Therapies Database

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

Selective TKI that binds to EGFR

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

Potential direct tubular injury

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

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

in patients with CRS, decrease perfusion vs ATN

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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increase in serum Cr

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

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No reported true AKI

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

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

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

Unclear

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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ATN (Acute tubular necrosis)

AIN reported and glomerular sclerosis

Water/electrolyte disturbances

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

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Unclear mechanism of AKI.

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

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

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

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

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

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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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ATN (Acute tubular necrosis), Water/electrolyte disturbances

Water/electrolyte disturbances

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

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

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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

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

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

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

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

AKI not well described

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

Inhibition of active tubular secretion of creatinine without clinically meaningful alteration in renal function.

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AIN (Acute interstitial nephritis)

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

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n/a

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

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

unclear cause of AKI.

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

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