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Renal Failure-Measuring the Glomerular Filtration Rate



Chronic renal disease is common, and its prevalence is rising. Its main causes are hypertension and diabetes mellitus. An abnormally low glomerular filtration rate (GFR) often escapes medical notice in the earliest, most treatable stage, so that an increasing number of patients progress to end-stage renal failure. Early recognition of low GFR would thus be an important clinical advance. The authors selectively review the literature retrieved by a PubMed search on the topic and also present their own clinical and laboratory data. Chronic renal failure can be detected early by direct measurement of the GFR with the aid of an exogenous filtration marker. Such techniques are costly and time-consuming and are therefore indicated only for patients at special risk. Chronic renal disease can also be diagnosed early with the aid of the endogenous filtration markers creatinine and cystatin C, which serve as indicators of a low GFR. The serum levels of these two substances are not taken as measures of GFR in themselves, but are rather entered into predictive equations for the estimation of GFR. Cystatin C-based equations seem to be more sensitive indicators of low GFR than creatinine-based equations. Creatinine- and cystatin C-based equations for the estimation of GFR are valuable tools for the early diagnosis of chronic renal disease and for disease staging according to the US National Kidney Foundation criteria.
Renal Failure—Measuring the
Glomerular Filtration Rate
Christian Thomas, Lothar Thomas
Background: Chronic renal disease is common, and its
prevalence is rising. Its main causes are hypertension and
diabetes mellitus. An abnormally low glomerular filtration
rate (GFR) often escapes medical notice in the earliest,
most treatable stage, so that an increasing number of
patients progress to end-stage renal failure. Early
recognition of low GFR would thus be an important
clinical advance.
Methods: The authors selectively review the literature
retrieved by a PubMed search on the topic and also
present their own clinical and laboratory data.
Results: Chronic renal failure can be detected early by
direct measurement of the GFR with the aid of an
exogenous filtration marker. Such techniques are costly
and time-consuming and are therefore indicated only for
patients at special risk. Chronic renal disease can also be
diagnosed early with the aid of the endogenous filtration
markers creat inine and cystatin C, which serve as
indicators of a low GFR. The se rum levels of these two
substances are not taken as measures of GFR in themselves,
but are rather entered into predictive equations for the
estimation of GFR. Cystatin C-based equations seem to be
more sensitive indicators of low GFR than creatinine-based
Conclusions: Creatinine- and cystatin C-based equations
for the estimation of GFR are valuable tools for the early
diagnosis of chronic renal disease and for disease staging
according to the US National Kidney Foundation criteria.
Key words: renal failure, chronic disease, nephropathy,
hypertension, diabetes mellitus
Cite this as: Dtsch Arztebl Int 2009; 106(51–52): 849–54
DOI: 10.3238/arztebl.2009.0849
hronic renal disease (CRD) is defined as a glo-
merular filtration rate (GFR) of <60 (mL × min
per 1.73 m
body surface area) for at least three months,
whatever the cause and regardless of the presence of
kidney damage (1). Patients in whom signs of damage
are found on diagnostic imaging or renal biopsy and
those with albuminuria also have nephropathy, even if
their GFR is >60. Patients without signs of kidney
damage whose GFR is >60 are highly unlikely to be
nephropathic (2). CRD is classified into five stages
according to the GFR (Table 1) (1). In the USA (3)
approximately 10% of adults are estimated to be in an
early stage of impaired renal function, of whom 40%
have a GFR <60 and 60% show elevated albumin
excretion (>30 mg/g creatinine) (e1). According to a
European study (4), the prevalence of CRD stage 4 and
5 is 1% in hospital patients under the age of 30 years
and 12% in those over 80 years of age.
Persons with impaired renal function are at greater
risk of cardiovascular morbidity and mortality (5), and
the prevalence is considerably higher in older people
(6). The latter generally display an annual GFR
decrease of <1 (7), but a yearly drop of >3, regardless
of baseline GFR, has proved to be an independent risk
factor for increased mortality (8).
The GFR is considered the best marker for renal
function (1). The early stages of renal function impair-
ment are clinically silent and are diagnosed only by
measuring GFR by means of external filtration markers
(measured GFR, mGFR) (9). Once GFR has decreased
to <60, functional impairments can be detected by
determining internal filtration markers and calculating
the estimated GFR (eGFR) (10). The complications of
CRD increase with decreasing GFR and may progress
from gradual reduction in renal function to end-stage
renal failure. The goal of GFR determination is to
detect CRD early in order to slow its progress.
The determination of mGFR and eGFR is indicated
as an isolated measurement to assess renal func-
tion at a particular point in time, e.g., in patients
with high prevalence of GFR <60;
to evaluate the progression of CRD;
to assess the efficacy of function-preserving treat-
ment measures.
GFR can be determined using exogenous and endo-
genous markers of filtration (Box 1). Measurements
employing exogenous filtration markers (mGFR) yield
Laboratoriumsmedizin, Krankenhaus Nordwest, Frankfurt am Main: Prof. Dr.
med. Lothar Thomas
The Prostate Centre at VGH, Vancouver BC: Dr. med. Christian Thomas
Deutsches Ärzteblatt International
Dtsch Arztebl Int 2009; 106(51–52): 849–54
reliable results and represent the gold standard.
