A quick rehash of cardiorenal syndrome Type 1 for IM docs

AttendingDocNJ

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Cardiorenal syndrome, a frustrating diagnostic entity

We have all been there as doctors, when a patient comes in with acute heart failure exacerbation and the Cr is noticeably elevated from the baseline. A nephrologist simply mutters, “This is all cardiorenal syndrome- carry on with diuresis.” A cardiologist nods in agreement and the only frustrating person in the group hurdle is you, who is left scratching your head. When you ask for more explanation, it usually begins “Well there are 5 different types” and then cardiologist immediately launches into bringing up the Frank-Starling curve, which is supposed to solve all the mysteries of the universe. Instead, you get more lost and just state, “Forget it, let’s just call it a cardiorenal syndrome and move on.”

So, what exactly is cardiorenal syndrome? Let’s call it a relationship between the heart and the kidneys in which one organ’s behavior causes acute and chronic changes in the other organ and vice versa, usually. Yes, very broad and vague definition. Stick with me here. Now, there are 5 types of cardiorenal syndromes as aforementioned and here they are:

Type 1-Acute heart failure exacerbation causes acute kidney injury (Heart→ Kidneys).

Type 2-Chronic heart failure causes progressive chronic kidney disease (Heart→ Kidneys).

Type 3-Sudden and worsening kidney function causes acute heart failure (Kidneys→ Heart).

Type 4-Primary chronic kidney disease causes cardiac issues in forms of heart failure, coronary heart disease, or arrhythmia. (Kidneys→ Heart).

Type 5-External systemic disorders (such as sepsis or diabetes) affect both the heart and the kidneys). (Systemic disorders→ Heart and Kidneys).

Allow me to confuse you further: Heart failure is common in elderly population and unfortunately, measurement of creatinine as a marker of the kidney function in that age group is not always accurate. Why? Because with age, you tend to lose muscle mass (unless you weightlift) and hence, decrease in creatinine production. So, the glomerular filtration rate in elderly people may be reduced but the serum creatinine may remain in normal range.

Now, let’s do a clinical scenario: A 60-year old male presents with acute congestive heart failure exacerbation and on basic metabolic panel, he is noted to have mild elevation in Cr of 1.5. You review your records and unfortunately, this is a new patient in your system so you have no previous Cr. One way to distinguish if this is chronic kidney disease or cardiorenal syndrome type 1 (Remember: Heart→ Kidneys and pre-renal etiology) is to order a UA and renal ultrasound.

A UA which shows proteinuria, or active urine sediment, and/or a renal ultrasound which shows small kidneys will give you hints that this is chronic kidney disease. In pure cardiorenal syndrome type 1, you should have a normal urinalysis. In acute heart failure exacerbation, strictly by textbook definition, you should have elevated BUN/Cr ratio as this is a prerenal cause. Fractional excretion of urine sodium should be less than 1% because given that heart failure is a pre-renal etiology, the body wants to retain sodium. HOWEVER, usually by the time you see the patient, ED has given Lasix 40mg IV and diuretic therapy (loop diuretic) causes sodium excretion. Hence, fractional excretion of sodium will be inaccurate and better measurement would be fractional excretion of urea.

Intermission: We do not and I repeat, do NOT need any lab markers to make diagnosis of heart failure as it is a clinical diagnosis. Also, if patient is volume overloaded especially with pulmonary edema, we have to give diuretic therapy in face of elevated Cr provided that patient is making urine. Otherwise, in advanced or end-stage chronic kidney disease, patient may need urgent hemodialysis in setting of oliguria or worse, anuria.

You may be wondering about what exactly is the pathophysiology of cardiorenal syndrome. Here’s an explanation that I am sure you have heard: that impaired forward flow of the heart causes reduced renal perfusion and thereby, causing reduced GFR manifesting as increased Cr. This is where the famous abovementioned Frank Starling Curve comes into play. However, studies have NOT corroborated the theory! Instead, increased renal venous pressure may be the main culprit here! Increased central venous pressure thereby causing increased renal venous pressure causes worsening renal function. You can see that it’s the lack of forward flow from the big bad right ventricle (right ventricular failure) which plays a larger role here than the left ventricle. When the right ventricle gets distended with fluid, it starts pushing on the left ventricle causing decrease in left ventricular cavity. This leads to decreased forward flow. Also, there is backflow of fluid into the superior vena cava and the venous system. So in the end, the goal of diuretic therapy is to reduce the right ventricular filling pressure→ decrease central venous pressure→ decrease renal venous pressure→ improve the GFR!

Source: UpToDate
 
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UnoMas

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Cardiorenal syndrome, a frustrating diagnostic entity

We have all been there as doctors, when a patient comes in with acute heart failure exacerbation and the Cr is noticeably elevated from the baseline. A nephrologist simply mutters, “This is all cardiorenal syndrome- carry on with diuresis.” A cardiologist nods in agreement and the only frustrating person in the group hurdle is you, who is left scratching your head. When you ask for more explanation, it usually begins “Well there are 5 different types” and then cardiologist immediately launches into bringing up the Frank-Starling curve, which is supposed to solve all the mysteries of the universe. Instead, you get more lost and just state, “Forget it, let’s just call it a cardiorenal syndrome and move on.”

So, what exactly is cardiorenal syndrome? Let’s call it a relationship between the heart and the kidneys in which one organ’s behavior causes acute and chronic changes in the other organ and vice versa, usually. Yes, very broad and vague definition. Stick with me here. Now, there are 5 types of cardiorenal syndromes as aforementioned and here they are:

Type 1-Acute heart failure exacerbation causes acute kidney injury (Heart→ Kidneys).

