Cardiorenal Syndrome

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As cardiorenal syndrome (CRS) in medicine simultaneous disease of heart and kidney called, in the acute or chronic impairment of an organ leads to an impairment of other organ.

history

Like the hepatorenal syndrome , the cardiorenal syndrome is also counted among the extrarenal kidney syndromes according to Wilhelm Nonnenbruch . Irrespective of this, the term cardiorenal syndrome was originally only used for the condition in which the therapy of heart failure (heart failure ) is limited by an increasing deterioration in kidney function ( renal failure ). Due to its high practical relevance, this definition continues to be used frequently in everyday clinical practice. In 2008 the term KRS was expanded by the Acute Dialysis Quality Initiative (ADQI) so that it encompasses the entire spectrum of mutual influences between the two organs. To distinguish, the term cardiorenal syndrome (in the narrower sense) is used when a heart disease leads to damage to the kidneys, and the term renocardial syndrome when, conversely, a kidney disease damages the heart. This creates a perpetrator-victim constellation: Renocardial insufficiency - cardiorenal insufficiency. Also included is the condition in which an underlying systemic disease leads to simultaneous damage to the kidneys and heart.

Epidemiology

There are hardly any data on the epidemiology of the KRS. In patients with stable heart failure, chronic kidney failure is also present in 20-60% of cases . If there is an acute decompensation of the heart failure, simultaneous renal failure is much more common at almost 70%. Heart failure is the leading cause of death in patients with end-stage renal disease.

Classification

The current classification of the KRS was made by Ronco et al. proposed and accepted at an ADQI consensus conference in 2008. It distinguishes 5 types according to pathogenetic aspects and the time course.

Type Underlying disease Secondary illness example
Type 1 acute cardiorenal syndrome Acute heart failure Acute kidney failure Arrhythmia , acute coronary syndrome , cardiogenic shock , myocarditis
Type 2 Chronic Cardiorenal Syndrome Chronic heart failure Chronic renal failure Cardiomyopathy , valvular heart disease
Type 3 acute renocardial syndrome Acute kidney failure Acute heart disease (e.g. heart failure, acute coronary syndrome, cardiac arrhythmia, cardiogenic shock, pulmonary edema ) Contrast-induced kidney failure , interstitial nephritis , urinary obstruction
Type 4 Chronic Renocardial Syndrome Chronic renal failure Chronic heart failure (systolic or diastolic), acute heart failure, acute coronary syndrome Glomerulonephritis , cystic kidneys
Type 5 secondary cardiorenal syndrome Systemic disease Heart failure (acute or chronic), acute coronary syndrome, acute kidney failure, chronic kidney failure Sepsis , diabetes mellitus , lupus erythematosus , amyloidosis

A clear assignment is often not clinically possible. Chronic heart failure and kidney failure often occur together because they are largely based on the same risk factors. So type 5 is very common. If, for example, type 5 has an acute worsening of heart failure, type 1 can be present at the same time.

Pathophysiology

When KRS develops, there is a reciprocal influence between the heart and the kidneys in the sense that heart failure restricts the function of the kidneys, while kidney failure in turn impairs the function of the heart.

Cardiorenal influences (type 1 and 2)

Why heart failure worsens kidney function has not yet been conclusively clarified. According to the original explanation, the kidneys are poorly supplied with blood due to the reduced pumping function of the heart (forward failure), the resulting kidney failure is called prerenal kidney failure . However, no connection between the extent of renal insufficiency and the pumping function of the heart could be established in studies, so that this mechanism has meanwhile been given little importance. Rather, kidney failure occurs in particular in those patients in whom increased pressure was measured in the large veins opening into the heart. It is therefore assumed that the backflow of blood in front of the heart (backward failure) is of greater importance. The backflow of blood in front of the heart leads to an increase in pressure in the venous vessels and thus also to venous congestion of the kidneys. It is assumed that the pressure inside the Bowman capsule space increases and the pressure difference between glomerular capillaries and the capsule space decreases as a result. Because this difference is a driving force behind the production of primary urine , intrarenal kidney failure occurs. Another theory says that venous congestion leads to increased interstitial pressure in the kidney, which triggers an oxygen deficiency ( hypoxia ) in the tissue. As a result, the kidney cells can no longer work properly or even die.

