Annals of Oncology Advance Access originally published online on March 9, 2007
Annals of Oncology 2007 18(5):950-958; doi:10.1093/annonc/mdm055
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© 2007 European Society for Medical Oncology
supportive care |
Monitoring of renal function in cancer patients: an ongoing challenge for clinical practice
1 Department of Hematology and Oncology, Medical Center
2 Department of Statistics and Biometry/Institute of Medical Biometry and Medical Informatics
3 Department of Nephrology, Medical Center
4 Central Laboratory, University of Freiburg, Freiburg, Germany
* Correspondence to: Prof Dr M. Engelhardt, Hematology and Oncology Department, Freiburg University Medical Center, Hugstetterstrasse 55, D-79106 Freiburg, Germany. Tel: +49 761 270 3256; Fax: +49 761 270 3318; E-mail: monika.engelhardt{at}uniklinik-freiburg.de
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Abstract |
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Background: Renal impairment (RI) has been shown to be one major risk factor in a number of diseases and is associated with a dismal clinical outcome. However, the influence of milder degrees of renal disease is less well defined, particularly not in patients with malignant diseases.
Patients and methods: We analyzed 167 patients with solid tumors and hematological malignancies. Besides disease-specific parameters, serum creatinine, cystatin C and the estimated glomerular filtration rate (eGFR) [‘modification of diet in renal disease’ equation (MDRD)/Cockcroft-Gault (CG)] were determined. Patients were compared within eGFR, creatinine and cystatin C groups.
Results: The median MDRD, CG, creatinine and cystatin C levels of all patients were 88 ml/min/1.73 m2, 89 ml/min, 1 mg/dl and 0.9 mg/l, respectively. Patients with chronic kidney disease stage 2 still showed normal creatinine and cystatin levels of 1 mg/dl and 1.1 mg/l, respectively, although mild RI was frequent. Those cancer patients with decreased eGFR (MDRD) (<60 ml/min/1.73 m2) had increased odds ratios (ORs) to have more concurrent diagnoses [OR 3.4; 95% confidence interval (CI) 1.5–8.1], a body mass index >24 kg/m2 (OR 2.1; 95% CI 1.0–4.5) and an elevated (>245 pg/ml) pro-brain natriuretic peptide level (proBNP) (OR 9.2; 95% CI 3.0–28.3).
Conclusions: These observations suggest that grouping cancer patients according to renal function, especially eGFR, may be one way to determine specific risk groups.
Key words: cancer patients, comorbidities, renal impairment
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introduction |
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TopAbstractintroductionpatients and methodsresultsdiscussionAcknowledgementsReferences |
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With use of chemotherapeutic agents in patients with solid tumors (STs) or hematological malignancies (HMs), kidney function should be monitored in order to recognize renal impairment (RI) as early as possible. The glomerular filtration rate (GFR) is the best measure of overall renal function [1–3]. Normal GFR varies according to age, sex and body size between 120 and 130 ml/min/1.73 m2 and declines with age [2]. A decline in GFR is of high predictive value for RI and leads to enhanced drug toxicity through reduced excretion of active drugs or active metabolites. GFR can be measured by urinary clearance of a filtration marker, such as iothalamate, inulin or iohexol which is the gold standard. However, as this is cumbersome in clinical practice, serum creatinine as an endogenous filtration marker has been used to assess GFR. The National Kidney Disease Education Program of the National Institute of Diabetes and Disease of the Kidney, National Kidney Foundation (NKF) and the American Society of Nephrology (ASN) recommend estimating GFR from serum creatinine using the ‘modification of diet in renal disease’ (MDRD) study equation [4, 5], which incorporates age, race, gender and serum creatinine level. The MDRD equation is currently one way of transforming creatinine levels into estimated glomerular filtration rate (eGFR) values in adults [2] and provides an improvement over serum creatinine alone [1]. It is more accurate and precise than the Cockcroft-Gault (CG) equation for persons with a GFR less than
90 ml/min/1.73 m2 [2, 5, 6]. Creatinine, an amino acid derivative with a molecular mass of 113 Da is freely filtered by the glomerulus. Serum creatinine is influenced by inflammation, age, gender and muscle mass, and has limits to detect mild RI. With the GFR varying between 90 and 60 ml/min/1.73 m2, creatinine levels do not significantly increase due to enhanced tubular secretion and glomerular filtration. Moreover, tubular secretion of creatinine differs among and within individuals. For these reasons, the relationship between creatinine and GFR varies substantially and creatinine clearance (CrCl) exceeds the GFR [7]. The urinary clearance of endogenous filtration such as creatinine (CrCl) itself, widely used as another marker of renal function, is influenced by timed urine collection, its volume and patients' sampling errors, combined with blood sampling during the collection period, which has created substantial difficulties in clinical practice. According to the guidelines of the NKF, the use of 24-h urine collection for the estimation of GFR has consistently been shown to be no more, and often less reliable than serum creatinine-based equations [1].
