Introduction:
IgA nephropathy (IgAN) is the most common form of glomerulonephritis worldwide and a leading cause of end-stage renal disease. When combined with chronic liver disease (CLD), it creates a complex clinical environment where both renal and hepatic dysfunction exacerbate one another. Despite the frequency of this coexistence, the interaction between these conditions and their influence on renal outcomes remains underexplored. This study investigates the clinical profile, renal outcomes, and the therapeutic efficacy of immunosuppressive therapy in patients with IgAN and CLD, aiming to fill this gap in clinical research.
Methods:
We conducted a prospective cohort study involving 50 patients with biopsy-proven IgAN and CLD, recruited from the nephrology and hepatology departments of a tertiary care hospital. Baseline data were collected, including demographics, renal function (serum creatinine, eGFR, UPCR), liver disease severity (MELD-Na, Child-Pugh score), and comorbidities. Immunosuppressive therapy with corticosteroids and mycophenolate sodium was administered to 76% of patients. Renal and hepatic parameters were monitored every three months over a nine-month period. Statistical analysis using the Friedman test and linear regression models was performed to evaluate correlations between liver and renal outcomes.
Results:
The patient cohort, predominantly male (94%), had a mean age of 49.9 years. Alcoholic liver disease (52%) and non-alcoholic steatohepatitis (42%) were the leading causes of CLD in this group. Comorbidities were observed in 56% of patients, with 52% requiring antihypertensive therapy. Notably, 52% were classified as Child-Pugh Class B, with a median MELD-Na score of 17. Nearly half (48%) exhibited a 90-day mortality risk of <2%. Histopathological analysis revealed crescentic glomerulonephritis in 34% of cases and moderate interstitial fibrosis and tubular atrophy (IFTA) in 58%. Immunosuppressive therapy resulted in marked improvement in renal function, evidenced by significant reductions in serum creatinine (p<0.001), eGFR (p<0.001), and UPCR (p<0.001) over nine months. Despite these improvements, regression analysis did not show a significant correlation between liver disease severity (MELD-Na, Child-Pugh scores) or IFTA with renal recovery, suggesting that renal outcomes may be modulated independently of hepatic dysfunction.
Conclusions:
This study highlights the significant renal impairment in patients with IgAN and CLD and the beneficial impact of immunosuppressive therapy in improving renal outcomes. Interestingly, liver disease severity did not predict renal recovery, suggesting that renal outcomes in this cohort may be driven by factors independent of liver disease progression. Early identification and intervention in IgAN patients with CLD are crucial for optimizing renal outcomes. Further research is needed to evaluate the long-term efficacy of immunosuppressive therapy and better understand the interplay between liver and renal dysfunction in this unique population.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.