Case Presentation:
A 49-year-old female was admitted to our hospital on May 9, 2023, chiefly complaining of bilateral lower limb edema that had persisted for six months. The edema was symmetrical, pitting, and had developed without an identifiable cause.
Approximately six months prior to admission, the patient sought evaluation at a local hospital following the onset of edema. Urinalysis at that time revealed significant abnormalities: Protein 3+, Occult Blood 2+, with a urine microalbumin level of 2014 mg/L. Laboratory studies also showed mild anemia, with a hemoglobin level of 92 g/L. Five days before admission, she was diagnosed with hypertension, with a peak blood pressure recording of 157/107 mmHg. Antihypertensive therapy with Allisartan Isoproxil was subsequently initiated. The patient was transferred to our institution for a definitive renal biopsy. Throughout the course of her illness, she reported no significant changes in diet, sleep patterns, bowel habits, or urinary function, and denied any other associated systemic symptoms.
Her past medical history was non-contributory. Personal, gynecological, and family histories were unremarkable.
Physical examination upon admission recorded the following vital signs: temperature 36.3°C, pulse 94 beats per minute, respiratory rate 18 breaths per minute, and blood pressure 130/92 mmHg. Cardiopulmonary and abdominal examinations were within normal limits; shifting dullness was negative. Bilateral pitting edema of the lower extremities was confirmed.
Admission Laboratory Investigations:
Urinalysis consistently showed Protein 3+ and Occult Blood 3+. The 24-hour urinary protein quantification was 3.04 g/day. Serum immunoglobulin A (IgA) was mildly elevated at 4.02 g/L, and the patient was hypoalbuminemic with an albumin level of 32.7 g/L. Renal function, however, remained within the normal range (serum creatinine 53 μmol/L, estimated glomerular filtration rate [eGFR] 107 mL/min/1.73m²). No other significant abnormalities were detected in the initial laboratory workup.
Renal Biopsy Findings:
A renal biopsy was performed for definitive diagnosis.
Immunofluorescence microscopy:
revealed strong (3+) mesangial staining for IgA, mild (1+) staining for IgM, moderate (2+) staining for C3, and was negative for IgG.
Light microscopy:
Examination of 19 glomeruli revealed global sclerosis in 2. The remaining glomeruli showed mild mesangial hypercellularity and matrix expansion without significant endocapillary hypercellularity; capillary lumens were patent. Fuchsinophilic deposits were observed in the mesangial areas. Five small cellular fibrotic crescents and adhesions between the glomerular tuft and Bowman's capsule were noted in individual glomeruli. Tubulointerstitial changes included vacuolar and granular degeneration of tubular epithelial cells, accompanied by occasional protein casts. Additional findings included mild tubular dilation, focal brush border loss, and focal tubular atrophy (affecting approximately 10% of the cortical area). The interstitium exhibited patchy areas of inflammatory cell infiltration accompanied by fibrosis. There was mild thickening of the walls of small arteries.
Diagnosis:
The histological features were consistent with a diagnosis of Focal Proliferative Sclerosing IgA Nephropathy, classified as Lee Grade IV and Oxford Classification M1E0S1T0C2.
Treatment and Clinical Course:
The initial treatment regimen consisted of intravenous methylprednisolone (240 mg/day for 3 consecutive days), followed by oral prednisone (40 mg/day), and mycophenolate mofetil (0.5 g twice daily). Adjunctive therapies included sodium restriction and allisartan isoproxil (240 mg once daily) for blood pressure control. The mycophenolate mofetil was gradually tapered and discontinued after six months.