Cystatin C, a cysteine protease inhibitor produced by nearly all human cells, has been suggested as an alternative marker of the GFR. With a molecular weight of 13 kDa, cystatin C is freely filtered in glomeruli and almost completely reabsorbed and catabolized by the proximal renal tubular cells [8]. Prior studies suggested cystatin C to be superior to serum creatinine for detecting a decreased CrCl and to be a stronger risk predictor for cardiovascular events and death compared with creatinine or GFR, especially among elderly persons [9, 10]. This is of interest, since prior studies have demonstrated that RI is independently associated with an increased risk of death, cardiovascular events or hospitalization [11]. However, it is less certain whether the measurement of cystatin C is an improvement over creatinine-based equations for estimating the GFR [7].
Both brain natriuretic peptide (BNP) and its circulating plasma form pro-BNP (NT-pro-BNP) are secreted in equimolar amounts during mechanic and neurohumoral stimulation of the heart. Both have been developed as markers of heart failure, since they are closely connected with symptoms of MI and left ventricular dysfunction [12]. In addition, both markers are used for risk stratification of acute congestive heart failure. Vickery et al. [13] have shown that BNP and pro-BNP levels are independently associated with renal function. In their multivariate analysis of patients with chronic renal failure and no clinical history of heart failure, the extents of RI and left ventricular mass index were independently correlated with BNP and NT-pro-BNP levels. These results suggest that elevated BNP levels cannot simply be attributed to reduced renal function and that subclinical cardiac dysfunction, and not RI itself, raises BNP levels. Nevertheless, the parameters pro-BNP, BNP and renal function may suggest an increased risk of death, or for composite end points of death from cardiovascular causes, such as reinfarction or stroke.
RI in cancer patients is often multifactorial and it is clinically useful to consider cancer-independent comorbidities as underlying causes, such as pre-, intrinsic- or post-RI that may decrease patients' outcome [14, 15]. The aim of this study was to determine, whether and to which extent consecutive cancer patients show RI and milder degrees of RI and which parameter of creatinine, cystatin C or eGFR (determining both MDRD- and CG-based eGFRs) is most suitable to determine risks for secondary end points, such as concurrent diagnoses, hypertension, diabetes, MI and stroke. Analysis of creatinine, cystatin C and eGFR and determination of their relevance to detect early RI seem valuable in order to screen for preclinical disease and for guidance in the selection of pharmacologic/chemotherapeutic agents in cancer patients.
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patients and methods |
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patient description and study design
In this retrospective study, we analyzed 167 consecutive patients (108 males and 59 females; median age 59 years; range 18–91) with ST or HM using medical charts and electronic records from August 2004 to March 2005. We determined patients' Karnofsky index (KI), number of concurrent diagnoses apart from the tumor, cardiovascular risk factors, such as body mass index (BMI), presence of stroke or transient ischemic attack (TIA) and comorbidities, described by the methods of Satariano and Ragland [16] on the basis of seven relevant prognostic comorbid conditions [heart disease, MI, diabetes, respiratory conditions, liver conditions, gall-bladder and cancer (other than underlying)].
