Acute kidney injury following coronary angiography is associated with a long-term decline in kidney function
2010; Elsevier BV; Volume: 78; Issue: 8 Linguagem: Inglês
10.1038/ki.2010.258
ISSN1523-1755
AutoresMatthew T. James, William A. Ghali, Marcello Tonelli, Peter Faris, Merril L. Knudtson, Neesh Pannu, Scott Klarenbach, Braden Manns, Brenda R. Hemmelgarn,
Tópico(s)Chronic Kidney Disease and Diabetes
ResumoTo determine whether acute kidney injury results in later long-term decline in kidney function we measured changes in kidney function over a 3-year period in adults undergoing coronary angiography who had serum creatinine measurements as part of their clinical care. Acute kidney injury was categorized by the magnitude of increase in serum creatinine (mild (50–99% or ≥0.3 mg/dl) and moderate or severe (≥100%)) within 7 days of coronary angiography. Compared to patients without acute kidney injury, the adjusted odds of a sustained decline in kidney function at 3 months following angiography increased more than 4-fold for patients with mild to more than 17-fold for those with moderate or severe acute kidney injury. Among those with an estimated glomerular filtration rate after angiography less than 90 ml/min per 1.73 m2, the subsequent adjusted mean rate of decline in estimated glomerular filtration rate during long-term follow-up (all normalized to 1.73 m2 per year) was 0.2 ml/min in patients without acute kidney injury, 0.8 ml/min following mild injury, and 2.8 ml/min following moderate to severe acute kidney injury. Thus, acute kidney injury following coronary angiography is associated with a sustained loss and a larger rate of future decline in kidney function. To determine whether acute kidney injury results in later long-term decline in kidney function we measured changes in kidney function over a 3-year period in adults undergoing coronary angiography who had serum creatinine measurements as part of their clinical care. Acute kidney injury was categorized by the magnitude of increase in serum creatinine (mild (50–99% or ≥0.3 mg/dl) and moderate or severe (≥100%)) within 7 days of coronary angiography. Compared to patients without acute kidney injury, the adjusted odds of a sustained decline in kidney function at 3 months following angiography increased more than 4-fold for patients with mild to more than 17-fold for those with moderate or severe acute kidney injury. Among those with an estimated glomerular filtration rate after angiography less than 90 ml/min per 1.73 m2, the subsequent adjusted mean rate of decline in estimated glomerular filtration rate during long-term follow-up (all normalized to 1.73 m2 per year) was 0.2 ml/min in patients without acute kidney injury, 0.8 ml/min following mild injury, and 2.8 ml/min following moderate to severe acute kidney injury. Thus, acute kidney injury following coronary angiography is associated with a sustained loss and a larger rate of future decline in kidney function. Acute kidney injury (AKI) following coronary angiography is often transient, with improvement in kidney function observed within days to weeks.1.Guitterez N.V. Diaz A. Timmis G.C. et al.Determinants of serum creatinine trajectory in acute contrast nephropathy.J Interv Cardiol. 2002; 15: 349-354Crossref PubMed Scopus (113) Google Scholar, 2.Pannu N. Wiebe N. Tonelli M. Prophylaxis strategies for contrast-induced nephropathy.JAMA. 2006; 295: 2765-2779Crossref PubMed Scopus (319) Google Scholar, 3.Barrett B.J. Parfrey P.S. Clinical practice. Preventing nephropathy induced by contrast medium.N Engl J Med. 2006; 354: 379-386Crossref PubMed Scopus (484) Google Scholar Although severe AKI that requires dialysis is a rare event in this setting,4.McCullough P.A. Wolyn R. Rocher L.L. et al.Acute renal failure after coronary intervention: incidence, risk factors, and relationship to mortality.Am J Med. 1997; 103: 368-375Abstract Full Text Full Text PDF PubMed Scopus (1400) , 5.Gruberg L. Mintz G.S. Mehran R. et al.The prognostic implications of further renal function deterioration within 48 h of interventional coronary procedures in patients with pre-existent chronic renal insufficiency.J Am Coll Cardiol. 