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Int Urol Nephrol

DOI 10.1007/s11255-014-0687-0

NEPHROLOGY - ORIGINAL PAPER

Relative lymphocyte count as a marker of progression of chronic


kidney disease
So Mi Kim Hyun Woo Kim

Received: 18 August 2013 / Accepted: 26 February 2014


Springer Science+Business Media Dordrecht 2014

Abstract
Background Although low relative lymphocyte count
(RLC) is associated with poor outcomes in patients with
chronic kidney disease (CKD), the relationship between
low RLC and progression of CKD is poorly defined. The
aim of this study was to determine the association between
low RLC and the progression of CKD.
Methods Between January 2003 and December 2009, 288
CKD patients were analyzed. RLC was calculated as the
ratio between lymphocyte and total white blood cell
counts.
Results The median RLC was 29.1 % [interquartile range
(IQR) 24.134.1]. When the patients were compared
according to a level below or above the median value for
RLC, the rate of CKD progression to end-stage renal disease (ESRD) was greater in patients with low RLC count
than in patients with high RLC (48 vs. 25 %, p \ 0.001)
during the median follow-up of 5.5 years (IQR 3.57.6).
The variables found to be predictive of progression to the
ESRD included younger age, smoking, diabetes, higher
systolic blood pressure, no use of angiotensin-converting
enzyme inhibitors (ACEIs) or angiotensin II receptor
blockers (ARBs), lower hemoglobin and serum albumin
levels, higher low-density lipoprotein cholesterol concentration, presence of proteinuria, and low RLC in the univariate Cox proportional hazards regression analysis.
However, after adjustment, younger age, male, higher

S. M. Kim  H. W. Kim (&)


Division of Nephrology, Department of Internal Medicine,
Jeju National University, School of Medicine, Jeju National
University Hospital, Ara 1-dong, 1753-3, Jeju-si,
Jeju-do 690-767, Korea
e-mail: andrewmanson@naver.com;
andrewmanson@jejunuh.co.kr

systolic blood pressure, no use of ACEIs or ARBs, lower


hemoglobin and serum albumin concentrations, higher
proteinuria, and lower RLC were significantly associated
with progression to ESRD in multivariate analysis.
Conclusions Low RLC is independently associated with
increased rate of progression in patients with CKD.
Keywords Chronic kidney disease  End-stage renal
disease  Lymphocyte

Introduction
Individuals with chronic kidney disease (CKD) experience
higher overall and cardiovascular disease-associated mortality than the general population [1]. It also has been
known that diabetes, hypertension, hyperlipidemia, and
vascular disease by which CKD patients are often combined
are associated with high cardiovascular mortality and CKD
progression [2, 3]. However, such factors do not entirely
explain this high rate of mortality and CKD progression.
It has been reported that CKD may constitute a chronic
inflammatory state demonstrated by increase in various
growth factors, inflammatory mediators and/or inflammatory markers such as C-reactive protein (CRP), interleukin6 (IL-6), tumor necrosis factor-alpha (TNF-a), or monocyte
chemoattractant protein-1 concentration [46]. These data
suggest that systemic inflammation may lead to progressive
loss of kidney function and development of cardiovascular
disease [6, 7]. Moreover, markers of nutritional deficiency
and/or inflammation are some of the most powerful predictors of poor outcomes in epidemiologic studies of CKD
patients [8]. Thus, various markers such as CRP, IL-6, or
TNF-a have been introduced to measure systemic inflammation in patients with CKD [46]. Two recent studies

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Int Urol Nephrol

reported that increased neutrophil to lymphocyte (N/L)


ratio is associated with standard inflammatory biomarkers
and an independent predictor for rapid disease progression
in patients with CKD, suggesting that a simple calculation
of N/L ratio might be a surrogate marker for evaluation of
inflammation and used as an additional parameter for the
preliminary approach of monitoring patients with CKD in
clinical practice [9, 10]. Likewise, cumulative evidence
supports the use of a low relative lymphocyte count (RLC)
as a marker of malnutrition and inflammation in patients
with CKD [11], and low RLC has been shown to be robust
predictors of mortality in CKD patients [12]. However, it is
obscure whether low RLCs are related with CKD progression as with N/L ratio. The aim of the present study
was to determine the association between low RLC
(assessed 6 months after the time of the first visit) and
CKD progression.

