Advances in Transplantology
Kidney transplantation
Incidence of Contrast-induced Nephropathy in Kidney Transplant Recipients

https://doi.org/10.1016/j.transproceed.2015.01.008Get rights and content

Highlights

  • Contrast induced nephropathy (CIN) is characterized by the development of acute kidney injury (AKI) after the administration of intravascular iodinated radio-contrast in the absence of any other etiology of AKI. Incidence of CIN for those without pre-existing renal impairment ranges from 0.6%–2.3%, however, risk increases to 12–26% for those with risk factors for CIN. Common risk factors are pre-existing renal impairment, DM, advanced age, peri-procedural intravascular volume-depletion, congestive heart failure and concomitant use of other nephrotoxic drugs. Patients who develop CIN have high morbidity and mortality in the short and long term.

  • We proposed that Kidney transplant recipients (KTRs) may be at higher risk of CIN, due to high prevalence of CKD, DM, CVD and the concurrent use of a nephrotoxic calcineurin-inhibitor (CNI) for immunosuppression. CNI are used in more than 95% of KTR. Very little information is available about incidence of CIN in KTRs. To our knowledge, only 4 studies (all retrospective) exist and were published in 1975, 1983 and 2000. Only one of these studies was done after the introduction of CNIs. There are no prospective studies of CIN in KTRs.

  • As such, we felt the need to explore this area in the CNI era. Important contrast based testing is often avoided in KTR for fear of CIN. We found that the risk of CIN is not elevated, despite being on calcineurin inhibitors, in patients with relatively high GFR. This finding will hopefully reassure the clinicians and help perform important testing that may involve contrast in a selective group of KTR.

Abstract

Contrast-induced nephropathy (CIN) is responsible for one-third of acute kidney injuries (AKI) in the hospital setting. The incidence of CIN varies from 3% to 30%, depending on the preexisting risk factors, with higher incidence noted with diabetes mellitus, chronic kidney disease, and older age. Though CIN risk factors are common in kidney transplant recipients (KTRs), data about incidence of CIN in this population are sparse.

Methods

We retrospectively analyzed 124 consecutive patients transplanted at our center between January 2002 and December 2013 and received iodinated intravascular contrast with stable kidney function prior to contrast administration. CIN was defined as either an absolute rise in serum creatinine of ≥0.5 mg/dL or a ≥25% drop in estimated glomerular filtration rate (eGFR) after contrast administration.

Results

Seven of 124 (5.64%) patients developed CIN. Kidney function returned to baseline in 5 of the 7 patients within 3 weeks. In 2 patients serum creatinine remained elevated due to recurrent AKI episodes from other causes. Dialysis was not required in any patient. Calcineurin inhibitors (CNIs) were being used in 95% patients at the time of contrast administration. Diabetes mellitus, baseline serum creatinine, age, race, gender, and the use of ACE inhibitor, angiotensin receptor blocker, diuretic, or prophylaxis with intravenous hydration ± N-acetylcysteine did not affect the incidence of CIN.

Conclusion

Incidence of CIN in KTRs was low in our study (5.6%), much less than previously reported. This low incidence may be related to the high baseline eGFR (>70 mL/min/1.73 m2) and use of hypo-osmolar contrast in our patients. In KTRs with baseline eGFR >70 mL/min, the incidence of CIN is low despite the concurrent use of nephrotoxic CNI.

Section snippets

Methods

We retrospectively identified from our institutional database 124 consecutive KTRs (transplanted between 2002 and 2013) who received intravascular contrast and had stable kidney function before contrast administration. Patients received contrast either for CT scan (77%), pulmonary angiogram (18%), or cardiac catheterization (4.8%).

We collected the following demographic data from patients: race, age, gender, date and type of contrast study, date and type of transplantation, type and volume of

Results

CIN developed in 7/124 patients (5.64%). The baseline characteristics of patients and risk factors for CIN stratified by the presence or absence of CIN are shown in Table 1. Because of the low overall event rate, the study was not adequately powered to examine the discriminatory power of individual variables as predictors of contrast nephropathy. Nevertheless, there was no significant association between CIN and any of the following: age, race, gender, DM, hypertension, baseline serum

Discussion

Controversy still persists over the incidence of AKI resulting directly from exposure to contrast in KTRs. Contrast causes vasoconstriction of the afferent glomerular arterioles and reduction in renal blood flow and GFR. Renal vasoconstriction and direct tubular epithelial toxicity are 2 major mechanisms by which contrast causes acute kidney injury. Immediately after contrast administration, there is a transient increase in renal blood flow followed by a prolonged period of reduced flow

Conclusion

In KTR with eGFR >70 mL/min/1.73 m2, administration of hypo-osmolal contrast does not appear to be associated with a high incidence of CIN. Even when CIN develops, it is usually mild and largely reversible. As patients with more advanced renal dysfunction were not included in our study, the safety of contrast administration in such patients can not be assumed from our results.

References (10)

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