Kidney Disease Treatment - T2DM: Diabetic Retinopathy, Chronic Kidney Disease

Kidney Disease Treatment




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https://www.youtube.com/watch?v=KB4VFOJoLBg


T2DM: Diabetic Retinopathy, Chronic Kidney Disease




Hello, I'm Norman Swan.
Welcome to this program in our series
on guidelines and type 2 diabetes.
Every year there are
about 3.8 million deaths globally
attributable to diabetes.
In Australia, type 2 diabetes is
the fastest-growing chronic disease,
with the total number of Australians
with diabetes and pre-diabetes
estimated at a whopping 3.2 million,
and it's the sixth-leading
cause of death.
This program looks at two NHMRC
evidence-based guidelines that are new
and address complications
and comorbidity in type 2 diabetes.
They are the evidence-based guidelines
for diagnosis and management
of kidney disease in type 2 diabetes,
and the guidelines for the management
of diabetic retinopathy.
For those of you
watching on your computers,
you can type your questions directly in
to the studio.
Just click on the LiveTalk tab at the
top of the web page you're looking at.
That also means, of course,
that we can ask questions of you.
Here's one to get you going:
Click away on that one, and we'll
give you results of that in a moment.
As usual, there are a number
of useful resources available
on the Rural Health Education
Foundation's website:
Now let me introduce our panel to you.
Stephen Twigg is an endocrinologist
at the University of Sydney
and President
of the Australian Diabetes Society.
- Welcome, Stephen.
- Good evening.
Alan Cass is the senior director
of the George Institute
for International Health,
and director of the Poche
Indigenous Health Centre
at the University of Sydney.
- Welcome, Alan.
- Good evening, Norman.
Paul Mitchell is
Professor of Ophthalmology
at the University of Sydney,
and runs the Blue Mountains Eye Study.
- Welcome, Paul.
- Thanks, Norman. Good to be here.
And David Guest is a rural general
practitioner in Goonellabah in NSW.
- Welcome.
- Thanks, Norman.
David, challenging,
dealing with comorbidities
in general practice, I assume.
It's a growing area.
It's a bigger and bigger problem.
It's something that's taking
more and more of GPs' time.
If you get systems in place, you can
probably cope with the challenge.
Talk to me about the trends
that are going on, Stephen.
As you've mentioned already,
diabetes is on the rise.
We believe that approximately
100,000 people per year in Australia
are developing diabetes.
It's very similar
to the worldwide trend.
There are a number of factors that
are probably critical in the process
in terms of the development of diabetes.
The prevalence changes
in different groups in Australia?
Yes, there are certainly
higher-risk groups,
particularly an ageing population.
There are certain ethnic groups that
are at higher risk than others.
There are also issues
to do with lifestyle change.
As we can see on this slide - this data
is from the turn of the millennium -
approaching a million people, or 7.4%
of adults aged over 25 had diabetes
in Australia at that time, well over 90%
of it being type 2 diabetes.
The other conditions, impaired fasting
glucose and impaired glucose tolerance,
or as you referred to them,
the pre-diabetes conditions,
also extremely common.
So approaching one in four
Australian adults have some form
of glucose abnormality.
NORMAN: Extraordinary.
It's a remarkable figure.
NORMAN: It's also age-dependent?
Yes, very much so.
If we dissect this out further,
the same study, the AusDiab study,
demonstrated a strong age-dependence
for diabetes, indicating that
the ability of the pancreas to produce
insulin tends to deteriorate with time.
Approaching one in four Australian
adults in their 70s will have diabetes
in comparison to a much lower percentage
of people earlier in their life.
We're trending upwards faster
than we thought?
Very much so.
World Health Organisation data,
recent trends have suggested,
rather than seven million people
per year developing diabetes,
it's more like ten million people.
We're going to hear about that
in the more recent estimates,
in the next year 2010 data
from the International
Diabetes Federation and WHO.
NORMAN: This graph shows we're
tracking faster than we thought.
And the Australian data, very similar.
In the AusDiab study,
whilst 'e' on the far right
is an estimate
based on previous decades,
in the last decade, the late '90s,
then into the 2000s,
the figures are well above what
the estimates were on the trend line.
A study from the Australian Institute
of Health and Welfare 2006 indicated
it's more like 1.5 million people
who have diabetes,
then increasingly, 100,000 a year.
So really, even off that scale,
if we look at more recent estimates
of diabetes in the Australian community.
We're talking here about absolute risk,
global risk,
just as much
as we're talking about glucose?
Definitely.
Glucose, if you like, is the marker.
People with diabetes have
two- to fourfold
the rate of cardiovascular disease
as the general community.
As you've pointed out, it does
emphasise global cardiovascular risk
and the importance of tight
blood pressure and cholesterol control.
David, on the day of broadcast,
yesterday's Medical Journal of Australia
described the fact that
general practitioners are not measuring
absolute risk
to the rate they should be.
What are the barriers
to measuring absolute risk?
It's a GP-education problem
to start with.
There are tools available now
that make it much easier.
I have a preference for a computerised
electronic health record.
Getting data out of the computer makes
these sort of assessments much easier.
A website which I think is the one
recommended by various colleges
to assess absolute cardiovascular-
disease risk is available on the web
and available on the desktop.
That's a very useful tool for GPs.
You've got an example of this risk tool
that's in the guideline?
That's right, Norman.
If we look at the next slide,
this is an example.
This is for people with diabetes.
The charts are divided into those
with and without diabetes.
People with diabetes
are a high-risk group.
They can be stratified on the basis
of their cardiovascular risk
in terms of looking at
their systolic blood pressure,
their cholesterol,
HDL total cholesterol, HDL ratio,
gender status and smoking status.
It's possible then to identify
whether a person would be deemed
at a high cardiovascular risk,
in which case the intensity of the
management of their surrogate markers -
their blood pressure, their cholesterol,
their glucose
and also antiplatelet therapy
can be modified appropriately.