Type 2-Chronic heart failure causes progressive chronic kidney disease (Heart→ Kidneys).

Type 3-Sudden and worsening kidney function causes acute heart failure (Kidneys→ Heart).

Type 4-Primary chronic kidney disease causes cardiac issues in forms of heart failure, coronary heart disease, or arrhythmia. (Kidneys→ Heart).

Type 5-External systemic disorders (such as sepsis or diabetes) affect both the heart and the kidneys). (Systemic disorders→ Heart and Kidneys).

Allow me to confuse you further: Heart failure is common in elderly population and unfortunately, measurement of creatinine as a marker of the kidney function in that age group is not always accurate. Why? Because with age, you tend to lose muscle mass (unless you weightlift) and hence, decrease in creatinine production. So, the glomerular filtration rate in elderly people may be reduced but the serum creatinine may remain in normal range.

Now, let’s do a clinical scenario: A 60-year old male presents with acute congestive heart failure exacerbation and on basic metabolic panel, he is noted to have mild elevation in Cr of 1.5. You review your records and unfortunately, this is a new patient in your system so you have no previous Cr. One way to distinguish if this is chronic kidney disease or cardiorenal syndrome type 1 (Remember: Heart→ Kidneys and pre-renal etiology) is to order a UA and renal ultrasound.

A UA which shows proteinuria, or active urine sediment, and/or a renal ultrasound which shows small kidneys will give you hints that this is chronic kidney disease. In pure cardiorenal syndrome type 1, you should have a normal urinalysis. In acute heart failure exacerbation, strictly by textbook definition, you should have elevated BUN/Cr ratio as this is a prerenal cause. Fractional excretion of urine sodium should be less than 1% because given that heart failure is a pre-renal etiology, the body wants to retain sodium. HOWEVER, usually by the time you see the patient, ED has given Lasix 40mg IV and diuretic therapy (loop diuretic) causes sodium excretion. Hence, fractional excretion of sodium will be inaccurate and better measurement would be fractional excretion of urea.

Intermission: We do not and I repeat, do NOT need any lab markers to make diagnosis of heart failure as it is a clinical diagnosis. Also, if patient is volume overloaded especially with pulmonary edema, we have to give diuretic therapy in face of elevated Cr provided that patient is making urine. Otherwise, in advanced or end-stage chronic kidney disease, patient may need urgent hemodialysis in setting of oliguria or worse, anuria.

You may be wondering about what exactly is the pathophysiology of cardiorenal syndrome. Here’s an explanation that I am sure you have heard: that impaired forward flow of the heart causes reduced renal perfusion and thereby, causing reduced GFR manifesting as increased Cr. This is where the famous abovementioned Frank Starling Curve comes into play. However, studies have NOT corroborated the theory! Instead, increased renal venous pressure may be the main culprit here! Increased central venous pressure thereby causing increased renal venous pressure causes worsening renal function. You can see that it’s the lack of forward flow from the big bad right ventricle (right ventricular failure) which plays a larger role here than the left ventricle. When the right ventricle gets distended with fluid, it starts pushing on the left ventricle causing decrease in left ventricular cavity. This leads to decreased forward flow. Also, there is backflow of fluid into the superior vena cava and the venous system. So in the end, the goal of diuretic therapy is to reduce the right ventricular filling pressure→ decrease central venous pressure→ decrease renal venous pressure→ improve the GFR!

Source: UpToDate
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iaskdumbquestions

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This is great, thank you for taking the time to write it up.

Question, regarding Type I being pre-renal, it just seems conceptually weird to me. I'm sure you're right, but maybe you can clarify. If the problem is venous congestion then I suppose I could see that GFR is down from lack of forward flow due to high back pressure, but the treatment is complete opposite of what we'd typically do in pre-renal AKI no? Fluids vs Diuresis? Does this sit in a true pre-renal cause?

Thanks for the clarification.
 

NITRAS

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Pre-renal means just that. That the problem is before the intrinsic filtration system. NSAIDs also can give you both a pre renal (and renal ) injury due to constriction of afferent arterioles. If you clamp renal artery, you are going to get a pre-renal injury. Fluids don’t fix those.

Fluids are for hypovolemia. Diuretics are for hypervolemia. Labs can be helpful, but the volume status is ultimately a clinical judgement.
 
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iaskdumbquestions

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Pre-renal means just that. That the problem is before the intrinsic filtration system. NSAIDs also can give you both a pre renal (and renal ) injury due to constriction of afferent arterioles. If you clamp renal artery, you are going to get a pre-renal injury. Fluids don’t fix those.

Fluids are for hypovolemia. Diuretics are for hypervolemia. Labs can be helpful, but the volume status is ultimately a clinical judgement.
Thank you, this helps. I guess my thought process was that in a pre-renal acute kidney injury it's generally (though not always) a fluid issue. That's why I said fluids. But I see your point.
 

Chemist0157

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Thank you, this helps. I guess my thought process was that in a pre-renal acute kidney injury it's generally (though not always) a fluid issue. That's why I said fluids. But I see your point.

Prerenal is often volume depletion but certainly not always and also not always fluid related. In CRS, it is a fluid issue but hypervolemia instead of hypovolemia. Consider as an analogy with GFR being reduced during CRS, that echo parameters such as EF canoften be worse if checked during a HF exacerbation and can look better when volume status is optimized.
 
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