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
glycolβassociated 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.
list, was recently established and includes 681 unique drugs or drug combinations that are renally dosed,
This evidence-based, standardized list of medications will be useful to harmonize future epidemiologic
studies and medication quality improvement initiatives.
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.
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.