Cardiorenal syndrome: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
====Cardiorenal Syndrome Type 1==== | ====Cardiorenal Syndrome Type 1==== | ||
*Acute | *[[Acute heart failure]] leading to [[acute kidney injury]] | ||
*Decreased | *Decreased [[cardiac output]], increased venous pressure, kidney congestion, hyperkalemia <ref name="ronco"></ref> possibly preventing the use of ACE-I, ARB, and Spironolactone. | ||
====Cardiorenal Syndrome Type 2==== | ====Cardiorenal Syndrome Type 2==== | ||
*Chronic | *Chronic heart dysfunction causing chronic kidney disease | ||
*Erythropoetin deficiency and anemia | *[[Erythropoetin]] deficiency and anemia | ||
*Neurohormonal abnormalities with over production of vasoconstrictors | *Electrolyte imbalances<ref>Jie, J., Verhaar, M., Cramer, M., & et al. (2006). Erythropoietin and the cardiorenal syndrome: Cellular mechanisms on the cardiorenal connectors. American Journal of Physiology - Renal Physiology, 291:F932-F944.</ref><ref>Fu, P., & Arcasoy, M. (2007). Erythropoietin protects cardiac myocytes against anthracycline-induced apoptosis. Biochemical and Biophysical Research Communications, 354:372-378.</ref> | ||
*Altered sensitivity to endogenous vasodilators <ref name="ronco"></ref>. | *Neurohormonal abnormalities with over production of vasoconstrictors | ||
*Altered sensitivity to endogenous vasodilators.<ref name="ronco"></ref>. | |||
====Cardiorenal Syndrome Type 3==== | ====Cardiorenal Syndrome Type 3==== | ||
*Acute | *[[Acute kidney injury]] leading to acute cardiac dysfunction, typically due to bilateral [[renal artery stenosis]]<ref name="ronco"></ref> | ||
*Fluid overload, neurohormonal activation, pericarditis, acidemia, hyperkalemia<ref>Blake, P., Hasegawa, Y., Khosla, M., Fouad-Tarazi, F., Sakura, N., & Paganini, E. (1996). Isolation of “myocardial depressant factor(s)” from the ultrafiltrate of heart failure patients with acute renal failure. ASAIO Journal, 42:M911-M915.</ref><ref name="ronco"></ref><ref>Meyer, T., & Hostetter, T. (2007). Uremia. The New England Journal of Medicine, 257:1316-1325.</ref> | *Fluid overload, neurohormonal activation, pericarditis, acidemia, hyperkalemia.<ref>Blake, P., Hasegawa, Y., Khosla, M., Fouad-Tarazi, F., Sakura, N., & Paganini, E. (1996). Isolation of “myocardial depressant factor(s)” from the ultrafiltrate of heart failure patients with acute renal failure. ASAIO Journal, 42:M911-M915.</ref><ref name="ronco"></ref><ref>Meyer, T., & Hostetter, T. (2007). Uremia. The New England Journal of Medicine, 257:1316-1325.</ref> | ||
====Cardiorenal Syndrome Type 4==== | ====Cardiorenal Syndrome Type 4==== | ||
*Primary chronic kidney disease leading to gradual decreased cardiac function | *Primary [[chronic kidney disease]] leading to gradual decreased cardiac function | ||
*Electrolyte imbalances with | *Electrolyte imbalances with chronic kidney disease | ||
*Fluid overload. | |||
====Cardiorenal Syndrome Type 5==== | ====Cardiorenal Syndrome Type 5==== | ||
*Combined cardiac and renal dysfunction due to acute or chronic systemic disorders (Sepsis, diabetes, amyloidosis, | *Combined cardiac and renal dysfunction due to acute or chronic systemic disorders ([[Sepsis]], [[diabetes]], [[amyloidosis]], [[lupus]], [[sarcoidosis]]) | ||
*Primary trigger causes simultaneous or sequential damage to both organs | *Primary trigger causes simultaneous or sequential damage to both organs | ||
*Injury to heart and kidneys cause of vicious cycle of further injury to each other <ref name="ronco"></ref> | *Injury to [[heart]] and [[kidneys]] cause of vicious cycle of further injury to each other. <ref name="ronco"></ref> | ||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 02:59, 26 November 2012
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate-Editor(s)-in-Chief: Yazan Dabboul; Rim Halaby
Overview
Cardiorenal Syndrome (CRS) comprises a group of disease states that involve simultaneous kidney and heart failure or disorder. Because the kidney and the heart lead a “symbiotic” bi-directional relationship; the vitality of one organ ultimately and inevitably depends on the vitality of the other [1]. Cardiorenal syndromes have recently earned major clinical significance because of their complex management challenges and their profound prognostic indication of mortality in patients suffering from concomitant heart and kidney diseases [2]. The term “cardiorenal syndromes” has only been recently clearly defined in the literature; where prior use of the term had witnessed several misconceptions and wrongful utilization in the past. Cardiorenal syndromes are a unique disease entity of complex and poorly understood pathophysiology, etiology, and management. Perhaps the greatest challenge a clinician faces with cardiorenal syndromes is the therapeutic approach and pharmacological intervention required in favor of a CRS patient with known poor prognosis. Today’s management approaches, despite proven efficacy, remain notorious for their injurious effects on the target organs of CRS. Individualized treatment remains up till now an optimal modality of approach pending the understanding of CRS, pathophysiology, and effective prevention.