2000; 36: 1542-1548Abstract Full Text Full Text PDF PubMed Scopus (642) Google Scholar even AKI of lesser severity has been consistently associated with adverse outcomes including death.6.Levy E.M. Viscoli C.M. Horwitz R.I. The effect of acute renal failure on mortality. A cohort analysis.JAMA. 1996; 275: 1489-1494Crossref PubMed Scopus (0) Google Scholar, 7.Chertow G.M. Burdick E. Honour M. et al.Acute kidney injury, mortality, length of stay, and costs in hospitalized patients.J Am Soc Nephrol. 2005; 16: 3365-3370Crossref PubMed Scopus (2256) Google Scholar Patients with preexisting chronic kidney disease (CKD) constitute a high-risk group for AKI in the setting of radiocontrast administration.2.Pannu N. Wiebe N. Tonelli M. Prophylaxis strategies for contrast-induced nephropathy.JAMA. 2006; 295: 2765-2779Crossref PubMed Scopus (319) Google Scholar Furthermore, CKD itself is associated with graded increases in risk of mortality with incremental reductions in glomerular filtration rate (GFR).8.Go A.S. Chertow G.M. Fan D. et al.Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization.N Engl J Med. 2004; 351: 1296-1305Crossref PubMed Scopus (8250) Google Scholar, 9Wattanakit K. Coresh J. Muntner P. et al.Cardiovascular risk among adults with chronic kidney disease, with or without prior myocardial infarction.J Am Coll Cardiol. 2006; 48: 1183-1189Abstract Full Text Full Text PDF PubMed Scopus (45) Google Scholar, 10.Hemmelgarn B.R. Southern D.A. Humphries K.H. et al.Refined characterization of the association between kidney function and mortality in patients undergoing cardiac catheterization.Eur Heart J. 2006; 27: 1191-1197Crossref PubMed Scopus (34) Google Scholar These observations suggest that the long-term effects of AKI on the development and progression of CKD are important to understand. The long-term trajectory of kidney function following an episode of AKI remains unclear. The majority of what is currently known relates to the risk of developing end-stage renal disease (ESRD) requiring dialysis among survivors of severe AKI.11.Ishani A. Xue J.L. Himmelfarb J. et al.Acute kidney injury increases risk of ESRD among elderly.J Am Soc Nephrol. 2009; 20: 223-238Crossref PubMed Scopus (809) Google Scholar, 12.Hsu C.Y. Chertow G.M. McCulloch C.E. et al.Nonrecovery of kidney function and death after acute on chronic renal failure.Clin J Am Soc Nephrol. 2009; 4: 891-898Crossref PubMed Scopus (287) Google Scholar, 13.Wald R. Quinn R.R. Luo J. et al.Chronic dialysis and death among survivors of acute kidney injury requiring dialysis.JAMA. 2009; 302: 1179-1185Crossref PubMed Scopus (506) Google Scholar The effects of lesser degrees of AKI have not been characterized, nor have the long-term effects of AKI on kidney function based on the rate of decline in estimated GFR (eGFR) after hospital discharge. Furthermore, the effects of AKI on serial post-procedure measurements of kidney function have not been examined following coronary angiography specifically, an event which is particularly relevant given the high cardiovascular risk and use of this procedure in patients with or at risk for CKD. Identification of patients at high risk for progressive loss of kidney function after these procedures would provide important prognostic information to guide subsequent patient care. The purpose of this study was to examine the association between AKI and long-term changes in kidney function following coronary angiography. We hypothesized that a graded association would exist between the severity of an AKI episode and loss of kidney function at 3 months after angiography. We also hypothesized that AKI would be an independent predictor of the subsequent rate of decline in GFR beyond 3 months following coronary angiography. We identified 19,022 Alberta residents 18 years of age or older undergoing