Concept Map: AKI in patients with Chronic Liver Disease

 

Concept map of AKI associated with chronic liver disease. Made using biorender.com 
Inspired by an article in CJASN

Consult Rounds: Cholemic nephrosis or Bile cast nephrpathy or should we say Jaundice associated nephropathy

Bile cast nephropathy or also called cholemic nephrosis represents a spectrum of renal injury from proximal tubulopathy to intrarenal bile cast formation found in patients with severe liver dysfunction. Bile can be toxic directly to the tubule or can form casts and have similar damage as myeloma cast nephropathy.

Recently this entity has gained some interest in the literature.

1.      Classically seen with patients with acute or chronic liver disease

2.      Usually, the total bilirubins are over 20 and conjugated over 16 is the cases that had bilirubin casts on kidney biopsies

3.      The LFTS were also higher in these patients

4.      The cause of liver disease doesn’t matter

The mechanisms responsible for tubular dysfunction include uncoupling of mitochondrial phosphorylation (thereby decreasing ATPase activity) by bilirubin  and oxidative damage of tubular cell membranes as well as inhibition of Na-H and Na-K pumps in the tubular cell membranes by bile acids. Cholemic nephrosis is reversible provided bilirubin levels are reduced early. This recovery is however delayed if there is extensive bile cast formation.

Some have suggested jaundice-related nephropathy as a replacement for cholemic nephrosis. Based on their definition, jaundice-related nephropathy would encompass the spectrum of injury that ranges from proximal tubulopathy to extensive tubular injury and tubular pigment. 

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.
The Hall's stain confirms bilirubin presence.

Other interesting articles on this topic

http://www.kidney-international.org/article/S0085-2538(15)56212-1/fulltext

http://onlinelibrary.wiley.com/doi/10.1111/hdi.12169/pdf

http://www.ajkd.org/article/S0272-6386(16)30488-7/abstract

https://www.karger.com/Article/Pdf/371689

Concept Map: AKI in Liver Failure

This concept map was created by Dr Daniel Ross based on the Kidney International Article

TOPIC DISCUSSION: Cirrhosis, Hyponatremia and the role of Vaptans?

CHF and SIADH has clear indications for use of vaptans. What is the data and evidence in cirrhosis associated hyponatremia?


1. No drug has been approved to treat hyponatremia of cirrhotics as of yet
2. Studies from Europe using lixivaptan and satavaptan have shown that short term effects of using them have had increased serum NA levels in cirrhotics and sustained for 1-2 weeks.
3. Unfortunately , only 27-54% had complete normalization of the Na
4. All studies showed increased urinary Na levels
5. Only one study has shown long term effects of captains in cirrhotics and that is using satavaptan. 
The main finding was that the improvement in serum Na obtained in first days of therapy was maintained for one year.
6. Thirst was the biggest side effect.
7. To avoid rapid correction, use of D5W after reaching a certain threshold and matching urine output cc by cc is recommended as risk of ODS is there but not been reported thus far.
8. Patients awaiting liver transplantation should get treatment for Hyponatremia as there have been situations were Na corrects rapidly as the transplant is replaced and subsequently causing neurological sequelae. 


Ref:
http://onlinelibrary.wiley.com/doi/10.1002/hep.22418/pdf
http://www.ncbi.nlm.nih.gov/pubmed/19797900
http://www.ncbi.nlm.nih.gov/pubmed/12671890

http://www.ncbi.nlm.nih.gov/pubmed/18508290