Classification
Five subgroups have been identified and further approved by the Acute Dialysis Quality Initiative (ADQI) in 2010 on the basis of the following:
- Pathophysiology
- Acute vs. Chronic
- Concomitance of cardiac and renal dysfunction
For descriptive purposes, the five cardiorenal syndromes have also been named differently [1] as shown in the table below:
| Type | Name |
| Type 1 | Acute cardiorenal syndrome |
| Type 2 | Chronic cardiorenal syndrome |
| Type 3 | Acute renocardiac syndrome |
| Type 4 | Chronic renocardiac syndrome |
| Type 5 | Secondary cardiorenal syndrome |
Pathophysiology
Cardiorenal Syndrome Type 1
- Acute heart failure leading to acute kidney injury
- Decreased cardiac output, increased venous pressure, kidney congestion, hyperkalemia [3] possibly preventing the use of ACE-I, ARB, and Spironolactone.
Cardiorenal Syndrome Type 2
- Chronic heart dysfunction causing chronic kidney disease
- Erythropoetin deficiency and anemia
- Electrolyte imbalances[4][5]
- Neurohormonal abnormalities with over production of vasoconstrictors
- Altered sensitivity to endogenous vasodilators.[3].
Cardiorenal Syndrome Type 3
- Acute kidney injury leading to acute cardiac dysfunction, typically due to bilateral renal artery stenosis[3]
- Fluid overload, neurohormonal activation, pericarditis, acidemia, hyperkalemia.[6][3][7]
Cardiorenal Syndrome Type 4
- Primary chronic kidney disease leading to gradual decreased cardiac function
- Electrolyte imbalances with chronic kidney disease
- Fluid overload.
Cardiorenal Syndrome Type 5
- Combined cardiac and renal dysfunction due to acute or chronic systemic disorders (Sepsis, diabetes, amyloidosis, lupus, sarcoidosis)
- Primary trigger causes simultaneous or sequential damage to both organs
- Injury to heart and kidneys cause of vicious cycle of further injury to each other. [3]
Pathophysiology
Diagnosis
Treatment
References
{Reflist|2}
- ↑ 1.0 1.1 Ronco, C., Haapio, M., House, A., Anavekar, N., & Bellomo, R. (2008). Cardiorenal Syndrome. Journal of the American College of Cardiology, 52(19):1527-1539.
- ↑ Heywood, J. (2004). The cardiorenal syndrome: Lessons from the ADHERE database and treatment options. Heart Failure Review, 9:195–201
- ↑ 3.0 3.1 3.2 3.3 3.4
- ↑ Jie, J., Verhaar, M., Cramer, M., & et al. (2006). Erythropoietin and the cardiorenal syndrome: Cellular mechanisms on the cardiorenal connectors. American Journal of Physiology - Renal Physiology, 291:F932-F944.
- ↑ Fu, P., & Arcasoy, M. (2007). Erythropoietin protects cardiac myocytes against anthracycline-induced apoptosis. Biochemical and Biophysical Research Communications, 354:372-378.
- ↑ Blake, P., Hasegawa, Y., Khosla, M., Fouad-Tarazi, F., Sakura, N., & Paganini, E. (1996). Isolation of “myocardial depressant factor(s)” from the ultrafiltrate of heart failure patients with acute renal failure. ASAIO Journal, 42:M911-M915.
- ↑ Meyer, T., & Hostetter, T. (2007). Uremia. The New England Journal of Medicine, 257:1316-1325.