Does your sympathetic nervous system get activated when you notice acute kidney injury in patients with cirrhosis? Ever wonder how to really diagnose hepatorenal syndrome (HRS)? Think you have the bile-acid-stones to start diuretics on a patient requiring pressor support for kidney failure? You have come to the right place! Listen to @kidney_boy Joel Topf, HRS expert Juan Carlos Velez (@veleznephhepato), and self-proclaimed most-handsome-nephrologist Bill Whittier (@TWhittier_RUSH) tackle the complex pathophysiology and treatment of hepatorenal syndrome in this NephMadness 2019 special episode!
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Written and produced by: Justin Berk MD, Nora Taranto MS4
Infographic by: Alex M @nephroguy
Hosts: Matthew Watto MD
Edited by: Matthew Watto MD, Emi Okamoto MD
Guests: Joel Topf MD, Juan Carlos Velez MD, Bill Whittier MD
Low urine sodium can help suggest hepatorenal syndrome (HRS) as a contributing factor (but does not rule other causes).
Patients with cirrhosis and elevated bilirubin may have stained hyaline casts (discolored by bilirubin) that are misinterpreted as muddy brown granular casts see in ATN.
History and physical exam are crucial for determining volume status and guiding decisions for diuresis or volume resuscitation.
In decompensated cirrhosis, vasodilators increase splanchnic blood flow which activates the renin-angiotensin-aldosterone system (RAAS) causing renal arteriole constriction, decreasing kidney perfusion.
In patients with cirrhosis and acute kidney injury (AKI), colloid resuscitation is usually preferred (expert opinion).
While a 5:2 ratio of spironolactone:furosemide is dogma for refractory ascites, spironolactone can be dangerous when kidneys are failing.
Any small change in clinical status (peritonitis, UTI, encephalopathy, large volume paracentesis) may be a trigger for HRS.
Albumin increases the circulatory volume and may also mitigate the pathogenesis of hepatorenal syndrome by binding the vasodilator factors caused from cirrhosis! Who knew?
Vasoconstrictors address splanchnic vasodilation, increase mean arterial pressure and kidney perfusion, and “reset the signal” to decrease RAAS-mediated constriction of renal blood flow.
Hemodynamic insults (poor kidney perfusion) commonly lead to acute kidney injury (AKI).
Dr. Velez: “You cannot underestimate a good history and physical.”
Urinalysis can help distinguish between parenchymal kidney damage and decreased perfusion.
Urine eosinophils are not a high yield test in practice (BUT, they’re helpful on the boards to diagnose acute interstitial nephritis).
Urine sodium or fractional excretion of sodium can also help distinguish etiology.
Renal ultrasound can evaluate for post-renal obstruction. Though lower yield and unclear if cost-effective, our nephrologists all agree that it is low-risk, inexpensive, and they use it to rule out easily reversible causes of AKI. Post-void residuals using a bladder scanner, while useful to rule out obstruction in other patients, are often difficult to obtain in patients with cirrhosis. Dr Whittier notes foley catheter can be considered (diagnostic and therapeutic for obstruction).
“It’s a test with no risk to the patients and rare cause of AKI that is immediately fixable… Treatment of obstruction should not be dialysis.”
Joel Topf gives us his expert opinion on why it’s unacceptable to miss acute urinary obstruction as a cause of AKI.
Advanced cirrhosis can lead to circulatory dysfunction, specifically splanchnic vasodilation causing blood to pool in the mesenteric circulation and low effective circulatory volume. This leads to increased sympathetic and renin-angiotensin-aldosterone system (RAAS) activation in an attempt to increase systemic blood pressure. In decompensated cirrhosis, the RAAS activation is enough to constrict renal arterioles & decrease kidney perfusion. BUT, this activation cannot successfully increase mean arterial pressure (MAP).
Both activations of the renin angiotensin system lead to the release of vasoconstrictors (norepinephrine and angiotensin), which ultimately decreases blood flow to kidneys.
Volume status is very difficult to assess. Trial resuscitation or diuresis and monitor response.
Fluid resuscitation trials help determine if the cause of AKI is pre-renal. AKI should improve with euvolemia. Most patients with cirrhosis have ascites and peripheral edema. Lack of edema may suggest hypovolemia.
In patients with cirrhosis, colloid resuscitation is preferred over crystalloid.
Please recall that our chief of hepatology, Scott Matherly, recommends using crystalloids for fluid resuscitation in a cirrhotic patient with variceal hemorrhage and hypotension (in addition to blood products) or sepsis to maintain pressure –episode 142 Cirrhosis TIPS.
Often patients with cirrhosis have water and volume overload and can benefit from diuresis.
Furosemide is typical diuretic to help remove fluid. Dr. Topf expert dosing equation: 20 multiplied by the creatinine.
Kashlak Pearl: Decreased muscle mass and decreased creatinine production from liver disease cause relatively low creatinine and GFR is often overestimated. Therefore, a higher dose may be needed.
Spironolactone (an aldosterone antagonist) can be helpful to combat the effects of the RAAS activation.
LVP is indicated if lots of fluid needs to be removed. The goal is euvolemia.
Hepatorenal syndrome should be considered in patients with cirrhosis and ascites who present with an acute kidney injury not explained by other causes. It does not respond after a trial of volume expansion.
The International Club of Ascites has diagnostic criteria, which lack specificity for HRS.
Are bile acid casts pathologic or incidental in renal injury? Check out the NephMadness site for discussion!
Type 1: Acute kidney injury within 2 weeks. Almost all inpatient AKI from HRS is type 1.
Type 2: Subacute / insidious worsening of chronic kidney disease. These often present in clinic, not the hospital.
Albumin increases the circulatory volume and may mitigate the pathogenesis of hepatorenal syndrome by binding the vasodilator factors caused from cirrhosis.
Vasoconstrictors (e.g. octreotide, norepinephrine, midodrine) may address splanchnic vasodilation and “reset the signal” to therefore actually decrease RAAS-mediated constriction of renal blood flow.
Volume management should be continued (as discussed above).
Initiate treatment as soon as HRS is diagnosed.
The goal of treatment is to increase overall mean arterial pressure (MAP):
Initiating hemodialysis can be considered but is a difficult decision. The prognosis of HRS is often poor.
Listeners will develop a general understanding of hepatorenal syndrome and understand the diagnosis, pathophysiology, and treatment modalities for this condition.
After listening to this episode listeners will…
Dr. Velez, and Dr. Whittier report no relevant financial disclosures. Dr Topf lists the following disclosures on his website “I have an ownership stake in a few Davita run dialysis clinics and a vascular access center. Takeda Oncology made a donation to MM4MM the program that is taking me to Mount Everest in 2018”. The Curbsiders report no relevant financial disclosures.
The Curbsiders are partnering with VCU Health Continuing Education to offer FREE continuing education credits for physicians and other healthcare professionals. Visit curbsiders.vcuhealth.org and search for this episode to claim credit.
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