Index
Module 9 • Nephrology
Acute Kidney Injury & Kidney Replacement Therapy
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Acute Kidney Injury & Kidney Replacement Therapy
Paige Garber Bradshaw ~3 min read Module 9 of 20
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Acute Kidney Injury and Kidney Replacement Therapy in the Critically Ill Patient

Examples of drugs that contribute to immune-mediated glomerular diseases include hydralazine

and propylthiouracil. Drugs that contribute to direct glomerular cell toxicity include lithium,

NSAIDs, sirolimus, anabolic steroids, anti-angiogenesis drugs (i.e., bevacizumab, sunitinib,

sorafenib), chemotherapeutics (i.e., mitomycin C, gemcitabine), calcineurin inhibitors,

interferon, thienopyridines (i.e., clopidogrel, prasugrel), and quinine.

ii.

Management of drug-induced glomerular disease includes identifying the subtype and

discontinuing the offending agent. These injuries are often type B reactions, subacute or chronic,

and may partly be irreversible. Immunosuppressants and plasmapheresis may be indicated for

treatment.

d.Osmotic nephrosis: Drugs such as mannitol; hydroxyethylstarch; immunoglobulins, especially those

containing sucrose; and dextrans may lead to osmotic nephrosis. In these cases, drug molecules

undergo pinocytosis and cellular accumulation, and the cells become swollen and vacuolated,

leading to tubular lumen obstruction.

Crystalluria/nephrolithiasis: Certain medications are insoluble in the urine and can result in

crystalline nephropathy and/or kidney stones. Suggestive diagnostics include crystalluria on urinary

analysis, overt nephrolithiasis, and ultrasound findings indicative of obstruction. Examples of drug

culprits include antibiotics, acyclovir, methotrexate, antiretrovirals, triamterene, and ethylene

glycol–associated calcium oxalate crystal precipitation.

Altered electrolyte handling/tubular dysfunction: Drugs may alter how the kidney handles

electrolytes, tubular proteins, and water. Example patterns include the syndrome of inappropriate

antidiuretic hormone, an acquired Fanconi syndrome; renal tubular acidosis; and nephrogenic

diabetes insipidus. Serum and urine electrolyte abnormalities, altered serum and urine osmolality,

and an altered acid-base profile may each indicate this type of DIKD. Examples of drug causes include

antiretrovirals, lithium, selective serotonin reuptake inhibitors, antiepileptics, and vincristine.

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A comprehensive medication list, titled the β€œAcute Kidney Intervention and Pharmacotherapy (AKIP)”

list, was recently established and includes 681 unique drugs or drug combinations that are renally dosed,

potentially nephrotoxic, or both in the acutely ill population (Ann Pharmacother. 2025;59(4):371-377).

This evidence-based, standardized list of medications will be useful to harmonize future epidemiologic

studies and medication quality improvement initiatives.

G.AKI Survivorship
1

Recently, increased emphasis has been placed on AKI survivor care. AKI survivor care focuses on

patients with an episode of AKI during hospitalization who are being discharged. Individuals have tried

specific AKI survivor clinics to improve comprehensive kidney care follow-up to limit the burden of

CKD.

2The landmark FUSION randomized controlled trial (Clin J Am Soc Nephrol. 2021;16:1005-14) enrolled

patients who survived an episode of stage 2 or 3 AKI and randomized them to either early nephrology

follow-up with a bundled care intervention or usual care. Although process outcomes were improved

with bundled care (increased nephrology visits, kidney function monitoring, medication reconciliation

completion and review), clinical outcomes, including a major acute kidney event at 1 year, were no

different. More research is needed to determine the optimal method for follow-up in AKI survivors that

is aligned with best practices and patient-centeredness.

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