NORMAN: You're arguably more likely
to save their life
by managing those other factors
than their sugar?
It's not one or the other,
but it's both.
All of them are important.
For example, diabetic retinopathy
glucose is the major factor
that will contribute
to that complication.
In terms of cardiovascular disease
in people with diabetes,
the risk is probably approaching 15%
to 20% of the variation
in risk will be glucose, depending upon
the degree of glycaemic control.
And cholesterol and blood-pressure
control, very important in that setting.
How important, Paul, are these
other risk factors than glucose?
We know that glucose control
can help diabetic retinopathy,
but those other risk factors?
- There's growing evidence, isn't there?
- That's right.
The effect of good diabetes
glucose control
on preventing the development
and progression of diabetic retinopathy
has been shown both in type 1
and in type 2 in the UKPDS.
That latter study, UKPDS,
actually demonstrated almost
an equivalent effect in type 2 diabetes
of blood-pressure management.
Indeed, recent studies,
the ACCORD studies and the RASS study,
just recently published,
have shown that in fact
really tight blood-pressure control,
perhaps
with modern blood-pressure agents, ARBs,
can actually reduce the incidence
of diabetic retinopathy
and may result in regression
of existing retinopathy lesions.
And in kidney disease, Alan Cass?
Again, the key factors to control
are blood pressure.
Also, how well you control glycaemia
is a key factor
in terms of progression
of kidney disease.
NORMAN: What's the management challenge,
Stephen?
Diabetes, as we know,
is extremely challenging.
There's the combination of lifestyle
management and pharmacotherapy.
There's the importance of vigilance
with respect to diabetes management,
because, as we know, targets can
be difficult to maintain over time.
When we look at the optimisation
of care, in terms of patient care,
we have tight blood pressure,
blood glucose and cholesterol targets
monitoring for complications.
This slide indicates that in general,
we will achieve a lot
if we have a generic,
crowd-based approach.
If we go on to the one which shows the
management challenge to optimise care,
once we can assess cardiovascular risk
for the individual
and we can target more appropriately
lipids and blood pressure and glycaemia
for the particular person -
the career stage of their diabetes -
then we can expect to achieve
even better outcomes
when we customise
or individualise the care.
Whilst the world is obsessed
with obesity, it's not the whole story?
Definitely not.
We have these other major risk factors,
we have to target those.
We try and bring our waists in
and reduce body weight
if not stop it going higher,
but there's a lot we can do to prevent
end-organ damage from diabetes.
Alan, you've got a lot of experience
working with Indigenous communities.
Indigenous rates of type 2 diabetes
and complication rates are enormous.
Is it a different disease or just worse?
I think the evidence is that
it's not a different disease,
that the issues of poverty,
poor access to care,
a whole series of factors come together
that make the same common problems
of diabetes
and related chronic illnesses worse
rather than an entirely different
approach being needed.
What are the targets
we should be aiming for?
The RACGP has generic targets,
as shown here -
glycaemia, total cholesterol
and blood pressure.
In general, these will work well for
patients and for health professionals.
So, the A1C target,
less than or equal to 7%.
Total cholesterol, less than 4.
These days, we focus on LDL cholesterol,
less than 2.5, if not down to 2.
Then blood pressure,
less than or equal to 130/80.
However, if we do customise
or individualise it
for the person
who has significant proteinuria,
we want a tighter blood-pressure target
than that.
People with known
ischemic heart disease,
we want a tighter LDL cholesterol level
- less than 1.8.
And depending upon the stage
of the person's diabetes,
early on we know that
tight glycaemic control can
reap rewards decades down the track.
There's even quite a push
for HbA1c levels 6% to 6.5%
early on after the diagnosis.
That's controversial.
If you look at the most recent type 2
diabetes guidelines
for glycaemic control, which
you might address in subsequent weeks -
I know we're not addressing those
today -
the generic targets,
A1C, less than 7.0%,
and we know we can achieve that
for a lot, if not all, of our patients.
We can achieve it for a lot.
There's increasing data,
again from ACCORD and ADVANCE
and VADT, a number of studies
over the last 18 months, 2 years,
that early on in the diagnosis -
and also from the UKPDS follow-up -
early on, we need to aim for very tight
glycaemic control, get in early.
We know that in general,
type 2 diabetes is a delaying diagnosis
of four to five years
between when it develops
and when it's diagnosed.
We're missing years there
when we can help achieve tight control
of these surrogate markers
for our patients.
Paul, you've been following this group
of people in the Blue Mountains
for many years,
many of whom have diabetes.
Getting them early
makes a difference?
Absolutely. In fact, one of the messages
that has come out in the last year
is this issue of metabolic memory.
So, good control of diabetes
in the first period of diabetes
is really important.
It's been shown in the UKPDS
in type 2 diabetes
that good diabetic control
over the period of the study persisted,
despite the fact that
the haemoglobin A1C levels
in intensive versus routine control...
We've got a graph to that effect
to show.
That metabolic memory effect
was shown initially in the DCCT
and is now being shown in UKPDS
for retinopathy
and for other complications.
That probably tells us
where the challenge is.
We know that on average,
we're picking people up with diabetes
several years after
the diabetes is established.
For primary care
and the health system generally,
what can we do to opportunistically
pick up people?
For example, coming each year,
most Australians do attend
a general practitioner's at least once.
There is strong evidence
in the Australian context
that if we opportunistically screen
50- to 69-year-olds for diabetes,
we can pick it up earlier
and intervene
and prevent heart attacks, strokes
and premature mortality.
Are you doing that, David?
Putting you on the spot.
Yes, probably indirectly.
A lot of patients
have lots of blood tests.
You'll flip through and see that
the sugars are in the 6s
or occasionally higher,
and it behoves us to concentrate on that
and get a fasting glucose,
get a two-hour glucose-tolerance test
done and see where we're up to.
