Experimental studies show that acute kidney injury induces cardiac complications independently of excretory kidney dysfunction via inflammation, redox dysbalance, apoptosis, and mitochondrial dysfunction.
Experimental models of cardiorenal syndrome type 3 demonstrate that acute kidney injury induces cardiac damage through systemic inflammation, mitochondrial dysfunction, and oxidative stress, independent of fluid retention or uremia.
BACKGROUND: The concept of cardiorenal syndrome (CRS) has been established more than 10 years ago. Five distinct types of CRS have been defined. In CRS type 3, acute kidney injury (AKI) induces cardiac complications such as ventricular decompensation due to arrhythmias, myocardial ischemia, or fluid retention with or without arterial hypertension. The risk of cardiovascular events in AKI has been known for many years, even long before the introduction of the CRS concept. However, epidemiological and clinical studies published in recent years increasingly emphasized CRS type 3 (and the remaining four types also) as separate entity which requires particular therapeutic attention in an interdisciplinary manner. However, only a limited number of experimental studies specifically addressed CRS type 3 so far. Our review aims to summarize experimental studies on the pathological mechanisms in CRS type 3. METHODS: The following search criteria were employed in order to identify articles published on the topic: "cardiorenal syndrome 3" OR "cardiorenal syndrome type 3" OR "CRS type 3" OR "CRS 3" AND "experimental" OR "mouse" OR "mice" OR "rats" OR "animals"; additional criteria were "myocardium" AND "ischemia" AND "kidney" OR "renal". By applying the search criteria mentioned earlier, 10 references were finally selected. RESULTS: By applying the search strategy, 10 experimental studies were finally selected. All included cardiac outcome analysis in AKI animals. The data clearly provide evidence for cardiac complications that evolve independently from excretory kidney dysfunction. Pathological processes that emerge in the heart of animals subjected to renal ischemia involve inflammation, a dysbalance of redox components, pro-apoptotic processes, and mitochondrial dysfunction. CONCLUSION: The findings may explain why AKI increases the risk of acute cardiac complications even if dialysis treatment has been initiated.
Patschan et al. (Sat,) conducted a review in Cardiorenal Syndrome Type 3. Acute Kidney Injury vs. Control animals without AKI was evaluated on Cardiac complications and pathological mechanisms. Experimental studies show that acute kidney injury induces cardiac complications independently of excretory kidney dysfunction via inflammation, redox dysbalance, apoptosis, and mitochondrial dysfunction.