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.
Highlights
Cholemic nephropathy (CN) is the clinical manifestation of hyperbilirubinemia that encompasses acute kidney injury (AKI) with characteristic histological changes in the distal segment of the nephron and intraluminal casts in jaundiced patients [1]
Since the pioneer studies of Hecher and Schroeder, it has been known that impairment of kidney function is a common event in the clinical course of cirrhosis, and it is associated with poor prognosis [2, 3]
AKI was attributed to hyperbilirubinemia based on the following rationale: (i) alternative diagnoses were actively ruled out; (ii) the onset of AKI coincided with the onset of severe hyperbilirubinemia; (iii) renal pathology showed large bile tubular casts and a marked tubular necrosis; and (iv) serum creatinine (sCr) dramatically decreased when bilirubin levels improved [25]
Summary
Cholemic nephropathy (CN) is the clinical manifestation of hyperbilirubinemia that encompasses acute kidney injury (AKI) with characteristic histological changes in the distal segment of the nephron and intraluminal casts in jaundiced patients [1]. It should be noted that the use of sCr in patients with cirrhosis is affected by decreased formation of creatinine from creatine in muscles secondary to muscle wasting, increased renal tubular secretion of creatinine, increased volume distribution that could dilute sCr, and interference of elevated serum bilirubin with assays of sCr [17, 18].
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