Just take us through quickly
the algorithm
to remind us of the basic management
of the glycaemic side of things
before we move on to the complications.
The algorithm involves
intensive lifestyle management.
That is both the diet
and regular physical activity.
We do find in most people
as time goes on
they do require pharmacological agents
in addition to focusing on lifestyle.
In terms of the HbA1c targets
that will help determine what type
of additional medications are needed
and when, following the initial
lifestyle intervention,
metformin is our first-line agent.
It certainly is effective
at lowering blood-glucose levels,
has a relatively low
side-effect profile, well tolerated,
and on top of that,
in the UKPDS we've referred to,
had good outcomes in terms of
cardiovascular
and microvascular outcomes.
Subsequent to that though,
as time goes on,
HbA1cs often deteriorate and people need
more than metformin alone.
Sulphonylureas in Australia for decades
have been our second port of call.
Then, multiple third-line options.
Each of the third-line options will
sit on that line
because they are newer agents
which might be less well studied
than sulphonylureas,
or they have challenges
associated with them, for example,
injections, as in the case of insulin.
NORMAN: We've got the results
of your first poll question.
We asked where you were located:
Here are the findings.
16% evenly split between metropolitan,
regional and remote.
And that big one, the blue one,
is rural.
Welcome to you all.
It's good to see such an even split
and an appropriate split
in terms of your location.
I'm going to ask the second question
now, which is:
So, we'll get your answers to that
while I ask David Guest,
what is the general practice
annual cycle of care
when you've got somebody with diabetes?
With patients with established diabetes,
it's a protocol
with which to manage them.
It involves clinical measures
that we probably should do
every time we see the patient,
but certainly six-monthly,
you need to check the blood pressure,
the weight and hopefully the feet,
but that's sometimes something
we don't get around to.
Annual tests needed,
HbA1c certainly annually,
more frequently
depending on the level of control.
We want to know
what the lipids are doing,
and HDL in particular in relation to
some new risk-factor calculators.
With diabetic nephropathy,
we want to keep an eye on
the albumin in the urine.
There's also the necessity for
second-yearly eye examination,
either yourself or more commonly
where I come from,
with optometrists and ophthalmologists.
Keep on eye on the social factors -
smoking, alcohol, exercise, diet areas.
If you get yourself into
a regular pattern with that,
either on your own
or with the help of your team,
you can keep your diabetic patient
under control.
Take us through the issues
in terms of chronic kidney disease.
Chronic kidney disease is common
in diabetes.
Chronic kidney disease is
manifest evidence of kidney damage.
The way that this is picked up is either
through a simple blood test,
then estimation
of the glomerular filtration rate,
where the GFR is less than 60ml
per minute,
evidence of significant kidney damage.
The other way is through
picking up protein leakage
into the urine - microalbuminuria -
through to more overt nephropathy.
When we think about how
we measure these things
in terms of the serum creatinine
on one hand,
how much protein in the urine
on the other hand
and the estimation of GFR,
it's sometimes complex.
Some of the keys to be cognisant of
is that often
leakage of albumin into the urine,
microalbuminuria,
is one of the earliest markers.
This usually occurs when
someone has normal renal function.
NORMAN: How best to measure that?
There are different ways
in which that's measured.
Ways that are felt to be equally valid
would be a spot,
particularly morning urine
for albumin-creatinine ratio
or a timed urine collection,
again, looking for albumin.
We were originally trained
in terms of 24-hour urines,
but in terms of common use
in primary care,
both of those methods are commonly used.
NORMAN: That should be part
- of the annual cycle of care?
- Yes.
Today's patients expect
fasting blood tests,
so during the urine test at the same
time has become part of the protocol,
part of the routine.
So that's...
You've knocked off a lot of your kidneys
before your creatinine rises.
Absolutely right. That's the way to pick
it up early, focusing on the albumin.
A key thing with the creatinine,
a common measure -
we do it on many patients -
is that you might have lost
half of your kidney function
before you get an abnormally elevated
creatinine measure.
That's where the simple calculation
of the estimated GFR,
which is done routinely by labs
throughout Australia now,
will provide a more ready measure
of the amount
of renal dysfunctional damage.
Why are we interested in that?
Both of those are important.
Both the level of albumin in the urine
and the level of kidney dysfunction
are known predictors of events
for people with diabetes.
In other words, chronic kidney disease
predicts heart attacks and strokes.
Correct. Why are we interested?
It's very common.
From AusDiab, perhaps a quarter
of people with diabetes
have evidence of chronic kidney disease.
And of all people
with chronic kidney disease,
what's the diabetes in relation to
the cause for end-stage kidney disease?
Diabetes is now the leading cause of
end-stage kidney disease in Australia
and in similar countries
throughout the world,
and interestingly
also in developing countries.
That relentless drive of diabetes
contributing to end-stage kidney disease
is quite clear
in the Australian context.
The ADVANCE study
related cardiovascular disease risk
with albuminuria and renal disease.
Absolutely correct.
The ADVANCE study was a large,
randomised-control trial
with over 11,000 type 2 diabetics
looking at blood-pressure control
and glycaemic control.
There is quite clear evidence there
that both of these markers are
predictors of heart attacks and strokes
and progression of kidney disease
to renal death or dialysis.
Both independently and together,
they add one to the other,
so people at highest risk are people
with reduced kidney function and
significant albumin leakage in urine.
NORMAN: Do they go hand in hand?
They do go hand in hand.
The figure that one in four people
with diabetes
probably has some early kidney disease
is about the figure for retinopathy.
It used to be thought that retinopathy
occurred before kidney disease.
That's before we measured kidney disease
properly.
They do go hand in hand.
We know that once kidney disease
really starts to accelerate,
retinopathy really gets a hold on
particularly macular oedema.
People,
as their creatinine starts to rise,
that's when we see retinopathy,
if it hadn't already needed treatment,
really become aggressive.
