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Effects of glycaemic management on diabetic kidney disease
#MMPMID28572879
MacIsaac RJ
; Jerums G
; Ekinci EI
World J Diabetes
2017[May]; 8
(5
): 172-186
PMID28572879
show ga
Hyperglycaemia contributes to the onset and progression of diabetic kidney
disease (DKD). Observational studies have not consistently demonstrated a glucose
threshold, in terms of HbA1c levels, for the onset of DKD. Tight glucose control
has clearly been shown to reduce the incidence of micro- or macroalbuminuria.
However, evidence is now also emerging to suggest that intensive glucose control
can slow glomerular filtration rate loss and possibly progression to end stage
kidney disease. Achieving tight glucose control needs to be balanced against the
increasing appreciation that glucose targets for the prevention of diabetes
related complications need be individualised for each patient. Recently,
empagliflozin which is an oral glucose lowering agent of the sodium glucose
cotransporter-2 inhibitor class has been shown to have renal protective effects.
However, the magnitude of empagliflozin's reno-protective properties are over and
above that expected from its glucose lowering effects and most likely largely
result from mechanisms involving alterations in intra-renal haemodynamics.
Liraglutide and semaglutide, both injectable glucose lowering agents which are
analogues of human glucagon like peptide-1 have also been shown to reduce
progression to macroalbuminuria through mechanisms that remain to be fully
elucidated. Here we review the evidence from observational and interventional
studies that link good glucose control with improved renal outcomes. We also
briefly review the potential reno-protective effects of newer glucose lowering
agents.
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