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Review
. Mar-Apr 2017;69(2):255-265.
doi: 10.1016/j.ihj.2017.01.005. Epub 2017 Jan 22.

Pathophysiology of the Cardio-Renal Syndromes Types 1-5: An Uptodate

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Free PMC article
Review

Pathophysiology of the Cardio-Renal Syndromes Types 1-5: An Uptodate

L Di Lullo et al. Indian Heart J. .
Free PMC article

Abstract

According to the recent definition proposed by the Consensus conference on Acute Dialysis Quality Initiative Group, the term cardio-renal syndrome (CRS) has been used to define different clinical conditions in which heart and kidney dysfunction overlap. Type 1 CRS (acute cardio- renal syndrome) is characterized by acute worsening of cardiac function leading to AKI (5, 6) in the setting of active cardiac disease such as ADHF, while type - 2 CRS occurs in a setting of chronic heart disease. Type 3 CRS is closely link to acute kidney injury (AKI), while type 4 represent cardiovascular involvement in chronic kidney disese (CKD) patients. Type 5 CRS represent cardiac and renal involvement in several diseases such as sepsis, hepato - renal syndrome and immune - mediated diseases.

Keywords: Acute kidney injury; Cardiorenal syndrome; Chronic kidney disease; Heart failure; Sepsis.

Figures

Fig. 1
Fig. 1
Timing of acute kidney injury in the setting of acute decompensated heart failure.
Fig. 2
Fig. 2
Non-hemodynamic network of pathophysiological interactions in CRS type 1. Note the emerging potential role of macrophages/monocytes as mediator of sodium and fluid retention. Reproduced with permission from ADQI.
Fig. 3
Fig. 3
Pathophysiological pathways of type-4 cardiorenal syndrome. It has been highlighted the role of uremia in developing minor and major cardiovascular complications referring to main CKD-related cardiovascular risk factors such as secondary hyperparathyroidism, anemia, accelerated atherosclerosis and chronic inflammation.
Fig. 4
Fig. 4
Clinical correlation between kidney and heart disease. This is a summary of close relationship between renal failure main features and equivalent heart involvement with particular focus on uremia effects on systolic and diastolic left ventricular function.
Fig. 5
Fig. 5
Pathophysiology of sepsis induced organ dysfunction. It has been focused attention on immunologic pathways leading to toxic damage on target organs since complement and coagulation cascade activation and endothelial and epitelial damage.
Fig. 6
Fig. 6
Pathophysiology of cirrhosis induced CRS-5.

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