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Therapies Database

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Abemaciclib (Verzenio)

CDK4/6 inhibitors

ATN (Acute tubular necrosis), ATIN (Acute tubulointerstitial nephritis), Water/electrolyte disturbances, Increase in serum creatinine which is likely caused by inhibition of tubular creatinine secretion, increase incidence of urinary tract infections

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Afatinib

Anti-angiogenesis

Selective TKI that binds to EGFR

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Aflibercept

Anti-angiogenics

TMA (thrombotic microangiopathy) (systemic/kidney limited), Podocyte Injury

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Atezolizumab

Immune check point inhibitors (ICPIs)

AIN (Acute interstitial nephritis), ATN (Acute tubular necrosis), Water/electrolyte disturbances, Glomerular injury, Tubular injury, Podocyte Injury, Chronic interstitial Nephritis

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Avelumab

Immune check point inhibitors (ICPIs)

AIN (Acute interstitial nephritis), ATN (Acute tubular necrosis), Water/electrolyte disturbances, Glomerular injury, Tubular injury, Podocyte Injury, Chronic interstitial Nephritis

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Axicabtagene ciloleucel // Yescarta

CAR-T ( Chimeric antigen receptor -T cell therapy)

in patients with CRS, decrease perfusion vs ATN

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Axitinib

Tyrosine kinase inhibitors

AIN (Acute interstitial nephritis), TMA (thrombotic microangiopathy) (systemic/kidney limited). HTN; vascular endothelial growth factor (VEGF) signaling pathway inhibition . Reduction of vasodilator production such as NO and enhance production of vasoconstriction such as endothelin 1

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Bendamustine

Non-platinum based Alkylating Agents

increase in serum Cr

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Bevacizumab

VEGF receptor monoclonal antibody

TMA (thrombotic microangiopathy) (systemic/kidney limited), Glomerular injury, cryoglobulinemic MPGN, collapsing FSGS

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Bosutinib

Tyrosine kinase inhibitors

No reported true AKI

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Brexucabtagene autoleucel// TECARTUS

CAR-T ( Chimeric antigen receptor -T cell therapy)

In the clinical trials no mention/ in package insert mention AKI in 6% patient in ZUMA-3. I would think is possible same mechanism with other CAR-T therapies, from CRS leading to hypoperfusion

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Capecitabine

Anti-metabolite

Not commonly associated with AKI may cause dehydration and pre-renal AKI

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Carboplatin

Platinum based Alkylating agents

AIN (Acute interstitial nephritis), ATN (Acute tubular necrosis), TMA (thrombotic microangiopathy) (systemic/kidney limited), Water/electrolyte disturbances, CKD, has significant emetic potential leading to pre renal state like nausea, vomiting diarrhea

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Cemiplimab

Immune check point inhibitors (ICPIs)

AIN (Acute interstitial nephritis), ATN (Acute tubular necrosis), Water/electrolyte disturbances, Glomerular injury, Tubular injury, Podocyte Injury, Chronic interstitial Nephritis

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Cetuximab

Anti-angiogenesis

Unclear

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Cisplatin

Platinum based Alkylating agents

Cellular toxicity of S3 segment PCT. Vasoconstriciton. PCT apoptosis (ATI). PCT-incresed uptake by OCT, decreased expression of sodium dep glucose transports. Decreased expression of magnesium transports. Generation of reactive ox species. Fanconi and TMA

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Cyclophosphamide

Non-platinum based Alkylating Agents

ATN (Acute tubular necrosis)

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Dabrafenib

Anti-neoplastic

AIN reported and glomerular sclerosis

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Dasatinib

Tyrosine kinase inhibitors

Water/electrolyte disturbances

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Durvalumab

Immune check point inhibitors (ICPIs)

AIN (Acute interstitial nephritis), ATN (Acute tubular necrosis), Water/electrolyte disturbances, Glomerular injury, Tubular injury, Podocyte Injury, Chronic interstitial Nephritis

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Etoposide

Topoisomerase inhibitor

Unclear mechanism of AKI.