coronary angiography with ≥1 outpatient serum creatinine measurement performed in both the pre- and greater than 3-month post-angiography time periods. We excluded 327 patients receiving renal replacement therapy before study entry, and 616 patients who underwent coronary artery bypass surgery within 7 days following angiography. Of the remainder, 11,249 (62.2%) had a serum creatinine measurement within 7 days following coronary angiography, and were included in the final cohort (Figure 1). The mean age of the cohort was 63.6 years, 69.6% were men, and the mean eGFR before coronary angiography was 73.8 ml/min per 1.73 m2. A total of 853 participants (7.6%) developed AKI following coronary angiography; 716 (6.4%) with mild AKI (increase in serum creatinine 50–99% or by ≥0.3 mg/dl) and 137 (1.2%) with moderate or severe AKI (increase in serum creatinine ≥100%). Patients who developed AKI were older, more likely to be women, with lower pre-angiography eGFR, proteinuria, and several comorbidities including diabetes mellitus, hypertension, and heart failure (Table 1).Table 1Characteristics of patients undergoing coronary angiography, according to AKI statusNo AKI (n=10,396)Mild AKI (n=716)Moderate or severe AKI (n=137)P-valueaANOVA or χ2-test.Age, years, mean (s.d.)63.3 (12.2)68.3 (11.8)66.8 (12.0)<0.0001Sex, male, no. (%)7263 (69.9)490 (68.4)79 (57.7)0.007Pre-angiography eGFR, ml/min per 1.73 m2, mean (s.d.)74.0 (19.8)62.4 (24.3)61.8 (26.2)<0.0001Pre-angiography eGFR, categories, no. (%) ≥90 ml/min per 1.73 m21897 (18.2)84 (11.7)16 (11.7)<0.001 60–89 ml/min per 1.73 m26195 (59.6)280 (39.1)49 (35.8) 30–59 ml/min per 1.73 m22196 (21.1)315 (44.0)59 (43.1) <30 ml/min per 1.73 m2108 (1.0)37 (5.2)13 (9.5)Proteinuria, no. (%) Absent6779 (65.2)424 (59.2)71 (51.8)<0.001 Microalbuminuria1225 (11.8)161 (22.5)50 (36.5) Proteinuria40 (3.8)11 (1.5)1 (0.7) Unmeasured2352 (22.6)120 (16.8)15 (10.9)Comorbidities, no. (%) Diabetes mellitus2730 (26.3)265 (37.0)62 (45.2)<0.001 Hypertension7024 (67.6)537 (75.0)93 (67.9)<0.001 Hyperlipidemia8098 (77.9)538 (75.1)90 (65.7)0.001 Heart failure1450 (13.9)224 (31.3)60 (43.8)<0.001 Cerebrovascular disease751 (7.2)83 (11.2)25 (18.2)<0.001 Peripheral vascular disease786 (7.6)84 (11.7)20 (14.6)<0.001 Chronic pulmonary disease1709 (16.4)190 (26.5)29 (21.1)<0.001 Liver disease141 (1.4)14 (2.0)5 (3.6)0.014 Malignancy451 (4.3)41 (5.7)8 (5.8)0.16 Current smoker3030 (29.1)166 (23.2)25 (18.2)<0.001Procedures following diagnostic angiogram, no. (%) Percutaneous coronary intervention5356 (51.5)329 (45.9)50 (36.5) 3 months after angiography was 3 (IQR 2, 4), with a median interval between measurements of 7 months (IQR 1, 11 months). During follow-up beyond 3 months after coronary angiography, 638 participants (5.7%) died, whereas 46 (0.4%) initiated chronic renal replacement therapy. The proportion of patients with a sustained loss of kidney function (serum creatinine concentration >50% or 0.3 mg/dl above pre-angiography concentration >3 months following the procedure) increased with greater severity of AKI, occurring in 5.9% of patients without AKI, 28.2% of patients with mild AKI, and 59.1% among patients with moderate or severe AKI (Table 2). In the final model adjusted for age, sex, pre-angiography eGFR, proteinuria, comorbidities, and revascularization procedures, compared with patients without AKI, the odds of a decline in kidney function by 3 months increased more than 4-fold for subjects with mild AKI Stage (odds ratio (OR) 4.74, 95% confidence interval (CI) 3.92–5.74), and more than 17-fold for those with moderate or severe AKI (OR 17.31, 95% CI 12.03–24.90).Table 2Sustained loss of kidney function at 3 months following coronary angiographyNo AKIMild AKIModerate or severe AKINo. of patients10,396716137No. serum creatinine measurements per patient, median (IQR)6 (3, 9)8 (5, 14)7 (4, 17)Decline in kidney functionaLoss of kidney function=serum creatinine >50% or 0.3mg/dl above pre-angiography concentration on all measurements obtained 