Because they're parallel processes
according to severity?
Probably a parallel process,
but certainly people
who have got significant proteinuria
have a major increased risk
for macular oedema.
What are the other risk factors
for diabetic retinopathy?
The principal risk factor is
glycaemic control,
but in type 2 diabetes,
it looks like blood pressure control
is probably almost or as important.
Lastly, blood lipid control
might also be important.
Data from field studies suggests that
an aggressive approach to blood lipids
might also be helpful,
although that's not so solid.
We certainly know that
elevated lipids are associated with
macular oedema specifically.
The nice thing about that is,
it's blood pressure
and glycaemic control
that are also related to progression
of kidney disease.
So similar approaches to management of
these factors that complicate diabetes
can reap the rewards
in terms of keeping people's vision
and keeping their kidney function.
How reversible is diabetic retinopathy?
It's quite reversible
in the early stages.
The recent data on this came from the...
Got a blank on the study?
It'll come to you later.
One of the most recent study of ARBs
showed that if you had retinopathy
at the first two stages,
microaneurysms only or a few
microaneurysms and retinal haemorrhages,
those stages were reversible with
really tight blood-pressure control.
But once the retinopathy became
slightly more advanced than that,
then it was not reversible.
These are the direct study findings.
We'll come back to do more
on diabetic retinopathy in a moment.
I've got the answer
to the poll question, which is:
The red is six-monthly, and it's 27%.
18% said it depends on the patient.
54.5% said annually.
What's the right answer,
Professor Twigg?
STEPHEN: I would say annually,
but it depends on the patient.
You're happy with both?
You've got a thinking physician there.
I'd prefer a thinking physician any day.
Annually is the cycle of care.
NORMAN: So most people
have got it right.
As is recommended
in the NHMRC guidelines,
which Stephen co-wrote.
Just testing, just testing.
We've talked about screening,
just to go back to kidney disease.
We've talked about the test that you do.
What about albumin-excretion rates?
What validity does that have?
People use both albumin-creatinine
ratios and albumin-excretion rates
in screening for damage to the kidney
causing albumin leakage into the urine.
Both are tests that are valid
and have good sensitivity
and specificity in terms of
their role in screening
and measuring response to therapy
for diabetics.
What are confounders
when you're doing urine tests?
It's critical that there are a number
of key confounders.
Urine infection, menstruation in women,
people who might have exercised
significantly in the preceding 24 hours.
Many Australians
who eat high-protein diets,
these people will have artificially
elevated readings, for example,
and some medications,
for example nonsteroidals
and others that are commonly taken.
When you're talking about
blood pressure control,
are we talking about angiotensin
receptor blockers and ACE inhibitors
or others work as well?
The answer is both.
Yes, there is accumulating evidence
from a number of trials
that for people who have,
in terms of prevention of early
chronic kidney disease in diabetes
and people with early stages
that ACE inhibitors and ARBs
might have a particular protective role.
As well as that, it's the overall level
of blood pressure control.
Indeed,
there now seems to be added evidence
that even for people
who are normotensive with diabetes
that there is the same benefit
as people with any level
of blood pressure
in lowering their blood pressure
in terms of kidney disease, for example.
As you implied earlier, Paul,
similar findings now
for diabetic retinopathy?
Certainly the UKPDS didn't differentiate
between different blood pressure agents,
and there's never really been
fantastic data suggesting
that one class of blood pressure
lowering medication would be better.
Recent studies of ACE inhibitors
and ARBs
seem to show the best effects,
but there hasn't been
a head-to-head comparison.
Stephen?
I agree. You look at all the national
and international guidelines
and first-line for hypertension
for people with diabetes
is an ACE inhibitor or ARBs.
As Paul and Alan mentioned though,
the critical issue is
tight blood pressure control.
Lipid control is not as strong
but still worth doing?
Lipid control is important,
because people with diabetes
have high cardiovascular risk.
There is not strong evidence that
lipid control prevents progression
of kidney disease.
But they are at high risk
of heart attack and stroke,
therefore require good lipid control
in that context.
David, were you going to say something?
Just agreeing that at the macrovascular
level, that's what you're looking for.
The place of aspirin in patients?
Does aspirin help with kidney
or eye disease?
Here we go. Put on your seatbelts.
We're in for a rough trip now.
Perhaps I can address the issue
of lipids.
No, let's have the aspirin question.
Professor Twigg?
For secondary prevention,
there's no question antiplatelet therapy
is critically important,
and that gets back to
the cardiovascular link.
You've got to have an event
before you start the aspirin
- for it to be of benefit?
- Yes.
For primary prevention,
this is where cardiovascular risk tables
can be extremely helpful.
If a person is deemed
to be at high risk,
you'd be prone to use antiplatelet
therapy. I would under those conditions.
NORMAN: But there's no evidence for it.
- That's for cardiovascular protection.
There is, but you have to extrapolate.
There was the Hypertension
Optimal Treatment study,
which had 1,700 with type 2 diabetes
in it,
but they're only 10% of that population.
Aspirin worked very well there.
There was also the Physicians'
Health Study for primary prevention.
From a cardiovascular point of view,
there's a basis for using aspirin
under those conditions.
It is complex in people with diabetes.
There's some evidence that maybe
aspirin resistance occurs -
resistance to the action of aspirin.
And what is the correct dosage?
From the point of view
of kidneys and eyes,
we'll move on to my esteemed colleagues.
But from the cardiovascular
point of view,
tables can be helpful
for antiplatelet therapy.
I'll come back to Paul
'cause I so rudely interrupted him.
To go on the aspirin point,
one of the original diabetic retinopathy
studies, the ETDRS,
looked at whether aspirin was beneficial
for people with diabetic retinopathy.
It really showed no benefit
over no aspirin.
Of course, in people who needed aspirin
for cardiovascular reasons,
there was no contraindication
to giving aspirin
because there was
no increase in haemorrhages,
even in people with severe retinopathy.
