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| Etiology | Pathophysiology | Management/potential therapeutic options |
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| Sepsis | Vasodilatation and reduced renal blood flow resulting in ischemia and direct renal tubular insult by inflammatory cytokines | Treatment of sepsis with appropriate medication |
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Nephrotoxic medication
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Amphotericin B
| Vasoconstriction of renal vasculature resulting in hypoperfusion and renal tubular epithelial damage | Measurement of urinary UNGAL levels may serve as early biomarker of AKI.
Restricting amphotericin use only for documented fungal infections.
Use of antifungals with minimal nephrotoxicity such as itraconazole, fluconazole, and voriconazole. |
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Acyclovir
| Formation of crystals in renal tubules and collecting ducts resulting in obstruction especially with IV administration in high doses | Demonstration of birefringent needle shaped crystals in urinary sediment under polarizing microscopy helps in diagnosis.
Slower IV administration, hydration, and renal dose adjustments are recommended |
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Aminoglycosides
| Intracellular accumulation in proximal tubules and change in cellular permeability | Measurement of alanine aminopeptidase and N-acetyl-beta-D glucosaminidase in urine may serve as an early biomarker of nephrotoxicity.
Reduction in dosage frequency is the mainstay of management |
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| Cyclosporine A | Renal vasoconstriction secondary to renin-angiotensin system activation.
Increased production of VEGF.
Downregulation of renal Klotho and increased oxidative stress causing renal endothelial damage.
Thrombotic microangiopathy.
Impaired glucose metabolism | Potential treatment options are aliskiren, valsartan, and switching to alternative immunosuppressant such as sirolimus |
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| Hepatic SOS | Damage to hepatic sinusoidal endothelial cells by chemotherapeutic agents and subendothelial deposition of fibrin and other blood products resulting in venular obstruction.
Glutathione depletion due to chemotherapeutic drug detoxification by glutathione pathway resulting in hepatocellular necrosis and fibrosis | Circulating endothelial cells (CECs) and plasminogen activator inhibitor-1 are potential biomarkers.
Modification of conditioning regimens and use of defibrotide |
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| Thrombotic microangiopathy | Renal endothelial injury by cytokines released in GVHD.
Decreased levels of VEGF.
Exposure to calcineurin inhibitors, TBI, and infections | Measurement of serum NETs level may serve as early biomarker for TMA.
Continuing acute GVHD treatment may be of benefit.
Plasma exchange has a limited role.
Eculizumab may be a potential treatment option |
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| Marrow infusion toxicity | Exposure to cryoprecipitants causes hemolysis and heme precipitation in distal renal tubules resulting in tubular obstruction | Alkalinization of urine and mannitol induced diuresis |
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| Tumor lysis syndrome | Lysis of tumor cells releasing intracellular products into circulation resulting in hyperuricemia, hyperphosphatemia, hyperkalemia, and hypocalcemia.
Precipitation of calcium phosphate and urate crystals causes damage to renal tubules.
Vasoconstriction of renal arterioles and exposure to inflammatory cytokines causes injury to renal tubules | Mainstay of management involves IV hydration, rasburicase, and allopurinol.
Low phosphate diet and phosphate binders for hyperphosphatemia.
Medical management of hyperkalemia and renal replacement therapy in resistant cases and severe AKI |
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| Infections | | |
BK virus
| Immunosuppression reactivates dormant virus in urinary tract causing renal tubular injury and hemorrhagic cystitis | Reducing immunosuppression is the mainstay of treatment.
Supportive care for cystitis. |
| Adenovirus | Tubulointerstitial nephritis and cystitis | Supportive care.
Intravesical cidofivir is potential treatment option for cystitis |
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