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Diabetic nephropathy is the most common cause of proteinuria in patients with longstanding type 2 diabetes mellitus (T2DM). However, the assumption that all proteinuria in diabetics is due to diabetic kidney disease (DKD) may delay diagnosis and appropriate treatment of coexisting or alternative pathologies, such as membranous nephropathy (MN). Identifying non-diabetic kidney disease (NDKD) is essential, particularly in patients with atypical clinical or laboratory features.
A 58-year-old woman with a 25-year history of T2DM and a 10 year history of hypertension was referred for evaluation of nephrotic-range proteinuria. Her medications included biphasic human insulin 20 units in the morning and 12 units at night, empagliflozin 10mg daily, vildagliptin/metformin 50/500 once daily, telmisartan 40 mg once daily, and atorvastatin 80 mg at night . Glycemic control was sub-optimal (HbA1c 7.8%) and fundoscopy revealed no evidence of diabetic or hypertensive retinopathy.She reported intermittent joint pains without arthritis or constitutional symptoms.
On examination, she was hemodynamically stable with bilateral pedal edema. The rest of the physical exam was unremarkable with no rash, no lymphadenopathy, or signs of systemic disease.
Urinalysis showed increased proteinuria of 4+ and 2+ glucose and the renal function tests were normal. A fasting lipid profile revealed elevated total cholesterol of 8.6mmol/L and LDL cholesterol of 5.78mmol/L. Autoimmune evaluation showed weakly positive antinuclear antibody (ANA) titers of 1:100, negative anti-dsDNA, negative extractable nuclear antigen (ENA) profile and negative anti-cyclic citrullinated peptide (anti-CCP).
Anti-phospholipase A2 receptor (anti-PLA2R) antibody test was done which was positive. Renal ultrasound demonstrated normal sized kidneys. Given the heavy proteinuria, preserved renal function, and absence of retinopathy, non-diabetic kidney disease was suspected, and a renal biopsy was performed. Histopathology confirmed diffuse membranous nephropathy with granular IgG and C3 deposits along the glomerular basement membrane. There was no evidence of diabetic nephropathy, confirming primary membranous nephropathy. The patient was initiated on the modified Ponticelli regimen, consisting of oral corticosteroids alternating with oral cyclophosphamide. After the first cycle of steroids, repeat urinalysis showed a reduction in proteinuria from 4+ to 2+, with stable renal function. The patient is tolerating the regimen well, with no adverse effects reported during initial treatment.
This case highlights the importance of having a high index of suspicion for non-diabetic kidney disease in diabetic patients presenting with atypical features. The absence of retinopathy, preserved renal function, rapid onset or disproportionate proteinuria should prompt further investigations for alternative etiologies. Membranous nephropathy can occur independently of diabetes and requires specific immunosuppressive treatment. Early detection using PLA2R serology and renal biopsy can significantly alter management and prognosis
Not all proteinuria in diabetic patient is due to diabetic kidney disease.This case highlights how the value of careful clinical assessment and comprehensive laboratory evaluation in identifying non-diabetic kidney disease and prompt therapy can lead to improved outcomes. A high index of suspicion, serologic workup, and renal biopsy helped uncover primary membranous nephropathy in a diabetic patient, allowing timely immunosuppressive therapy with promising early response. Clinicians should, therefore, maintain vigilance for atypical presentation in diabetic patients to ensure accurate diagnosis and individualized care.
