Case Presentation: A 70-year-old male with past medical history of hypertension, history of cerebrovascular accident, hyperlipidemia, right carotid stenosis status post carotid endarterectomy, obesity, tobacco use, and chronic sinusitis presented with a 3-month history of intermittent facial discomfort, difficult nasal inhalation, productive cough, orthopnea, and an episode of gross painless hematuria 4 days prior to admission. Outpatient workup by his PCP was unrevealing.On presentation, he presented tachycardic with hypertensive emergency. Labs were significant for BUN 32 mg/dL, creatinine 4.42 mg/dL (baseline 1.3), WBC 13.7 thou/cmm, hemoglobin 11.7 g/dL, platelets 348 thou/cmm, and urinalysis with 5+ blood and 3+ protein. CT abdomen showed a 1.5 cm renal stone in the left kidney. Chest x-ray revealed right lower lobe infiltrate/atelectasis. He was admitted to medicine and treated with intravenous fluids and antibiotics.Nephrology was consulted for acute kidney injury in the setting of hematuria/proteinuria. Creatinine peaked at 6.09 mg/dL. Renal ultrasound and angiography showed no renal artery stenosis. Urine protein was 1.5 g. Serologies revealed elevated free kappa/lambda ratio with normal complements. Kidney biopsy was performed showing IgA nephropathy with acute tubular necrosis.He was treated with intravenous solumedrol 1000 mg daily for 3 days followed by oral prednisone 60 mg daily. With improvement in blood pressures, he was discharged on hospital day nine on prednisone with creatinine down to 4.98 mg/dL. Outpatient creatinine two months post-discharge remained elevated at 3.74 mg/dL.
Discussion: This case illustrates an atypical presentation of IgA nephropathy: AKI after an episode of hematuria. The patient’s AKI with rapid decline in kidney function is uncommon in IgA nephropathy. IgA nephropathy’s hallmark is mesangial IgA deposition, often presenting with asymptomatic hematuria and proteinuria. Patient’s extensive medical history, including a chronic sinusitis raised questions about contributing factors to IgA nephropathy. The diagnosis hinged on clinical features and a kidney biopsy justified by persistent proteinuria and elevated serum Cr. This case reinforces that IgA nephropathy should remain on the differential diagnosis for AKI even in older adults when associated with hematuria. Prompt diagnosis and treatment is key to improve renal outcomes in atypical cases.
Conclusions: The most prevalent form of primary glomerulonephritis is IgA nephropathy, which most commonly impacts males between the ages of 20 and 30 years old. It classically presents with episodes of gross hematuria associated with upper respiratory infections, along with asymptomatic microscopic hematuria and proteinuria between episodes. Definitive diagnosis requires a kidney biopsy. This case of IgA nephropathy is unique given the patient’s older age at presentation and the severity of the acute kidney injury (AKI), which is uncommon with IgA nephropathy. It highlights the importance of considering IgA nephropathy in the differential diagnosis of AKI even in older adults when associated with hematuria. Prompt diagnosis and treatment is essential to prevent progression to CKD in atypical cases.