Chronic Kidney Disease Pathway Document Description Presented ...

Glycaemic Control
CKD and Diabetes
Diabetes mellitus is the most common cause of chronic kidney disease
worldwide (Burrows-Hudson 2005) (Levy et al 2006) and at least 20-30% of
people with diabetes will have some evidence of the disease (Audit Commission
2002). There is a variation in the incidence of diabetes among racial and ethnic
groups, with people of South Asian, African and African-Caribbean descent
having a higher than average risk of type 2 diabetes (DOH 2001). The risk of
nephropathy is related to the duration of diabetes with microalbuminuria being
the first sign, progressing to albuminuria then nephropathy. The presence of
urine albumin whether microalbuminuria or albuminuria strongly increases the
person’s cardiovascular risk (University Hospital of Leicester 2006). Thereby a
person with diabetes should not be assessed in isolation for kidney disease but
also for lipid lowering, anti-platelet therapy and hypertension in tandem. Optimal
glycaemic control should be the cornerstone of all treatment for diabetes care.
For guidance please see Dudley Diabetes Management Guidelines for Adults
2006.
Persistent hyperglycaemia results in the thickening of the basement membranes
and accumulation of proteins in the glomeruli (Levy et al 2006). Research studies
suggest that intensive glycaemic control can reduce the rate of microalbuminuria,
proteinuria and nephropathy (Gross et al 2005) and improvement in glycaemic
control may reduce the risk of patients with diabetes developing both
macrovascular and microvascular complications (DOH 2001). Studies relating to
hypertension control also suggest similar results in relation to prevention of renal
failure (DOH 2001) recommending the use of ACE inhibitors (Angiotension
Converting Enzyme Inhibitors) or ARBs (Angiotension Receptor Blockers) to
delay the onset of diabetic nephropathy in people with microalbuminuria.
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