Home' Australian Pharmacist : April 2011 Contents Vol. 30 -- April #04
Reduction of salt intake for the prevention
and treatment of diabetic kidney disease
By Hanan Khalil
The purpose of this evidence
summary is to present the best
available evidence for reducing salt
intake in diabetic patients based
on a systematic review published
by the Cochrane collaboration.6
For the full review see http://dx.doi.
Diabetic kidney disease (DKD) is
the largest cause of chronic kidney
disease in this group of patients.1
Moreover, these diabetic patients
form the largest group on dialysis
programs which in turn places a huge
burden on our healthcare system.2
Interventions that aim to prevent and
slow kidney diseases will result in a
huge improvement to the well being
of these individuals and show benefits
in reducing the costs on our health
Diabetic patients have a lower
incidence of renin state and higher
plasma renin activity. Therefore the
(RAAS) is not functioning normally
to maintain salt and water balance.
It has been suggested that this lack
of suppression of the RAAS with a
high salt diet may play a part in the
development of high blood pressure
(BP).4 Lowering salt intake reduces
urinary protein excretion in several
populations and not only is this an
important marker of cardiovascular
disease, but also of DKD. Reducing
BP significantly results in slowing the
progression of DKD.5 Currently there
is no consensus in restricting salt
intake in diabetic patients.
Dr Hanan Khalil is an evidence synthesis
group member of the Chronic Disease
Management Centre for the Joanna Briggs
Institute, School of Rural Health, Department
of Rural and Indigenous Health, Monash
University. She is also a consumer reviewer
for the Cochrane Collaboration.
Characteristics of studies
The participants selected for the
systematic review were adults
(18 years or older) with type 1 diabetes
or type 2 diabetes mellitus. Children
and pregnant women were excluded.
The interventions considered in the
systematic review included studies
where comparisons between low
and high salt intake were stated.
Several outcomes were retrieved
from the included studies and
these were divided into primary and
secondary outcomes. The primary
outcomes addressed included net
change in 24 hour urinary sodium
concentration and blood pressure.
Secondary outcomes included data on
urinary albumin excretion, creatinine
clearance or glomerular filtration rate,
effective renal plasma flow, body
weight, body mass index and glycated
Thirteen studies (254 diabetic
individuals) were included in the
systematic review on which this
evidence summary is based:
75 individuals had type 1 diabetes
and 158 had type 2 diabetes.
Quality of the research
All studies included in this
systematic review were randomised
control trials in which all participants
• The mean reduction in urinary Na
was 11.9 g/day in type 1 diabetes
and 7.3 g/day in type 2 diabetes.
• The mean duration of salt reduction
was one week in both type 1 and
type 2 diabetes.
• BP was reduced in both type 1 and
type 2 diabetes.
• There was a greater reduction in BP
in normotensive patients, possibly
due to a large decrease in salt
intake in this group.
• Reducing salt intake by 8.5 g/day
lowered BP by 7/3 mm Hg.
• Public health guidelines recommend
reducing dietary salt intake to less
than 5--6 g/day and people with
diabetes would benefit from reducing
salt in their diet to at least this level.
Implications for research
The results presented in this evidence
summary are based on 13 randomised
control trials. The majority of the
studies had short duration of follow
up ranging from 5 days to 12 weeks.
Studies with longer duration of follow
up are needed to ascertain the real
benefit of long term salt reduction in
diabetic patients with kidney disease.
The most up to date evidence
suggests that lowering salt intake
has apparent benefits by reducing
BP in type 1 and 2 diabetics who
have normal or high BP. Additional
pharmacological interventions are
also important to successfully slow
the rate of DKD to end stage renal
failure as it is difficult to control BP to
the recommended current guidelines
using non pharmacological treatment.
1. Giunti S, Barit D, Cooper M. Mechanisms of diabetic
nephropathy: role of hypertension. Hypertension. 2006;
2. He FJ, MacGregor GA. How far should salt intake be
reduced? Hypertension. 2003; 42(6):1093--9.
3. He FJ, MacGregor GA. Effect of modest salt reduction
on blood pressure: a meta-analysis of randomized
trials. Implications for public health. Journal of Human
Hypertension. 2002; 16(11):761--70.
4. Harvey JN. Trends in the prevalence of diabetic
nephropathy in type 1 and type 2 diabetes. Current
Opinions in Nephrology & Hypertension. 2003; 12:317--22.
5. Price DA, De'Oliveira JM, Fisher ND, et al. The
state and responsiveness of the rennin angiotensin-
aldosterone system in patients with type II diabetes
mellitus. American Journal of Hypertension. 1999;
6. Suckling RJ, He FJ, MacGregor GA. Altered dietary
salt intake for preventing and treating diabetic kidney
disease. Cochrane Database of Systematic Reviews
2010. Issue 12. Art. No.: CD006763.
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