However, they are costly, time-consuming, and labor-
intensive, can be performed only in specialized labora-
tories, and are therefore indicated primarily in patients
displaying nephrological symptoms. Simpler, but less
precise, is estimation of GFR (eGFR) by means of the
endogenous filtration markers creatinine and cystatin
C.The aim of this review is to depict the methods used
to determine GFR and—by sifting the nephrological,
internal medical and clinical chemistry literature avail-
able in PubMed—ascertain their reliability in the detec-
tion and monitoring of CRD.
Measuring GFR by means of exogenous
filtration markers (mGFR)
The clearance of various markers of filtration, such as
Cr-EDTA, iohexol, iothalamate, and
Tc-diethylenetriaminepentaacetic acid (DTPA), is
determined. The GFR is either expressed in absolute
terms as mL × min
or standardized to 1.73 m
, the
body surface area of a person weighing 70 kg. The unit
of measurement is: mL × min
× (1.73 m
. Age- and
gender-specific reference values for GFR can be found
in Table 2 (11). The reduction in GFR correlates with
the extent of functional impairment of the nephrons and
thus with the degree of renal failure. A patient whose
GFR falls below 15 usually requires dialysis. Never -
theless, in certain cases GFR is insensitive to the loss of
functioning nephrons. In the early stage of diabetes-
related kidney disease, for instance, characterized by
microalbuminuria, the renal hypertrophy and hyperper-
fusion mean that GFR is normal or raised; thus, deter-
mination of GFR is of no value in the diagnosis of
incipient diabetic nephropathy (e2). The different
methods for mGFR do not show full agreement: at GFR
values >80, GFR
gives lower readings than
, but below this threshold GFR
is lower
than GFR
Measuring GFR by means of endogenous
filtration markers (eGFR)
Internal markers of filtration such as creatinine and cys-
tatin C are endogenous substances that are almost com-
pletely filtered out by the glomeruli. Increasing serum
levels of these parameters indicate decreasing GFR. It
is recommended that whenever creatinine is determined
the eGFR should be calculated and reported along with
the serum value (14). Equations frequently used to
ascertain eGFR based upon creatinine and cystatin C
are presented in Box 2.
Serum creatinine
Determination of creatinine in serum is the method
most frequently used to evaluate renal function. Creati-
nine derives from the muscular metabolism of creatine
and phosphocreatine. As such, the synthesis of creati-
nine at a daily rate of approximately 20 mg/kg body
weight reflects muscle mass and varies little from day
to day.
Classification of chronic renal failure, modified from (1)
GFR, glomerular filtration rate; GFR in mL × min
× (1.73 m
89 to 60
59 to 30
29 to 15
Renal disease
With normal GFR
With mild functional
With moderate fail-
With severe failure
With end-stage renal
Confirm diagnosis,
inhibit progression
Inhibit progression
Confirm diagnosis, treat secondary
Prepare for renal replacement
Institute renal replacement treatment
Methods for determination and estimation
of GFR and their evaluation
Clearance of exogenous substances
Inulin, iohexol,
Tc-diethylenetriaminepenta -
acetic acid (DTPA)
Evaluation: Precise and accurate, but costly, time-consuming, and labor-inten-
Clearance of endogenous blood substances
Serum creatinine
Evaluation: Insufficiently sensitive for detection of chronic renal disease (CRD)
Creatinine clearance
Evaluation: No longer recommended due to errors in urine collection
Exception: Patients with highly abnormal muscle mass or vegetarian diet
(e8, e9)
Serum cystatin C
Evaluation: More sensitive than serum creatinine for detection of GFR
reduction in the range 70 to 40; better than creatinine in children
Estimated GFR (eGFR)
Creatinine-based and use of patient-specific data
Counahan-Barratt equation
Evaluation: Only suitable for children, overestimates GFR by ca. 20% to 30%
Cockcroft-Gault equation
Evaluation: Only suitable for adults, slightly overestimates GFR, well suited for
estimation of GFR changes during pharmacotherapy
MDRD (Modification of Diet in Renal Disease) equation
Evaluation: Practicable in adults with CRD; not suitable for children
Cystatin C-based eGFR
No patient-specific data required
Evaluation: In the range 70 to 40, estimates GFR more sensitively than
creatinine-based equations
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Creatinine synthesis is age-dependent. As measured
by urinary excretion, it decreases with increasing age,
falling from a mean 23.8 mg/kg body weight in men
aged 20 to 29 years to 9.8 mg/kg body weight in men
aged 90 to 99 years (e2). The essential reason is reduc-
tion in muscle mass.
When renal function is normal, creatinine is filtered
out by the glomeruli and 15% of it is secreted by the
tubuli (e3). There is a reciprocal non-linear relationship
between GFR and serum creatinine, such that a decrease
in GFR to around 40 often does not lead to an increase to
above the upper limit of normal (e4). If no previously
obtained values are available, a concentration within the
normal range cannot be interpreted as potentially showing
a decrease in GFR. In acute renal failure serum creatinine
rises within 2 days as a direct result of retention within
the body. In CRD the increase in serum is only 30% to
50% of what would be expected from the prevailing
GFR. The reason for this is that, depending on the extent
of GFR reduction, 16% to 66% of creatinine is eliminated
extraglomularly (e5). Tubular secretion and intestinal
elimination reach their maximum when GFR falls to
15. Noteworthy extra renal patient-related factors that
influence creatinine synthesis and thus the concentration
in serum include sex, age, ethnicity, muscle mass,
chronic illness, and the consumption of cooked meat.
