Cardiorenal syndrome

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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. 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

Cardiorenal Syndrome Type 2

  • Chronic heart dysfunction causing chronic kidney disease
  • Erythropoetin deficiency and anemia
  • Electrolyte imbalances[3][4]
  • Neurohormonal abnormalities with over production of vasoconstrictors
  • Altered sensitivity to endogenous vasodilators.[1].

Cardiorenal Syndrome Type 3

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. [1]

Diagnosis

Cardiorenal Syndrome Type 1

  • Blood and Urine Neutrophil gelatinase-associated lipocalin (NGAL) [7]
  • Cystatin C is a good early predictor of GFR[8][9]
  • Serum Creatinine elevates 48-72 h later[10]

Cardiorenal Syndrome Type 2

  • Serum creatinine to measure renal function
  • Classical makers of heart failure (eg. BNP) and measurement by ultrasound of systolic and diastolic ventricular dysfunction and ejection fraction [11]

Cardiorenal Syndrome Type 3

  • Cardiac troponins for ischemia[12] and BNP for heart failure[13]

Cardiorenal Syndrome Type 4

  • Classical diagnosis of CKD and HF[1]

Cardiorenal Syndrome Type 5

  • Diagnosis of primary disease

Treatment

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 Ronco, C., Haapio, M., House, A., Anavekar, N., & Bellomo, R. (2008). Cardiorenal Syndrome. Journal of the American College of Cardiology, 52(19):1527-1539.
  2. Heywood, J. (2004). The cardiorenal syndrome: Lessons from the ADHERE database and treatment options. Heart Failure Review, 9:195–201
  3. 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.
  4. Fu, P., & Arcasoy, M. (2007). Erythropoietin protects cardiac myocytes against anthracycline-induced apoptosis. Biochemical and Biophysical Research Communications, 354:372-378.
  5. 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.
  6. Meyer, T., & Hostetter, T. (2007). Uremia. The New England Journal of Medicine, 257:1316-1325.
  7. Mishra, J., Ma, Q., Prada, A., & et al. (2003). Identification of neutrophil gelatinase-associated lipocalin as a novel early urinary biomarker for ischemic renal injury. Journal of American Society of Nephrology, 14: 2534-2543.
  8. Dharnidharka, V., Kwon, C., & Stevens, G. (2002). Serum cystatin C is superior to serum creatinine as a marker of kidney function: a meta-analysis. American Journal of Kidney Diseases, 40:221-226.
  9. Vandevoorde, R., Katlman, T., Ma, Q., & et al. (2006). Serum NGAL and cystatin C as predictive biomarkers for acute kidney injury. Journal of American Society of Nephrology, 17:404A.
  10. Wagener, G., Jan, M., Kim, M., & et al. (2006). Association between increases in urinary neutrophil gelatinase-associated lipocalin and acute renal dysfunction after adult cardiac surgery. Anesthesiology, 105:485-491.
  11. Palazzuoli, A., Silverberg, D., Iovine, F., & et al. (2007). Effects of beta-erythropoietin treatment on left ventricular remodeling, systolic function, and B-type natriuretic peptide levels in patients with the cardiorenal anemia syndrome. American Heart Journal, 154:645e9-15.
  12. Cameron, S., Sokoll, L., Laterza, O., Shah, S., & Green, G. (2007). A multi-marker approach for the prediction of adverse events in patients with acute coronary syndromes. Clinica Chimica Acta, 376:168-173.
  13. Forfia, P., Lee, M., Tunin, R., Mahmud, M., Champion, H., & Kass, D. (2007). Acute phosphodiesterase 5 inhibition mimics hemodynamic effects of B-type natriuretic peptide and potentiates B-type natriuretic peptide effects in failing but not normal canine heart. Journal of American College of Cardiology, 49:1079-1088.