SA JOURNAL OF DIABETES & VASCULAR DISEASE
VOLUME 13 NUMBER 2 • DECEMBER 2016
Alteration in kidney function predominated in patients with a
longer duration of diabetes, enhancing the effect of both chronic
hyperglycaemia and the ageing process.
The latter is associated
with changes in vascular structure and function due to clustering of
multiple risk factors, including insulin resistance/hyperinsulinaemia,
oxidative stress and inflammation.
Arterial stiffness, an independent
predictor of morbidity and mortality, has been reported to increase
with age and is associated with high systolic and pulse pressure.
Moreover, the decrease in the number of nephrons, which occurs
with ageing, may result in hyperfiltration, hypertrophy and elevation
in glomerular capillary pressure.
The high prevalence of LVH in CKD patients found in our study
agrees with that of other studies.
LVH in CKD is thought to
result partly from uraemia-associated risk factors such as anaemia,
calcium-phosphate products and hyperhomocysteinaemia.
Moreover, renal dysfunction activates the renin–angiotensin–
aldosterone system, with subsequent formation of angiotensin
II, known to be essential for the development and progression
The risk of CVD and death increases with the decline
in glomerular filtration rate (GFR) and the major increase in risk
occurs at a GFR < 60 ml/min per 1.73 m
LVH has been reported to predispose to ischaemic heart
disease, arrhythmias and congestive heart failure.
indicate that patients with severe CKD had higher proportions of
abnormal LV geometry, with concentric remodelling and concentric
hypertrophy as the most frequent pattern. Both eccentric and
concentric hypertrophy may occur in individuals with CKD.4
Eccentric hypertrophy is thought to result from volume overload,
leading to cardiomyocyte drop out. Concentric hypertrophy
is typically the result of hypertension and increased afterload
and is exacerbated by anaemia, hyperparathyroidism and high
angiotensin II concentrations. Eccentric and concentric hypertrophy
have different impacts on the prognosis.
confers the worst prognosis, followed by eccentric hypertrophy and
Moderate CKD and a high proportion of hypertension could
explain the pre-eminence of concentric hypertrophy observed
in the present study. In Nigerian hypertensive patients, Aje
reported greater systolic, diastolic, pulse and mean blood pressure
among patients with concentric hypertrophy in comparison with
those with normal geometric patterns.
In our study, hyperuricaemia emerged as the only predictor
of LVH in CKD patients. The mechanisms that could account
for increased uric acid levels in CKD include overproduction to
counteract oxidative stress and endothelial dysfunction, the severity
of diabetes and/or hypertension, impaired renal uric acid clearance,
and insulin resistance/hyperinsulinaemia-induced proximal renal
tubular reabsorption of sodium and urate.
between hyperuricaemia and LVH could rely upon an association of
uric acid with other risk factors, either isolated or combined in the
The coexistence of hyperuricaemia and LVH
has been recognised as an independent and powerful predictor of
The interpretation of the results of our study is confounded by
some limitations. The cross-sectional design of the work precludes
any causal relationship between CKD and associated risk factors.
Moreover, the sample size did not allow sufficient power to
detect additional associations. One wonders to what extent the
conclusions of this clinic-based study could be extrapolated to the
general population, given the bias in the referral of patients. The
findings of our study bear, however, some clinical implications for
CKD identification, treatment protocol and estimated prognosis in
This study has shown that LVH is common among type 2 diabetes
patients with CKD. Concentric LVH was the geometric LV pattern
most frequently encountered and its frequency increased with the
decline in renal function. Hyperuricaemia emerged as the unique
independent predictor of the risk of LVH.
The authors thank Prof JJ Muyembe, head of the National Institute
of Biomedical Research/Ministry of Health, for the facilities
obtained for the measurements of cholesterol and its sub-fractions.
Particular thanks go to Prof E Kintoki, Division of Cardiology and Dr
M Lelo, Division of Radiology and Imaging, Department of Internal
Medicine, University of Kinshasa Hospital for their contribution to
the evaluation of left ventricular mass and geometry.
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