There was no increase
in vitreous haemorrhage.
So it's safe, but there are
no protective effects on its own.
Can I add to that?
Stephen talked about the HOT trial.
There was a recent analysis,
presented this year
at the World Congress of Nephrology,
showing that people in that trial
who had chronic kidney disease -
people we're talking about here
with chronic kidney disease
in the context of diabetes -
had the greatest absolute benefit from
aspirin therapy of the entire group.
Because they're at much higher
cardiovascular risk.
Even though they had some increase
in some risks,
the added benefit in terms of
the prevention of, in that case,
heart attack and vascular events
outweighed that.
So people with CKD had
particular benefit from aspirin therapy.
And smoking cessation
affects the kidneys and eyes?
Smoking has been looked at a lot
in terms of retinopathy,
but no good data suggests that cessation
of smoking benefits retinopathy.
NORMAN: So smoke doesn't get
in your eyes?
I'm sure it does, and it's great to stop
if you've got diabetes.
It gets in your eyes from macular
degeneration rather than anything else.
- What about kidneys?
- There is evidence people who smoke
are at greater risk of progression
of chronic kidney disease.
What about protein restriction
with grade 3 renal disease?
I wouldn't advocate that now.
That was something...
So generations of people
with impaired kidneys
have been eating that horrible stuff
all that time?
Correct. The evidence of benefit is
that it might at best delay the onset
of dialysis by one or two months.
And you feel every month of that.
The clinical care guidelines
are very helpful here
in terms of the points
that Paul has raised
about aspirin not being a risk
in terms of intercurrent retinopathy.
They are nicely covered
in the guidelines,
and as Alan points out,
the smoking issue too.
Even the executive summary,
I'd encourage people to go online
and have a look at it.
Excellent marketing, Professor Twigg.
We're most impressed.
What about salt reduction in kidney
disease? Does that have any benefit?
Salt reduction is becoming increasingly
an issue of focus in Australia.
In general we eat a high-salt diet.
A lot of that is about not salt
that we add but that salt is in...
..takeaway foods and foods
that we buy at the supermarket.
It's quite clear that the high-salt diet
has implications for hypertension.
Therefore, I think it will be an area
of increasing focus -
how can we reduce that
in terms of interaction
with the food industry, for example,
so we can lower blood pressure?
That will be very relevant
for management of diabetes.
A question from New South Wales -
'What is the incidence of chronic kidney
disease with gestational diabetes?'
Maybe I can answer
the gestational diabetes part,
then pass on to the colleagues
for chronic kidney disease.
Gestational diabetes by definition
is diabetes that develops in pregnancy,
then usually resolves
shortly afterwards.
You wouldn't expect kidney disease
with it?
Yes. It does affect about 5%
of the pregnant population.
After saying that, pregnancy-induced
hypertension and pre-eclampsia
and eclampsia, they do cosegregate
with gestational diabetes,
probably through body weight
and equivalent risks.
In terms of renal disease per se,
in some of the renal disease-related
conditions, there is some link.
I'll stop there and pass on to others.
The actual risk
of significant renal disease
at the time of gestational diabetes
or pre-eclampsia, for example, is low.
People who might already have
overt diabetic nephropathy
at the time of becoming pregnant
and high blood pressure and things
are at more risk
in that condition
of worsening of renal function
and of having greater difficulty
in managing those comorbid conditions.
There are a lot of people interested in
following people
after having the pregnancy,
having a baby,
in terms of their then ongoing risk
of developing type 2 diabetes
and related chronic kidney disease,
where it does appear that there is,
in long-term, some increased risk.
Another question is,
'How does steroid abuse
influence the incidence
of chronic kidney disease
in existing type 2 diabetes?'
I assume we're talking
anabolic steroid abuse here.
That's not something
I have any particular knowledge about.
You haven't got many muscled-up...
What about steroids
as in corticosteroids?
There's obviously concerns about obesity
and its interaction with diabetes
as to whether that's a risk factor
for development and progression
of chronic kidney disease in diabetes.
But again, it's not something
that features steroid use,
in terms of development
of chronic kidney disease.
Let's have a look at
our first case study.
Back a while, back about 10, 11 years,
I was working in the coal fields then.
I went to the doctor because the
diabetes had sort of caught up with us,
the high blood pressure and that.
The doctor had taken blood tests
and that and said, oh, yeah,
there's something wrong with
your kidneys.
So I had to go to Townsville.
They took a biopsy on the kidney.
They thought it was a diseased kidney.
They took a biopsy, and the result of
that was, neither kidney was diseased.
We had to go and see a dietitian
in Mackay when he came back.
They said, don't eat this and
don't eat that. Eat this and eat that.
So he did it, but nobody ever said,
you've got to follow it up.
It wasn't until about five years ago
that he started feeling down.
He said he was feeling a bit tired
a lot.
I said, you need a good sleep.
Stop eating so much.
He got the flu.
He was away working in a mine.
He used to fly in and out.
And then he got sick.
He flew back in, and I couldn't believe
he was a person when I opened the gate.
I thought, what's wrong with you?
He said, I'm really sick.
Jeez, it nearly killed me.
It was just something unbelievable.
That's when he asked his doctor
if he could get his kidneys checked,
and lucky he did do that.
Next I know,
I'm at the renal area of the doctor's.
It just went from there.
I knew something was wrong when
he didn't come out.
I kept seeing people going out,
and I thought, something's wrong.
Then I thought, oh, no.
When I walked in and saw the faces,
I knew then.
It just hits you like a brick.
It all happened so quick.
It obviously was over a long period
of time.
Probably the good life caught up.
Personally, it gets back to the way
you're brought up, I guess.
The foods that you eat when
you're in your younger days,
grog, everyone does it.
A lot of people overindulge.
It just depends.
It gets back to your diet
and the way you look after your body.
I didn't show him,
I'd just go out and cry.
I couldn't handle it.
