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

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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 (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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Rifampin-induced Acute Kidney Injury Is Associated With Hemolysis and Drug Re-exposure.

Junaid A Wali1, Yaseen A Jamal1, Mustafa Al-Kawaaz2

  • 1Department of Pathology, Stanford University School of Medicine, Stanford, CA.

Kidney Medicine
|January 9, 2026
PubMed
Summary

Rifampin can cause acute kidney injury and hemolysis, especially with re-exposure. This study highlights acute tubular necrosis with hemoglobin casts as a key finding in rifampin-induced kidney injury, emphasizing the need for awareness.

Keywords:
Acute interstitial nephritisAcute kidney injury (AKI)Drug-induced hemolysisHemoglobin cast nephropathyHemolysisKidney biopsyRifampicinRifampinTuberculosis

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Area of Science:

  • Nephrology
  • Pharmacology
  • Infectious Diseases

Background:

  • Rifampin is a crucial antibiotic for treating tuberculosis and other infections.
  • Acute kidney injury and hemolysis are rare but serious adverse effects associated with rifampin, particularly upon re-exposure.
  • The precise clinical, laboratory, and pathological correlations of rifampin-induced kidney injury require further elucidation.

Purpose of the Study:

  • To investigate the association between rifampin exposure and acute kidney injury (AKI) in a contemporary patient cohort.
  • To comprehensively correlate clinical presentations, laboratory findings, and kidney biopsy results in patients with suspected rifampin-induced nephrotoxicity.
  • To identify specific histopathological features indicative of rifampin-related kidney damage.

Main Methods:

  • A retrospective case series was conducted, identifying adult patients who underwent kidney biopsy for AKI while on rifampin between 2012 and 2023.
  • Clinical data were extracted from electronic medical records, and biopsy pathology reports were analyzed.
  • Correlation of clinical, laboratory, and histopathological findings was performed.

Main Results:

  • Eighteen patients presented with AKI and hemolysis during rifampin therapy, with nine having prior rifampin exposure.
  • Common symptoms included gastrointestinal and flu-like illness following rifampin (re)exposure.
  • Kidney biopsies revealed acute tubular injury in all patients, with 11 showing pigmented casts (9 hemoglobin, 2 myoglobin), and 15 exhibiting evidence of hemolysis. Acute tubular necrosis with hemoglobin casts emerged as a significant finding.

Conclusions:

  • Rifampin-induced hemolytic anemia and hemoglobin cast nephropathy are rare but severe complications that can lead to AKI.
  • Clinicians and patients must be vigilant for these potential side effects.
  • Avoiding interruption of rifampin therapy may be crucial in preventing severe adverse events.