7 days to 3 months following angiogram. No. (%)613 (5.9)202 (28.2)81 (59.1) Crude odds ratio (95% CI)1 (reference)6.30 (5.25–7.56)23.20 (16.34–32.94) Adjusted odds ratio (95% CI)bFinal model adjusted for age, sex, pre-angiography eGFR, proteinuria, comorbidities (diabetes mellitus, hypertension, heart failure, cerebrovascular disease, chronic pulmonary disease), revascularization following coronary angiogram (percutaneous coronary intervention or coronary artery bypass surgery).1 (reference)4.74 (3.92–5.74)17.31 (12.03–24.90)Abbreviations: AKI, acute kidney injury; CI, confidence interval.a Loss of kidney function=serum creatinine >50% or 0.3 mg/dl above pre-angiography concentration on all measurements obtained 7 days to 3 months following angiogram.b Final model adjusted for age, sex, pre-angiography eGFR, proteinuria, comorbidities (diabetes mellitus, hypertension, heart failure, cerebrovascular disease, chronic pulmonary disease), revascularization following coronary angiogram (percutaneous coronary intervention or coronary artery bypass surgery). Open table in a new tab Abbreviations: AKI, acute kidney injury; CI, confidence interval. Among the 10,418 (92.6%) patients with a post-angiography eGFR <90 ml/min per 1.73 m2 more than 3 months following angiography, those who had developed AKI had lower eGFR at 3 months, as well as further decline in eGFR during subsequent long-term follow-up (Figure 2). The unadjusted mean annual rate of decline in eGFR during long-term follow-up was 0.1 (95% CI -0.1 to 0.2) ml/min per 1.73 m2 per year among patients without AKI, 1.0 (95% CI 0.4–1.5) ml/min per 1.73 m2 per year among patients with mild AKI, and 3.1 (95% CI 2.0–4.2) ml/min per 1.73 m2 per year among patients with moderate or severe AKI. After adjustment for age, sex, proteinuria, and comorbidities, the adjusted rate of decline in eGFR was 0.2 (95% CI -0.4 to 0.8) ml/min per 1.73 m2 per year in patients without AKI, 0.8 (95% CI 0.1–1.6) ml/min per 1.73 m2 per year in those who had developed mild AKI, and 2.8 (95% CI 1.7–4.1) ml/min per 1.73 m2 per year in patients who had experienced moderate to severe AKI (P-trend <0.001). The odds of rapid progression of kidney disease during the long-term follow-up period also increased in a graded manner with increasing severity of AKI (Table 3). The test for interaction between AKI and post-angiogram eGFR was nonsignificant (P-interaction 0.24) suggesting that AKI was associated with similar risks of subsequent rapid progression of kidney disease regardless of the eGFR at the start of long-term follow-up.Table 3Long-term changes in kidney function beyond 3 months following coronary angiography among patients with post-angiography eGFR 4 ml/min per 1.73 m2 per year, no. (%)333 (3.4)58 (7.8)22 (16.0) Initiated chronic renal replacement therapy, no (%)21 (0.2)18 (2.4)8 (5.8)Composite outcomebComposite outcome=decline in eGFR >4ml/min per 1.73m2 per year or initiation of chronic renal replacement therapy. Crude odds ratio (95% CI)1 (reference)2.81 (2.15–3.67)6.52 (4.22–10.07) Adjusted odds ratio (95% CI)cFinal model adjusted for age, sex, baseline eGFR, proteinuria, comorbidities (diabetes mellitus, hypertension, heart failure, cerebrovascular disease, peripheral vascular disease, chronic pulmonary disease, liver disease, malignancy, and current smoking).1 (reference)1.60 (1.19–2.14)3.12 (1.95–4.99)Abbreviations: AKI, acute kidney injury; eGFR, estimated glomerular filtration rate; IQR, interquartile range.a Final model adjusted for age, sex, and comorbidities (diabetes mellitus, hypertension, proteinuria, and heart failure).b Composite outcome=decline in eGFR >4 ml/min per 1.73 m2 per year or initiation of chronic renal replacement therapy.c Final model adjusted for age, sex, baseline eGFR, proteinuria, comorbidities (diabetes mellitus, hypertension, heart failure, cerebrovascular disease, peripheral vascular disease, chronic pulmonary disease, liver disease, malignancy, and current smoking). Open table in a new tab