Subjects and methods


Patients
The records of 445 outpatients who had CKD and were
evaluated and treated at our hospital between 2003 and
2009 were retrospectively reviewed. At enrollment, the
patients had to be at least 18 years old and have CKD, as
defined by an estimated glomerular filtration rate (eGFR) of
\60 ml/(min 1.73 m2), determined using the Modification
of Diet in Renal Disease formula [13]. The major exclusion
criteria were as follows: stage V CKD, cancer, hematologic
disturbances, autoimmune disease, acute infection, and
treatment with corticosteroids or immunosuppressants.
Patients with white blood cell (WBC) count of
[20,000 cell/mm3 were also excluded because these
patients may have had a subclinical infection. Finally, we
examined a total of 288 patients with CKD. This study was
approved by an institutional review board (no. JEJUNUH
2012-10-014).
Data collection
Laboratory results, such as those for total WBC, neutrophil,
lymphocyte, and monocyte counts, were averaged over
6 months after the first visit and were obtained using an
automated blood cell counter. The RLC was calculated as
the ratio of lymphocyte and total WBC counts. Proteinuria
was defined by a score of 1? or greater on a dipstick urine
test during the first 6 months of follow-up. The primary
end point was the progression to end-stage renal disease
(ESRD), defined as the initiation of maintenance renal
replacement therapy or kidney transplantation.

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Statistical analysis
The patients were divided into two groups on the basis of
having RLC values greater or less than the median value of
29.1 %. Continuous variables have been expressed in terms
of mean standard deviation (SD) or median with the
interquartile range (IQR). Categorical variables have been
represented as frequencies and percentages. Students t test
or the MannWhitney U test was used to compare differences in continuous variables. The chi-square test or
Fishers exact test was used to compare categorical variables. Renal survival was measured from the date of patient
enrollment to the date of initiation of dialysis. The renal
survival of patients was estimated using the KaplanMeier
method, and the log-rank sum test was used to assess the
statistical difference among patients divided into two or
three groups based on the RLC. The relationships of various factors with the development of ESRD were examined
using Cox regression analysis. Variables that were significant in the univariate models (p \ 0.05), and known risk
factors for CKD progression such as gender, body mass
index, baseline blood pressure, and eGFR were analyzed in
a multivariate model with the use of a backward-selection
procedure. A p value of \0.05 was considered significant.
All statistical analysis was performed using SPSS, version
15.0.

Results
Between January 2003 and December 2009, 288 CKD
patients were analyzed. The mean age at enrollment was
59 12 years, and 191 (66 %) patients were male. The
mean eGFR was 37 11 ml/(min 1.73 m2). All patients
had stage III (31 %) or IV (69 %) CKD. The causes of
renal insufficiency in the patients were as follows: diabetic
nephropathy (132 cases, 46 %), hypertensive nephrosclerosis (92 cases, 32 %), chronic glomerulonephritis (40
cases, 14 %), chronic interstitial nephritis (10 cases, 3 %),
and others (14 cases, 5 %). Eighty-seven percent of the
patients had hypertension, 49 % had diabetes mellitus, 8 %
had coronary artery disease, and 12 % had a history of
cerebrovascular accident.
The median values for the total WBC, neutrophil, and
monocyte counts were 7,007 cell/mm3 (IQR 5,8008,325 cell/
mm3), 4,140 cell/mm3 (IQR 3,2225,093 cell/mm3), and
505 cell/mm3 (IQR 388560 cell/mm3), respectively. The
mean lymphocyte count was 2,078 624 cell/mm3, and the
median RLC was 29.1 % (IQR 24.134.1 %). When the
patients were compared on the basis of an RLC value greater or
lesser than the median value of 29.1 %, no obvious differences
were observed in age, gender distribution, initial GFR, or the
prevalence of diabetes mellitus, hypertension, coronary artery

Int Urol Nephrol


Table 1 Baseline characteristic
of patients with chronic kidney
disease

Characteristics

Patients with RLC of


B29.1 % (n = 144)

Patients with RLC of


[29.1 % (n = 144)

p value

Age (years)

60.3 11.6

58.4 12.6

0.178

Age C 65 years [n (%)]

60 (42)

58 (40)

0.811

Male [n (%)]

96 (67)

95 (66)

0.901

2a

Body mass index (kg/m )

24.1 (21.727.0)

24.4 (22.626.4)

0.339

Smoking [n (%)]

27 (19)

28 (19)

0.881

Diabetes mellitus

73 (51)

