Journal of Clinical Medicine Research, ISSN 1918-3003 print, 1918-3011 online, Open Access
Article copyright, the authors; Journal compilation copyright, J Clin Med Res and Elmer Press Inc
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Volume 14, Number 1, January 2022, pages 22-27

Experimental Cardiorenal Syndrome Type 3: What Is Known so Far?


Figure 1.
Figure 1. Selection process of references cited in the study.
Figure 2.
Figure 2. Molecular mechanisms involved in myocardial dysfunction in CRS type 3. The figure summarizes the essential findings described in the article. Acute kidney injury of various origin triggers mitochondrial dysfunction in cardiomyocytes, an aberrant (systemic and local) immune response, and systemic vasomodulatory disturbances. CRS: cardiorenal syndrome.


Table 1. Characteristics, Pathophysiological Hallmarks, and Treatment Strategies of CRS Types 1-4
CRS typeCharacteristicsPathophysiological hallmarksTreatment strategy
The table exclusively summarizes the most important information. CRS: cardiorenal syndrome; AHF: acute heart failure; AKI: acute kidney injury; CHF: chronic heart failure; CKD: chronic kidney disease; FGF-23: fibroblast growth factor-23; RAS: renin-angiotensin system.
IAHF induces AKICardiac output ↓, venous congestion, activation of renin-angiotensin-aldosterone and sympathetic nervous system → impaired renal perfusionTreatment of respective cause, anti-congestive therapy, vasopressors if mandatory, fluid removal by hemodialysis/hemodiafiltration/slow extended daily dialysis/peritoneal dialysis if mandatory
IICHF aggravates progression of CKDLow cardiac output and prolonged venous congestion → renal ischemia and subsequent endothelial cell dysfunctionTreatment of respective cause, management of CHF according the current recommendations (beta-blocker, mineralocorticoid antagonist, gliflozine, RAS inhibitor or sacubitril/valsartan), anti-progressive CKD treatment according to current recommendations, kidney replacement therapy if mandatory
IIIAKI induces acute cardiac complications (e.g., arrhythmias, left ventricular insufficiency, myocardial ischemia)Hyperhydration due to oligo-anuria, hyperkalemia, metabolic acidosis, intrarenal inflammation with subsequent systemic inflammationTreatment of respective cause, treatment of electrolyte disturbances if mandatory, treatment of infections, avoidance of nephrotoxic substances, kidney replacement therapy if mandatory
IVCKD aggravates CHFRetention of sodium and water, retention of phosphorus, increase of blood FGF-23, renal anemia, CKD-associated endothelial cell dysfunctionTreatment of respective cause, anti-progressive CKD treatment according to current recommendations, particularly: blood pressure control, phosphorus-lowering therapy, bicarbonate supplementation, control of renal anemia, kidney replacement therapy if mandatory