AbstractPDF
Abstract
Before the introduction of renin-angiotensin-aldosterone
system (RAAS) inhibitors in the 1980s, non-steroidal
anti-inflammatory drugs (NSAIDs) were the only class
of drugs available for the reduction of symptomatic
proteinuria. Long-term data from those days suggested
sustained renoprotective properties in proteinuric chronic
kidney disease (CKD), but this potential has not been
further explored, due to the adverse effects of NSAIDs,
and due to the successful introduction of RAAS blockade
for blood pressure control and renoprotection. The
renoprotective potential of NSAIDs may seem surprising
for the present generation of clinicians, as NSAIDs
are well known for their adverse effects on the kidney.
Interestingly, the newer selective COX-2 inhibitors (coxibs), such as non-selective (ns) NSAIDs, exert an antiproteinuric effect in CKD patients. This review discusses the role of NSAIDs as a class of drugs representing an old concept for renoprotection in the light of current insights on renoprotection. It has become increasingly clear during the last two decades, from evidence obtained almost exclusively in studies using RAAS blockade, that not only reduction of blood pressure, but also of proteinuria is a prerequisite for
long-term renoprotection. Ns-NSAIDs and coxibs reduce
proteinuria without reduction of blood pressure. Their
possible role as an adjunct in individualised treatment
strategies, particularly for individual patients resistant or
intolerant to current therapy, will be discussed.