Biochemical assays included serum creatinine, cystatin C and N-terminal pro-BNP. The eGFR for quantifying renal function was estimated by the use of the simplified four-component MDRD equation which incorporates age, race, gender and serum creatinine level, thereby resulting in an eGFRMDRD (ml/min/1.73 m2) = 186 x [serum creatinine level (in mg/dl)]–1.154 x [age (in years)]–0.203 x (0.742 if female, 1.21 if black) [5, 6]. According to the guidelines of the NKF [1], the distribution of eGFRMDRD was divided into five categories: 
90 ml/min/1.73 m2 (I), 89–60 ml/min/1.73 m2 (II), 59–30 ml/min/1.73 m2 (III), 29–15 ml/min/1.73 m2 (IV) and <15 ml/min/1.73 m2 (V). In addition, eGFRMDRD was compared with the GFR as estimated by the CG equation [eGFRCG (ml/min)] = [(140 – age) x weight (kg)]/(72 x Scr in mg/dl) x 0.85 (if female), where age is given in years and Scr is the serum creatinine concentration [1]. Cystatin C was measured by means of a particle-enhanced immunonephelometric assay (Dako, Hamburg, Germany) with a nephelometer (Immage, Beckman, Krefeld, Germany). Serum creatinine was determined by enzymatic method (Modular Hitachi, Roche Diagnostics GmbH, Mannheim, Germany), and pro-BNP levels by using a chemiluminescent immunoassay kit (Roche Diagnostics, E170 Hitachi). RI was defined by creatinine levels >1.1 mg/dl, cystatin C >1.0 mg/l or eGFR <60 ml/min/1.73 m2 (for 3 months with or without renal damage). The study and analysis were carried out according to the guidelines of the Declaration of Helsinki and good clinical practice. All patients gave their written informed consent for institutional-initiated research studies and specifically for retrospective analyses of clinical outcome studies conforming to our institutional review board guidelines.
statistical analysis
All data analyses were performed using SAS statistical software version 8.2. (SAS Institute Inc., Cary, NC). Median and ranges are given in order to describe the distribution of continuous variables; Pearson correlation coefficients are calculated in order to investigate the relationship between two continuous variables. We further categorized the parameters under investigation, eGFRMDRD in five, and cystatin C and creatinine in three categories for descriptive purposes. Odds ratios (ORs) were calculated from categorizations into two classes and are accompanied by 95% confidence intervals (CIs) and continuity-adjusted 
2 tests. A P value of <0.05 was considered to indicate statistical significance.
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correlation between eGFRMDRD and serum creatinine
The analysis of eGFRMDRD and serum creatinine demonstrated a close correlation in our cancer patients, whereby with decreasing eGFRMDRD, creatinine levels also increased. The relationship showed that greater eGFR variations between the critical range of mild RI (90–60 ml/min/1.73 m2) only insignificantly (or to a much lesser degree) affected serum creatinine levels (Figure 1).
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correlation analysis among measurements of renal function (creatinine and cystatin levels, eGFRMDRD and cystatin levels)
The analysis of serum cystatin and creatinine levels demonstrated a positive correlation (r = 0.73) as depicted in Figure 2A. Besides, there was a negative correlation between eGFRMDRD and cystatin C-levels (r = –0.60) (Figure 2B). This confirmed that elevated creatinine and cystatin levels reveal impaired renal function. The relation between creatinine and eGFR is given by the MDRD equation, thereby was not formally analyzed via correlation analysis.
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patients' characteristics
The consecutive patients (as summarized in Table 1) showed a typical age of cancer patients, predominance of male patients and equal distribution of ST and HT patients. Despite 131 (78%) patients having advanced (metastatic or disseminated) disease, our patient cohort showed a low risk profile, since their median BMI was normal, their KI almost normal, their comorbidity (Satariano) index (SI) low and median concurrent diagnoses were limited (3, range 0–8). Forty-six percent of patients showed a normal eGFRMDRD (
90 ml/min/1.73 m2) which was similar to median eGFRCG values. This was in line with median creatinine and cystatin levels within normal ranges. Comparing chronic kidney disease (CKD) stages 1–5 with the use of the MDRD versus CG equation, both were comparable, with 46% versus 50% having CKD stage 1, and 54% versus 50% CKD stages 2–5, respectively (Table 1). Twenty-two percent of patients met the criteria for CKD with eGFRMDRD/CG<60 ml/min/1.73 m2 for three or more months [1]. In all patients, the median pro-BNP level was elevated with 245 pg/ml. Baseline patient characteristics were also analyzed within different subgroups of declining eGFRMDRD (Tables 2 and 3), and increasing cystatin C (Table 4) and creatinine (Table 5) levels.