Not only my father died,
his father died of it.
I've got aunties on my mother's side
that have died of it
down in South Australia.
So you think, he's got it,
so I must have it.
It knocked the whole lot of us.
Really knocked the family.
The grandkids just couldn't believe
Poppy could get sick,
not their poppy.
Not a good story there, David.
No, no.
Like he said, it happened so quick,
but it really is something
over a decade or more, isn't it?
I think it's probably a good idea when
we have patients with diabetes early on
that we have our registers set up
so we can keep track of them.
It would be even better
if we could negotiate some plan
on how we're going to manage it
according to the cycle of care
so they don't get away from us.
And using a team.
And using a team to ease the burden,
particularly on rural GPs
who don't have much time.
He looked as if he was trucking along
with a haemoglobin of about 9.
I think that's right.
They talk about the devastating impact
of diabetes and kidney disease
on the family.
The key issue is multiple
missed opportunities for engagement
in the management of the diabetes.
He talked about all the factors
we know are crucial -
his blood pressure, diet,
all of the approaches to management
that could have made a difference
and prevented his severe kidney failure.
This problem is writ large
again and again across the country.
I'm going to ask you another question.
How would you rate your understanding of
correlation between serum lipid levels,
good blood glucose control
and blood pressure control
and eye complications?
It's probably a bit better since we've
been speaking about it for a while.
Let's see how you rate it now.
While you're answering those questions,
we've got another case study to watch.
Let's look at Darren's story.
My name's Darren Dorey.
In September, I'll be 43.
I live in Warrnambool,
in the south-west corner of Victoria.
It's approximately 300km
or three hours from Melbourne,
a little seaside town that is
a nice, little friendly community.
I was diagnosed with type 2 diabetes
when I was 27.
I was told to change diet,
and I was put on some tablets.
But as time went by
and I didn't feel any different,
I got more and more slack with it.
Probably for the next ten years,
I lost focus on control of the diabetes.
At the time I was told,
you have to have your eyes checked.
OK, well, that's pretty serious.
I drive a truck for a living,
so I've got to keep on top of the eyes.
After a couple of years of going,
yep, your eyes are fine,
you stop worrying about it.
Around about 2001
I was starting to struggle a little bit
with seeing some road signs.
I went in to the optometrist's
to get some glasses.
She had a look in my eyes and said,
you've got a massive bleed in the eye.
She said, you need laser surgery
and you need it now.
I walked out
of the ophthalmologist's rooms
after having something like 300, 400
shots of laser in the eye.
I ended up having a vitrectomy.
Probably 18 months later,
I developed a cataract,
which I had out in about 2006,
in the left eye.
That brought back vision beautifully.
It was like, wow, a whole new world.
This is all good.
In 2007
I'd actually gone back to truck driving.
I guess going back into trucks was,
for the diabetes,
one of the worst things I did.
I did a lot of travel where
you'd take off for a few days' trip
and forget to take your medications
with you.
I noticed it was getting harder
to read the paperwork,
and the headlights of cars started
to become more glarey -
the lights would flare.
I thought, I'd better
go back to the ophthalmologist.
He looked at my eyes and said,
'Are you still in sales?'
I said, 'No, I'm a truck driver.'
He just said, 'Not anymore you're not.
Hand in your licence tomorrow.'
I then had to go home to my wife
and four kids and say,
'I don't have a job, and it looks like
I might be going blind.'
The same day,
our landlord called over to mention that
he'd put the house on the market
and we'd have to move.
Yeah, life just crumbled.
Paul Mitchell, entirely preventable?
I think that blindness from diabetic
retinopathy should be preventable.
There really should not be any cases
of people who go blind from this disease
anymore.
There are still people going blind
from it,
and there will still be some people.
But if you look at every one
of those cases,
you can really detect what went wrong.
Clearly, in the early stages of his
diabetes, he was poorly managed.
He put his head in the sand.
Maybe his doctors didn't impress on him
the absolute importance
of having regular checks,
but it should have been prevented.
After he had that first lot of therapy,
it looks like he again lost contact.
He should have had pretty intense
follow-up after that first therapy.
But he didn't go,
and he went back to driving again.
If you look at Darren's story, there are
many circumstances where really,
the wrong path was taken, and
his blindness, or severe vision loss,
could have been prevented.
How do you screen your patients
for retinopathy, David?
Do you send them to the optometrist?
I send them off to the optometrist
or ophthalmologist,
probably a 50/50 split, or a bit more
to the ophthalmologist where we are.
Question from Michael Stuckey
in Queensland -
'Why not annual retinopathy screening?'
Paul?
It's been looked at.
Around the world, most diabetes
associations recommend annually,
but in fact, the development
of retinopathy occurs relatively slowly.
It's been shown that two-yearly is
actually sufficient.
If someone has
difficult-to-control diabetes,
if they've already got
other complications,
of course they need
to be seen more frequently,
even if they have no retinopathy.
How good are the screening tests?
This is ophthalmoscopy?
Yeah, this is ophthalmoscopy.
The eye doctor, or optometrist, wouldn't
use a handheld ophthalmoscope.
He would use a slit lamp
with a much wider area,
being able to screen the retina
much more effectively
than the handheld ophthalmoscope.
We also have the potential availability
for clinics
of non-mydriatic photography.
This is what they're using in some
Aboriginal communities?
That's right. That's very effective.
You see a blown-up picture,
you can immediately see
if there are any retinopathy lesions.
The standard though, at the moment,
would be pupil dilation?
Yeah. The standard is pupil dilatation,
then examination of the retina
by someone who can do it properly -
an ophthalmologist, an optometrist
or a well-trained GP or physician.
What are the criteria for referral
to an ophthalmologist?
Certainly non-ophthalmologists
can manage people with diabetes
in terms of retinal screening
until the point at which any significant
retinopathy is present -
anything more than the occasional
haemorrhage or microaneurysm.