59 (41)

Hypertension

44 (31)

48 (33)

Chronic glomerulonephritis

13 (9)

27 (19)

Chronic interstitial nephritis

3 (2)

7 (5)

Others
Underlying diseases

11 (7)

3 (2)

Hypertension [n (%)]

125 (87)

125 (87)

Causes of chronic kidney disease

Values are expressed as mean


(SD), n, or percentage unless
otherwise specified
ACEIs angiotensin-converting
enzyme inhibitors, ARBs
angiotensin II receptor blockers,
HMG-CoA 3-hydroxy-3methylglutaryl-coenzyme A,
RLC relative lymphocyte count
a

Median (intequartile range)

Table 2 Laboratory data of


patients with chronic kidney
disease

0.103

Diabetes mellitus [n (%)]

78 (54)

62 (43)

0.059

Coronary artery disease [n (%)]

14 (10)

9 (6)

0.277

Cerebrovascular accident [n (%)]

17 (12)

18 (13)

0.857

Glomerular filtration rate (ml/min/1.73 m2)

35.8 11.2

38.1 10.9

0.080

ACEIs or ARBs

97 (67)

98 (68)

0.900

b-Blockers

47 (33)

33 (23)

0.066

Calcium channel blockers

79 (55)

70 (49)

0.289

Diuretics

67 (47)

53 (37)

0.094

HMG-CoA reductase inhibitors

46 (32)

50 (35)

0.677

Anti-platelet agents

64 (44)

55 (38)

0.281

Baseline medications [n (%)]

Laboratory data

Patients with RLC of


B29.1 % (n = 144)

Median (intequartile range)

p value

7,520 (6,2869,155)

6,700 (5,8007,875)

\0.001

Neutrophil (mm3a)

4,859 (4,1276,164)

3,486 (2,8974,258)

\0.001

Lymphocyte (mm3)

1,784 524

2,372 577

\0.001

Monocyte (mm3)

560 211

498 191

0.010

Hemoglobin (g/dL)

11.8 2.0

12.3 2.1

0.043

217 66

218 66

0.337

LDL low-density lipoprotein,


RLC relative lymphocyte count

Patients with RLC of


[29.1 % (n = 144)

White blood cells (mm3a)

Platelets (1,000/mm3)

Values are expressed as mean


(SD), n, or percentage unless
otherwise specified

1.000

Serum creatinine (mg/dL )

1.8 (1.62.4)

1.8 (1.62.3)

0.134

Serum albumin (g/dL)

3.7 0.7

3.9 0.6

0.047
0.277

Total cholesterol (mg/dL)

203 58

195 48

Triglyceride (mg/dLa)

147 (113208)

161 (114208)

0.028

LDL cholesterol (mg/dL)


Corrected total calcium (mg/dL)

130 57
9.1 0.5

126 39
9.2 0.4

0.661
0.603

Proteinuria (dipstick positive) [n (%)]

102 (71)

83 (58)

0.019

disease, or cerebrovascular accident between the two groups


(Table 1). The medications taken by the patients have been
listed in Table 1. The two groups did not significantly differ
with respect to the use of angiotensin-converting enzyme
inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs),
b-blockers, calcium channel blockers, diuretics, anti-platelet

agents such as aspirin and clopidogrel, and 3-hydroxy-3methylglutaryl-coenzyme A reductase inhibitors (statins).
Patients with low RLC had higher total WBC, neutrophil, and
monocyte counts than patients with high RLC. However, the
lymphocyte counts and the hemoglobin and serum albumin
concentrations were lower in patients with low RLC than in

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Int Urol Nephrol

Fig. 1 Renal survival curves in patients with chronic kidney disease


according to relative lymphocyte count. a Renal progression-free
survival was significantly higher in patients with high relative
lymphocyte count (RLC [ 29.1 %) than in patients with low relative
lymphocyte count (RLC B 29.1 %, p \ 0.001). b When the patients

were divided into three groups based on the tertiles of RLC (lower
tertile \26.1 %; middle tertile 26.132.6 %; upper tertile [32.6 %),
higher levels of RLC were associated with faster progression to endstage renal disease (p for trend across tertiles = 0.002)