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patients' characteristics according to eGFRMDRD
The baseline characteristics according to eGFRMDRD analyzed in subgroups of
90, 89–60, 59–30, 29–15 and <15 ml/min/1.73 m2 (Table 2) confirmed that patients with decreasing eGFRMDRD (eGFR < 60 ml/min/1.73 m2) had increasing creatinine and cystatin levels, as well as decreasing eGFRCG values. Moreover, we noted an increased BMI, more concurrent diagnoses and clinical signs of left ventricular systolic dysfunction (as suggestive with substantially increasing pro-BNP levels with RI). Of note, the SI did not change with RI. A decreased eGFRMDRD was associated with increasing age, reflecting the fact that age is incorporated in the eGFRMDRD equation.
patients' characteristics within different eGFRMDRD stages
As depicted in Table 3, grouping cancer patients into CKD 1 versus 2–5 and CKD 1–2 versus 3–5 allowed to detect substantial differences. Patients with eGFRMDRD <90 ml/min/1.73 m2 (CKD stages 2–5) as compared with CKD stage 1 showed an increased age (P < 0.0001), elevated creatinine and cystatin C levels, as well as decreased eGFR values as calculated by the CG equation. Comparing CKD stages 1–2 versus 3–5 patients demonstrated in the latter group more concurrent diagnoses and increased pro-BNP levels. Patients with decreasing eGFRMDRD had higher rates of hypertension, diabetes, MI and stroke or TIA, albeit without reaching statistical significance (Tables 3 and 6), most likely due to limited patient numbers with these concurrent diseases.
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patients' characteristics according to cystatin C
For the analysis of baseline characteristics of patients according to cystatin C levels, these were categorized into three groups of <1.0 mg/l, 1.0–1.28 mg/l and >1.28 mg/l as shown in Table 4. Similar to decreasing eGFRMDRD rates (Tables 2 and 3), other renal parameters, such as rising creatinine and declining eGFR by MDRD and CG equations confirmed elevated cystatin C levels. With elevated cystatin C levels, patients tended to be older, had more concurrent diagnoses and rising pro-BNP levels. Patients with increasing cystatin C also had a higher rate of diabetes and hypertension, although without statistical significance (Table 6).
patients' characteristics according to creatinine
Patients were grouped into three categories of <1.1, 1.1–1.3 and >1.3 mg/dl according to their creatinine levels (Table 5). Patients with increasing creatinine tended to be older, had similar or more concurrent diagnoses, higher BMI and pro-BNP. Again, patients with higher creatinine levels showed increasing cystatin C and decreasing eGFR levels by MDRD and CG. Moreover, risks for hypertension, diabetes and MI seemed to increase, which for the latter reached significance (Table 6).
comparison of decreased eGFR (MDRD and CG), elevated cystatin C and creatinine as predictor variables
Overall, eGFRMDRD showed a strong association with increasing creatinine, cystatin C levels, declining eGFRCG values and vice versa (all P < 0.0001; continuity-adjusted 2 tests; Table 6). Noteworthy, eGFR calculated by MDRD in stages eGFRMDRD <90, 60 ml/min/1.73 m2 showed an OR of 47 for eGFR stages by CG (eGFRCG <90, 60 ml/min) (Table 6). Comparing different clinical parameters within the groups of patients with eGFRMDRD (<90, <75, <60 ml/min/1.73 m2), eGFRCG (<90, <60 ml/min), cystatin C (>1.0 mg/l) or creatinine (>1.1 mg/dl), we observed no association with a specific gender risk, diagnosis of ST versus HM, more advanced disease or comorbidity (SI) (also depicted in Tables 2, 4 and 5).
