Intrarenal Infusions Aid AKI Recovery

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Infusion of high-dose fenoldopam directly into the kidneys helps patients regain renal function.

HOLLYWOOD, Fla.— Using a novel drug-delivery system to infuse fenoldopam and other vasodilators directly into the kidneys may improve recovery from acute kidney injury (AKI), according to a small study showing that this approach dramatically reduced 28-day mortality when compared with historical outcomes.

At the 21st annual International Symposium on Endovascular Therapy (ISET) here, James A. Tumlin, MD, professor of medicine at the University of Tennessee at Chattanooga and director of clinical research at Southeast Renal Research Institute, also in Chattanooga, told attendees that 61% of subjects recovered renal function within four days after treatment.

Much of the kidney dysfunction in early AKI involves reduced blood flow at the corticomedullary junction. Previous studies have attempted to use fenoldopam and other vasodilators to reverse this effect, but the onset of systemic hypotension prevented investigators from reaching target doses and potentially produced additional damage to the kidneys.

Dr. Tumlin and colleagues attempted to address this problem by threading catheters from the groin into the aorta and then cannulating the renal arteries under fluorescent-imaging guidance. Using the intrarenal approach, Dr. Tumlin and colleagues were able to safely infuse doses of fenoldopam as high as 0.8 µg/kg/min directly into the renal arteries.

Of 28 AKI patients enrolled in the study, 10.7% regained renal function—defined as the production of two times the baseline urine output—within two days. Another 36% of subjects recovered function within three days, and 14.3% recovered kidney function within four days. Creatinine levels peaked at 2.5 mg/dL and decreased to about 2.05 at Day 7.

“It is difficult for me to convey from the podium the severity of illness of these patients,” Dr. Tumlin said. Of the 28 patients enrolled in the study, 92% were diagnosed with oliguria and 90% were unresponsive to diuretic therapy. Unresponsiveness was defined as failure to produce twice the baseline urine after an IVbolus of furosemide (80-120 mg).

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