent predictor of AKI, not %CysC12h.

Conclusions:

  • Serum Cystatin C shows a significant difference in infants developing AKI post-CPB, but it was not an independent predictor in this study.
  • Lower urine output emerged as a significant independent predictor of AKI in infants following CPB.
  • Further research with larger, homogenous populations is warranted to elucidate the role and variability of CysC as an AKI biomarker in infant CPB.