Those cancer patients with decreased eGFRMDRD (<90, <75, <60 ml/min/1.73 m2) had increased OR to be older, for more concurrent diagnoses, elevated BMI and pro-BNP levels. With eGFRMDRD <60 ml/min/1.73 m2, patients had increased OR of 4.8 to be older, of 3.4 for concurrent diagnoses, of 2.1 for a BMI >24 and 9.2 for an elevated pro-BNP. In addition, patients with an eGFRCG (<60 ml/min) showed—similarly to eGFRMDRD <60 ml/min/1.73 m2—elevated OR of 9.9 to be older, of 2.4 for concurrent diagnoses and of 7.7 for higher pro-BNP levels. Increased ORs were evident for all decreasing eGFRMDRD/CG rates [<90, (<75) and <60 ml/min/1.73 m2] and thereby already detectable with mild RI. Cystatin C >1 mg/l and creatinine >1.1 md/dl levels also increased OR for those risk factors as depicted in Table 6, albeit were lower when compared with eGFRMDRD <60 ml/min/1.73 m2 OR in terms of age, concurrent diagnoses and pro-BNP levels. Decreasing eGFRMDRD/CG and increasing creatinine and cystatin C levels affected OR for hypertension, diabetes, MI and stroke, although these (for most) failed to reach significance, since case numbers were small.
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discussion |
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The prevalence of end-stage renal disease (ESRD) continues to rise, especially in persons >65 years. Several prior studies suggested that RI increases the risk of death and complications from cardiovascular disease and hospitalization [11, 17, 18]. The reciprocal relationship between GFR and serum creatinine (as demonstrated in Figure 1) offers difficulties for the clinicians to detect early stages of RI by monitoring serum creatinine alone. This is, however, important for early adjustment of medication [19], such as chemotherapy. Therefore, close collaboration of hematologists and oncologists with nephrologists is essential. In our study, we used the simplified four-variable MDRD equation for eGFR values in comparison to eGFR by CG, and creatinine and cystatin C levels for determining the prevalence of early RI in cancer patients.
Our results suggest that consequent monitoring of renal function by eGFR (MDRD or CG) seems to be warranted already in CKD stage 2 (eGFRMDRD 89–60 ml/min/1.73 m2) in order to avoid further kidney damage and to focus on additional patient-related risk factors. We observed, that cancer patients with barely decreased eGFRMDRD (<90, <75 ml/min/1.73 m2) had already increased OR for more concurrent diagnoses, elevated BMI and pro-BNP levels, which substantially increased with deteriorating eGFR rates. Of interest (and thereby confirming our results) is that increased BMI, age, deteriorating eGFR, in combination with hypertension and diabetes mellitus, have previously been shown to increase the risk of cardiovascular disease [20–22]. Furthermore, one study has examined the relationship between higher BMI and risk for ESRD: in a retrospective study of 320 252 adults, the rate of ESRD increased with higher BMI (starting at a BMI of 25 kg/m2), even in people without diabetes or hypertension, illustrating again that this risk factor and others (often being numerous in cancer patients) increase the risk for early, but also ESRD [22].
Risk stratification according to comorbidity scores is widely used in cancer patients. Comorbidities are associated with a decreased life expectancy and have repetitively been found to be an independent prognostic factor for cancer outcome. In addition, comorbidities may decrease the tolerance of cancer chemotherapy [23] and are thus being recommended to be assessed for the most adequate guidance of intensive chemotherapy regimens in frail patients. In our study, we used the SI which includes a number of conditions that may influence patients' survival. We chose the SI rather than the more commonly used Charlson index, since the former does not include renal disease within its comorbidity factors, thereby independently allowing determining its correlation with eGFR, cystatin and creatinine levels as well as other parameters. Despite an increased number of concurrent diagnoses with decreased eGFRMDRD, we found no difference in the SI. This might have failed to show due to (i) our limited patient number, (ii) our patients showing a low median SI and/or (iii) indeed no close correlation of the SI with mild or moderate RI.