Abbreviations: AKI, acute kidney injury; eGFR, estimated glomerular filtration rate; IQR, interquartile range. There were 5,478 (59.2%) patients who also had estimates of GFR available spanning >1 year before angiography with which to estimate the pre-angiography rate of decline in kidney function. The annual rate of decline in eGFR was similar for the pre- and the post-angiography time periods for patients without AKI or with mild AKI. For patients who experienced moderate or severe AKI, there was a statistically significant increase in the rate of decline in kidney function following the episode of AKI by 1.8 (95% CI 0.6–3.0) ml/min per 1.73 m2 per year, compared with the pre-angiography rate. Sensitivity analyses were conducted to explore the impact of the number and frequency of serum creatinine measurements on results. For the analysis of kidney function at 3 months, we restricted the cohort to patients who had ≥2 creatinine measurements obtained between 7 days and 3 months following angiography, which produced similar findings to our primary analysis. For the analysis of long-term progression of kidney function beyond 3 months following angiography, we stratified the cohort according to the number of serum creatinine measurements during the follow-up period (≤ 2, 3, or ≥4 measurements). Although the subsequent rate of decline in eGFR increased with greater number of serum creatinine measurements across all categories of AKI, the relative increases in rate of decline in eGFR, and odds of rapid progression with mild and moderate or severe AKI were comparable across all strata to those observed in the primary analyses. In this large cohort undergoing coronary angiography, a loss of kidney function at 3 months following coronary angiography was common after AKI. Among patients with an eGFR <90 ml/min per 1.73 m2 following angiography, the long-term risk of further progressive loss of kidney function also increased with greater severity of AKI. Furthermore, patients with moderate or severe AKI experienced acceleration in the rate of eGFR decline following an episode of AKI compared with their pre-angiography rate of progression. These results show that patients who develop AKI following coronary angiography are at increased risk for progressive long-term loss of kidney function following angiography. Although the short-term adverse effects of AKI during hospitalization are well recognized,7.Chertow G.M. Burdick E. Honour M. et al.Acute kidney injury, mortality, length of stay, and costs in hospitalized patients.J Am Soc Nephrol. 2005; 16: 3365-3370Crossref PubMed Scopus (2256) Google Scholar, 14.Coca S.G. Peixoto A. Garg A.X. et al.The prognostic importance of a small acute decrement in kidney function in hospitalized patients: a systematic review and meta-analysis.Am J Kidney Dis. 2007; 50: 712-720Abstract Full Text Full Text PDF PubMed Scopus (169) Google Scholar, 15.Rihal C.S. Textor S.C. Grill D.E. et al.Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention.Circulation. 2002; 105: 2259-2264Crossref PubMed Scopus (1370) Google Scholar the long-term effects of AKI on renal outcomes have been unclear because comparisons to patients without AKI have been lacking, the confounding effects of preexisting CKD have not been controlled for, or identification of progression of kidney disease has been based solely on receipt of treatment for ESRD.16.Lo L. Liu K.D. Hsu C.Y. Long-term outcomes after acute kidney injury: where do we stand and how can we move forward?.Am J Kidney Dis. 2009; 53: 928-931Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar, 17.Coca S.G. Yusuf B. Shlipak M.G. et al.Long-term risk of mortality and other adverse outcomes after acute kidney injury: a systematic review and meta-analysis.Am J Kidney Dis. 2009; 53: 961-973Abstract Full Text Full Text PDF PubMed Scopus (728) Google Scholar Elderly patients hospitalized with diagnosis codes for AKI superimposed on CKD11.Ishani A. Xue J.L. Himmelfarb J. et al.Acute kidney injury increases risk of ESRD among elderly.J Am Soc Nephrol. 