Background

Diabetic kidney disease (DKD) is a complication of diabetes mellitus ultimately characterized by decreasing GFR and gradually increasing levels of proteinuria. In patients with T2DM and proteinuria studies have shown 53% of patients receive a pathologic diagnosis of non-diabetic renal disease when a biopsy is obtained. For this reason, it is important to consider kidney biopsy in diabetic patients with kidney injury and proteinuria whose presentation differs from typical DKD.

Case Presentation

A 77-year-old man with a past medical history including insulin-dependent type 2 diabetes mellitus, hypertension, and stage IV CKD presented with worsening left lower extremity weakness and pain. A history of diabetic retinopathy was notably absent. Additional testing showed an AKI with creatinine of 2.76 mg/dl (baseline of 2.11 mg/dl), hypoalbuminemia of 2.1 g/dl, protein of greater than 1000 mg/dl on urinalysis, and blood pressure of 192/104. A protein/creatinine ratio was elevated at 14.5, from 0.3 one year prior. A 24-hour urine protein was 11g, demonstrating nephrotic range proteinuria. A serologic workup for glomerulonephritis resulted normal C3 and C4, normal kappa/lambda ratio, negative ANA, ANCA, HBsAg, HBc IgM, HCV Ab, HIV, MPO and PR3 ANCA, PLA2R antibody and serum immunofixation demonstrating only hypoalbuminemia and hypogammaglobulinemia. HbA1c over the previous two years had been well controlled, between 5.3 and 6.8%. The patient’s creatinine remained stable at 2.8 mg/dl over the next week, and he was discharged on oral furosemide with plans for kidney biopsy. The presenting lower extremity symptoms were attributed to mild L5-S1 spinal stenosis and left tibial artery disease found on workup. Two weeks later the patient was readmitted with new onset shortness of breath, a 14kg weight gain and a creatinine of 3.99 mg/dl. Physical examination now showed 3+ bilateral lower extremity pitting edema and bibasilar crackles on lung auscultation. Aggressive diuresis was begun. Subsequent kidney biopsy showed C3 glomerulonephritis. The patient was discharged on an appropriate diuretic regimen with plans for outpatient management by nephrology.

Discussion

We present a case of rapidly progressive nephrotic range proteinuria in the setting of longstanding DKD which was secondary to biopsy proven C3 glomerulonephritis. This case underscores the importance of renal biopsy in patients with T2DM who develop renal disease in a pattern atypical of DKD, such as rapid onset nephrotic syndrome or severe kidney disease in the absence of diabetic retinopathy.