In accordance with previous studies, our results emphasize that GFR estimated by the use of the creatinine-based MDRD equation seems more accurate than serum creatinine or cystatin C alone [1, 4] and is comparable to the eGRF by CG equation. Albeit being aware of limitations of the MDRD and CG equation, it helps clinicians to interpret GFR estimates. Moreover, the utilization of equations is efficient and cost-effective in centralized computer systems, compared with calculation by clinicians themselves [1]. Therefore, laboratories should closely work with physicians in: (i) making the best choice of GFR equation, (ii) defining indications of eGFR (either only to be measured if requested or each time when serum creatinine is also determined) and (iii) communicating additional information (normal values for age and gender, GFR levels for Kidney Disease Outcomes Quality Initiative (K/DOQI) CKD stages) [1]. Due to our results and evidence from other publications, we have decided to use the MDRD equation at our institution instead of timed 24-h urine collections and cystatin C [1, 7, 18].
In this study, we also confirmed the closer correlation between creatinine and cystatin C and lower correlation between eGFRMDRD and cystatin C [9]. The additional use of cystatin C as a marker for RI seemed limited, especially as it appears to be influenced by the effect of thyroid function [24]. Furthermore, the unforeseen influence of pharmacokinetics, metabolism and pharmacodynamics of antineoplastic drugs on cystatin C levels is unclear and less well reported, especially not in large numbers of cancer patients. The extent of the specific cancerous disease may also influence the concentration of cystatin C and other renal parameters. Some have suggested an improved prediction of decreased CrCl and thereby RI by determination of serum cystatin C as compared with creatinine in cancer patients [25], nevertheless, the study was limited due to its sample size and lack of inclusion of a variety of tumor patients (having included only malignant melanoma, gastric and ovarian cancer), so that further studies on cystatin C and other renal parameters are warranted in larger cohorts.
Our comparison of creatinine, cystatin C and eGFR levels suggested that the latter seemed remarkably valuable for determining early stages of RI. In addition, we confirmed that creatinine and cystatin C levels remain within normal ranges in CKD stage 2, so that early detection of slow progression to possible end-stage RI might be more reliably drawn with eGFR values (and may also influence cancer patients' outcome). These findings reinforce the importance of using a practical and cost-effective way to determine RI and—if our results are confirmed in future studies—to speculate that eGFR is an alternative, useful and prognostic determinant to detect early stages of RI as compared with CrCl, serum creatinine or cystatin C.
Albeit for this analysis being adequate in number, our study may be criticized for its still limited consecutive patients, especially of those with RI. This reduced our statistical power to determine specific risk factors with deteriorating eGFR, creatinine or cystatin C levels. Furthermore, eGFR by the use of creatinine-based equation has also been assessed critically [4]. Finally, we did not measure RI within a follow-up analysis, so that the role of nephropathy induced by different chemotherapies or radiocontrast agents remains as yet unclear. Forthcoming longitudinal analyses are being planned with longer follow-up and inclusion of disease outcome in a more homogeneous patient group, such as multiple myeloma patients with different eGFR equations. This current analysis already highlights the importance of future longitudinal analyses with extended follow-up and inclusion of disease outcome to assess RI as a potential prognostic marker in cancer patients.
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Acknowledgements |
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We thank for the critical reading of the manuscript of Prof. Dr Hartmut Peter Hermann. Neumann (Department of Nephrology, University of Freiburg), the anonymous internal reviewer of our department (Med I, Hematology/Oncology) and the insightful as well as helpful comments of the reviewers of Annals of Oncology that have substantially inspired our manuscript. We are grateful to Prof. Dr R. Mertelsmann's continuous support.
Received for publication April 13, 2006. Revision received September 27, 2006. Revision received November 30, 2006. Accepted for publication January 15, 2007.
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1. National Kidney Foundation. Kidney Disease Outcome Quality Initiative (K/DOQI) clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis (2002) 39(Suppl 1):1–266.[CrossRef][Web of Science][Medline]
2. Levey AS, Coresh J, Balk E, et al. National kidney foundation practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Ann Intern Med (2003) 139:137–147.
3. Smith HW. Comparative physiology of the kidney. In: The Kidney: Structure and Function in Health and Disease—Smith HW, ed. (1951) New York, NY: Oxford University Press. 5250–5274.
