Cardiorenal syndrome is as a newly discovered syndrome including anemia, intractable congestive heart failure and end-stage kidney disease. Unfortunately, reaching this diagnosis can happen later.
May be in the very early stages so,the mandatory needs of innovating new classifications of newly discovered entity of cardiorenal disease long before the emergence of this very complex preplexing syndrome where all moda;ities also fail to treat the failure
Iron deficiency must be investigated and treat it (better with iv iron)
But b vitamin deficit must be discarded (it is not unfrequent chronic intravascular hemolysys, and B9 (folic acid) supplement coud be benefit, but always if B12 deficit is not present)
Of course, in case of anemia secondary to chronic kidney disease all international guidelines recommend EPO administration if Hb level is under 100 g/L (but used with iv iron, after iron overload discarded)
It is interesting to see that on a topic where much is published on in scientific journals, so little is discussed in a forum like this one. The question is important, but despite much effort, no satisfactory answer can be given. The very short answer by Dr. Valadez is actually what we have today. Investigating the cause (that is also what the different classes of cardio-renal syndrome are doing) and (try to) treat it!
Still, the question remains if there is more than this. Based on the literature and focusing on the heart as primary cause, increasing evidence suggests that venous congestion can be important and this should be treated first. If not helpful and importantly also on the long-term intensifying therapy that improves cardiac function is crucial. Unfortunately, often the opposite is being done. Thus, ACE-inhibition and spironolactone / eplerenone are being reduced or stopped. There are no prospective data on the effects of keeping using these drugs despite worsening renal function, as far as I am aware of. Indirect evidence, however, suggests that this should be done. There are some publications suggesting that treating the heart matters and not considering the kidneys too much is the best for heart failure patients (at least if LVEF is reduced). A retrospective, not yet published analysis of our TIME-CHF data suggests the same: significant worsening of renal function in patients with high doses of loop diuretics is bad, in those with high doses ACE-inhibitors /beta-blockers and/or on spironolactone does not matter much.
Obviously, we would need prospective studies investigating interventions in this clinically important syndrome. In the meantime, the inderect evidence discussed above is all we have got. So, proper dignostics (what is the reason for renal dysfunction / cardiac dusfunction and can this be treated?) and if heart failure is the cause, then treat venous congestion (often by using iv diuretics), but thereafter reduce diuretic therapy and intensify the therapy proven to improve prognosis in HFrEF even if renal function deteriorates is the way to go.
My doctoral dissertation is on cardiorenal syndrome and the role of inflammation. From my original research, I have found that there is a major role that inflammation plays in deterioration of the condition of cardiorenal syndrome. While the treatment seems to help one organ at the expense of the other, one of the solutions seem to be the use of biologic agents. These can decrease inflammation and damage to both organs at the same time. I agree with Dr. Brunner-La Rocca that currently more prospective studies are necessary in order to fully understand different therapies that work.