2009; 20: 223-238Crossref PubMed Scopus (809) Google Scholar as well as patients with increases in creatinine following hospitalization with myocardial infarction have been shown to be at increased risk for enrollment in ESRD programs in the United States.18.Newsome B.B. Warnock D.G. McClellan W.M. et al.Long-term risk of mortality and end-stage renal disease among the elderly after small increases in serum creatinine level during hospitalization for acute myocardial infarction.Arch Intern Med. 2008; 168: 609-616Crossref PubMed Scopus (233) Google Scholar Severe AKI leading to dialysis during hospitalization has recently been shown to be associated with an increased risk for chronic renal replacement therapy in later life,12.Hsu C.Y. Chertow G.M. McCulloch C.E. et al.Nonrecovery of kidney function and death after acute on chronic renal failure.Clin J Am Soc Nephrol. 2009; 4: 891-898Crossref PubMed Scopus (287) Google Scholar, 13.Wald R. Quinn R.R. Luo J. et al.Chronic dialysis and death among survivors of acute kidney injury requiring dialysis.JAMA. 2009; 302: 1179-1185Crossref PubMed Scopus (506) Google Scholar whereas patients with diagnosis codes for acute tubular necrosis or dialysis-requiring AKI have also been reported to be at risk for earlier identification of stage 4 or 5 CKD.19.Lo L.J. Go A.S. Chertow G.M. et al.Dialysis-requiring acute renal failure increases the risk of progressive chronic kidney disease.Kidney Int. 2009; 76: 893-899Abstract Full Text Full Text PDF PubMed Scopus (404) Google Scholar, 20.Amdur R.L. Chawla L.S. Amodeo S. et al.Outcomes following diagnosis of acute renal failure in US veterans: focus on acute tubular necrosis.Kidney Int. 2009; 76: 1089-1097Abstract Full Text Full Text PDF PubMed Scopus (221) Google Scholar This analysis expands upon the findings of previous studies by identifying both AKI and subsequent changes in kidney function using serial measurements of serum creatinine and eGFR. This is a significant advantage given the limitations in sensitivity and specificity when using administrative codes to define AKI and CKD in isolation or combination.21.Winkelmayer W.C. Schneeweiss S. Mogun H. et al.Identification of individuals with CKD from Medicare claims data: a validation study.Am J Kidney Dis. 2005; 46: 225-232Abstract Full Text Full Text PDF PubMed Scopus (172) Google Scholar, 22.Garg A.X. Parikh C.R. Yin and Yang: acute kidney injury and chronic kidney disease.J Am Soc Nephrol. 2009; 20: 8-10Crossref PubMed Scopus (7) Google Scholar, 23.Waikar S.S. Wald R. Chertow G.M. et al.Validity of International Classification of Diseases, Ninth Revision, Clinical Modification Codes for Acute Renal Failure.J Am Soc Nephrol. 2006; 17: 1688-1694Crossref PubMed Scopus (343) Google Scholar Furthermore, the use of pre- and post-angiography estimates of GFR allowed for the confounding effects of preexisting CKD (and its severity) to be accounted for in these analyses.16.Lo L. Liu K.D. Hsu C.Y. Long-term outcomes after acute kidney injury: where do we stand and how can we move forward?.Am J Kidney Dis. 2009; 53: 928-931Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar A number of mechanisms may explain the associations between AKI and progressive loss of kidney dysfunction following coronary angiography. First, the association may be due to numerous comorbidities (that is, hypertension, diabetes mellitus, proteinuria, or later stages of CKD) in patients who develop AKI. However, the magnitude of the associations that remained after statistical adjustment suggests that confounding by these characteristics is unlikely to explain our findings. Second, patients who develop AKI may be more likely to have a serum creatinine measurement obtained during follow-up, thus introducing potential for ascertainment bias. However, we observed similar results when analyses were stratified by the number of serum creatinine measurements performed during follow-up, suggesting that the clinical decisions that lead to the measurement of serum creatinine do not explain our findings. Third, patients who develop AKI may be susceptible to other processes that lead to progressive kidney disease following angiography such as atheroemboli.24.Thadhani R.I. Camargo C.A.J. Xavier R.J. et al.Atheroembolic renal failure after invasive procedures: natural history based on 52 histologically proven cases.Medicine (Baltimore). 