I think the most direct way to answer your question is that while sodium is what me measure that goes down with SIADH, the free water that is retained is distributed across all compartments, thus excess water is in the interstitial, the vasculature, and intracellular spaces thus reducing solute concentrations in all these spaces. However overall plasma volume is regulated by sodium excretion and thus the patient remains for the most part euvolemic. Imagine for example a patient develops SIADH, his overall volume status is slightly increased by let's say 1 liter, roughly 2/3s of this is intercellular and would have no effect on edema, 1/3 is extracellular and the split the quantity and split of this 1/3 between intra and extra vascular determines the presence of edema. So therefore you would think the SIADH and the resultant free water retention might be able to cause some edema by just increasing extra vascular volume as a whole, but remember that you haven't changed the balance between intra and extra vascular volume, just the total in the intercellular compartment. Therefore the transient intravascular expansion will trigger renal salt excretion and thus volume reduction back to euvolemia albeit with reduced body wide solution concentrations. Hope that was clear enough