Cardiorenal syndrome (CRS) occurs when acute or chronic dysfunction of the heart or kidneys induces acute or chronic dysfunction of the other organ. CRS is classified into 5 types based on pathophysiology. Type 1 is acute CRS where cardiac dysfunction causes acute kidney injury. Type 2 is chronic CRS where chronic cardiac issues lead to chronic kidney disease. Type 3 is acute reno-cardiac syndrome where acute kidney problems induce cardiac dysfunction. Type 4 is chronic reno-cardiac syndrome due to primary chronic kidney disease damaging the heart over time. Type 5 is secondary CRS occurring due to an underlying condition affecting both organs. Management depends on the CRS type and involves treating the underlying causes, cardiac and renal
2. INTRODUCTION
➢ Cardiac and renal diseases are common and frequently
coexist to significantly increase mortality, morbidity, and
the complexityand cost of care.
➢Primary disorders of 1 of these 2 organs often result in
secondary dysfunction or injury to the other.
➢Such interactions represent the pathophysiological basis
for a clinical entity called cardiorenal syndrome (CRS) .
3. WHAT IS CRS ?
• CRS can be generally defined as a patho
physiologic disorder of the heart and kidneys
whereby acute or chronic dysfunction of one
organ may induce acute or chronic dysfunction of
the other. - European Heart Journal (2010)
4. CLASSIFICATION
World congress of nephrology classified cardiorenal
syndromes into 5 subtypes based on patho-
physiology:
• CRS type 1 : acute cardio-renal syndrome
• CRS type 2 : chronic cardio-renal syndrome
• CRS type 3 : acute reno-cardiac syndrome
• CRS type 4 : chronic reno-cardiac syndrome
• CRS type 5 : secondary cardio-renal syndrome
5. EPIDEMOLOGY
• Epidemiology and Outcomes in Combined Cardiorenal
Disease
• Prevalence of Renal Disease in Patients With HF
• In the Acute DecompensatedHeart Failure National
Registry (ADHERE) of 1,05,000 individuals admitted for
acute decompensatedHF, 30% had a history of renal
insufficiency, 21% had serum creatinine concentrations
>2.0 mg/dL, and 9% had creatinine concentrations >3.0
mg/dL.
6. IMPACT OF RENAL DISEASE
ON HF PATIENTS !
• Impact of Renal Disease on Clinical Outcomesin Patients
With HF
• Renal dysfunction is one of the most important
independent risk factors for poor outcomesand all-cause
mortality in patients with HF.
• Baseline glomerular filtration rate (GFR) appears to be a
stronger predictor of mortality in patients with HF than
left ventricular ejection fraction or NYHA functional class.
• Both elevated serum creatinine on admission and
worsening creatinine during hospitalization predict
prolonged hospitalization, rehospitalization, and death.
7. HF OUTCOMES !
Patients with chronic renal insufficiency
are at strikingly higher risk for myocardial
infarction, HF with systolic dysfunction,
HF with preserved left ventricular
ejection fraction, and death resulting
from cardiac causes compared with
individuals with normal GFR.
8. MECHANISMS IN CRS !
1. RAAS
2. INCREASED SNA
3. REACTIVE OXYGEN SPECIES
4. INFLAMMATION
5. ENDOTHELIN EFFECT
6. ARGININEVASOPRESSIN EFFECTS
7. BNP EFFECTS
9.
10. CRS TYPE-1
➢CRS type 1 (acute CRS)--is characterized by a rapid
worsening of cardiac function, leading to acute kidney
injury (AKI).
➢Acute heart failure (HF) may be divided into 4 subtypes:
• Hypertensive pulmonary edema with preserved left
ventricular (LV) systolic function,
• Acutely decompensatedchronic HF,
• Cardiogenic shock, and
• Predominant right ventricular failure.
12. CRS TYPE-2
➢CRS type 2 (chronic CRS) is characterized by chronic
abnormalities in cardiac function (e.g., chronic
congestive HF) causing progressive CKD.
➢Worsening renal function in the context of HF is
associatedwith adverse outcomes and prolonged
hospitalizations.
➢The prevalence of renal dysfunction in chronic HF has
been reported to be approximately 25%.
➢Even slight decreases in estimated glomerular
filtration rate (GFR) significantlyincrease mortality
risk and are considered a marker of severity of
vascular disease.
13. MANAGEMENT (CRS-2)
1. Diuretics – volume expanded state
2. ACEI
3. ARBs block RAAS ---decrease LVH, proteinuria,
decrease progression of CKD .
4. Vasodilators may also be useful.
14. CRS TYPE-3
➢CRS type 3 (acute renocardiac syndrome)- is
characterized by an abrupt and primary worsening
of kidney function (e.g., AKI, ischemia, or
glomerulonephritis), leading to acute cardiac
dysfunction (e.g., HF, arrhythmia, ischemia).
➢ Type 3 CRS appears less common than type 1
CRS, but this may only be due to the fact that,
unlike type 1 CRS, it has not been systematically
studied.
16. CRS TYPE- 4
➢ CRS type 4 (chronic renocardiac syndrome)- is
characterized by a condition of primary CKD (e.g.,
chronic glomerular disease) contributing to
decreased cardiac function, ventricular
hypertrophy, diastolic dysfunction, and/or
increased risk of adverse cardiovascular events.
17. MANAGEMENT
(CRS-4)
1. Cessationof smoking, control of diabetes,
HTN.
2. Correction of anemia –iron supplements
and erythropoietin
3. Hb 11-12 gm % hct >36%
4. Loop diuretics ,ACEI, ARB s, Beta blockers
5. Calcium-phosphate ionic product to be
kept below 50 mg2/m2
6. Sevelamer .
7. Statins
8. Vitamin E
18. CRS TYPE- 5
➢CRS type 5 (secondary CRS)- is characterized by
the presence of combined cardiac and renal
dysfunction due to acute or chronic systemic
disorders.
➢Several acute and chronic diseases can affect
both organs simultaneously and that the disease
induced in one can affect the other and vice versa.
Examples include sepsis, diabetes, amyloidosis,
systemic lupus erythematosus, and sarcoidosis.
➢ Several chronic conditions such as diabetes and
hypertension may contribute to type 2 and 4 CRS.