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Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
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Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
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All neuromuscular blocking agents are injected intravenously because they are poorly absorbed from the GI tract. Rapid onset is achieved with intravenous administration, although absorption is also adequate from an intramuscular injection. Since these agents are highly ionized, they do not readily penetrate cell membranes or cross the blood-brain barrier.
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Once the process of glomerular filtration is completed, blood carrying unfiltered drug molecules traverses through efferent arterioles and makes its way into the peritubular capillaries in the proximal tubule. A variety of carriers play a pivotal role in actively secreting drugs from these peritubular capillaries into the tubular fluid. The organic anion transporter transfers acidic drugs, against an electrochemical gradient, from the peritubular capillaries into the renal tubule cells and...
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Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
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Related Experiment Video

Updated: Jun 27, 2025

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Polymyxin B-induced Bartter syndrome.

Bhavesh Mohan Lal1, Nimisha Musthafa Hafeesa1, Naval Kishore Vikram1

  • 1Department of Medicine, All India Institute of Medical Sciences, New Delhi, Delhi, India.

BMJ Case Reports
|May 3, 2024
PubMed
Summary

Acquired Bartter syndrome can be drug-induced. This case report highlights polymyxin B-induced nephrotoxicity, causing Bartter syndrome symptoms that resolved upon drug withdrawal and recurred upon reintroduction.

Keywords:
Adult intensive careDrugs: infectious diseasesFluid electrolyte and acid-base disturbancesUnwanted effects / adverse reactions

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Area of Science:

  • Nephrology
  • Clinical Pharmacology
  • Genetics

Background:

  • Bartter syndrome is a genetic disorder with metabolic alkalosis, hypokalemia, hypomagnesemia, and hypercalciuria.
  • Acquired Bartter syndrome can be induced by medications like polymyxins and aminoglycosides.
  • Polymyxin B and colistin (polymyxin E) are clinically used, with colistin more frequently linked to nephrotoxicity.

Observation:

  • A middle-aged male patient presented with symptoms mimicking Bartter syndrome.
  • The patient developed acquired Bartter syndrome attributed to polymyxin B treatment.
  • Symptoms resolved upon discontinuation of polymyxin B and reappeared upon its reintroduction.

Findings:

  • Polymyxin B can cause nephrotoxicity leading to acquired Bartter syndrome.
  • Kidney handling differences between polymyxin B and colistin may influence their nephrotoxic potential.
  • This case demonstrates a reversible drug-induced Bartter syndrome.

Implications:

  • Clinicians should be vigilant for polymyxin B-induced nephrotoxicity, especially in patients presenting with Bartter syndrome-like symptoms.
  • Monitoring kidney function is crucial during polymyxin B therapy.
  • Understanding drug-induced nephrotoxicity is vital for patient safety and effective treatment strategies.