Lack of standardization of methods also impacts
negatively on the validity of serum creatinine for
assessment of GFR. Medications such as cimetidine and
trimethoprim inhibit creatinine secretion and increase the
serum concentration without affecting GFR. It must also
be realized that serum creatinine is not suitable for
evaluation of rapid changes in GFR: The estimated GFR
is too high in swiftly decreasing renal function and too
low when function recovers.
Serum cystatin C
Cystatin C is a plasma protein with a molecular weight
of 13.4 kDa and belongs to the cysteine protease in-
hibitors. It is synthesized at a constant rate by all
nucleated cells, excreted into plasma, filtered by the
glomeruli, and reabsorbed and metabolized by the
proximal tubule cells. In the age group from 1 to 50
years, the serum concentration is independent of
muscle mass, sex, and age .
Reference values for GFR (11)
* (mL × min
× [1,73 m
Premature births
Children (2 to 8 weeks)
Children (3 to 12 months)
Children/adolescents (1 to 20 years)
Adults (age group, years)
>0.5 mL × min
× kg
>10 mL × min
× [m
16.3 to 44.6 (mL × min
× [1.73 m
>70 (mL × min
× [1.73 m
>80 (mL × min
× [1.73 m
Creatinine- and cystatin C-based equations for calculation of eGFR
Counahan-Barratt equation (e14) Creatinine-based
eGFR (mL × min
) = 0.43 × height (cm) × (S
Equation according to Cystatin C-based
Grubb et al. (24) eGFR (mL × min
× [1.73 m
) = 84.69 × (S
cystatin C
[mg × L
× 1.384 (in children <14 years)
Cockcroft-Gault equation (19) Creatinine-based
(mL × min
) = (140 – age [years]) × (S
[mg × dL
× (BW [kg] × [72]
Correction factor: for women × 0.85
MDRD equation (10) Creatinine-based
eGFR (mL × min
× [1.73 m
) = 175 × (S
standardized [mg × dL
× (age [years])
Correction factor: for women × 0.742
f or blacks × 1.18
Equation according to Cystatin C-based
Hoek et al. (25) eGFR (mL × min
× [1.73 m
) = 80.35 × (S
cystatin C
[mg × L
] – 4)
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These properties show that cystatin C is a good
marker for assessment of renal function. Comparably
with serum creatinine, there is an inverse, non-linear
relationship between GFR and serum cystatin C. In
comparison with serum creatinine, the proportional
increase of cystatin C is higher when GFR falls to a
level between 70 and 40 (Figure) (17). Cystatin C rises
age-dependently from the age of 50 years and corre-
lates with the decrease in GFR.
Cystatin is not always a reliable marker of renal
function, as its synthesis is increased in smokers,
patients with hyperthyroidism, and those on glucocorti-
coid therapy and decreased in hypothyroidism (e6).
According to a meta-analysis, however, cystatin C is a
more reliable parameter than creatinine for detection of
CRD (18).
Creatinine-based eGFR
eGFR is determined by means of equations that take
account of empirically patient-related parameters and
thus permit more precise and accurate assessment of
GFR. All of the equations employed for estimating
GFR were developed using cross-sectional data from
patient collectives. The Cockcroft-Gault equation (19)
and the Modification of Diet in Renal Disease (MDRD)
equation (20) are recommended (Box 2). The former
incorporates age, body weight, sex, and serum creati-
nine concentration, while the latter considers age,
ethnicity, sex, and serum creatinine concentration. The
Counahan-Barratt equation is recommended for
Cockcroft-Gault equation
The Cockcroft-Gault equation estimates creatinine
clearance in mL × min
, but not GFR, and is not stan-
dardized to the body surface area of 1.73 m
. In relation
to GFR it systematically overestimates clearance
because tubular creatinine secretion is not taken into
account (19, 20). Because this equation includes body
weight, it is particularly recommended for the monitor-
ing of renal function during treatment with medications
that influence kidney performance.
MDRD equation
The MDRD equation includes age, sex, and ethnicity to
take account of differences among population sub-
groups. Therefore reductions in GFR are detected ear-
lier than with serum creatinine.
Because the MDRD equation was developed exclu -
sively using data from patients with CRD, a GFR of
>60 should be reported not as an absolute value but as
eGFR >60 mL = (mL × min
× [1.73 m
) (20, 21).
