| AUTHOR & YEAR OF PUBLICATION |
TYPE OF STUDY & # OF PATIENTS |
PURPOSE OF STUDY |
CONCLUSION |
| Clementi et al. [1] 2019 |
Review |
Neurohormonal, endocrine, immune dysregulation and inflammation mechanisms in CRS |
To insinuate the need for novel drug therapies that cover new mechanisms in CRS. |
| Virzì et al. [18] 2014 |
Review |
Heart--kidney cross-talk and role of humoral signaling in critical illness |
Damaged cardiac myocytes and renal tubular epithelium promote activation of innate and adaptive immune systems strengthening the humoral response. |
| Colombo et al. [20] 2012 |
Review |
Inflammatory activation: cardiac, renal, and cardio-renal interactions in patients with cardiorenal syndrome |
To highlight the sustained inflammatory response that is responsible for the functional deterioration of patients with CRS. Existing anti-inflammatory treatment methods have been disappointing to date necessitating new studies. |
| Virzì et al. [32] 2018 |
Review |
The role of dendritic and endothelial cells in CRS |
Heart and kidney Dendritic cells are involved in tissue remodeling. Additionally, endothelial cells act as antigen-presenting cells and act as a bridge between innate and adaptive immune systems. |
| Bonventre [45] 2003 |
Review |
Dedifferentiation and proliferation of surviving epithelial cells in acute renal failure. |
The renal epithelium can regenerate and replace dead tubular cells after ischemic-repercussion injury. |
| Laxmanan et al. [46] 2005 |
In vitro study |
CD40: a mediator of pro- and anti-inflammatory signals in renal tubular epithelial cells. |
CD40 serves a dual purpose, promoting inflammatory ROS and anti-inflammatory heme oxygenase-1. Finding the balance between these two effects has a therapeutic purpose in inflammatory renal disease. |
