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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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