From Initiation to Recovery: A Longitudinal Analysis of Polymyxin B-Induced Kidney Injury in Clinical Practice

Gui-Xiang Zhang1, Meng-Ru Zhang2, Qiang Qu3

  • 1Department of Pharmacy, The Second People's Hospital of Hunan Province (Brain Hospital of Hunan Province), Changsha, Hunan, People's Republic of China.

Abstract

Insights

Identifying risk factors for Polymyxin B (PMB)-associated nephrotoxicity is crucial. Concurrent use of vancomycin, aminoglycosides, amphotericin B, high-dose furosemide, and higher PMB loading doses increase AKI risk.

Area of Science:

  • Pharmacology and Nephrology
  • Clinical Medicine
  • Drug Safety

Background:

  • Polymyxin B (PMB) is vital for treating severe infections but carries a risk of nephrotoxicity.
  • Identifying factors contributing to PMB-induced kidney damage is essential for patient safety and improved treatment outcomes.

Purpose of the Study:

  • To identify risk factors associated with Polymyxin B-induced acute kidney injury (AKI).
  • To evaluate the impact of these risk factors on renal function recovery in patients receiving PMB therapy.

Main Methods:

  • Retrospective analysis of 325 patients treated with intravenous PMB.
  • Logistic regression analyses to identify risk factors for AKI and factors influencing renal recovery.
  • AKI diagnosis and staging based on KDIGO criteria using serum creatinine levels.

Main Results:

  • 34.5% of patients developed AKI. Independent risk factors included concurrent vancomycin, aminoglycosides, amphotericin B, furosemide (>20 mg/day), and higher PMB loading dose.
  • Median time to AKI onset was 7 days.
  • Renal recovery occurred in 41.1% of AKI patients; vasoactive agent use was negatively associated with recovery.

Conclusions:

  • Concurrent use of vancomycin, aminoglycosides, amphotericin B, high-dose furosemide, and PMB loading dose are key risk factors for AKI.
  • Close serum creatinine monitoring within the first week of PMB therapy is critical.
  • Minimizing nephrotoxic agents and stabilizing hemodynamics are crucial for optimizing renal recovery.

Related Concept Videos

Acute Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

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...
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

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...
Drug Accumulation During Multiple Dosing: Intermittent IV Infusions01:24

Drug Accumulation During Multiple Dosing: Intermittent IV Infusions

Intermittent intravenous (IV) infusion is a method of drug administration where medications are delivered over short infusion periods followed by intervals of no drug delivery. This approach helps to prevent sustained high drug concentrations in the bloodstream, reducing the risk of adverse effects associated with prolonged exposure. Unlike continuous infusion, steady-state concentrations may not be achieved during a single dosing cycle but can be reached through repeated...
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

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...
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

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...
Acute Kidney Injury V: Interprofessional Care01:20

Acute Kidney Injury V: Interprofessional Care

Acute Kidney Injury (AKI) requires a collaborative healthcare approach to restore renal function and prevent complications. Essential management strategies involve monitoring fluid and electrolyte balance, adjusting medications, initiating dialysis when necessary, and providing nutritional support.Fluid and Electrolyte ManagementFluid Monitoring: Regularly monitoring body weight, central venous pressure, and urine output helps detect fluid imbalances early. Patient intake and output are...