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APPRAISAL
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DOI:10.5301/JN.2010.2030
t of
and
Renal
ABSTRACT
1- 10
TABLE I
ESTIMATED PREVALENCE OF LEFT VENTRICULAR HYPERTROPHY (LVH) IN PATIENTS WITH CHRONIC
KIDNEY DISEASE IN SOME DIFFERENT STUDIES
Author
Year of
publication
Number
of patients
LVH prevalence
GFR
Definition of LVH
LVMI >131
g/m2
in men
and >100 g/m2
in women
Mean
39
ml/min
Method to
estimate GFR
Creatinine
clearance
Tucker et al (33)
1997
85
16%-38%
Levin et al (36)
ml/min
1999
318
34%
Not defined
<40
Cockcroft-Gault
equation
2002
2,257
16.4%
Not defined
<8 ml/min
MDRD equation
36 ml/min
Cockcroft-Gault
equation
Paoletti et al (37)
2005
244
74%
LVMI >134
g/m2
in men
and >110 g/m2
in women
LVMH2.7 >49.2
g/m in men and >46.7
2.7
Peterson et al (38)
2007
599
69.4%
g/m2.7
in women
44 ml/min/1.73 m2
Nardi et al (31)
2009
293
47.1%
LVMI >125
g/m2
in men
and >110 g/m2
in women
39 ml/min/1.73 m2
Cockcroft-Gault
equation
GFR = glomerular filtration rate; LVH = left ventricular hypertrophy; LVMI = left ventricular mass indexed by body surface area;
MDRD = Modification of Diet in Renal Disease.
Fig. 1 - Prevalence of patterns of left ventricular hypertrophy (LVH) in patients with essential hypertension and normal
renal function, and in hypertensives with chronic kidney disease (CKD).
study, regardless of the stage of CKD, remained substantially higher than in the rest of the literature (45).
In the African American Study of Kidney Disease (AASK)
(38), the prevalence and the correlates of LVH were
evaluated in 599 nondiabetic hypertensive African
Americans. Mean age was 60 years, and mean GFR was
44 ml/min per 1.73 m2. Of note is the fact that in this
study, GFR was estimated by means of a different
equation developed from baseline data in the AASK trial
(39). LVM was indexed by height el- evated to a power of
2.7 (LVMH2.7) (47) and LVH was defi
as LVMH2.7 >49.2 g/m2.7 in men and >46.7 g/m2.7 in women.
The variables independently associated with LVH, the
global prevalence of which was 69.4%, were daytime and
night- time ambulatory BP, GFR and younger age (38).
A recent study by our group (31) evaluated the prevalence
of LVH and LV geometry in a group of 293 hypertensive
Fig. 3 - Possible mechanisms connecting chronic kidney disease, inflammation and left ventricular hypertrophy (LVH).
CRP = C-reactive protein; CT1 = cardiotrophyn-1; NADPH =
nicotinamide adenine dinucleotide phosphate; NO = nitric
ox- ide; PICP = carboxy-terminal propeptide of collagen
type I; ROS = reactive oxygen species.
feature of Em measured by TDI is its relative preload independence. Consequently, Em remains reduced even in
those stages of diastolic dysfunction characterized by
increased preload compensation. Moreover, Em has been
demonstrat- ed to be inversely related to the degree of fi
osis in isch- emic as well as in normal myocardial
segments (83).
CONCLUSIONS
CV diseases are highly prevalent in patients with CKD, and
represent the major hazard for mortality in this population.
Anomalies of LV structure and function are very frequent
too among CKD patients, and show a negative impact on
CV prognosis.
Early detection of LVH and LV dysfunction is recommended, as early and aggressive treatment can yield
an improvement in the adverse CV outcomes of CKD
patients. Furthermore, treatment of major determinants
of LV growth in CKD, such as hypertension and anemia, should be of benefit. It has been demonstrated in
hypertensive patients that echocardiographic finding of
LVH regression may have positive prognostic relevance
(84-87).
On the other hand, studies regarding the effect of
treatment of anemia on LV growth in CKD patients have
reached con- flicting results (88-92).
However, it is timely to remark that, despite the established
evidence that CKD patients are exposed to a very high CV
risk, they are often undertreated in clinical practice. In this
regard, in a large cohort of more than 130,000 elderly patients, it has been demonstrated that patients with renal
insufficiency were less likely to receive appropriate cardioprotective treatments (93).
11.
13.
14.
15.
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