KDIGO Clinical Practice Guideline for Acute Kidney Injury
Recommendations and Rationale

Chapter 4.5: Effects of hemodialysis or hemofiltration

• 4.5.1: We suggest not using prophylactic intermittent hemodialysis (IHD) or hemofiltration (HF) for contrast-media removal in patients at increased risk for CI-AKI. (2C)

Rationale

Contrast media are excreted mainly by glomerular filtration and there is a significant correlation between both total body and renal clearances of contrast media and GFR; the renal excretion of contrast media will thus be delayed in patients with renal failure (for review, see Deray).⁵¹⁶ Contrast media can be efficiently removed from blood by IHD and a single session effectively removes 60–90% of contrast media.^516,517 On the basis of these observations, several studies have explored the prophylactic value of IHD in patients at high risk, but most of these studies have not demonstrated a reduced incidence of CI-AKI.^516,518 For example, Vogt et al.⁵¹⁸ recorded renal function and other parameters, IHD requirements, and relevant clinical events before and during 6 days after administration of contrast media in 113 patients with a baseline SCr > 2.3 mg/dl ( > 203 µmol/l). Eight out of 55 patients in the prophylactic IHD group and three in the non-IHD group (P = 0.12), required IHD after contrastmedia examination. Reinecke et al.⁵¹⁹ performed a prospective single-center trial in 424 consecutive patients with SCr concentrations between 1.3–3.5 mg/dl (115–309 µmol/l) who underwent elective coronary angiography. Patients were randomized to one of three treatment strategies with all patients receiving pre- and postprocedural fluids: one group received no additional therapy, patients in the second group were hemodialyzed once, and the third group received oral NAC. The frequency of CI-AKI (defined as an increase in SCr ≥ 0.5 mg/dl or ≥ 44.2 µmol/l) from 48 to 72 hours after catheterization was 6.1% in the fluids-only group, 15.9% with IHD treatment, and 5.3% in the NAC group (intentionto- treat analysis; P = 0.008). There were no differences between the treatment groups with regard to increased SCr ≥ 0.5mg/dl (≥ 44.2 µmol/l) after 30–60 days (4.8%, 5.1%, and 3.1%, respectively; P = 0.700). Analyses of long-term followup (range 63–1316 days) by Cox regressions models of the study groups found quite similar survival rates (P = 0.500). This large study concluded that IHD, in addition to fluids, for the prevention of CI-AKI provided no evidence for any outcome benefit but showed evidence for probable harm.

A retrospective but important cohort study of 391 patients (age 69 ± 8 years, with chronic renal insufficiency [SCr ≥ 1.3 mg/dl; ≥ 115 µmol/l]) who underwent cardiac catheterization, also did not find any beneficial preventive effect.⁵²⁰ By contrast, Lee et al.⁵²¹ presented a prospective RCT indicating that prophylactic IHD might be useful in patients scheduled for coronary angiography or coronary intervention with severely impaired renal function (baseline CrCl of 13 ml/ min per 1.73 m²). Patients were treated with normal saline at 1 ml/kg/h for 6 hours before and 12 hours after contrastmedia administration and randomized to receive IHD for 4 hours as soon as possible after angiography or control treatment. Four days after angiography, SCr concentrations were lower in the IHD group compared to the control group. Out of 42 patients, one patient (2%) in the IHD group but 14 (35%) out of 40 patients in the control group required temporary IHD after coronary angiography. Furthermore, none of the 42 patients in the IHD group, but five (13%) out of 40 patients in the control group, required maintenance IHD after discharge from the hospital (P < 0.05).

A recent meta-analysis of studies using periprocedural extracorporeal blood purification techniques⁵¹⁷ concluded that such treatments did not decrease the incidence of CI-AKI. It could theoretically be anticipated that high-flux membranes used in HF or hemodiafiltration (HDF) modalities should be able to remove contrast media more efficiently than low-flux membranes used in routine IHD. However, recent publications on this topic have added to the controversy about the role of IHD or HF to prevent CI-AKI (Suppl Tables 28 and 29). Marenzi et al.⁵²² studied 114 consecutive patients with CRF (SCr concentration > 2 mg/dl or > 177 µmol/l) who were undergoing coronary interventions. Fifty-eight patients were assigned to either HF starting before the contrast-medium administration and continuing for up to 24 hours after, while 56 patients were treated with isotonic saline at a rate of 1 ml per kilogram of body weight per hour, given in a step-down unit over the same time interval. In-hospital mortality was 2% in the HF group and 14% in the control group (P = 0.02), and the cumulative 1-year mortality was 10% and 30%, respectively (P = 0.01). Temporary RRT was required in 25% of the control group and in only 3% of the patients in the HF group. An increase in the SCr concentration of > 25% from the baseline value after the coronary intervention occurred less frequently among patients in the HF group than among the control patients (5% vs. 50%, P < 0.001). The effective removal of creatinine during HF or IHD makes it difficult to be certain that an observed lower incidence of CI-AKI is not related to the transport removal of creatinine during the procedure.

In a subsequent study, the same authors⁵²³ randomized 92 patients with CKD (CrCl ≤ 30 ml/min) to three different prophylactic treatments: i.v. isotonic saline (control group); i.v. saline for 12 hours before contrast-media exposure, followed by HF for 18–24 hours after contrast-media exposure; and a third group where HF was performed for 6 hours before and for 18–24 hours after contrast-media exposure. The incidence of CI-AKI ( > 25% increase in SCr) and the in-hospital clinical course were compared in the three groups. In-hospital mortality was 20%, 10%, and 0%, respectively, in the three groups; IHD was required in nine (30%), 3 (10%), and zero (0%) patients, respectively (P = 0.002). According to these results, pre-HF is required to obtain the full clinical benefit, suggesting that among different mechanisms possibly involved, high-volume controlled volume expansion before contrast-media exposure plays a major role in prevention. This study further suggests that bicarbonate exposure with HF may ultimately have been the mechanism for the lower CI-AKI incidence (Suppl Table 29). In summary, the evidence profile for IHD vs. HF showed low-quality evidence and an uncertain benefit vs. harm balance of HF/IHD in preventing CI-AKI in patients with severe CKD. Given the costs and logistical difficulties, the use of HF modalities for CI-AKI prevention can only be advocated if future studies will convincingly show clear benefit.