A 70-year-old female with a past medical history of hypertension, type 2 diabetes, and hypothyroidism presented with a 2-month history of epigastric pain associated with abdominal distention, nausea, and generalized malaise. She also noted facial and bilateral leg swelling. Despite reporting decreased appetite, she had gained approximately 20 pounds in 1 month. She denied hematuria, fevers, night sweats, joint pain, vomiting, diarrhea, or changes in stool color or caliber. Admission vital signs were within normal range. Physical examination was remarkable for a mildly distended abdomen without evidence of ascites or peritoneal signs. Her lungs were clear and she had no jugular venous distention. There was 3+ pretibial pitting edema in her lower extremities bilaterally. Periorbital edema was also noted.Laboratory tests showed a normal electrolyte panel with a blood urea nitrogen of 2 mg/dL and creatinine of 0.7 mg/dL. Liver function tests were within normal limits. Serum albumin and protein were significantly depressed at 1.1 and 4.1 g/dL, respectively. Computed tomography of the abdomen was only remarkable for diverticulosis. Urinalysis showed 3+ protein, < 1 red blood cells, and no casts, and 24-hour urine protein was significantly elevated at 6426 mg/vol. Total cholesterol was elevated at 246 mg/dL, with an elevated triglyceride of 254 mg/dL. Hemoglobin A1c was 6.7%. Autoimmune workup was negative and systemic lupus erythematosus was excluded. Complement C3 was 126 mg/dL (normal 85-200 mg/dL) and complement C4 was 24 mg/dL (normal 17-46 mg/dL). Viral panel including acute hepatitis panel, HIV, cytomegalovirus, and herpes simplex virus was also negative. Immunoglobulin panel was checked and showed an immunoglobulin A level of 172 mg/dL (normal 85-350), immunoglobulin M (IgM) level of 99 mg/dL (normal 60-300), and immunoglobulin G level of 193 mg/dL (normal 696-1488). Doppler analysis of the renal vasculature was unremarkable. For work-up of her abdominal pain, esophagogastroduodenoscopy showed a normal esophagus and gastritis with prominent gastric folds. Gastric mucosa showed no evidence of inflammation or dysplasia but was remarkable for edema and congestion. Colonoscopy revealed diverticulosis without diagnostic mucosal alteration. Ultimately, biopsy of the left kidney was performed. Renal pathology was remarkable for mesangial proliferation and mild segmental sclerosis on light microscopy (Figure 1), diffuse IgM deposits in the mesangial area on immunofluorescence with areas of focal C1q, and diffuse C4d deposits in the mesangium (Figure 2). No light chain deposits were identified. Electron microscopy was remarkable for effacement of visceral epithelial cells (Figure 3).
C A S E R E P O R T
AbstractIgM nephropathy is a relatively rare cause of idiopathic nephrotic syndrome.
