Case 1: A 54 M s/p liver transplant for HCV, coinfected with HIV. Patient has recurrent HCV, cirrhosis, decompensated with ascites, jaundice and variceal bleeding. His baseline creatinine was 0.9 mg/dL, and rose to 1.7 upon presentation with a gastric variceal bleed. Interestingly, his baseline serum sodium was 136, and was just 128 at the time of his rise in creatinine.
Knowing that this patient has end stage liver disease, with ascites and hyponatremia, there was concern for HRS-type 1. Sure enough, urinalysis had no RBC, no protein and the creat failed to normalize after a 2-day volume challenge. He was given vasoactive medications and albumin.
The differential diagnosis is worth noting. Part of his immunosuppression regimen included tacrolimus, a calcineurin inhibitor; its level was supertherapeutic at 24.9 (goal of 6). Tacrolimus is well known to be neurotoxic and nephrotoxic. Acutely it can cause a reversible, ischemic-type injury through vasoconstriction and inhibition of vasodilators of the afferent arterioles; its chronic use results in irreversible damage to renal tubules. Therefore, it is possible that this drug played a confounding role in the acute setting.
Lastly, we learned that when dealing with HCV and acute kidney injury, always bear in mind the associations between the virus and kidney: cryoglobulinemia, membranous glomerulonephritis and MPGN.
Case 2: A 50 M with HCV cirrhosis, DM-2, HTN, CKD. He presented with decompensation – ascites/worse renal function, and encephalopathy. The question was raised: can a patient with previous renal disease have a diagnosis of HRS, considering the definition of HRS includes the documentation of healthy kidneys (bland urine sediment and normal retroperitoneal US)? The purpose of this diagnostic criteria for HRS is to prevent the clinician from concluding HRS if there is a better, alternative renal diagnosis. However, by no means does having hypertensive nephropathy, or diabetic nephropathy protect the patient from the extreme hemodynamic effects of afferent arteriolar vasoconstriction in end-stage liver disease. Therefore, a patient like this can still receive a diagnosis of HRS in the right clinical setting, when the other criteria are met.
With respect to the encephalopathy, the question arose: was it due to the uremia or the hepatic encephalopathy? After all, either of these can contribute to confusion and asterixis. His serum BUN was almost 100. Sometimes it is difficult to tell the two apart, and hemodialysis can theoretically improve either. In the future, you can aggressively treat the hepatic component with lactulose and rifaximin, and if the asterixis persists along with uremia, the underlying cause can be parsed.