From that point people should
see an ophthalmologist.
Marisa Pilla from North Queensland asks,
'Is there any ACE inhibitor
that's superior to the others
in helping to prevent retinopathy
or the worsening of the condition?'
We don't know.
There are two recent studies
looking at two different ARBs
and they both showed beneficial effects,
but there's been
no head-to-head comparison.
She also asks about antioxidants.
The AREDS study suggested
that a certain cocktail might
help macular degeneration.
Does it help in diabetic retinopathy?
There's no evidence that
it helps diabetic retinopathy.
Talk us through
laser photocoagulation here.
There are some new therapies coming on
when you've got microaneurysms
and bleeds.
Once ophthalmologists take over
follow-up and management
of people with diabetes,
what they're really critically
interested in doing is
evaluating the patient at an interval
so that they would detect
vision-threatening retinopathy
and could apply laser treatment
at the optimal time.
The indications for laser treatment are
the presence of either new vessels,
and this is an advanced stage
of the background type of retinopathy.
New vessels are fragile, they bleed,
they don't really help,
they don't bring new blood to the area.
The second is macular oedema.
This is the more frequent and
more important complication to detect.
That is harder to detect
with ophthalmoscopy.
That's why you really need
an ophthalmologist or optometrist
to examine the patient.
And the treatment of macular oedema?
The treatment of macular oedema is
currently laser treatment
using the guidelines
that have been around for 25 years.
It's reasonably effective
but not brilliantly effective.
Certainly many people will still
lose vision.
We now have some other
adjunctive therapies that can help.
The main one is anti-VEGF therapy.
This is vascular
endothelial growth factor.
- This is like Avastin or Lucentis.
- That's right.
These agents are an adjunct to therapy.
They don't do away with
the need for laser,
but they can help to dry out the macula
until laser treatment
can be a bit more effective.
Laser treatment is probably
more effective if it's applied
when the macular oedema is resolved.
And the role of fluorescein angiography?
Becoming less and less.
Fluorescein is not a particularly
pleasant test to have done.
We actually do it very rarely.
We might do it at the onset,
before we start laser treatment
for macular oedema, once,
but we rarely repeat it these days.
We don't do it at all for screening
or for the follow-up of people
with diabetic retinopathy.
Unlike retinal detachment,
vitrectomy has a different reason.
You're trying to get rid of
the haemorrhage from the vitreous?
There are two circumstances.
The first is to get rid of
the haemorrhage and scar tissue,
because new vessels that bled
will then develop scarring,
and that scarring will cause traction
on the retina.
Because retinal detachment
is increased in diabetes?
Correct, and it's a tractional type
of retinal detachment.
The other type of need
for vitrectomy surgery
is for traction on the macula itself,
which can cause macular oedema
to persist and be chronic.
But we are doing less and less
vitrectomies now
because physicians are managing people
with diabetes much better.
We're seeing less people
presented at Act V, Scene IV,
and we're needing to do
a lot less vitrectomy surgery.
Just to explain, the vitrectomy involves
microdissection to remove scar tissue.
Correct. It involves usually two ports
on the side of the eye
with instrumentation which can dissect
and peel off membranes
and coagulate blood vessels.
People have said that doing cataract
surgery can also damage the retina.
What risks are there
in cataract surgery and diabetes?
This is an important issue,
and it's still important.
We know that people with diabetes
develop cataract much earlier
than people without diabetes.
There's a direct effect of glucose
on the lens in the eye.
The type of cataract they get
is a cortical cataract -
the spokes when you dilate the pupil -
you can see them quite easily
with an ophthalmoscope -
or an opacity on the back of the lens.
The problem is that when people
with diabetes develop cataract,
they may also be developing retinopathy.
If there is any early macular oedema
or moderate retinopathy,
then you can develop macular oedema
after cataract surgery,
perhaps as a response to
the inflammation of the surgery itself.
One of the issues that
all ophthalmologists know
is that we must stabilise
the retinopathy before cataract surgery
as much as we possibly can.
What about access to
good ophthalmological care
when you're living in
a small country town?
This is always difficult.
Ophthalmologists like
to live in the nicer suburbs,
and don't necessarily go to the country
so often.
But in all country areas in Australia,
there is some degree of access.
It always needs to be better,
but there is reasonable access.
And if there isn't,
you need to let us know
so the College of Ophthalmologists
can look at this.
Local ophthalmologists
in some of the larger rural areas
will be prepared
to travel to smaller areas
if they think there's a reasonable need.
This non-mydriatic screening can
be transmitted for people to look at.
Correct. Right now there's another
application to the Medicare group
to consider funding
non-mydriatic photography.
This would produce a fantastic way
of screening people.
It means
they wouldn't have to travel a long way
to see an optometrist or eye doctor.
GPs themselves
could read the photographs quite well
with relatively minor training.
That has not yet been approved,
but we're hoping it will be.
Let's have a look at Darren's story
again, and what his life is like now.
My left eye has
been left with 25% vision.
The right eye, about 10%.
The hardest thing with the eyes
is that they see totally differently.
I describe it as being like
the old fun mirrors at Luna Park,
where everything is distorted,
or fog up your windscreen,
jump in your car of a cold morning,
going for a drive
without a clean windscreen.
Then put a few little lines
and black dots into your line of vision
then go cross-eyed so you've got
double vision on top of that.
I was never actually told
about the correlation between diabetes
and depression.
If my sugar levels were high,
my moods would swing.
But once I lost the sight, the
depression came in like a tidal wave.
It became all-encompassing
to the fact where I attempted suicide.
I lost all self-esteem,
I lost all self-worth.
It cost me my marriage. I haven't
seen my children for two years.
October '07, my life fell into a hole -
a very, very deep black hole.
It took me another six months to crawl
my way out of it and restart my life.
One of the biggest things that helped me
get my life back on track,
or helped me out of the hole
that I was in,
I made an appointment to see my GP
and couldn't get in,
so they said, we've got another doctor
here with an appointment open.
