How would you treat a patient with alcoholic cirrhosis and IgA nephropathy with high risk features including nephrotic range proteinuria, microscopic hematuria, and declining eGFR?

Cirrhosis is a well-known cause of secondary IgA nephropathy. Impaired removal of IgA-containing complexes by the Kupffer cells in the liver is thought to predispose to IgA deposition in the kidney (Amore et al., PMID 8302021). As in primary IgAN, polymeric IgA1 appears to be the dominant IgA isoform deposited. Therefore, the pathogenesis of the kidney injury, if not the source of immune complexes, appears to be similar in cirrhosis-associated IgAN and primary IgAN, and thus theoretically treatm...

This was a generic question, and as I do not know the patient, I can only provide a generic answer. Do you think this is secondary IgAN from cirrhosis?

How are patient's blood pressures? Can we optimize the patient on a RAAS blocker or sparsentan? Can SGLT2 inhibitors be added? With the history of alcohol cirrhosis, has he quit drinking? Do you think he is a reliable patient? Do you think he will be able to handle immunosuppression?

If yes, we could do a targeted release of budesonide or prefera...