patients with high RLC. Furthermore, proteinuria was noted


more frequently in the low RLC group than in the high RLC
group (Table 2).
The median duration of follow-up was 5.5 years (IQR
3.57.6 years). Over the year of follow-up, 105 of 288
patients (37 %) progressed to ESRD. Decreased absolute
lymphocyte counts were associated with accelerated rate of
GFR decline in simple correlation analysis (r = 0.133;
p = 0.024), indicating that lymphocyte count may be
reflected to CKD progression. When progression to ESRD
was compared between patients with low or high RLC, the
low RLC group showed significantly greater progression to
ESRD than the high RLC group (Fig. 1a). In addition,
when the patients were divided into three groups based on
the tertiles of RLC (lower tertile \26.1 %; middle tertile
26.132.6 %; upper tertile [32.6 %), higher levels of RLC
were associated with slower progression to ESRD (p for
trend across tertiles = 0.002, Fig. 1b). Compared with the
lower tertile, the upper tertile of RLC level was associated
with a hazard ratio (HR) of 0.39 (0.240.63, p \ 0.001)
and the middle tertile with a HR of 0.54 (0.350.84,
p = 0.007), respectively.
Tables 3 and 4 show the results of Cox proportional
hazards modeling. The factors associated with increased
progression to ESRD included younger age, smoking,
diabetes, higher systolic blood pressure, no use of ACEIs or
ARBs, higher low-density lipoprotein (LDL) cholesterol
level, lower hemoglobin and serum albumin levels at
baseline, presence of proteinuria, and low RLC during the
first 6 months of follow-up (Table 3). Higher eGFR is
associated with a tendency toward reduced progression to
ESRD (p = 0.111). However, after adjustment, smoking,

diabetes, and higher LDL cholesterol level were no longer


associated with the progression of CKD to ESRD. Multivariate analysis showed that younger age, male, higher
systolic blood pressure, no use of ACEIs or ARBs, lower
hemoglobin and serum albumin concentrations, higher
proteinuria, and lower RLC were significantly associated
with increased progression to ESRD (Table 4). As expected, the relative risk of progression to ESRD among
patients who had proteinuria during the first 6 months of
follow-up was 3.7-fold higher than that among patients
who did not have proteinuria during this period [HR 3.685,
95 % confidence interval (CI) 1.4379.499, p = 0.007].
Furthermore, the risk of progression to ESRD among
patients whose RLC was less than 29.1 % was higher than
that for patients whose RLC was greater than or equal to
29.1 % (HR 1.796, 95 % CI 1.0693.016, p = 0.027).

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Discussion
The aim of the present study was to investigate the association between low RLC and CKD progression. We found
that RLC was inversely associated with the progression of
CKD to ESRD. Younger age, male, higher systolic blood
pressure, no use of ACEIs or ARBs, lower hemoglobin and
serum albumin concentrations, and proteinuria were also
associated with an increased risk for renal replacement
therapy or kidney transplantation.
Patients with CKD are reported to have lower lymphocyte counts than individuals without CKD [14]. However,
the relationship between low lymphocyte counts and
patient outcomes is unclear. Several studies have reported

Int Urol Nephrol


Table 3 Univariate predictors for progression of chronic kidney
disease to end-stage renal disease

Table 4 Multivariate predictors for progression of chronic kidney


disease to end-stage renal disease

Covariate

HR (95 % CI)

Covariate

HR (95 % CI)

Age (years)

0.980 (0.9650.995)

0.010

Age (years)

0.959 (0.9360.983)

0.001
0.018

p value

Gender, male/female

1.160 (0.7701.749)

0.478

Gender, male/female

2.412 (1.1615.011)

Body mass index (kg/m2)

0.950 (0.8981.004)

0.071

Body mass index (kg/m2)

0.992 (0.9271.061)

0.810

Smoking

1.775 (1.1332.780)

0.012

Smoking

1.555 (0.8412.875)

0.160

Systolic blood pressure (mmHg)

1.033 (1.0231.043)

\0.001

Systolic blood pressure (mmHg)

1.036 (1.0181.054) \0.001

Diastolic blood pressure (mmHg)

1.001 (0.9961.005)

0.699

Diastolic blood pressure (mmHg)

1.001 (0.9871.015)

0.912

Diabetes mellitus
Coronary artery disease

1.801 (1.2202.658)
1.189 (0.5772.448)

0.003
0.639

Diabetes mellitus
ACEIs or ARBs

1.107 (0.6032.032)
0.469 (0.2420.911)

0.743
0.025

Cerebrovascular accident

1.306 (0.6802.506)

