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Kidney Week

Abstract: PO0135

A Case of Secondary IgA Nephropathy and Response to Steroids

Session Information

Category: Trainee Case Report

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Javed, Zain A., MacNeal Hospital, Berwyn, Illinois, United States
  • Shah, Arooj F., Shifa College of Medicine, Islamabad, Pakistan
Introduction

Secondary IgA nephropathy a lesser known variant of primary IgA, has been reported to occur after a bacterial illness. These have led to rapid progression towards kidney failure. Victims of the disease are likely to become dialysis dependent shortly after acquiring the disease process.

Case Description

Patient is an 87 year old male with past medical history of DMT2, CKD IIIb, Prostrate Ca, Bladder Ca and a recent admission for sepsis due to MSSA bacteremia, was admitted to an elevated Cr to 3. His symptoms comprised only of fatigue and confusion with no decrease in urine output. Admission labs showed BUN of 78 and Cr of 4.13 and >300 protein on UA. Urine studies showed FEUrea of 59.3% and 24 hour Urine protein of 5g. Renal U/S and CT abdomen and pelvis did not reveal any obstructive process.
Patient was placed on IV fluids while a GN workup was in progress followed by a biopsy and was discharged to be followed up on outpatient. Biopsy demonstrated IgA nephropathy with diffuse proliferative glomerulonephritis with acute tubular injury without crescenteric involvement. There was also evidence of mild chronic tubulointerstial injury and global glomerulosclerosis. His Cr had up trended to 7.4 and BUN 146 without any signs of azothemia. Decision was made to start 500mg methylprednisone once daily for 3 days followed by 0.5mg/kg of oral steroids on discharge and 1 month follow up.
1 month later, Cr was found to have down trended to 5 with no electrolytes disturbances with improvement activities of daily living with adequate urine output. Decision was made to continue oral steroids in an attempt to delay dialysis.

Discussion

Post infectious IgA nephropathy is rare but continues to be responsible for progression towards ESRD. The infections responsible include E Coli Sepsis and Osteomyelitis. Variable approaches have been made which revolve around the inflammatory infiltrates.
Immuno-suppressive therapies like cyclophosphamide and rituximab have been typically used for crescenteric glumerolonephritis but have shown limited response. Their use in secondary IGA nephropathy has been limited to transplant recipents.
Our case demonstrated one of the rare instances in which there was presence of active inflammatory infiltrate in absence of any crescent formation which guided our decision to initiate steroids. In this process, dialysis was delayed as the patient continued to have adequate renal function.