Kidney Week 2014: The Kidney-Liver Service

The first two talks of this session were by Robert Schrier on hepatorenal syndrome and by Anthony Chang on bile cast nephropathy

Dr. Schrier reviewed the patho-physiology of HRS and reminded us that it’s the renal vasoconstriction that is the end result of cirrhosis. The overfill hypothesis is the current thought (there is increased plasma volume) and increased ascites leading to the elevation in hormones that activate the RAAS.

Some key points:

1. Precipitating factors of HRS: SBP, paracentesis without albumin, GI bleed, alcoholic hepatitis, unknown

2. Hyponatremia is an early surrogate of HRS

3. Criteria for HRS diagnosis criteria (all criteria are required to diagnose HRS)

  • Low GFR, indicated by a serum creatinine level higher than 1.5 mg/dL or 24-hour creatinine clearance lower than 40 mL/min
  • Absence of shock, ongoing bacterial infection and fluid losses, and current treatment with nephrotoxic medications
  • No sustained improvement in renal function (decrease in serum creatinine to <1.5 mg/dL or increase in creatinine clearance to >40 mL/min) after diuretic withdrawal and expansion of plasma volume with 1.5 L of plasma expander
  • Proteinuria less than 500 mg/d and no ultrasonographic evidence of obstructive uropathy or intrinsic parenchymal disease

(these are subject to change based on an upcoming guidelines meeting that is going to be published soon)


Dr. Chang then discussed an entity that has been recently been described called bile cast nephropathy.

1. As bile passes via tubules, there is pigment nephropathy. Pathology findings include: extensive acute tubular injury with bile stained tubular casts. Macroscopic findings will include bile stained yellowish discoloration of the kidneys in jaundiced patients which become dark green after formalin fixation. Most of the damage is distal nephron related. The Hall’s stain confirms bilirubin presence. In one series from the speaker’s institution of liver dysfunction patients, 50% of jaundiced patients had intra renal bile casts and 12% of the autopsy cases had extensive involvement of both proximal and distal tubules. 85% of patients with hepatorenal syndrome had bile casts.  In the same series, bile casts were seen in 100% of patients with alcoholic cirrhosis. The injury is similar to cast nephropathy seen with myeloma.

2. The level at which they saw more of this entity was a bilirubin of around 26.

3. Many case reports have then been published regarding this entity as well.


Given the above findings, it might be very important to rule out this entity in our cirrhotic patients for two reasons: some might get misdiagnosed as HRS and get inappropriate treatment and secondly, if truly this is an intrinsic renal entity, perhaps these patients do better with a liver-kidney transplant than the liver alone.
I would suggest that the guideline makers of HRS include total bilirubin <20 or 25 be a criteria to diagnose someone with HRS as above 25, perhaps the risk of bile cast nephropathy exists and biopsy might be indicated to confirm.

Post by Dr. Kenar Jhaveri, eAJKD Editor.

Check out more of eAJKD’s coverage of Kidney Week 2014! Also, follow @eAJKD on Twitter for live updates!

3 Comments on Kidney Week 2014: The Kidney-Liver Service

  1. The criteria for HRS were changed in 2007 as below. The above criteria are the old ones.

  2. Thanks for the reference. Amazing to see that an ascites club exists. What do you think regarding including bilirubin in the light of bile cast nephropathy?

    • I think its a tough call because if you don’t treat a patient as HRS because of the bilirubin level cut off basically you are not doing anything except referring them for combined liver-kidney transplant . The use of vasopressors as part of the treatment of HRS may or not be beneficial but at least you are potentially preventing further hypotension induced renal ischemia. There are patients who have reversible liver failure and also those whose bilirubin is high due to a high delta fraction even though their synthetic function is improving otherwise – these patients may eventually not need a transplant and if the AKI is due to HRS or bile cast nephropathy may eventually be reversible ? Too many confounding variables to use just a bilirubin as a determinant of possible bile cast nephropathy – further how many MDs will feel comfortable requesting a kidney biopsy with a bilirubin of 30 (and the concurrent coagulopathy/thrombocytopenia/anemia).

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