Key result
Short-course prednisone curbs procedure-induced rise in KIM-1 compared to hydration alone.
Why the study?
There is no optimal therapy for preventing and treating contrast-induced nephropathy and related renal complications in cardiology procedures.
Does oral prednisone plus hydration reduce biomarkers of renal tubular damage compared to hydration alone in patients at risk of CI-AKI undergoing cardiovascular procedures?
RCT (n=38)
1:1
Does oral prednisone plus hydration reduce biomarkers of renal tubular damage compared to hydration alone in patients at risk of CI-AKI undergoing cardiovascular procedures?
A short course of peri-procedural oral prednisone may reduce biomarkers of renal tubular damage in patients at risk for contrast-induced nephropathy.
Supports adjunctive prednisone for tubular injury reduction in CI-AKI risk; extends RCT biomarker data but leaves clinical outcomes open.
BACKGROUND: Contrast-induced nephropathy (CI-AKI) is a complication of diagnostic/therapeutic hemodynamic procedures in cardiology, which may also cause renal cholesterolinic atheroembolism. Despite the severe clinical impact of these complications, there is no optimal therapy for preventing and treating them. We suggest a short course of high-dose steroids as an effective preventive measure. METHODS: Patients at risk of CI-AKI (n = 38) undergoing cardiovascular procedures were assigned 1:1 to 1 of 2 experimental arms (prednisone+hydration vs. hydration alone). Oral prednisone 1 mg/kg was administered 12 hours before, at 6 am on the same day, and 24 hours following the procedure. Serum creatinine was tested immediately before and again 24-48 hours after the procedure; neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), protein and albumin were assayed in spot urine before and 6 hours after the procedure. RESULTS: NGAL and KIM-1 tended to rise after the procedure, but to a lesser degree in the prednisone group (delta NGAL: hydration = +128%, prednisone = +46%; p = 0.26; delta KIM-1: hydration = +99%, prednisone = +11%; p = 0.02). Proteinuria and albuminuria decreased significantly in the prednisone group. In 5 patients developing CI-AKI, their delta NGAL and delta KIM-1 did not differ from the values seen in patients without CI-AKI. Hypertension, peripheral arteriopathy and use of low-dose aspirin or diuretics were positive predictors of baseline NGAL, while treatment with calcium channel blockers and statins were negative predictors. Statins were negative predictors of baseline KIM-1. CONCLUSIONS: A short course of prednisone reduces the procedure-induced changes in biomarkers of renal tubular damage. This study suggests that steroids had a tubule-protecting effect.
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Ribichini et al. (2013) conducted an RCT in Contrast-induced nephropathy (CI-AKI) risk (n=38). Prednisone vs. Hydration alone was evaluated on delta KIM-1 (change in kidney injury molecule-1) (p=0.02). A short course of prednisone significantly reduced the procedure-induced rise in kidney injury molecule-1 compared to hydration alone (+11% vs +99%; p=0.02).
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