Author + information
- Kenji Okumura, MD⁎ (, )
- Takahito Sone, MD,
- Shuji Morikawa, MD,
- Hideyuki Tsuboi, MD,
- Hiroaki Mukawa, MD,
- Itsuro Morishima, MD,
- Michitaka Uesugi, MD,
- Yasuhiro Morita, MD,
- Yasushi Numaguchi, MD and
- Toyoaki Murohara, MD
- ↵⁎Cardiovascular Research Medicine, Nagoya University School of Medicine, Nagoya, Aichi 466-8550, Japan
Contrast-induced nephropathy (CIN) involves both glomerular filtration failure and tubular dysfunction. However, CIN is defined only using the value of serum creatinine, or estimated glomerular filtration rate (eGFR) calculated from serum creatinine (1). Creatinine and cystatin C are endogenous markers of glomerular filtration, and all of them are contained in blood. By contrast, tubular dysfunction markers such as N-acetyl-β-D-glucosaminidase (NAG) and α1- and β2-microglobulin are collected from urine. A few reports regarding CIN estimated NAG and microglobulin (2). These reports showed that the markers of glomerular filtration failure seem to be more appropriate as CIN markers than tubular dysfunction markers, even if they were expressed after being adjusted by dividing by urine creatinine. We could not adjust the values of NAG and microglobulin by urine creatinine (3). This may be the reason that we detected no significant difference in NAG and β2-microglobulin. In our results, β2-microglobulin was significantly higher at 24 h from baseline in both atrial natriuretic peptide (ANP) and control groups (both p < 0.0001). In all patients combined, the decrease in eGFR was <1 ml/min/1.73 m2as pointed out, but the decrease in 19 patients with CIN was 9.1 ml/min/1.73 m2at 48 h.
In our study, only 1 patient in the control group required temporary dialysis. The long-term prognosis with treatment with ANP or nesiritide (B-type natriuretic peptide) should be estimated in a large, controlled multicenter study. In an integrated advanced algorithm for the management of CIN, treatment with N-acetylcysteine or ascorbic acid as an antioxidant is recommended in the case of eGFR in the range of 30 to 59 ml/min (1), but an analysis of studies using N-acetylcysteine demonstrated that significant benefits were observed in only one-half of the studies in patients with chronic renal insufficiency (4). As the algorithm says, adjunctive medications do not require all patients to undergo angiography—only the subjects already with renal insufficiency. If the number of patients with CIN were reduced to one-fourth by ANP as demonstrated in our study, the cost would be negligible.
We used Ringer solution containing 28 mEq for hydration without bicarbonate because volume supplementation with either intravenous normal saline or bicarbonate remains a better regimen for preventing CIN in moderate- to high-risk patients (1,5). We should pay more attention to high-risk patients with renal insufficiency during angiography. We recruited 272 patients with creatinine levels of ≥1.3 and <6 mg/dl, but excluded 11 before treatment was assigned, and 4 of them showed creatinine levels outside of the acceptable range.
Finally, we suggest again that in addition to hydration, treatment with a dose of ANP infusion that is calibrated so as not to reduce blood pressure too greatly helps to prevent CIN.
- American College of Cardiology Foundation