More recently individuals without CRD have also been
Proportional increase in serum creatinine (blue) and serum cystatin C (yellow) with
decreasing glomerular filtration rate (GFR)
Advantages of cystatin C-based
eGFR over creatinine-based eGFR
Patient category Advantage
Children (e23) Children have low levels of
creatinine and determina -
tion is unreliable in the
low er range of measure-
The elderly (e15) Owing to physiological re-
duction in renal function
and decrease in muscle
mass, cystatin C correlates
better than creatinine with
inulin clearance
Myasthenics, Because of the lower
leg amputees, muscle mass, creatinine
paraplegics (e16) synthesis is low and
creatinine- based eGFR is
late to detect renal failure
Diabetics (e17) Early stages of renal failure
are detected more reliably
with cystatin C based than
with creatinine-based
Liver cirrhosis (18) Creatinine methods are
slow to detect the decrease
in GFR because creatinine
metabolism in the liver is
Cytostatic treatment (e19) The nephrotoxicity of cis-
platin is dose-dependent
and a reduction in GFR is
detected earlier by cystatin
C-based than by creatinine-
based eGFR
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Dtsch Arztebl Int 2009; 106(51–52): 849–54
studied. The diagnostic reliability of the MDRD
equation for estimation of GFR can be summarized as
The eGFR can be 6% too high in CRD (11,
e7–e9), and may be 29% too low in individuals
without CRD (e10, e11).
In 90% of cases in the MDRD study group the
eGFR was within ±30% of the mGFR (21). For a
GFR of 60 (mL × min
× [1.73 m
) this would
mean a range of 42 to 78 (mL × min
× [1.73
). This degree of accuracy is considered ac-
ceptable provided eGFR is determined again after
3 months (22).
The MDRD equation over-stages patients in CRD
stages 2 and 3, but correctly classifies those in
stages 4 and 5 (4).
This overestimation of GFR by the MDRD equation
is important for the monitoring of CRD. Patients in
stage 3 are expected to exhibit an annual decrease in
GFR of 1.4 to 3.9. In a comparison of mGFR and
eGFR, however, 41.8% of patients showed a decrease
in eGFR that was less than that in mGFR by 2. Thus
monitoring of CRD by eGFR must be viewed critically
Any patient with eGFR <60 very probably has CRD.
Young patients with eGFR as low as this may have a
true GFR that is 29% higher, but will still probably
have impaired renal function (22). In such cases dem-
onstration of, for example, albuminuria is required for
the diagnosis of renal damage (1).
To ensure comparability of eGFR among labora-
tories it is important to use kinetic methods such as the
Jaffé reaction or enzymatic techniques to determine
creatinine. To this end calibrators and controls of the
tests carried out must be based on highly specific pro-
cedures for creatinine determination and specific ref -
erence materials (21).
Cystatin C-based eGFR
All that is needed for calculation of eGFR is the serum
concentration of cystatin C. This method is particularly
indicated in children (e12, e13), because the MDRD
equation cannot be used in this age group (e9), and in
the elderly (6). For children the equation according to
Grubb (24) has proved more reliable than the
Counahan-Barratt equation, and for adults the equation
according to Hoek (25) is more sensitive than the
MDRD equation (Box 2). In older age groups the
physiological decrease in GFR from year to year is reg-
istered more sensitively with cystatin C-based eGFR
than with the MDRD equation (6), and a drop of >3 is
associated with a higher subsequent risk of mortality
(8). Further indications for cystatin C-based determi-
nation of eGFR are listed in Box 3.
Serum creatinine and establishment of eGFR with the
MDRD equation are important basic investigations for
the diagnosis of CRD. The determination of cystatin C
and reporting of cystatin C-based eGFR offers advantages,
but on grounds of cost (determination of cystatin C is
20 to 30 times more expensive than that of creatinine) it
should be reserved for certain categories of patients.
Conflict of interest statement
The authors declare that no conflict of interest exists according to the guide-
lines of the International Committee of Medical Journal Editors.
Manuscript received on 5 March 2009, revised version accepted on 14 July
Translated from the original German by David Roseveare.
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Corresponding author:
Prof. Dr. med. Lothar Thomas
Krankenhaus Nordwest
Steinbacher Hohl 2–26
60488 Frankfurt am Main, Germany
For e-references please refer to:
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Dtsch Arztebl Int 2009; 106(51–52)
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Renal Failure—Measuring the
Glomerular Filtration Rate
Christian Thomas, Lothar Thomas
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... n women compared to men and affected by age (in older ages the glomerular filtrate rate is less). An abnormally low glomerular filtration rate (GFR) often escapes medical notice in the earliest, most treatable stage, so that an increasing number of patients progress to end-stage renal failure. Its main causes are hypertension and diabetes mellitus (Thomas et. al., 2009). In hypertension according to the literature, there are changes related to the arteries that supply the kidneys, their walls get thicker in order to withstand the high pressure. This leads to a narrow lumen, providing less blood and oxygen for the kidneys, damaging so the structural and functional parts of the kidneys (nephrons). The sa ...
... From our observations and data analysis of the observed parameters in this group, we can say that the degree of changes, in both hematological and biochemical parameters, depends on the severity of renal failure. Except the fact that it is difficult to point an abnormally low glomerular filtration rate (GFR), which often escapes medical notice in the earliest stage and leads to end-stage renal failure (Thomas et al., 2009), socioeconomic difficulties affect self examination and the frequencie one is going to the doctor for a routine check up , etc. (Zeng et al. 2018), leading so in severe forms of chronic kidney disease in the population. We found out that most of these patients are living in low income 42.1% (less than 200 euro and only 7.2% of the patients are living in the categorized high income living group (more than 400 euro per month). ...