Do you mind seeing someone else?
I said, I just need a script,
so that would be great.
I sat down with this new female doctor.
Very young, she was.
She had a look at my file and said,
you haven't had this test done for
a while. You haven't had this test.
What's going on here?
What's going on there?
We'd better take control of this.
It was almost a light-bulb moment
for me,
like, someone is listening,
someone is taking note.
The GP I was seeing,
we had a good rapport,
but it just became the usual,
yep, I've run out of tablets.
Can you help me here?
It was in and out, script in hand,
thanks very much, see you later.
She also linked me in with
the local psychiatric services
through the local hospital,
and I was given a case manager,
who, once again,
showed a lot of compassion and care
and was listening to me.
Also Vision Australia
really came on board
and helped me
with a lot of adaptive stuff.
They sent out a person
to help me learn how to walk again.
It sounds silly, but you learn to feel
the ground rather than see the ground.
I couldn't see the normal,
everyday things anymore,
simple things like how to put something
in the microwave, push the button to go.
I couldn't see that button.
I couldn't feel that button
'cause they're flat-panel.
Vision Australia said,
we've got these dots,
put them on the go and stop buttons.
I can't read how many minutes
I've got up,
so I count how many times it beeps.
It's just one of the little things
you take for granted
that suddenly become an issue.
It was the supports behind me
that helped me.
I'm now employed by
South West Healthcare,
Psychiatric Services Department.
Vision have come down from Melbourne
and put in a program
which helps with email,
it enlarges the font automatically.
I can't read normal-size font.
Also, enlarged keys or enlarged stickers
on the keyboard.
Without them, I've got no hope.
The main thing for someone
who's new to diabetes,
or even a doctor that's
treating a new diabetic,
is to emphasise what it is
and how it works.
Doctors need to emphasise,
you won't feel it coming.
As I said earlier,
I expected to have signs.
If there's any damage, I expected
to have the signs of it coming.
You don't feel it coming.
It creeps up very, very slowly
until suddenly it's out of control.
A lot of the things I did was, if
it's serious, they'll tell me about it.
Of course they think
you've understood it, so they let it go.
Suddenly it becomes a huge issue
down the track.
I honestly feel,
if it had been more of a team effort
between my GP and myself,
maybe I wouldn't have lost the sight.
Tragic, David.
DAVID: Yes.
You feel bad as a GP
when you see a story like that.
There's a place for having a register
of your diabetic patients
and reviewing that regularly
and getting your team to help you
in the management of these patients
and make sure they're not lost
to follow-up and you can keep on them.
I joke with our diabetes educator
who visits our surgery
that we play good cop, bad cop.
She tells them all the things they
have to do, then I come in and say,
Sharon says this, so you'd better do
the right thing for next time.
Let me get the results
of the poll question:
6% of you said you had no understanding.
Hopefully we've improved that tonight.
62% said you've got moderate,
and 31%, comprehensive.
So over 90% of you have
got a reasonable understanding,
at least on a self-assessment basis.
We won't be administering any
multichoice questionnaires tonight.
Paul, not a good story there,
but you're saying it's becoming rarer.
It's becoming rarer. One of the points
we could say about Darren
is that he's been through
the gamut of therapy.
Usually their vision is stable
from that point.
Usually there's no further progression,
because the disease becomes
relatively quiescent
after it's done all that damage.
He probably will hold his vision
from now on.
We should be looking at his case and
say, this should have been prevented.
We really need to work hard to prevent
all these cases, and I think we can.
We mustn't forget
the psychosocial issues.
Depression goes along with it.
It makes diabetes worse.
Absolutely.
It's an important part of the package.
We know people with diabetes
have a two- to threefold
higher prevalence rate of depression.
It's a vicious cycle.
What are your takeaway messages
for the audience, David?
Know who your diabetic patients are,
and keep them under careful,
close review.
Don't try and do it all yourself.
Your diabetes educators,
dietitians, podiatrists,
they're all there to help,
and make sure the necessary gets done.
- And get the targets right.
- Get the numbers right.
Paul?
At least two-yearly,
I review by competent examiner.
Make sure that you really work hard
at the control of diabetes
blood pressure and blood lipids.
- Alan?
- Chronic kidney disease is common.
It can be readily detected and followed
with simple blood and urine tests.
And again, blood pressure
and glycaemic control
are crucial to preventing progression.
For me, those two case histories show
that too many people
fall through the cracks.
Both as individuals
in our own clinical practice
and the health system generally,
we need to do something better
to prevent those disastrous outcomes.
- Stephen?
- Vigilance is key.
Diabetes does tend
to be a progressive condition,
and the complications.
We need to get to know our patients
well.
Work with them as one of the key members
of the team.
Recognise that we can prevent
at many different levels.
Hopefully we can prevent many people
from developing diabetes,
many others from diabetes complications
developing
once they've been diagnosed
with diabetes.
Even those who develop more severe
later-stage complications,
there's a lot that we can do.
Never give up,
prevent at multiple different levels
and get to know your patient.
Thank you all very much.
Very interesting and very important.
I hope you got a lot from the program
too.
The series of four programs we're
making on type 2 diabetes guidelines
will be available in December free
on DVD.
To order,
visit the Foundation's website.
Copies of the guidelines can be
downloaded from Diabetes Australia:
www.diabetes.com.au.
If you're obtaining
even more information
about issues raised
in tonight's program,
there are a number of resources
available
on the Rural Health Education
Foundation's website:
Don't forget to complete and send in
your evaluation forms
and register for CPD points
by completing the attendance sheet.
I'm Norman Swan.
From all of us, see you next time.
Funded by the Australian Government
Department of Families, Housing,
Community Services
and Indigenous Affairs.
Captions by
Captioning & Subtitling Internationa�

https://www.youtube.com/watch?v=W8n6R3qG5Nw