#3523 effect of immunosuppressive treatments on renal outcomes after gross hematuria-related acute kidney injury in iga nephropathy

Abstract Background and Aims Macroscopic hematuria bouts are one of the most characteristic presentations of IgA nephropathy (IgAN). Acute kidney injury (AKI) is a well-known complication of these episodes of gross hematuria. Although the first descriptions of AKI associated with macroscopic hematuria (AKI-MH) reported a good prognosis in young patients, more recent studies have shown that a substantial number of adult and elderly patients with this variant type of IgAN did not completely recover their baseline kidney function after AKI-MH. Although guidelines recommend a conservative approach for AKI-MH, immunosuppressive therapy (IT) is frequently used in real world clinical practice. Aim of this study was to analyse the influence of different therapeutic strategies (immunosuppressive or conservative) on kidney function recovery after an episode of biopsy-proven AKI-MH in IgAN ≥patients 40 years. Method Retrospective study including 91 IgAN patients from 17 nephrology departments who presented with AKI-MH. Secondary types of IgAN and IgA vasculitis were excluded. All the patients had at least one measurement of serum creatinine (Scr) and eGFR before AKI-MH. Kidney function recovery after AKI-MH was defined by the ratio between Scr value at a given time after AKI-MH and the last determination of Scr before AKI-MH onset (baseline Scr). No recovery was defined by a Scr > 75% of baseline Scr or the need of kidney replacement therapy (KRT); partial recovery by a Scr <75% and >25% of baseline Scr; and complete recovery by a Scr <25% of baseline Scr. End stage kidney disease (ESKD) was defined by an eGFR <15 ml/min/1.73 m2 or KRT. Outcomes were the proportion of patients with complete, partial or no recovery of kidney function at 6 and 12 months after MH-AKI and kidney survival (defined as a status free of ESKD or death) at 1, 2 and 5 years and at the end of follow-up. Follow-up was 59±36 moths. Results Mean age was 65±16 years and 72 patients (79%) were men. Mean Scr and eGFR before AKI-MH were 1.2±0.47 mg/dl and 65±24.9 ml/min/1.73m2, respectively, and 37 patients (41%) had CKD (eGFR <60 ml/min/1.73m2) at baseline. Mean Scr and eGFR at presentation were 4.3±2.8 mg/dL and 19.3±13.4 ml/min/1.73m2, respectively. Thirty-two patients (35%) required acute dialysis at presentation. The most remarkable histological lesions were intratubular erythrocyte casts and tubular necrosis in all the patients. In addition, mesangial proliferation was found in 64%, endocapillary hypercellularity in 25%, segmental glomerulosclerosis in 41%, T1-T2 tubular atrophy/interstitial fibrosis in 33% and crescents in 4%. Sixty-nine patients (76%) were treated with renin-angiotensin blockers. IT was prescribed to 52 (57%) patients: corticosteroids alone in 32 (61%), corticosteroids plus mycophenolate in 12 (23%) and corticosteroids plus cyclophosphamide in 8 (15%). Treated patients were significantly older (69.4±9.9 vs 59.9±20.1; p = 0.01), required acute dialysis in a greater proportion (46% vs 20%; p = 0.01) and had more glomerulosclerosis (51% vs 28%; p = 0.02) than non-treated patients. No differences were found in other clinical or histological parameters. There were no significant differences between treated and not treated patients in the number of cases with complete, partial or no recovery of kidney function at 6 months (25%, 33% and 42% vs 26%, 20% and 54% respectively) and 12 months (28%, 30% and 40% vs 35%, 20% and 43% respectively). Kidney survival at 1, 3, 5 years was similar among treated (75%,63%, 52%, respectively) and not treated patients (76%, 68%, 50%, respectively). Adverse events occurred in 27% of IT patients: infections (7 patients), diabetes mellitus and cytopenia (2) and vertebral collapse (1). At the end of follow-up, 27 patients (30%) had developed ESKD, with no differences between treated and untreated, and 17 patients had died, 10 among treated patients and 7 among untreated cases. Conclusion Prognosis is very poor in IgAN patients > 40 years who present with AKI-MH. IT does not change this unfavorable prognosis, so new therapeutic alternatives are needed.