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Related Concept Videos

Renal Failure: Dose Adjustments01:11

Renal Failure: Dose Adjustments

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In patients with renal impairment, drugs undergo significant changes in their pharmacokinetics, which require dosage adjustments to ensure safe and effective therapy.
Reduced renal clearance and elimination rate are common outcomes of renal impairment. These alterations lead to a prolonged elimination half-life and an altered apparent volume of distribution for drugs. As a result, dosage adjustments are typically necessary to maintain optimal drug levels in the body.
However, dosage adjustments...
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Renal Drug Excretion: Overview01:15

Renal Drug Excretion: Overview

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As primary excretory organs, the kidneys maintain homeostasis by removing waste substances from the bloodstream. They comprise over a million units called nephrons, which serve as the kidney's functional units.
A nephron consists of two primary structures: the renal corpuscle and the renal tubule. The renal corpuscle contains the glomerulus, a network of capillaries where the first step of renal excretion, glomerular filtration, occurs. Blood pressure forces water, ions, and small molecules...
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Renal Drug Excretion: Glomerular Filtration01:02

Renal Drug Excretion: Glomerular Filtration

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The kidney serves as the primary organ responsible for eliminating drugs and their metabolites from the body. This process, known as renal elimination, starts with glomerular filtration and results in urine formation. Each kidney houses millions of functional units called nephrons, where urine production occurs. A nephron has two main components: a renal corpuscle and a renal tubule.
Drugs gain access to the kidney via the renal artery, which progressively branches off into afferent arterioles....
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Renal Drug Excretion: Tubular Secretion01:28

Renal Drug Excretion: Tubular Secretion

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Active tubular secretion is a robust, energy-demanding process that utilizes carrier systems to transport drugs into renal tubules. The active renal secretion systems include the organic anion transporter (OAT) for weak acids and the organic cation transporter (OCT) for weak bases. Structurally similar drugs can compete for the same transporter, potentially leading to drug accumulation and toxicity. However, this principle can be exploited therapeutically. One example is probenecid (Probalan),...
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Renal Drug Excretion: Tubular Reabsorption01:25

Renal Drug Excretion: Tubular Reabsorption

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Tubular reabsorption, a process occurring post-glomerular filtration of drugs in the renal tubule, is a critical determinant of drug half-life. During the process of renal excretion, as the glomerular filtrate progresses to the distal convoluted tubule (DCT), drugs that are highly permeable, lipophilic, and nonionized undergo passive reabsorption from the tubular fluid into the surrounding peritubular capillaries. This reabsorption process restricts their elimination through the kidneys. This...
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Pharmacokinetics: Drug–Food and Drug–Viral Interactions01:26

Pharmacokinetics: Drug–Food and Drug–Viral Interactions

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A drug interaction occurs when the concurrent use of another drug, food, or an external substance alters the pharmacological activity of a drug. This interaction can modify the action of the original drug, affecting its effectiveness and safety.Drug–food interactions are significant as they impact drug absorption, metabolism, and excretion. For example, grapefruit juice is a well-known disruptor of drug metabolism. It inhibits the cytochrome P450 3A4 enzyme, crucial for the metabolism of...
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Updated: Mar 23, 2026

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
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[Tenofovir nephrotoxicity].

Corinne Isnard-Bagnis1, Blandine Aloy2, Gilbert Deray3

  • 1Service d'urologie néphrologie transplantation, groupe hospitalier universitaire Pitié-Salpêtrière-Charles-Foix, 47-83, boulevard de l'Hôpital, 75651 Paris cedex 13, France; Université Pierre-et-Marie-Curie, 4, place Jussieu, 75005 Paris, France.

Nephrologie & Therapeutique
|March 28, 2016
PubMed
Summary
This summary is machine-generated.

Tenofovir, an HIV medication, can cause kidney damage (nephrotoxicity), both acute and chronic. Early detection and dose adjustments are key to managing this risk in patients.

Keywords:
Acute kidney injuryAntiretroviralAntirétroviralChronic kidney diseaseDrug nephrotoxicityDrug side effectEffets secondaires médicamenteuxFanconi syndromeInsuffisance rénale aiguëInsuffisance rénale chroniqueSyndrome de FanconiToxicité rénaleTubulopathieTubulopathy

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Area of Science:

  • Nephrology
  • Virology
  • Pharmacology

Background:

  • Tenofovir is a primary nucleotidic reverse-transcriptase inhibitor for HIV treatment.
  • While generally well-tolerated, tenofovir is associated with significant nephrotoxicity.
  • Acute and chronic kidney toxicity mechanisms and manifestations require further understanding.

Purpose of the Study:

  • To characterize the acute and chronic nephrotoxicity of tenofovir.
  • To elucidate the cellular mechanisms underlying tenofovir-induced kidney damage.
  • To identify strategies for mitigating tenofovir-related renal risks.

Main Methods:

  • Review of clinical data and cohort studies on tenofovir nephrotoxicity.
  • Analysis of tenofovir's pharmacokinetic and pharmacodynamic properties related to renal excretion.
  • Examination of cellular pathways involved in tenofovir-induced mitochondrial dysfunction.

Main Results:

  • Acute tenofovir nephrotoxicity involves proximal tubular cell accumulation, mitochondrial DNA polymerase inhibition, and respiratory chain dysfunction, potentially leading to Fanconi syndrome and acute kidney failure.
  • Chronic tenofovir toxicity, characterized by accelerated glomerular filtration rate decline, is increasingly recognized despite unclear pathophysiology.
  • Reversibility of acute toxicity upon drug discontinuation is common, while chronic effects require further investigation.

Conclusions:

  • Tenofovir's renal toxicity, both acute and chronic, is a significant clinical concern.
  • Understanding tenofovir's cellular impact on kidney mitochondria is crucial for managing toxicity.
  • Implementing dose adjustments, risk factor identification, and drug level monitoring can reduce tenofovir-induced nephrotoxicity.