CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 3, May/June 2016
132
AFRICA
30 days of follow up. In addition, according to our findings,
diabetes mellitus and AKI were significant determinants of
mortality in patients undergoing iloprost infusion therapy.
This study has several limitations, many of which are inherent
in its retrospective design, including the possibility of missing
risk factors that could contribute to a confounding bias. In
addition, renal imaging studies were unavailable for all patients.
However, the association between iloprost-induced hypotension
and AKI was independent and clear. Our results clearly illustrate
that relative hypotension may play a key role in the development
of AKI during iloprost infusion therapy in patients with altered
renal function.
Conclusion
We conducted a retrospective study to evaluate the risk factors
for AKI development and mortality in patients with severe PAD
treated with iloprost. We found that patients who developed
AKI were more likely to have relative decreases in systolic,
diastolic and mean arterial pressures and worse baseline renal
function than unaffected patients. We suggest that patients with
a smoking habit and those not using ASA are at an increased
risk for AKI. In this group of patients we advise iloprost
dose reduction and close follow up for evidence of AKI, and
discontinuation of iloprost in patients with severe hypotension.
As patients with AKI have a higher mortality risk, we suggest
that iloprost treatment should be given to selected patients.
From our findings, we advise that iloprost should be avoided as
it is very likely to cause AKI in patients with CKD or low blood
pressure. In addition, we recommend iloprost dose reduction
or possible discontinuation for patients receiving iloprost who
show evidence of AKI or hypotension. Ultimately, prospective,
randomised studies will be needed to address the effects of
iloprost infusion therapy on renal outcomes in patients with
severe PAD.
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