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Chronic kidney disease is a serious, life threating health problem. It is also known as chronic kidney failure, as it is a process of irreversible loss of nephrons, which at the end stage leads to kidney failure. There are many different reasons that lead to kidney failure, such as: hypertension, diabetes, polycystic kidney disease, glomerulonephritis, parathyroid glands dysfunction, etc. The aim of this study was to evaluate the biochemical and hematological profile in a group of chronic kidney patients in Albania. A group of 247 chronic kidney disease patients is included in this study (170 adult males and 77 adult females). A group of biochemical parameters, such as urea, CRP, albuminemia, HbA1C, creatinine, ALT, AST, calcium, phosphate, CaxP product, sodium, potassium and hematological parameters, such as hemoglobin, red blood cells, white blood cells and PTH, where measured and compared to the findings from the control group. Results were analyzed statistically using SPSS 20 program for windows. From data analysis, we found a reduced count of red blood cells and hemoglobin, statistically significant change, compared to the control group (p0.05). High levels of PTH, serum urea, creatinine and hyperphosphatemia, accompanied by hypocalcemia, were found statistically significant compared to the control group (p0.05). From our observations, hypertension, diabetes and kidney stones were the main causes leading to chronic kidney disease. Evaluation of these parameters, results to be significant in the differentiation and management of the health state of these patients.
... Recent epidemiological studies suggest high prevalence rates ranging from 11 to 13% for the prominence of chronic kidney disease [1]. Typically, the disease is characterized by a reduction in the rate of glomerular filtration rate, i.e., ≤ 60 ml/min/ 1.73 m 2 [3], and has been reported to present itself with a range of manifestations of which anemia is the most prominent [4,5]. ...
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Purpose To meta-statistically compare the efficiency of hypoxia-induced factor prolyl hydroxylase inhibitor on hemoglobin, ferritin, hepcidin rate, and adverse events. Methods A systematic identification of literature was performed according to PRISMA guidelines on 4 academic databases: MEDLINE, Scopus, EMBASE, and CENTRAL. A meta-analysis evaluating the influence of hypoxia-induced factors was performed for patients undergoing/not undergoing hemodialysis. The analysis evaluated the efficacy of hypoxia-induced factors on hemoglobin, ferritin, hepcidin rate, and the number of adverse events. Results Out of 1052 records, 15 articles including 2045 patients (mean age 62.1 ± 5.4 years) were included in this review. The systematic review presents a 1a level of evidence supporting the use of hypoxia-induced factor for mediating anemia in patients with chronic kidney disease. The meta-analysis reveals medium to large beneficial effects of the hypoxia-induced factor on hemoglobin rate for patients receiving (0.72) and not receiving (1.04) hemodialysis. Moreover, the administration of hypoxia-induced factors was reported to reduce ferritin rate and the hepcidin rate, and the number of adverse events in patients with chronic kidney disease. Conclusion The current meta-analysis recommends the use of hypoxia-induced factor prolyl hydroxylase inhibitor for managing anemia in chronic kidney disease.
... концентрацій креатиніну та сечовини сироватки крові. Однак зазначені вище ниркові маркери мають недоліки та низьку інформативність щодо розвитку ранніх стадій пошкодження нирок, особливо у вагітних, що призводить до помилкових позитивних результатів [2,3]. На противагу сироватковий цистатин С не залежить від віку, статті і ваги та відображає швидкість клубочкової фільтрації (ШКФ) -від гіперфільтрації до ранніх стадій гіпофільтрації, тоді як зниження рівня ШКФ за креатиніном відображає переважно тяжкі стадії ренальної дисфункції [4]. ...
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Background. Placental ischemia and renal dysfunction are crucial elements of pre-eclampsia development. Thorough renal function control enables timely delivery and minimization of complications during pregnancy. It also enables pre-eclampsia diagnosing at the pre-clinical stage. The purpose was to study serum cystatin C levels and to evaluate its efficacy in pre-eclampsia prognosis compared to creatinine and urea serum levels in pregnant patients. Materials and methods. Thirty females at their first trimester of pregnancy were enrolled. Twenty females with a history of pre-eclampsia risk factors were included into the study group, 10 healthy females without any pre-eclampsia risk factors were included into the control group. Serum levels of cystatin C, creatinine and urea were studied at 22–36 weeks of gestation. Results. Comparison of mean values in a group of females, who subsequently developed pre-eclampsia (n = 8), and average values in females without pre-eclampsia (n = 12) demonstrated following cystatin C, creatinine and urea levels: 1.34 ± 0.11 mg/l vs 0.88 ± 0.03 mg/l, a significant difference for cystatin C has been demonstrated С (р < 0.001); 78.54 ± 3.68 μmol/l vs 69.06 ± 4.94 μmol/l, a significant difference for creatinine has been demonstrated (р
... One of the best markers to assess the renal function is the GFR. 12 Accurate estimation of GFR requires the use of invasive techniques which is difficult to perform routinely in daily practice. 13,14 To overcome this, endogenous biomarkers like serum creatinine and cystatin-C have been used as markers for estimation of GFR to assess the renal functional status. 15 Various formulae have been derived based on serum creatinine. ...
