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Chapter 11: Diabetes mellitus 457

Age Diabetic patients may have other causes for proteinuria
Increases with age. and renal failure, so particularly if there are atypical fea-
tures such as haematuria, rapid onset or absent retinopa-
Aetiology thy further investigation must be carried out to look for
Associated with hypertension, smoking and poor gly- another cause.
caemic control.
Management
Microalbuminuria and proteinuria require aggres-

Pathophysiology
sive treatment of hypertension (<130/75), better gly-
In addition to the other microvascular mechanisms
caemic control and cessation of smoking. ACE in-
hypertension can accelerate nephropathy by causing
hibitors and angiotensin II blockers appear to be most
further thickening of the capillary walls and reduced
effective in reducing protein loss and delaying pro-
glomerular filtration rate. This further increases hyper-
gression.
tension.
End-stage renal failure is treated as for non-diabetics.
Glomerular basement membrane (GBM) thickening
Haemodialysis may be more complicated because of
and glomerulosclerosis due to an increase in the mesan-
increased cardiovascular disease and autonomic neu-
gial matrix. It leads to diffuse sclerosis of the glomeru-
ropathy which exacerbates postural hypotension. Hy-
lus, which later condenses into nodular lesions, called
poglycaemia may occur because insulin and sulpho-
Kimmelstiel-Wilson lesions. The thickening of the base-
nylureas accumulate in renal failure.
ment membrane increases its permeability to albumin.
Renal transplantation is the preferred option in
As the disease progresses, the amount of protein lost in-
younger patients, and pancreatic-renal transplants
creases.
may be of value in reducing diabetic complications.
The glomerular filtration rate is initially normal, but
falls with progressive renal damage and chronic renal
failure occurs around 5–7 years after macroalbuminuria Diabetic neuropathy
occurs. Definition
Nerve damage is one of the microvascular complications
Clinical features of diabetes mellitus.
The condition is asymptomatic until chronic renal fail-
ure or nephrotic syndrome develops. Patients should be Incidence/prevalence
screened annually for all diabetic complications and hy- Diabetesisthemostcommonmetabolicdisordercausing
pertension. neuropathy: 10% of diabetics have significant symptoms
and 30% have evidence on testing.
Microscopy
The GBM is thickened (can be seen on electron mi- Aetiology
It is thought to be secondary to hyperglycaemia and mi-
croscopy). There are exudative lesions on the surface
crovascular disease.
of the glomerulus, which are masses of red-staining fib-
There are three main types of diabetic neuropathy:
rinprotein. The mesangial matrix is expanded and there
Symmetrical peripheral neuropathy: Affecting sen-
are round hyaline areas in the glomeruli (Kimmelstiel-
Wilson nodules). sory and motor function diffusely, particularly in the
lower limbs. This can be a painful neuropathy.
Focal and multifocal neuropathy: Affecting one or

Investigations
more cranial or peripheral nerves.
Annual screening of urine for microalbuminuria.
Autonomic neuropathy: Affecting the sympathetic
Amount of albumin lost per 24 hours:
and parasympathetic nerves.
30–300 mg/24 hours Microalbuminuria
>300 mg/24 hours Proteinuria Pathophysiology
>3.6 g/24 hours Hypoalbuminaemia and Hyperglycaemia may damage nerves through non-
Nephrotic syndrome enzymatic glycosylation of proteins or through the