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Fluorouracil

Anti-metabolite

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Gemcitabine

Anti-metabolite

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Ibandronate sodium, Boniva

Bisphosphonates

ATN (Acute tubular necrosis), Water/electrolyte disturbances, Glomerular injury, Podocyte Injury

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Ibrutinib

Anti-angiogenesis

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Idecabtagene vicleucel // ABECMA

CAR-T ( Chimeric antigen receptor -T cell therapy)

renal injury seems to be related to CRS - decreased kidney perfusion vs ATN (but unsure from this drug as no studies done to determined the cause)

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Ifosfamide

Non-platinum based Alkylating Agents

AIN (Acute interstitial nephritis), ATN (Acute tubular necrosis), Fanconi syndrome , and nephrogenic DI

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Imatinib

Tyrosine kinase inhibitors

ATN (Acute tubular necrosis), Crystalline Nephropathy/Tubular obstruction

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Ipilimumab

Immune check point inhibitors (ICPIs)

AIN (Acute interstitial nephritis), ATN (Acute tubular necrosis), Water/electrolyte disturbances, Glomerular injury, Tubular injury, Podocyte Injury, Chronic interstitial Nephritis

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Irinotecan

Topoisomerase inhibitor

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Lisocabtagene maraleucel // Breyanzi

CAR-T ( Chimeric antigen receptor -T cell therapy)

74% patients with CRS - AKI (26%) from kidney hypoperfusion vs ATN

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Methotrexate

Anti-metabolite

Crystallization of MTX in the kidney tubular lumen. Other possible mechanisms; vasoconstriction of afferent capillary and direct effects on renal tubular cells

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Nedaplatin

Platinum based Alkylating agents

ATN (Acute tubular necrosis), Water/electrolyte disturbances

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Nilotinib

Tyrosine kinase inhibitors

Water/electrolyte disturbances

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Nivolumab

Immune check point inhibitors (ICPIs)

AIN (Acute interstitial nephritis), ATN (Acute tubular necrosis), Water/electrolyte disturbances, Glomerular injury, Tubular injury, Podocyte Injury, Chronic interstitial Nephritis

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Oxaliplatin

Platinum based Alkylating agents

ATN (Acute tubular necrosis), ATIN (Acute tubulointerstitial nephritis), TMA (thrombotic microangiopathy) (systemic/kidney limited), Water/electrolyte disturbances

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Paclitaxel

Microtubule inhibitor

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Palbociclib (Ibrance)

CDK4/6 inhibitors

ATN (Acute tubular necrosis), ATIN (Acute tubulointerstitial nephritis), Water/electrolyte disturbances, Increase in serum creatinine which may be related to inhibition of tubular creatinine secretion, increase incidence of urinary tract infections

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Pamidronate disodium, Aredia

Bisphosphonates

ATN (Acute tubular necrosis), Water/electrolyte disturbances, Glomerular injury, Podocyte Injury

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Pazopanib

Tyrosine kinase inhibitors

TMA (thrombotic microangiopathy) (systemic/kidney limited), Glomerular injury

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Pembrolizumab

Immune check point inhibitors (ICPIs)

AIN (Acute interstitial nephritis), ATN (Acute tubular necrosis), Water/electrolyte disturbances, Glomerular injury, Tubular injury, Podocyte Injury, Chronic interstitial Nephritis

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Pemetrexed

Anti-metabolite

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Ponatinib

Tyrosine kinase inhibitors

TMA (thrombotic microangiopathy) (systemic/kidney limited), Glomerular injury possibly via VWF-mediated platelet adhesion and a secondary microvascular angiopathy

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Regorafenib

Tyrosine kinase inhibitors

AKI not well described

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Ribociclib (Kisqali)

CDK4/6 inhibitors

ATN (Acute tubular necrosis), ATIN (Acute tubulointerstitial nephritis), Water/electrolyte disturbances, Increase in serum creatinine which may be related to inhibition of tubular creatinine secretion, increase incidence of urinary tract infections

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Sorafenib

Tyrosine kinase inhibitors

AIN (Acute interstitial nephritis)

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Sunitinib

Tyrosine kinase inhibitors

AIN (Acute interstitial nephritis), TMA (thrombotic microangiopathy) (systemic/kidney limited)

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Temozolomide

Non-platinum based Alkylating Agents

n/a

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Tisagenlecleucel // Kymriah

CAR-T ( Chimeric antigen receptor -T cell therapy)

ATN (Acute tubular necrosis), injury from CRS leading to decreased perfusion.

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Topotecan

Topoisomerase inhibitor

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Trabectedin

Non-platinum based Alkylating Agents

ATN (Acute tubular necrosis), Rhabdomyolysis , CPK elevation ,Isolated increase in Serum Cr is noted without AKI phenotype

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Vandetanib

Tyrosine kinase inhibitors

unclear cause of AKI.

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Venetoclax

Anti-neoplastic

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Vinblastine

Microtubule inhibitor

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Vincristine

Microtubule inhibitor

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Zoledronic Acid, Reclast, Zometa

Bisphosphonates

ATN (Acute tubular necrosis), Water/electrolyte disturbances, Glomerular injury, Podocyte Injury

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tepotinib

TKI- MET Inhibitor

pseduo-AKI; competitive inhibition of creatinine secretion in the renal tubules

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