0.423

Hemoglobin (g/dL)

0.764 (0.6470.902)

0.001

ACEIs or ARBs

0.587 (0.3720.927)

0.022

Serum albumin (g/dL)

0.646 (0.4470.934)

0.020

b-Blockers

1.292 (0.8521.960)

0.228

1.004 (0.9951.013)

0.422

Calcium channel blockers

1.239 (0.8421.821)

0.277

Low-density lipoprotein cholesterol


(mg/dL)

Diuretics

1.278 (0.8701.786)

0.211

0.991 (0.9661.016)

0.478

HMG-CoA reductase inhibitors

1.260 (0.8411.889)

0.263

Estimated glomerular filtration rate


(ml/min/1.73 m2)

Anti-platelet agents

1.219 (0.8311.789)

0.311

Proteinuria (g/day)

3.685 (1.4379.449)

0.007

White blood cells (mm )

1.051 (0.9671.133)

0.061

Relative lymphocyte count (%)

0.965 (0.9380.992)

0.012

Neutrophil (mm3)

1.000 (1.0001.000)

0.079

Monocyte (mm )

1.000 (0.9991.001)

0.188

Hemoglobin (g/dL)

0.767 (0.6960.845)

\0.001

Platelet (1,000/mm3)

1.001 (0.9971.0044)

Serum albumin (g/dL)

0.365 (0.2820.471)

\0.001

Total cholesterol (mg/dL)


Low-density lipoprotein cholesterol
(mg/dL)

1.022 (0.9851.047)
1.008 (1.0011.014)

0.111
0.028

Triglyceride (mg/dL)

1.001 (0.9981.004)

0.420

Corrected total calcium (mg/dL)

1.084 (0.6471.818)

0.758

Estimated glomerular filtration rate


(ml/min/1.73 m2)

0.993 (0.9721.005)

0.111

Presence of proteinuria

7.411 (3.73414.708) \0.001

Relative lymphocyte count (29.1


vs. [29.1 %)

2.490 (1.6553.717)

0.647

\0.001

HR Hazard ratio, CI confidence interval, ACEIs angiotensin-converting enzyme inhibitors, ARBs angiotensin II receptor blockers,
HMG-CoA 3-hydroxy-3-methylglutaryl-coenzyme A

that low lymphocyte counts are associated with poor outcomes in CKD patients. Kovesdy et al. [12] reported an
inverse relationship between lymphocyte levels and allcause mortality among CKD patients who were not on
dialysis. Similarly, low lymphocyte counts are reported to
be associated with mortality among hemodialysis patients
[15, 16]. In a recent study, however, Agarwal et al. [14]
reported no independent association between decreases in
lymphocyte counts and subsequent ESRD or death. Previous studies, including above-mentioned reports, used allcause or cardiovascular mortality as the outcome measure;
however, relatively little data are available on the relationship between low lymphocyte counts and CKD progression. In our study, low RLC was found to be an

HR Hazard ratio, CI confidence interval, ACEIs angiotensin-converting enzyme inhibitors, ARBs angiotensin II receptor blockers

independent risk factor for progression to ESRD in patients


with stage III or IV CKD.
The exact pathophysiologic mechanism by which low
RLC causes CKD progression is uncertain, but several
mechanisms can be proposed. First, it has been reported
that CKD may constitute a chronic inflammatory state, as
demonstrated by the increase in CRP, IL-6, or TNF-a
concentrations irrespective of the cause of renal disease [6].
This suggests that inflammation induces endothelial cell
damage and dysfunction and predisposes the patient to
atherosclerotic plaque formation and ischemic organ
damage [17]. It is thus plausible that systemic inflammation
may lead to progressive loss of kidney function. Recently,
Okyay et al. [9] reported that N/L ratio is significantly
higher in CKD patients compared with healthy subjects and
positively correlated with well-established inflammatory
markers, IL-6 and high-sensitivity CRP levels. Furthermore, these markers of inflammation are the independent
factors for predicting of N/L ratio, suggesting that N/L
ratio is an inflammatory biomarker for CKD patients [9].
Another recent study also reported that increased N/L ratio
([3) is an independent predictor for rapid kidney function
decline in patients with CKD [10]. Moreover, serum
albumin levels are lower in CKD patients than in the
general population because of chronic metabolic acidosis
and chronic inflammation from concurrent illnesses [18,
19]. Although the mechanism by which hypoalbuminemia
leads to accelerated progression of CKD has not yet been
established, a few studies have observed an association
between hypoalbuminemia and accelerated CKD