4. Stevens LA, Levey AS. Frequently Asked Questions about GFR Estimates. (2004) New York, NY: National Kidney Foundation.
5. Levey AS, Bosch JP, Green T, et al. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Ann Intern Med (1999) 130:461–470.
6. Levey AS, Greene T, Kusek J, Beck G. A simplified equation to predict glomerular filtration rate from serum creatinine. J Am Soc Nephrol (2000) 11:155A.
7. Stevens LA, Coresh J, Greene T, Levey AS. Assessing kidney function measured and estimated glomerular filtration rate. N Engl J Med (2006) 354:2473–2483.
8. Jobsson B, Lignelid H, Bergerheim USR. Transthyretin and cystatin C are catabolized in proximal tubular epithelial cells and the proteins are not useful as markers for renal cell carcinomas. Histopathology (1995) 26:559–564.[Web of Science][Medline]
9. Shlipak MG, Sarnak MJ, Katz R, et al. Cystatin C and the risk of death and cardiovascular events among elderly persons. N Engl J Med (2005) 352(20):2049–2060.
10. Coll E, Botey A, Alvarez L, et al. Serum cystatin C as a new marker for noninvasive estimation of glomerular filtration rate and as a marker for early renal impairment. Am J Kidney Dis (2000) 36:29–34.[Web of Science][Medline]
11. Go AS, Chertow GM, Fan D, et al. Chronic kidney disease and the risk of death, cardiovascular events, and hospitalization. N Engl J Med (2004) 351:1296–1305.
12. Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N Engl J Med (2004) 350:647–654.
13. Vickery S, Price CP, John RI, et al. B-type natriuretic peptide (BNP) and amino-terminal ProBNP in patients with CKD: relationship to renal function and left ventricular hypertrophy. Am J Kidney Dis (2005) 46:610–620.[CrossRef][Web of Science][Medline]
14. Kapoor M, Chan GZ. Malignancy and renal disease. Crit Care Clin (2001) 17:571–598.[CrossRef][Web of Science][Medline]
15. da Silva J, Mesler D. Acute renal failure as a result of malignancy. In: Acute Renal Failure: A Companion to Brenner and Rector's The Kidney—Molitoris B, Finn W, eds. (2001) Indianapolis, IN: Harcourt. 312–321.
16. Satariano WA, Ragland DR. The effect of comorbidity on 3 year survival of women with primary breast cancer. Ann Intern Med (1994) 120:104–110.
17. Tokmakova M, Skali H, Solomon SD, et al. Moderate renal dysfunction augments cardiovascular risk after myocardial infraction. Presented at the European Society of cardiology Congress, Vienna, Austria, 31 August 2003.
18. Anavekar NS, McMurray JJV, Velazques EJ, et al. Relation between renal dysfunction and cardiovascular outcomes after myocardial infarction. N Engl J Med (2004) 351:1285–1295.
19. Shlipak MG. Pharmacotherapy of heart failure in patients with renal insufficiency. Ann Intern Med (2003) 138:917–924.
20. McCullough PA. Cardiorenal risk: an important clinical intersection. Rev Cardiovasc Med (2002) 3:71–76.[CrossRef][Medline]
21. Foley RN, Parfrey PS, Sarnak MJ. Epidemiology of cardiovascular disease in chronic renal disease. J Am Soc Nephrol (1998) 9:16–23.[CrossRef]
22. Hsu C-Y, McCulloch CE, Iribarren C, et al. Body mass index and risk for end-stage renal disease. Ann Intern Med (2006) 144:21–28.
23. Balducci L, Extermann M. Management of cancer in the older person: a practical approach. Oncologist (2000) 5:224–237.
24. Fricker M, Wiesli P, Brandle M, et al. Impact of thyroid dysfunction on serum cystatin C. Kidney Int (2003) 63:1944–1947.[CrossRef][Web of Science][Medline]
25. Stabuc B, Vrhovec L, Stabuc-Silih M, et al. Improved prediction of decreased creatinine clearance by serum cystatin C: use in cancer patients before and during chemotherapy. Clin Chem (2000) 46:193–197.
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