Eluxadoline is approved for the treatment of diarrhea‐predominant irritable bowel syndrome in the United States. The impact of renal impairment on the pharmacokinetic (PK) parameters of eluxadoline is currently unknown. This phase 1, open‐label, parallel‐group study evaluated the PK and safety profile of eluxadoline in 8 participants with renal impairment and 8 matched healthy controls. Of the participants with renal impairment, 2 had severe renal impairment (estimated glomerular filtration rate [eGFR] <30 mL/min/1.73 m2) and 6 had end‐stage renal disease while not yet on dialysis (eGFR <15 mL/min/1.73 m2). The primary objective was to assess plasma and urine PKs, and plasma protein binding of eluxadoline. In participants with renal impairment, mean plasma concentrations of eluxadoline were consistently higher compared with matched healthy controls: 1.4‐fold higher for mean maximum plasma concentration (Cmax) and 2.2‐fold higher for mean area under the plasma concentration‐time curve from time 0 to time t. The median time to Cmax was 2.5 hours in both groups. Although eluxadoline is a locally acting drug with low oral bioavailability, because of the increased systemic exposure in participants with renal impairment as a cautionary measure the lower approved dose of 75 mg twice daily is recommended for individuals with severe renal impairment and end‐stage renal disease while not yet on dialysis. Eluxadoline 100 mg single dose was well tolerated in participants with renal impairment and matched healthy controls.
Objective To assess the correlation of co-morbid ADHD and diabetes-related complications in patients with type-1-diabetes-mellitus (T1DM). Methods A retrospective cross-sectional study was conducted during 2018 using the Leumit-Health-Services(LHS) database. Diabetes-related complications were assessed in patients with T1DM and ADHD (T1DM-ADHD+) and compared with patients with T1DM alone (T1DM-ADHD−). Results Out of 789 adult-patients with T1DM, 75 (9.5%) were T1DM-ADHD+, matched to 225 T1DM-ADHD−. HbA 1 C levels were higher in T1DM-ADHD+ patients (8.1% ± 1.6 vs. 7.4% ± 1.2, p < .01), as well as diabetes-related complications: neuropathy (22.7% vs. 5.8%, p < .01), ulcers (8% vs. 0.9%, p < .05), limb amputation (5.3% vs. 0.9%, p < .05), albuminuria (15.5% vs. 2.8%, p < .01), chronic renal failure (10.6% vs. 2.5%, p = .01), and emergency room admissions rate (26.7% vs. 15.1%, p < .05). In sub-analysis, lower average HbA 1 C levels and diabetic ulcer rates were found among ADHD patients treated with stimulants, all p < .05. Conclusion Co-morbidity of ADHD and T1DM is associated with poor glycemic control and higher complication rates.
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Background We report patient characteristics, treatment pattern and one-year clinical outcome of nonvalvular atrial fibrillation (NVAF) from Kerala, India. This cohort forms part of Kerala Atrial Fibrillation (KERALA-AF) registry which is an ongoing large prospective study. Methods KERALA-AF registry collected data of adults with previously or newly diagnosed atrial fibrillation (AF) during April 2016 to April 2017. A total of 3421 patients were recruited from 53 hospitals across Kerala state. We analysed one-year follow-up outcome of 2507 patients with NVAF. Results Mean age at recruitment was 67.2 years (range 18-98) and 54.8% were males. Main co-morbidities were hypertension (61.2%), hyperlipidaemia (46.2%) and diabetes mellitus (37.2%). Major co-existing diseases were chronic kidney disease (42.1%), coronary artery disease (41.6 %), and chronic heart failure (26.4%). Mean CHA2DS2-VASc score was 3.18 (SD+ 1.7) and HAS-BLED score, 1.84 (SD+ 1.3). At baseline, use of oral anticoagulants (OAC) was 38.6% and antiplatelets 32.7%. On one-month follow-up use of OAC increased to 65.8 % and antiplatelets to 48.3%. One-year all-cause mortality was 16.48 and hospitalization 20.65 per 100 person years. The main causes of death were cardiovascular (75.0%), stroke (13.1%) and others (11.9%). The major causes of hospitalizations were acute coronary syndrome (35.0 %), followed by arrhythmia (29.5%) and heart failure (8.4%). Conclusions Despite high risk profile of patients in this registry, use of OAC was suboptimal, whereas antiplatelets were used in nearly half of patients. A relatively high rate of annual mortality and hospitalization was observed in patients with NVAF in Kerala AF Registry.
