There is some ambiguity about the ideal blood pressure target for people with CKD particularly those who also have
proteinuria or diabetes . The NZGG Cardiovascular Guidelines (2009) state that the target should be <125/75 mmHg
for people with diabetes and overt nephropathy, microalbuminuria or other renal disease, or CKD and significant albuminuria.
Elsewhere in the document it recommends the same target for all people with CKD in general. The Kidney Health New Zealand
Summary Guide recommends the blood pressure target for people with CKD should be <130/80 mmHg and <125/75 if
Proteinuria is present. Can the specialist clarify this?
Many people may have been surprised about the level of dietary salt intake that is recommended for patients with CKD – 80
mmol/day which is equivalent to only around one teaspoon of salt. The panel felt that it was useful to have a number
to work with as it is difficult to find information for patients on how much salt they should have. They also wondered
how to judge how much salt is being consumed as it is often hidden in food.
They queried whether people with hypertension should also aim for a salt intake of less than one teaspoon per day?
There was some discussion about the rationale for salt restriction in elderly people who are often hyponatraemic.
The panel queried whether it is unwise to recommend a reduced salt diet in these people?
The panel felt they had a good understanding of the concept of adjusting drug doses in renal failure, however commented
that in practice this is sometimes difficult to do on a consistent basis. Setting up a recall for an annual medication
review in CKD patients is recommended.
GPs generally tend to be timid with the dose of ACE inhibitors particularly in elderly people. How do you judge what
dose is sufficient? The panel would be interested in whether the dose of ACE inhibitor should be increased even if blood
pressure is well controlled? What are the benefits of this?
The first point I would make is that the recommendations for blood pressure should not be seen as a target. Rather
they should be seen as the minimum blood pressure to be achieved, if possible. Essentially the lower the blood pressure
the better the outcome. This clearly has to be assessed in the context of the individual. In an elderly patient with
long standing isolated systolic hypertension and CKD stage 3, dropping their blood pressure to below 130 systolic may
well precipitate a hypotensive fall and a subsequent hip fracture.
The presence of proteinuria and/or albuminuria increases the cardiovascular risk as well as the likelihood of renal
progression. A lower blood pressure is advantageous as this is usually associated with a reduction in proteinuria.
There are numerous clinical studies demonstrating the advantages of angiotensin converting enzyme inhibitors or angiotensin
receptor blocking agents in reducing proteinuria and improving renal outcomes. Most studies support titrating the dose
to the maximum possible dose that can be tolerated to achieve the best outcomes.
ACEI are not contraindicated in elderly people, just as renal artery stenosis is not an absolute contraindication
for the use of ACEI. Rather it is a question of caution and careful titration of the dose according to response. If
the individual is already on a diuretic then reduction in the diuretic dose or stopping the diuretic as the ACEI is
introduced may well be appropriate.
From an epidemiological perspective, increased dietary salt intake is clearly associated with increased hypertension
and cardiovascular risk. The WHO recommended daily intake of sodium is 80 mmol/day. In people with hypertension, a reduction
in salt intake down to this level can achieve a reduction in systolic blood pressure of about 8 – 10 mmHg (similar
to a single anti-hypertensive agent). It should therefore be part of the diet and lifestyle recommendations given to
all people with hypertension. With progressive kidney disease the impact of salt and hypertension becomes even more
significant with over 90% of individuals with CKD 4 and 5 (pre-dialysis) being very salt sensitive.
The majority of our dietary salt intake is derived from processed food. The amount added at the table probably accounts
for only 10%. The National Heart Foundation is working closely with the Food Industry in order to reduce the amount
of salt added to food. This has to be done in a controlled manner with a gradual reduction over time so as not to cause
major consumer resistance. This has already been successfully implemented in the UK. The best approach to assessing
dietary salt intake as well as providing education is to refer the patient to a dietitian.
With respect to elderly people, in most cases hyponatraemia is not due to salt restriction or depletion. Low plasma
sodium does not usually mean low total body salt. In most cases it is excessive water retention due to impaired free
water clearance, impaired cardiac function etc. Impaired free water clearance is commonly associated with thiazide diuretics
and non steroidal anti-inflammatory drugs. Stopping the thiazide and introducing an ACEI is more likely to correct the
hyponatraemia in an elderly person who is hypertensive and initially on a thiazide.
The panel would like to ask the specialist what sort of cases he sees referred by GPs? Does he have any key advice
for managing CKD in general practice?
In our practice we are happy to review any patient who has evidence of kidney disease, when advice with respect to
management and investigation is requested. Unless it is an urgent referral, we would request that there are several
checks of renal function: plasma creatinine and eGFR, urinalysis and if proteinuria is present a protein creatinine
ratio; along with documentation of blood pressure and associated cardiovascular disease and medication.
The control of blood pressure remains the most important part of management of CKD. Therefore assessment of this and
attempts to achieve the lowest tolerated blood pressure is important. For example in a 65 year-old with a eGFR of 40
mL/min secondary to hypertensive nephrosclerosis, if blood pressure is well controlled the decline in eGFR may be reduced
to < 1 mL/min/year. In this case it is unlikely the individual will process to ESKD (it will take 30 years to reach
an eGFR of 10 mL/min).