Lecture: Ward Rounds and Acute Kidney Injury
Dr. Sarah Faubel created this 2-hour lecture block. The idea was to look at four different theater of operations and look do a deep dive on how the causes and treatments of acute kidney injury differ. This is a salute to Bayesian logic and attempts to give doctors a refined view of pre-test probabilities for the etiologies of AKI depending on the clinical scenario. Great idea.
Dr. Sangeeta Hingoran is up next to speak about AKI after hematopoietic cell transplant. After familiarizing the audience with the language of hematopoietic cell transplant she shared the risk of various complications based on the type of transplant: myeloablative, autologous cell transplant has the lowest risk of AKI and no risk of graft versus host disease. Non-myeloablative conditioning, autologous cell transplant has the lowest risk of sinusoidal obstructive syndrome, previously known as veno-occlusive disease. The table came from one of her articles from 2007.
Hematopoietic cell transplants use a host of renal toxic medications including: calcineurin inhibitors, acyclovir, trimethoprim-sulfamethoxazole, ganciclovir, and foscarnet.
The timing of AKI ranges from 14 to 60 days after the transplant. The BMT community settled on an AKI system prior to the ADQI’s RIFLE criteria or the AKIN criteria. The system is pretty straightforward:
▪ Grade 0: Decrease in GFR of less than 25%
▪ Grade 1: Decrease in GFR from 25-50%
▪ Grade 2: More than a doubling of creatinine but no need for dialysis
▪ Grade 3: Grade 2 and the need for dialysis
Zager et al published their experience regarding AKI in 272 patients in AJKD. They found 24% required dialysis and 53% doubled creatinine. Risks for AKI included amphotericin B, weight gain >2kg, jaundice, pre-transplant Cr >0.7 mg/dL.
Dr. Hingorini, our speaker, found similar risk factors in a review of 147 patients: amphotericin (including liposomal), sinusoidal obstructive syndrome.
Lopes et al found that AKI predicted mortality. The hazard ratio for 5-year all-cause mortality was 2.36.
Ando et al found a graded increase in mortality with increasing degrees of renal failure:
▪ Risk: HR 1.64 (NS)
▪ Injury: HR 2.59
▪ Failure: HR 8.8
Parikh et al confirmed this finding in a meta analysis of 6 studies and 1,211 patients.
Gooley et al found a decreased incidence of AKI over time, going from 50 to 33% from 1993-1997 to 2003-2007. The decreasing frequency of sinusoidal obstructive syndrome is the driver for this improvement in patient care.
Treatment protocols have focused on controlling fluid overload.
Texas Children’s used an AKI protocol where they initiated dialysis quickly to prevent fluid overload. The protocol is interesting:
▪ AKI and 5% fluid overload: furosemide and low dose dopamine
▪ 10% fluid overload and 50% increase in creatinine or drop in urine output to half: start RRT
This was successful in reducing fluid overload but did not reduce mortality (Michael et al).
The last aspect she examined was the long-term complications that resulted from AKI. She reported the results of Hoffmeister et al, who found an increased rate of hypertension 30 years after dialysis.
Post by Dr. Joel Topf, eAJKD Advisory Board member