Мета дослідження – визначити показники рівня сироваткового цистатину С (sCc) й оцінити ефективність його використання у вагітних у діагностиці прееклампсії (ПЕ) на доклінічному етапі розвитку порівняно з традиційним визначенням за сироватковим креатиніном. Матеріали та методи. У дослідження було включено 30 жінок у першому триместрі вагітності, з них: 20 жінок з анамнестичними факторами ризику щодо розвитку ПЕ увійшли в основну групу (ОГ), контрольну групу (КГ) склали 10 жінок без екстрагенітальних захворювань і з необтяженим акушерсько-гінекологічним анамнезом. Подальший розподіл в ОГ на підгрупи базувався на рівнях sCc, дослідження якого проводили в період від 22 до 36 тижнів вагітності. У підгрупу Іц˃1 увійшли жінки з рівнем sCc більше 1,0 (n=10), у підгрупу Іц˂1-жінки з рівнем sCc менше 1,0 (n=10). Група Іа – вагітні, в яких у кінці вагітності розвинулась ПЕ (n=8) і Іб – пацієнтки, у яких не розвинулась ПЕ (n = 12). Результати дослідження та їх обговорення. За результатами було відзначено, що рівні sCc у вагітних в групі Іа склали 1,34±0,11 (95 % ДІ: 1,13–1,55), (p<0,001); у підгрупі Іц˃1 чутливість sCc у розвитку ПЕ дорівнює 87,5 %, специфічність – 100 %, що, в свою чергу, підтверджує високі діагностичні характеристики sCc як предиктора ПЕ. У підгрупі Іц˂1 із рівнем sCc 0,88±0,03 (95 % ДІ: 0,81 – 0,95), (p<0,001) – прееклампсія не розвинулась. При порівняльному аналізі показників швидкості клубочкової фільтрації (ШКФ) по sCc (ШКФцис) і ШКФ по креатиніну (ШКФкр) були відзначені статистичні відмінності значень у вагітних: в групі Іа рівень СКФцис склав 58,62±4,11 (95 % ДІ: 50,57 – 66,68) і значно знижений порівняно з ШКФкр – 88,25±5,76 (95 % ДІ: 76,96 – 99,54); у контрольній групі статистичної різниці ШКФцис (114,5±2,7 (95 % ДІ: 109,2 – 119,8)) і ШКФкр (112,5±4,1 (95 % ДІ: 104,47–120,53 )) не відзначено. Таким чином, найбільш істотна різниця в значеннях ШКФцис і ШКФкр має місце в групі Іа, що доводить ефективність використання ШКФцис у діагностиці порушення ниркової функції на доклінічному етапі ПЕ. Висновки. У результаті проведених досліджень доведено, що сироватковий цистатин С достовірно підвищений у вагітних у групі ризику щодо розвитку ПЕ і при значенні показника вище 1,0 є достовірним маркером розвитку прееклампсії на доклінічному етапі реалізації.
Die Labormedizin hat die Aufgabe, durch Messung physikalischer, hämatologischer, molekularbiologischer und (bio)chemischer Eigenschaften von menschlichem Untersuchungsmaterial gezielt gestellte ärztliche Fragen im Hinblick auf Diagnostik, Therapieverlauf, Prävention und Prognose von Krankheiten zu beantworten. Relevante Kenngrößen werden in dem Kapitel ebenso wie die Qualitätssicherung im medizinischen Labor vorgestellt.
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Objective:We evaluated the course of the renal function and potential risk factors for renal deterioration in patients who had undergone radical cystectomy with ileal conduit diversion.Materials and Methods:A retrospective study evaluated 121 patients, including 114 male and 7 female who underwent radical cystectomy with ileal conduit diversion. Estimated glomerular filtration rate (eGFR) was calculated and postoperative changes in renal function were reviewed. The clinical variables influencing renal function were evaluated.Results:The median follow-up period was 35.6 months (range, 12.2 to 139.6 months). The mean eGFR was 78.37±27.58 mL/min/1.73 m2 before surgery and 90.14±29.68 mL/min/1.73 m2 at 5 years postoperatively. The comparison of preoperative eGFR and the last follow-up eGFR showed the no statistically significant difference (p=0.195). Statistical analysis showed that development of postoperative urinary tract obstruction and postoperative urinary tract infection were significant adverse factors (p=0.008, p=0.026, respectively).Conclusion:Thirty two patients (53.3%) developed renal deterioration during the follow-up period. Development of urinary tract obstruction and urinary tract infection in the postoperative period were found to be significant adverse factors affecting renal function.
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A formula has been developed to predict creatinine clearance (Ccr) from serum creatinine (Scr) in adult males: (see article)(15% less in females). Derivation included the relationship found between age and 24-hour creatinine excretion/kg in 249 patients aged 18-92. Values for Ccr were predicted by this formula and four other methods and the results compared with the means of two 24-hour Ccr's measured in 236 patients. The above formula gave a correlation coefficient between predicted and mean measured Ccr's of 0.83; on average, the difference predicted and mean measured values was no greater than that between paired clearances. Factors for age and body weight must be included for reasonable prediction.
Nearly half of all patients on hemodialysis are diabetic. Epidemiologic studies indicate that hyperglycemia is an important factor for the development of diabetic nephropathy. The following pathogenetic mechanisms are discussed: (i), the extracellular ocurring glycation reaction and the resultant advanced glycation end (AGE) products, (ii), high glucose-induced activation of protein kinase C and (iii), the induction of cytokines. Particularly interesting is the induction of transforming growth factor β (TGF-β), since this factor induces the de novo synthesis of components of the extra-cellular matrix. The laboratory diagnosis of the diabetic nephropathy is still limited to only a few parameters. Besides the classical de termination of creatinine and urea in serum and the creatinine clearance, the determination of urinary albumin levels has been proven to be an important marker for the early detection of diabetic nephropathy. The presence of persistent microalbuminuria in type 1 diabetic patients indicates diabetic nephropathy with relatively high specificity. Microalbuminuria in type 2 diabetes may also be caused by other kidney diseases which should therefore be excluded. Several laboratories are currently investigating if increased TGF-β1 levels in urine of diabetic patients is of value for the prediction of the development of diabetic nephropathy. Up to now no genetic or molecular biology markers have been found to predict the susceptibility of an individual diabetic patient to develop diabetic nephropathy.