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progression, suggesting that a decrease in the serum albumin concentration of CKD patients may reflect not only
proteincalorie malnutrition but may also reflect activation
of the systemic inflammatory response, and consequently
may result in CKD progression [2022]. In our study,
patients with low RLCs had higher total WBC, neutrophil,
and monocyte counts than patients with high RLCs, and
RLC had negative correlations with log transformed CRP
(r = -0.044, p = 0.029), indicating that an increase in
inflammation leads to a decrease in the RLC. In addition,
similar to the study of Okyay et al. [9], a single serum
albumin concentration determined within several weeks of
the first visit and hemoglobin were positively associated
with RLC in simple correlation test (r = 0.149; p = 0.014
and r = 0.154; p = 0.009, respectively), and remained
potent independent markers for CKD progression in our
study, suggesting that inflammation combined with malnutrition, indicated by hypoalbuminemia, anemia, and low
RLC are associated with the progression of CKD. Second,
impaired host resistance, indicated by low lymphocyte
counts, may predispose the patient to infections, which are
in turn associated with increased CKD progression in
patients with low RLCs. Although we excluded patients
with WBC counts of [20,000/mm3 in our study, subclinical infection may be associated with low RLCs. Third, it
has been reported that once renal damage has been initiated, low-grade inflammation in the kidney could be
maintained by autoimmune reactivity such as natural thymotoxic autoantibody for circulating T-lymphocytes [23,
24]. This auto-attack could reduce T-lymphocyte levels and
activated T-lymphocytes could infiltrate into the kidney
causing progressive renal injury [25, 26]. Although we did
not measure autoantibody in the present study, it is possible
that decreased levels of circulating lymphocytes may be
due to autoantibody reaction.
We also identified younger age and male as independent
risk factors for the progression of CKD to ESRD. The
results of the present study correspond with those of earlier
studies which reported that old age or female gender are
associated with lower incidence of CKD progression,
showing that older patients are more likely to die than to
develop ESRD in contrast to younger patients [27, 28]. In
addition, anemia and hypoalbuminemia are associated with
progression of CKD in our study. Anemia in CKD is
associated with increased cardiovascular complications
such as increased left ventricular hypertrophy and cardiac
mortality [29]. However, only a few studies have investigated the role of anemia as an independent risk factor for
CKD progression [20, 21], and the effect of anemia correction on CKD progression is controversial. One study
reported that early treatment of anemia in renal failure
patients slowed the decline of renal function [30], but other
studies did not report any change in CKD progression [31,

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32]. In the present study, anemia during the first 6 months


was a strong predictor for progression to ESRD, even after
multivariate adjustment for other established risk factors.
However, because a very small proportion of patients with
anemia (2 %) were treated with erythropoiesis-stimulating
agents, we could not evaluate the effect of anemia correction on CKD progression.
This study has several limitations. First, it is a relatively
small (n = 288) single-center study that has the inherent
limitations of such studies. Thus, the results may not be
generalizable to other populations. Second, we did not
determine how low RLC translates into CKD progression.
Thus, it is also possible that low RLC is both a cause and a
consequence of CKD progression. Third, we could not
compare RLC with other inflammatory markers such as
tumor necrosis factor TNF-a, IL-6, fibrinogen, or myeloperoxidase because they were not routinely measured in
our study population. Fourth, proteinuria was not uniformly
determined by 24-h protein excretion at baseline in all
patients (missing values on 148 of 288). This fact precluded the use of this important predictive factor as a
continuous variable in the Cox model. We could therefore
not exclude the possibility that the serum albumin level
may act as a proxy for the degree of proteinuria.
In conclusion, younger age, male, higher systolic blood
pressure, anemia, hypoalbuminemia, proteinuria, and low
RLC are independently associated with an increased rate of
progression to ESRD in CKD patients. Because proteinuria
is highly associated with CKD progression, urinalysis is
one of the methods that can be used to identify subjects
who are likely to progress to ESRD. Similarly, although
routine monitoring of inflammatory markers in CKD
patients is not recommended by most guidelines, our
results suggest that measurement of complete blood count
with differential may be useful in assessing the risk profiles
for renal disease progression in CKD patients.
Acknowledgments This research was supported by the 2014 scientific promotion program funded by Jeju National University.

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