1995; 74: 350-358Crossref PubMed Scopus (188) Google Scholar Alternatively, the long-term decline in eGFR following AKI may be due to persisting renal damage after an episode of acute tubular injury. Animal studies suggest that chronic changes to the renal microvasculature may result from acute ischemic renal injury.25.Basile D.P. Donohoe D. Roethe K. et al.Renal ischemic injury results in permanent damage to peritubular capillaries and influences long-term function.Am J Physiol Renal Physiol. 2001; 281: F887-F899Crossref PubMed Scopus (527) Google Scholar, 26.Basile D.P. The endothelial cell in ischemic acute kidney injury: implications for acute and chronic function.Kidney Int. 2007; 72: 151-156Abstract Full Text Full Text PDF PubMed Scopus (318) Google Scholar Our observations that kidney function was less likely to recover to pre-angiography levels, and further declined at a faster rate following an episode of AKI, are in keeping with this hypothesis. There are limitations to our study resulting from its observational nature and the use of serum creatinine and eGFR to determine kidney function. First, because this study was conducted retrospectively, participant selection was limited to patients who had pre- and post-angiography serum creatinine measurements including measurements within 7 days of coronary angiography as part of their clinical care. Although many outpatients were thus excluded because of the inability to ascertain AKI, these patients had few risk factors for AKI and showed a low rate of CKD progression during follow-up (decline in eGFR 0.1 ml/min per 1.73 m2 per year). Therefore exclusion of these patients from the study and restriction of the control group to those with creatinine measurements are unlikely to have impacted our findings. Second, episodes of AKI and their severity may have been misclassified due to our dependence on existing creatinine measurements captured following coronary angiography. However, our approach to identification of AKI is most vulnerable to missing episodes of mild AKI or underestimating the severity of AKI in those who developed it. If such misclassification occurred, we anticipate this would have underestimated the risk of renal outcomes following moderate or severe AKI. Finally, measurement of long-term study outcomes required that patients survive beyond 3 months to obtain repeated measures of kidney function. Loss of patients due to death, ESRD, or loss to clinical follow-up may thus have influenced results. However, because patients with more rapid decline in kidney function are more likely to experience death or ESRD,27.Rifkin D.E. Shlipak M.G. Katz R. et al.Rapid kidney function decline and mortality risk in older adults.Arch Intern Med. 2008; 168: 2212Crossref PubMed Scopus (256) Google Scholar, 28.Stevens L.A. Greene T. Levey A.S. Surrogate end points for clinical trials of kidney disease progression.Clin Nephrol. 2006; 1: 874-884Crossref Scopus (104) Google Scholar our estimates of the rate of progression are likely conservative.29.Touloumi G. Pocock S.J. Babiker A.G. et al.Impact of missing data due to selective dropouts in cohort studies and clinical trials.Epidemiology. 2002; 13: 347-355Crossref PubMed Scopus (46) Google Scholar The associations between AKI and progressive kidney dysfunction have potentially important implications for clinical management of patients following coronary angiography, given the availability of strategies that may slow the progression of CKD.30.Wright J.T. Bakris G. 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