Case Presentation: A 36-year-old female with no prior medical history presented with progressive dyspnea, orthopnea, and bilateral lower extremity edema. On admission, she was severely hypertensive (BP 203/138 mmHg) and tachycardic (HR 103 bpm). Laboratory studies revealed hemoglobin 6.9 g/dL, serum creatinine 10.8 mg/dL (prior baseline 0.9 mg/dL), BUN 112 mg/dL, and urine protein-to-creatinine ratio of 6.1 g/g. Renal ultrasound showed normal-sized kidneys without obstruction. Initial echocardiogram demonstrated reduced ejection fraction (EF) of 25–30% and global hypokinesis. Serologic work-up for glomerulonephritis was negative. Renal biopsy revealed advanced IgA nephropathy (IgAN) with 60% interstitial fibrosis and tubular atrophy (IFTA), “onion skinning” and severe podocyte effacement. The patient was initially treated with high-dose corticosteroids but ultimately required maintenance hemodialysis, and a referral for renal transplant evaluation was submitted. After seven days of hemodialysis and blood pressure optimization, a repeat echocardiogram demonstrated improvement in the ejection fraction to 55–60%.
Discussion: IgAN is the most common form of glomerulonephritis worldwide. In our patient, the abrupt onset of nephrotic-range proteinuria, hematuria, and acute kidney injury reflects a mixed nephrotic–nephritic picture typical of advanced disease. Her biopsy findings (60% IFTA, “onion-skinning”, and severe podocyte effacement) explained both the heavy proteinuria and the rapid, irreversible decline in kidney function. These factors highlight how IgAN with extensive podocyte injury can mimic additional podocytopathies.Hypertension is common in IgAN, and this patient’s severe uncontrolled blood pressure likely accelerated her chronic glomerular damage and contributed to the dramatic elevation in creatinine at presentation. The combination of malignant hypertension, profound anemia, and uremia created significant physiological stress, predisposing her to acute cardiac dysfunction. Although Takotsubo cardiomyopathy (TCM) is classically associated with emotional stress, this patient’s reversible reduction in EF is consistent with stress-induced cardiomyopathy triggered by her hypertensive crisis and hemodynamic instability at presentation. Following the initiation of renal replacement therapy and effective blood pressure control, the physiological stressors resolved, and her EF rapidly recovered.
Conclusions: Severe, previously undiagnosed IgAN may present with catastrophic nephrotic-nephritic syndrome with advanced fibrosis, particularly when compounded by chronic uncontrolled hypertension. Hypertensive crises in this setting may trigger stress-induced cardiomyopathy such as TCM. Early diagnosis, aggressive blood pressure control, and coordinated multidisciplinary care are essential to prevent irreversible renal damage and optimize both cardiac and renal outcomes.