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IgA nephropathy (IgAN) is the most common glomerular disease worldwide. It usually affects young adults 16-35 yo, which account for approximately 80% of total patients. In up to 50% of IgAN patients, this disease progresses to the end-stage renal disease within 20 to 25 years, and the median age of patients starting renal replacement therapy is within 40-47 years. Despite of progressive course of IgAN, it`s treatment has become controversial, especially regarding immunosuppression. In this presentation, we describe our experience in the treatment of high-progressive IgAN.
The case of Mr.E.
Mr.E, 30 yo White IT-specialist, was referred for eGFR 46 ml/min/1.73 m2, proteinuria 1.8 g/day, UACR 1100 mg/g, macrohematuria, hyperuricemia 700 mqmol/l. First episode of hematuria was observed at the age of 16. Prior medical history did not include any significant condition. Body mass index was 24.9 kg/m2, he was a nonsmoker, and BP was 150/90 mm Hg. He did not take any BP-lowering medications. A kidney biopsy showed IgA nephropathy (MEST score M1, E1, S1, T1, C2). Olmesartan 20 mg was added, and the patient had prepared to participate in Zenith trial (with SLGT2i). The war has changed the treatment plan. After 3 month of supportive care with olmesartan (the patient could not participate in the study), despite of optimal BP control, IgAN has been progressed: eGFR downed on 22% (46 to 36 ml/min/1.73 m2), proteinuria raised to 2.8 g/day, UACR 2400 mg/g, Hb downed to 99 g/l, macrohematuria. Given the high progressive course of IgAN, a 6-month course of steroids was prescribed after discussion with the patient about possible treatment-emergent toxicity.
During the first month of methylprednisolone 48 mg/day, his kidney function improved, GFR raised to 49 ml/min/1.73 m2, proteinuria decreased to 1.6 g/day, UACR 686 mg/g, Hb stabilized on 115 g/l. Six month later, BP fell to levels below 120/80 mm Hg, eGFR was 49 ml/min, and proteinuria decreased to 0.32 g/d, UACR was 130.5 mg/g. Among adverse events were weight gain 6 kg, cosmetic skin defects (Cushingoid, stretch marks), recurrent upper RTIs. Any serious AE were not observed.
Catamnesis 6 month. Follow up visit showed moderate decline of kidney function, eGFR decreased to 40 ml/min/1.73 m2, proteinuria and UACR were 0.9 g/day and 454 mg/g respectively. Olmesartan maximized to 40 mg/day. In addition to olmesartan, SLGT2i dapagliflozin was added.
Catamnesis 12 month. Follow up visit showed stabilization of kidney function, eGFR is 40 ml/min/1.73 m2, proteinuria is 0.7 g/day, UACR 391.3 mg/g, Hb 123 g/l.
Changes in eGFR and proteinuria rates during the year are presented at figure 1 and 2 respectively.
Glucocorticoid therapy in the treatment of IgAN is controversial. Indeed, TESTING and STOP-IgAN trials have showed no difference between the supportive care and immunosuppression groups, in terms of annual decline in eGFR at 3 years, or the adapted primary endpoint of time to first occurrence of death, kidney failure, or decline in eGFR by 40% compared with baseline over a median follow-up of 7.4 years. Nevertheless, this clinical case shows that steroids may stabilize and even improve kidney function, especially in the condition of war-inducible extreme stress, because we could not predict what will be with his kidney function in rapid progressive IgAN under war-stress without steroids. Time will tell.