The “False Alarm:” Recognizing Pseudoacute Kidney Injury in Cancer Patients

Dear Editor, The introduction of targeted therapies has transformed cancer treatment and improved patient outcomes. However, their nephrotoxic effects present new challenges in nephrology. Both true and pseudo-acute kidney injury (AKI) can be caused by cancer drugs. It is important to know the distinction for effective therapy. Pseudo-AKI is an emerging phenomenon where serum creatinine (SCr) levels falsely elevate, mimicking actual kidney damage. SCr is the most used marker of kidney function and its levels vary with the rate of its production and elimination from the body. Its elimination relies not only on filtration but also on tubular secretion by transporters like organic cation transporter 2, organic cation transporter 3, organic anion transporter polypeptide 2, multidrug and toxin extrusion protein 1, and multidrug and toxin extrusion protein 2-K.[1,2] Certain medications, particularly targeted therapies, can interfere with these transporters, causing a harmless rise in SCr and a corresponding decline in estimated glomerular filtration rate (eGFR). This can erroneously be interpreted as AKI. Several classes of chemotherapy drugs, particularly targeted therapies, have been associated with pseudo-AKI [Table 1].[3,4]Table 1: Drugs causing Pseudo AKIPseudo-AKI is characterized by transient increase in SCr within the first 2 weeks of treatment initiation. Upon discontinuation or dose adjustment of the causative agent, SCr levels usually return promptly to baseline, demonstrating near-complete recovery of renal function. Urine analysis typically reveals no evidence of kidney injury, such as proteinuria, hematuria, or casts. Assessment of renal function using alternative methods, such as cystatin C-based eGFR or radioisotope techniques (e.g., 51Cr-EDTA and 99 mTc-DTPA), reveals that the “true” glomerular filtration rate remains largely unaffected, aligning with pretreatment estimates.[5] Measured GFR techniques, such as inulin clearance or iohexol plasma clearance, provide a more precise assessment of kidney function by directly measuring the actual filtration rate. Recognizing pseudo-AKI induced by targeted chemotherapy is important. Missed diagnosis of pseudo-AKI can lead to unnecessary tests, such as renal ultrasound examination or even kidney biopsies, which can be invasive and costly. The fear of true AKI may lead to dose reductions or even discontinuation of life-saving cancer therapies, potentially compromising treatment effectiveness and patient outcomes. Awareness of this phenomenon will help clinicians to adjust treatment plans accordingly, ensuring both effective cancer treatment and optimal kidney function. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

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Publication Details

Journal
Indian Journal of Kidney Diseases
Published
2025-01-01
DOI
https://doi.org/10.4103/ijkd.ijkd_48_24
Primary Topic
Acute Kidney Injury Research
Type
article
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article

The “False Alarm:” Recognizing Pseudoacute Kidney Injury in Cancer Patients

Anagha Auradkar, Jasmine Sethi
Indian Journal of Kidney Diseases
Acute Kidney Injury Research
article

The “False Alarm:” Recognizing Pseudoacute Kidney Injury in Cancer Patients

Anagha Auradkar, Jasmine Sethi
article en

Abstract

Dear Editor, The introduction of targeted therapies has transformed cancer treatment and improved patient outcomes. However, their nephrotoxic effects present new challenges in nephrology. Both true and pseudo-acute kidney injury (AKI) can be caused by cancer drugs. It is important to know the distinction for effective therapy. Pseudo-AKI is an emerging phenomenon where serum creatinine (SCr) levels falsely elevate, mimicking actual kidney damage. SCr is the most used marker of kidney function and its levels vary with the rate of its production and elimination from the body. Its elimination relies not only on filtration but also on tubular secretion by transporters like organic cation transporter 2, organic cation transporter 3, organic anion transporter polypeptide 2, multidrug and toxin extrusion protein 1, and multidrug and toxin extrusion protein 2-K.[1,2] Certain medications, particularly targeted therapies, can interfere with these transporters, causing a harmless rise in SCr and a corresponding decline in estimated glomerular filtration rate (eGFR). This can erroneously be interpreted as AKI. Several classes of chemotherapy drugs, particularly targeted therapies, have been associated with pseudo-AKI [Table 1].[3,4]Table 1: Drugs causing Pseudo AKIPseudo-AKI is characterized by transient increase in SCr within the first 2 weeks of treatment initiation. Upon discontinuation or dose adjustment of the causative agent, SCr levels usually return promptly to baseline, demonstrating near-complete recovery of renal function. Urine analysis typically reveals no evidence of kidney injury, such as proteinuria, hematuria, or casts. Assessment of renal function using alternative methods, such as cystatin C-based eGFR or radioisotope techniques (e.g., 51Cr-EDTA and 99 mTc-DTPA), reveals that the “true” glomerular filtration rate remains largely unaffected, aligning with pretreatment estimates.[5] Measured GFR techniques, such as inulin clearance or iohexol plasma clearance, provide a more precise assessment of kidney function by directly measuring the actual filtration rate. Recognizing pseudo-AKI induced by targeted chemotherapy is important. Missed diagnosis of pseudo-AKI can lead to unnecessary tests, such as renal ultrasound examination or even kidney biopsies, which can be invasive and costly. The fear of true AKI may lead to dose reductions or even discontinuation of life-saving cancer therapies, potentially compromising treatment effectiveness and patient outcomes. Awareness of this phenomenon will help clinicians to adjust treatment plans accordingly, ensuring both effective cancer treatment and optimal kidney function. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Indian Journal of Kidney DiseasesVol. 4(1)
Mathrusri Ramabai Ambedkar Dental College & Hospital (IN), Post Graduate Institute of Medical Education and Research (IN)
Openalex Percentile: Top 92%
Acute Kidney Injury Research
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