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Related Concept Videos

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...
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Renal Failure: Dose Adjustments

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.
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Chronic Kidney Disease III: Interprofessional Care01:28

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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...
Nephrons01:10

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Related Experiment Video

Updated: Jun 25, 2026

Induction of Nephrotic Syndrome in Mice by Retrobulbar Injection of Doxorubicin and Prevention of Volume Retention by Sustained Release Aprotinin
07:38

Induction of Nephrotic Syndrome in Mice by Retrobulbar Injection of Doxorubicin and Prevention of Volume Retention by Sustained Release Aprotinin

Published on: May 6, 2018

Calcineurin inhibitor nephrotoxicity.

Maarten Naesens1, Dirk R J Kuypers, Minnie Sarwal

  • 1Department of Nephrology and Renal Transplantation, University Hospitals Leuven, Herestraat 49, B-3000 Leuven, Belgium. maarten.naesens@uzleuven.be

Clinical Journal of the American Society of Nephrology : CJASN
|February 17, 2009
PubMed
Summary

Calcineurin inhibitors like cyclosporine and tacrolimus improve transplant outcomes but cause kidney damage. This review explores calcineurin inhibitor nephrotoxicity mechanisms, diagnosis, and factors influencing its development.

Related Experiment Videos

Last Updated: Jun 25, 2026

Induction of Nephrotic Syndrome in Mice by Retrobulbar Injection of Doxorubicin and Prevention of Volume Retention by Sustained Release Aprotinin
07:38

Induction of Nephrotic Syndrome in Mice by Retrobulbar Injection of Doxorubicin and Prevention of Volume Retention by Sustained Release Aprotinin

Published on: May 6, 2018

Area of Science:

  • Nephrology
  • Immunology
  • Pharmacology

Background:

  • Calcineurin inhibitors (cyclosporine, tacrolimus) are vital for transplantation success.
  • Chronic nephrotoxicity remains a significant challenge, impacting long-term graft survival.
  • Understanding calcineurin inhibitor nephrotoxicity is crucial for improving patient outcomes.

Purpose of the Study:

  • To review clinical features, diagnosis, and mechanisms of acute and chronic calcineurin inhibitor nephrotoxicity.
  • To critically evaluate the role of the calcineurin-NFAT pathway in nephrotoxicity.
  • To explore factors influencing susceptibility to calcineurin inhibitor-induced kidney damage.

Main Methods:

  • Comprehensive literature review of calcineurin inhibitor nephrotoxicity.
  • Analysis of clinical, histological, physiological, and molecular data.
  • Critical assessment of evidence linking drug levels and local factors to nephrotoxicity.

Main Results:

  • Calcineurin inhibitor nephrotoxicity involves reversible and irreversible kidney damage across all compartments.
  • The direct link between calcineurin-NFAT pathway activation and nephrotoxicity is not fully established.
  • Local drug exposure and factors like P-glycoprotein, CYP3A4/5, kidney age, and genetic polymorphisms influence susceptibility.

Conclusions:

  • Calcineurin inhibitor nephrotoxicity is a complex process with multifactorial causes.
  • Further research into underlying mechanisms is needed for targeted prevention and therapy.
  • Identifying susceptibility factors may allow for personalized immunosuppressive strategies.