Case Presentation: A 25-year-old Spanish-speaking man with a history of hypertension and post-streptococcal glomerulonephritis (PSGN) presented to the Emergency Department with abnormal kidney function tests. Two months earlier, his creatinine level was 2.68 mg/dL at an outside institution. He denied symptoms such as hematuria, dysuria, or edema. Physical examination revealed elevated blood pressure (172/92 mm Hg) and tachycardia (101 bpm), but he was otherwise asymptomatic. Laboratory evaluation showed significant worsening of renal function (creatinine 3.95 mg/dL, BUN 52 mg/dL), nephrotic-range proteinuria (3+), and hematuria (2+ blood, 20 RBCs/hpf). A renal ultrasound revealed normal-sized kidneys without hydronephrosis but findings consistent with underlying medical renal disease. Serologic workup, including autoimmune and infectious markers, was unremarkable. Nephrology consultation raised concerns for an active glomerular disease due to worsening renal function and nephrotic-range proteinuria. A kidney biopsy was performed, revealing IgA nephropathy with high chronicity and 90% interstitial fibrosis and tubular atrophy, consistent with advanced chronic kidney disease (CKD) and irreversible renal damage. The patient was started on prednisone 20 mg daily, which was later transitioned to budesonide. Additionally, an ACE inhibitor was initiated in the outpatient setting.
Discussion: This case underscores the importance of revisiting and critically evaluating prior diagnoses when faced with unexplained progression of renal dysfunction. The patient’s history of PSGN, diagnosed two years ago without a confirmatory biopsy, created an anchoring bias that likely delayed a more comprehensive exploration of his CKD etiology. While PSGN typically resolves in most patients, the progression of this patient’s renal dysfunction and the development of nephrotic-range proteinuria raised concerns for a different active glomerular disease. The decision to perform a kidney biopsy was pivotal, revealing advanced IgA nephropathy with significant interstitial fibrosis and tubular atrophy. IgA nephropathy can present with overlapping features, such as proteinuria and microscopic hematuria, that mimic PSGN. This case highlights the missed opportunity for earlier intervention, which might have altered the disease trajectory. It also emphasizes the importance of considering kidney biopsy in patients with worsening renal function and proteinuria, even when alternative diagnoses like PSGN are presumed. Achieving diagnostic clarity allows for more targeted management and improved outcomes, especially in young patients at risk of irreversible kidney damage.
Conclusions: This case highlights the diagnostic complexities in progressive CKD and the critical need to reevaluate prior conclusions. Anchoring on an earlier diagnosis of PSGN hindered the timely identification of the true etiology. In young patients with advancing CKD and inconclusive evaluations, clinicians must consider alternative or concurrent glomerular diseases and pursue biopsy when appropriate. Early and accurate diagnosis remains essential for mitigating CKD progression and improving patient outcomes.