Cholemic Nephropathy: Hyperbilirubinemia and its Impact on Renal Function

Abstract

Cholemic nephropathy represents a spectrum of renal injury, from proximal tubulopathy to intrarenal bile cast formation, found in patients with severe liver dysfunction. It is caused by hyperbilirubinemia, usually in jaundiced patients. Acute kidney injury is one of the most important complications in patients with end-stage liver disease. The relationship between liver disease and renal impairment, especially the effect of hyperbilirubinemia on renal tissue and renal function, has not been fully elucidated. These considerations deem necessary for nephrologists, when performing a clinical evaluation of patients with liver diseases, for the implementation of an integrated medical approach. This review focuses on the current knowledge on cholemic nephropathy with emphasis on the role of hyperbilirubinemia on renal impairment. The treatment strategies and outcome are also discussed.

A Donor With Green Kidneys—To Transplant or Not to Transplant: A Case Report

“…Renal dysfunction is a common complication of liver cirrhosis, which is of clinical relevance when considering this population as potential renal organ donors. 3 The clinical characteristics of the donor as well as the gross and microscopic findings of this case are consistent with previous reports addressing the potential consequences of CLD on renal function. [3][4][5][6] Both donor kidneys demonstrated IgAN likely secondary to cirrhosis and hepatic glomerulopathy, which has previously been associated with cirrhosis and hyperbilirubinemia.…”

“…3 The clinical characteristics of the donor as well as the gross and microscopic findings of this case are consistent with previous reports addressing the potential consequences of CLD on renal function. [3][4][5][6] Both donor kidneys demonstrated IgAN likely secondary to cirrhosis and hepatic glomerulopathy, which has previously been associated with cirrhosis and hyperbilirubinemia. [6][7][8][9] Oftentimes occult, IgAN associated with CLD is the most common cause of secondary glomerulonephritis in the developed world.…”

“…This is characterized by progressive renal insufficiency in the presence of elevated serum bile salts and hyperbilirubinemia. 3,4 The mechanisms responsible for tubular damage are thought to involve excess bilirubin that causes oxidative injury to cell membranes and uncoupling of mitochondrial phosphorylation. Bilirubin becomes saturated in the proximal tubule and causes cast formation, tubular obstruction, and tubular injury.…”

Novel Function for Bilirubin as a Metabolic Signaling Molecule: Implications for Kidney Diseases

“…Moderate increases in plasma bilirubin are protective to the kidney; however, higher levels can be detrimental in some conditions. For example, severely jaundiced patients with liver failure can exhibit cholemic nephropathy (97). Hyperbilirubinemia is also associated with postoperative AKI in patients undergoing cardiac surgeries (98).…”