Heart failure leads to the activation of the renin-angiotensin-aldosterone system (RAAS) at an early stage . The increased production of angiotensin II and aldosterone leads to excessive fluid reabsorption and thus to a further increase in venous pressure.

A rare cardiac cause of cardiorenal syndrome is heart transplantation in young children . The donated heart does not grow proportionally over the years . Heart failure occurs with reduced cardiac output and reduced renal perfusion . The glomerular filtration decreases; it comes to chronic kidney failure .

Renocardial influences (types 3 and 4)

Renal insufficiency leads to increased cardiac stress by increasing the preload and afterload , which means that the heart has to move more blood (increased preload) and has to exert greater pressure when it is ejected from the chambers (increased afterload). Activation of the sympathetic system leads to an increase in blood pressure and thus the afterload; activation of the RAAS increases the preload due to increased fluid reabsorption. The increased aldosterone concentrations caused by the RAAS activation furthermore directly favor fibrosis , hypertrophy (wall thickening) and dilation of the heart muscle (enlargement of the chamber diameter) and thus heart failure. Renal anemia ( anemia caused by kidney damage) typical of chronic kidney disease is also associated with hypertrophy and dilation of the left ventricle.

Whether kidney failure is a causal factor in the development of coronary heart disease (CHD) is debatable. A negative influence of uremia toxins (the body's own pollutants that accumulate in the blood in the event of renal insufficiency) on endothelial function as a risk factor for arteriosclerosis is discussed . Furthermore, disorders in the vitamin D / calcium-phosphate metabolism are associated with an increasing stiffness of blood vessels. Due to the many common risk factors of renal insufficiency and CAD, however, renal insufficiency is often interpreted as a sign of general vascular damage and not as an independent risk factor for CAD.

External influences (type 5)

A number of diseases lead to simultaneous damage to the heart and kidneys; Sepsis is the prototype . Patients with sepsis often develop impaired kidney function and signs of heart failure (e.g. elevated troponin levels). The causes are, on the one hand, microcirculation disorders in both organs and, on the other hand, toxic effects from significantly increased catecholamine concentrations. Other diseases that can damage both organs include diabetes mellitus, amyloidosis and lupus erythematosus.

clinic

The most common reason for hospital treatment for patients with CRS is acute fluid overload ( hydropic decompensation ). Classic symptoms are increasing edema of the extremities and shortness of breath due to pulmonary edema or pleural effusions . Furthermore, there may be abdominal pain during a Stauungsgastritis or congestive hepatopathy come.

Diagnosis

The diagnosis of KRS is based on the established diagnostic criteria for heart and kidney diseases. Heart failure is diagnosed using the criteria of the European Heart Association or the American Heart Association . An acute renal failure after the RIFLE criteria divided, chronic renal failure after the KDIGO / KDOQI criteria .

therapy

Therapy of cardiorenal syndrome (types 1 and 2)

Regulation of the fluid balance

To improve kidney function, it is crucial to optimally control the fluid balance. Especially in acute KRS (type 1) there is often an excess of fluid, which can be reduced by restricting the amount of water you drink and using diuretics ( water tablets ). Loop diuretics have the highest priority here . Since the absorption is reduced in the case of oral administration due to congestive gastritis that often occurs at the same time, this should preferably be done intravenously in the acute stage . A sequential nephron blockade (combination of a loop diuretic with a thiazide diuretic ) should be aimed for to improve the effectiveness . The kidney function and the electrolyte balance must be checked regularly by means of laboratory controls . Loop diuretics are only given in the case of end-stage renal insufficiency ( GFR <15 ml / min). A draining therapy with vasopressin antagonists ( vaptans ) is unusual and did not lead to any survival benefit .

Diuretic therapy treads a fine therapeutic line: If too much fluid is withdrawn, intravascular volume depletion and prerenal deterioration of renal insufficiency occur. If too little fluid is withdrawn, the increased renal-venous pressure leads to renal deterioration of the renal insufficiency and the pulmonary edema does not improve sufficiently .

