The Perfect Storm, page-100

Perfect storms sometimes have a habit of lasting for a very long time. For a storm to last it needs continual feeding from the outside . . . and this is what I see in Cellmid's IP portfolio.

A very recent paper by Malyszko et. al, that covers the role of midkine in Contrast Induced Kidney Injury caught my eye.

Midkine – A Novel and Early Biomarker of Contrast-Induced Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Interventions-PCI

My very rudimentary understanding is that the medications used to support imaging in angioplasty procedures can in a small percentage of cases lead to kidney damage due to an increase in the protein creatinine. I can't say more as I'm not qualified to do so.

They authors found that that:

" Midkine were significantly higher 2, 4 and 8 hours after PCI in patients with CIN, while NGAL levels were significantly higher in patients with CIN starting 2 hours after PCI (serum NGAL) or 4 hours (urinary NGAL). Cystatin C were higher only 8&24 hours after PCI in patients with CIN. "


They conclude:

" Since the “window of opportunity” is narrow in CI-AKI and time is limited to introduce proper treatment after initiating insult, particularly when patients are discharged within 24 hours after the procedure, midkine needs to be investigated as a potential early marker for renal ischemia and/or nephrotoxicity. Inhibition of midkine can prevent the migration of inflammatory cells to the injured epithelial layer, reducing the severity of renal damage. "

Clinical relevance to CDY would (IMO) appear to be:

- at a diagnostic level .... it indicate a post treatment/ post surgical problem exists; then
- at a therapeutic level ....perhaps a MK mab to reduce elevated midkine levels and thus the likelihood of significant injury (nephropathy).

The paper may point to the need for yet another clinical trial IMHO. For Cellmid, business risk relates more to (potential) overfeeding rather than the usual malnutrition.

Cheers