Background: The National Kidney Foundation has advocated the use of the abbreviated Modification of Diet in Renal Disease (MDRD) equation to estimate glomerular filtration rate (GFR) from serum creatinine measurements in clinical laboratories. However, healthy persons were not included in the development of the MDRD equation. Objectives: To assess the accuracy of the MDRD equation in patients with chronic kidney disease compared with healthy persons and to develop a new equation that uses both patients with chronic kidney disease and healthy persons. Design: Cross-sectional study. Setting: The Mayo Clinic, a tertiary-care medical center. Participants: Consecutive patients (n = 320) who had an iothalamate clearance test specifically for chronic kidney disease evaluation and consecutive healthy persons (n = 580) who had an iothalamate clearance test specifically for kidney donor evaluation. Measurements: Serum creatinine levels, GFR, demographic characteristics, and clinical characteristics were abstracted from the medical record. Results: The MDRD equation underestimated GFR by 6.2% in patients with chronic kidney disease and by 29% in healthy persons. Re-estimated coefficients for serum creatinine and sex were similar to the original MDRD equation in the chronic kidney disease series but not in the healthy series. At the same serum creatinine level, age, and sex, GFR was on average 26% higher in healthy persons than in patients with chronic kidney disease (P < 0.001). A quadratic GFR equation was developed to estimate logarithmic GFR from the following covariates: 1/SCr, 1/SCr 2 , age, and sex (where SCr = serum creatinine). Limitations: The new equation was not developed in a general population sample. Elderly and African-American persons were underrepresented. Conclusion: The MDRD equation systematically underestimates GFR in healthy persons. A new equation developed with patients who have chronic kidney disease and healthy persons may be a step toward accurately estimating GFR when the diagnosis of chronic kidney disease is unknown.
Background: Reliable serum creatinine measurements in glomerular filtration rate (GFR) estimation are critical to ongoing global public health efforts to increase the diagnosis and treatment of chronic kidney disease (CKD). We present an overview of the commonly used methods for the determination of serum creatinine, method limitations, and method performance in conjunction with the development of analytical performance criteria. Available resources for standardization of serum creatinine measurement are discussed, and recommendations for measurement improvement are given. Methods: The National Kidney Disease Education Program (NKDEP) Laboratory Working Group reviewed problems related to serum creatinine measurement for estimating GFR and prepared recommendations to standardize and improve creatinine measurement. Results: The NKDEP Laboratory Working Group, in collaboration with international professional organizations, has developed a plan that enables standardization and improved accuracy (trueness) of serum creatinine measurements in clinical laboratories worldwide that includes the use of the estimating equation for GFR based on serum creatinine concentration that was developed from the Modification of Diet in Renal Disease (MDRD) study. Conclusions: The current variability in serum creatinine measurements renders all estimating equations for GFR, including the MDRD Study equation, less accurate in the normal and slightly increased range of serum creatinine concentrations [<133 μmol/L (1.5 mg/dL)], which is the relevant range for detecting CKD [<60 mL · min⁻¹ · (1.73 m²)⁻¹]. Many automated routine methods for serum creatinine measurement meet or exceed the required precision; therefore, reduction of analytical bias in creatinine assays is needed. Standardization of calibration does not correct for analytical interferences (nonspecificity bias). The bias and nonspecificity problems associated with some of the routine methods must be addressed.
Background. Based on the data derived from the Modification of Diet in Renal Disease (MDRD) study, a new equation was developed for the estimation of glomerular filtration rate (GFR). This equation, which takes into account body weight, age, sex, serum creatinine, race, serum urea, and serum albumin, provided a more accurate estimation of GFR in patients with renal insufficiency. However, this prediction equation has not been validated in subjects with normal or supra‐normal GFR. Methods. In a cross‐sectional study, we measured GFR by inulin clearance in 46 healthy controls and 46 non‐complicated type 1 diabetic patients. In this study population, GFR was predicted by measured creatinine clearance, the Cockcroft–Gault formula, and the MDRD equation. Results. In the healthy subjects, mean GFR (±SD) was 107±11 as compared to 122±18 ml/min per 1.73 m2 in the diabetic patients. This difference in GFR was reflected by a lower serum creatinine (76±8 vs 71±8 μmol/l) in the diabetic patients. In the healthy controls, median absolute differences (and the 50th–75th–90th percentile of percentage absolute differences) between predicted and measured GFR were 5.2 ml/min per 1.73 m2 (4.9–9.8–18.5%) for creatinine clearance, 9.0 ml/min per 1.73 m2 (8.6–14.3–24.6%) for the Cockcroft–Gault formula, and 10.7 ml/min per 1.73 m2 (10.9–16.3–25.5%) for the MDRD equation. In the diabetic patients, these differences were 8.3 ml/min per 1.73 m2 (7.6–9.3–13.0%) for creatinine clearance; 11.8 ml/min per 1.73 m2 (10.1–16.0–22.5%) for the Cockcroft–Gault formula, and 18.8 ml/min per 1.73 m2 (16.0–24.2–31.9%) for the MDRD equation. Conclusions. In subjects with a normal or increased GFR, the new MDRD‐prediction equation of GFR is less accurate than creatinine clearance or the Cockcroft–Gault formula, and offers no advantage.