If fluid intake is restricted and adequate diuretic therapy is not sufficient, it is referred to as diuretic resistance. Dialysis therapy can break the vicious circle of mutually reinforcing cardiac and renal insufficiency by withdrawing volume. In this way, the time can be bridged until the drug therapy of heart failure shows sufficient effect.

Heart failure medication

Guideline-compliant heart failure medication is carried out as basic therapy . Since patients with advanced renal insufficiency were often excluded from clinical studies on heart failure, the data for patients with CRS are weak. In addition to the administration of beta blockers , blocking the RAAS with ACE inhibitors or AT1 antagonists is recommended. In particular, patients with moderate renal insufficiency (GFR around 45 ml / min) seem to benefit from ACE inhibitor therapy (CONSENSUS study). Since ACE inhibitors can lead to an increase in serum creatinine, careful dosing is recommended in order to avoid a deterioration in kidney function. Also aldosterone antagonists are used, but must be used due to the Hyperkaliämiegefahr especially in severe renal insufficiency caution and low doses.

In the context of acute hydropic decompensation, in addition to the dehydrating therapy, fast-acting vasodilators (vasodilators) such as nitroglycerin are used, which help stabilize the heart function by reducing the preload and afterload on the heart.

Therapy of renocardial syndrome (types 3 and 4)

Because these types of cardiorenal syndrome were only recently defined, there are no established therapeutic strategies.
Since acute renocardial syndrome (type 3) often occurs after exposure to contrast medium after cardiac surgery, the prevention of contrast medium-
induced kidney failure is of particular importance. Because the volume overload caused by acute kidney failure plays a decisive role in the development of heart failure, this should be prevented or remedied.

In chronic renocardial syndrome (type 4), cardioprotective heart failure medication (ACE inhibitors, beta blockers, see above) is carried out in addition to the treatment of the underlying renal disease. It is discussed whether treatment of the frequently present renal anemia leads to an improvement in heart failure. However, there is evidence that increasing hemoglobin (Hb) levels to normal in renal anemia leads to increased adverse cardiovascular events. Therefore, in the case of chronic renal insufficiency, it is currently recommended to raise the Hb value to a maximum of 11.5 g / dl (below the normal range).

Therapy of secondary cardiorenal syndrome (type 5)

The therapy of the secondary CRS depends on the underlying disease.

Individual evidence

  1. a b c d e f g h i Claudio Ronco, P. McCullough u. a .: Cardio-renal syndromes: report from the consensus conference of the acute dialysis quality initiative. In: European heart journal. Volume 31, Number 6, March 2010, pp. 703-711, ISSN  1522-9645 . doi : 10.1093 / eurheartj / ehp507 . PMID 20037146 . PMC 2838681 (free full text).
  2. ^ Wilhelm Nonnenbruch : The bilateral kidney diseases - Brightii disease , Ferdinand Enke Verlag, Stuttgart 1949, pp. 170-192.
  3. ^ Frank Evans: Cardio-Renal Connections in Heart Failure and Cardiovascular Disease . NHLBI Working Group. Retrieved on August 28, 2014.  ( Page no longer available , search in web archivesInfo: The link was automatically marked as defective. Please check the link according to the instructions and then remove this notice.@1@ 2Template: Dead Link / nhlbi.nih.gov  
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  5. Horst Brass et al. (Ed.): Cardiovascular diseases and kidney , Dustri-Verlag, Munich-Deisenhofen 2001, ISBN 3-87185-320-8 , p. 44.
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  7. ^ Herbert Renz-Polster, Steffen Krautzig (ed.): Basic textbook internal medicine , 5th edition, Urban & Fischer , Munich 2013, ISBN 978-3-437-41114-4 , p. 843.
  8. ^ A b W. Mullens, Z. Abrahams, GS Francis, G. Sokos, DO Taylor, RC Starling, JB Young, WH Tang: Importance of venous congestion for worsening of renal function in advanced decompensated heart failure. In: Journal of the American College of Cardiology. Volume 53, Number 7, February 2009, pp. 589-596, ISSN  1558-3597 . doi : 10.1016 / j.jacc.2008.05.068 . PMID 19215833 . PMC 2856960 (free full text).
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