Today, we discussed the fascinating case of a middle-aged man with HCV cirrhosis and ILD who presented with acute worsening of his renal function. This was a fascinating case to think about the causes of HCV-related kidney injury!
Quick pearls from Chi (Nephrology attending) and Harry
- Chi’s pearl (Ditty-related): When you’re trying to distinguish whether a patient’s renal failure is secondary to tumor lysis syndrome, a useful lab is the urine Uric acid/Creatinine ratio! If this ratio is not elevated, it is unlikely that the renal injury is secondary to uric acid precipitation.
- Harry’s pearl (Case-related): Can we have cryoglobulins in the absence of viremia? For the most part, no. There tends to be a correlation between direct inhibition of HCV replication and clinical improvement in cryoglobulinemic patients! – Check out this trial: Gragnani et al., Triple antiviral therapy in hepatitis C virus infection with or without mixed cryoglobulinemia: A prospective, controlled pilot study. Digestive and Liver Disease. 2014 Sept; 46(9):833-7.
HCV and Renal Disease
I. Pre-renal: Think in terms of volume response!
a. Dehydration (volume responsive): poor PO intake, sepsis, medication induced
b. Hepatorenal syndrome (volume unresponsive)
– Pathogenesis: arterial vasodilation in splanchnic circulation + fall in systemic vascular resistance à decline in renal perfusion à progressive decline in filtration rate.
– Diagnosis of exclusion after other apparent causes of renal disease are deemed unlikely
– Lack of improvement in renal function after volume expansion with IV albumin (1 g/kg of body weight per day up to 100 g/day)
– Treatment: multifold, including improving hepatic function (transplantation), midodrine/octreotide, TIPS (transjugular intrahepatic portosystemic shunt).
a. Glomerular Causes
– Membranoproliferative glomerulonephritis (MPGN)
– Mixed cryoglobulinemia syndrome: systemic vasculitis that typically present with nonspecific systemic symptoms, palpable purpura, arthralgias, fever, renal disease, and neuropathy
– Polyarteritis Nodosa: well described in patients with HBV but CAN occur in HCV in the absence of cryoglobulins
– FSGS (less common but can happen!)
– IgA nephropathy
b. Tubular Causes
– Acute tubular necrosis in the setting of preceding sepsis
– chronic tubulointerstitial nephritis can be secondary to glomerular and vascular processes.
c. Vascular causes
– Thrombotic microangiopathy syndrome in the setting of DIC or other systemic processes.
III. Post-renal: Don’t forget about common causes of obstruction, including kidney stones!