VOLUME 10 NUMBER 4 • NOVEMBER 2013
151
SA JOURNAL OF DIABETES & VASCULAR DISEASE
REPORT
athy. However, these effects are seen mainly
in incipient rather than overt disease. ‘In
the latter, blood pressure control is the key
concern, delaying progression and having a
beneficial effect on kidney function.’
Renin–angiotensin system (RAS) block-
ade is the mainstay of blood pressure treat-
ment in CKD patients, with angiotensin
converting enzyme inhibitors (ACEIs)
and angiotensin receptor blockers (ARBs)
reducing proteinuria and slowing disease
progression. Thiazide diuretics have a
lower efficacy in the kidney-impaired and
loop diuretics are preferred in the context
of proteinuria and ESRD. Statins can signifi-
cantly improve GFR or delay its decline in
type 2 diabetes, but need to be initiated
early as they have little effect when kidney
impairment is advanced.
Renal anaemia affects 20% of diabetes
patients with stage three CKD. It worsens
with disease progression, and low haemo-
globin levels increase the risk of all-cause
mortality. Patients need to be screened for
anaemia. Erythropoietin-stimulating agents
may be indicated, but need to be used with
caution as they do carry risk. Abnormalities
in bone mineral metabolism should also be
addressed.
Lifestyle measures should not be under-
estimated. ‘Smoking promotes the onset
and progression of diabetic kidney disease,
while cessation reduces cardiovascular
risk and prevents the progression of early
CKD. Weight loss reduces proteinuria and
microalbuminuria, and improves glycaemic
control. While there are less robust data for
dietary modification, protein restriction is
recommended. Exercise has been shown
to attenuate disease progression in animal
models and may therefore be of benefit.’
Summing up, Dr Trokis underscored that
timeous nephrology referral reduces cost,
hospitalisation and mortality. ‘We have the
knowledge and means to prevent unneces-
sary deaths. Screen routinely and actively.
Be aware of exceptions to stereotypes.
Consider non-diabetic causes of kidney
disease. Maintain glycaemic and lipid tar-
gets early, and never accept “almost there”
blood pressures.’
Neuropathy: a diagnosis?
Dr Brian Kramer, Centre for Diabetes and
Endocrinology, Johannesburg
When is neuropathy, neuropathy? ‘Cur-
rently it’s defined in terms of an alteration
in morphology and function that results
in a disturbance of the neurones,
affecting the axon and myelin’, said Dr
Kramer.
Neuropathy is common in longstanding
diabetes, with a lifetime risk of approxi-
mately 60%. The major consequences of
neuropathy are foot ulcers and amputa-
tions.
There is no universal consensus on what
defines neuropathy and how to detect it
and monitor its progress. Although hyper-
glycaemia plays an important role, the
mechanism of neural damage remains
poorly understood. As a result, it is difficult
to develop and implement effective pre-
ventive and treatment strategies. ‘Where
glycaemic exposure is concerned, a well-
controlled patient may nonetheless develop
neuropathy, and vice versa.’
There are various tools for detecting
neuropathy, including screening/scoring
systems and quality-of-life measures. ‘The
monofilament test appears to be the best
validated in respect of predicting future
ulceration’, observed Dr Kramer.
‘While we have reasonable ways of
detecting and scoring neuropathy and pre-
dicting risk, the question remains whether
we’re diagnosing diabetic neuropathy or
simply neuropathy occurring in a patient
with diabetes but not necessarily caused by
it’, concluded Dr Kramer. ‘The lack of spe-
cific tests to determine whether neuropathy
is indeed caused by diabetes means that
clinicians always need to bear other causes
in mind and exclude these in patients with
diabetes.’
The diagnosis of diabetic neuropathy
is therefore one of exclusion. Those other
possible causes include toxic neuropathy
(caused by alcohol and drugs), systemic
disease, malignancy, inflammatory/infective
conditions, deficiency states and hereditary
factors.
The debate renewed… Is bariatric
surgery a ‘cure’ for diabetes?
Drs Graham Ellis and Ray Moore went head
to head on the subject, making persuasive
cases for and against. However, the majority
of the audience remained steadfast in their
original views. Prior to the debate, 31%
answered ‘yes’ to the question as opposed
to 69% answering ‘no’. Afterwards, those
figures had changed only slightly: to 34
and 66%, respectively.
Yes!
Dr Graham Ellis, Helderberg Diabetes and
Medical Clinic, Somerset West
‘If you want to lose your butt, bypass your
gut’, quipped Dr Ellis. ‘We often treat glu-
cose at the cost of obesity and most clini-
cal trials ignore the obese diabetic patient;
those with a BMI > 35–40 kg/m
2
. The data
we use to extrapolate from may therefore
not be appropriate to this group of patients
with obesity-related co-morbidities.’
There is a correlation between weight
loss and insulin sensitivity, although it is
not a direct relationship. Bariatric surgery –
biliopancreatic diversion (BPD) or Roux-
en-Y – can improve insulin resistance by
50% and decrease BMI by 30%. Critically,
the changes in sensitivity precede the actual
weight loss. In a small group of patients,
BPD is associated with complete restoration
of the acute insulin response one month
post surgery.
‘Cure’ is defined as remission that is par-
tial, complete or prolonged. Partial remission
requires an HbA
1c
level < 6.15 µg/dl and fast-
ing plasma glucose (FPG) values between
5.6 and 7 mmol/l without pharmacotherapy
for a year. The same is required for com-
plete remission, except that FPG must be
5.6 mmol/l or lower. Prolonged remission is
defined as complete remission sustained for
five years.
Laparoscopic banding has been associ-
ated with 73% remission at two years. For
Roux-en-Y the figure is 75% and for BPD
95%. Bariatric surgery is also associated
with a significant reduction in medication
use, supporting the notion that it can ‘cure’
diabetes. And data show that it is well
maintained and compares favourably with
other interventions.
But is normalising blood glucose suf-
ficient, given that it is only a surrogate
marker? Turning to other outcomes – mor-
tality, microvascular complications and
cardiovascular disease – Dr Ellis noted
that medical therapy for weight loss may
increase mortality, where lifestyle interven-
tion usually produces only modest, short-
term results.
‘Indications are that bariatric surgery
in the severely obese can reduce all-cause
mortality by 21% at 16 years. Cardiovascu-
lar events and deaths are likewise reduced
at 15 years post surgery. Preliminary evi-
dence suggests that it improves retinopa-
thy and nephropathy. There is therefore a
growing body of data that it has a wide
