67 year old man presents with a 1-week history of anorexia, nausea, lassitude, and pedal edema. Past medical history reveals Longstanding hypertension, osteoarthritis. Medications: hydrochlorothiazide, amlodipine. ibuprofen. PE: BP 142/68mmHg, heart rate 72 bpm, Temp of 97.8OF. JVP 8 cm; normal cardiac and pulmonary examinations; and 2+ pitting edema. Urinalysis: SG 1.017, protein 4+, no blood, neg glucose. Urine sediment was bland. BUN 18 mg/dL; Cr 0.8 mg/dL; Sodium 137 mEq/L, Potassium4.4 mEq/L, Chloride 95 mEq/L, C02 21 mEq/L, Ca 9.2 mg/dL, Phos 3.6 mg/dL, UA 4.6 mg/dL; Alb 2.9 g/dL; HCT 38%. anti-dsDNA antibody level 0. Albumin to creatinie ratio 7.7. Renal ultrasound showed normal sized kidneys bilaterally without obstruction.
The glomeruli, on light microscopy, will most probably show:
A). Thickened loops with evidence of double contours
B). Swollen endothelial cells -- glomerular endotheliosis
C.) No changes
D.) Focal segmental sclerosis
E.) Mesangial proliferation
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The correct answer for GN Quiz of 10/1/11 is–D.) Membranous glomerulopathy
A 27-year-old man consults his family physician because of the recent onset of edema. He has no other relevant history and the physical examination is remarkable only for significant pitting edema in the lower extremities. His blood pressure is 135/80. The blood and urine tests reveal a BUN of 15 mg/dL, serum creatinine of 0.9 mg/dL. The serum albumin is 1.7 g/dL (normal = 3.5 to 5 g/dL), plasma glucose is 92 mg/dL. Urinalysis shows 4+ albumin and trace blood. The sediment shows oval fat bodies, occasional hyaline casts, rare red cells. The albumin to creatinine ratio is 10.8.
The most likely diagnosis is
–A.) Idiopathic focal segmental glomerulosclerosis
–B.) Diabetic nephropathy
–C.) Membranoproliferative glomerulonephritis
–D.) Membranous glomerulopathy
–E.) Minimal change disease
Membranous glomerulopathy (MGN)
This is epidemiologically the likeliest cause for primary nephrotic syndrome. 85% of MGN cases are classified as primary membranous glomerulopathy. A recent study from David Salant’s group at Boston University has identified antibodies to a 185-kD glycoprotein -- an M-type phospholipase A2 receptor in 70% (26 of 37) cases evaluated (1).
Morphologically, the key features of MGN are the presence of subepithelial immunoglobulin-containing deposits along the glomerular basement membrane (GBM). By light microscopy, the basement membrane is diffusely thickened. Using Jones stain the GBM appears to have a "spiked" or "holey" appearance. On electron microscopy, subepithelial deposits that nestle against the glomerular basement membrane cause of the thickening. The podocytes also lose their foot processes. As the disease progresses, the deposits will eventually be cleared, leaving cavities in the basement membrane. These cavities will later be filled with basement membrane-like material, and if the disease continues even further, the glomeruli will become sclerosed and finally hyalinized. Immunofluorescence microscopy shows typical granular deposition of immunoglobulins and complement along the basement membrane.
Tretament can be quite challenging and will be covered in another quiz.
References
References
1. Beck LH Jr, Bonegio RG, Lambeau G, Beck DM, Powell DW, Cummins TD, Klein JB, Salant DJ. M-type phospholipase A2 receptor as target antigen in idiopathicmembranous nephropathy. N Engl J Med. 2009 Jul 2;361(1):11-21. PubMed PMID:19571279; PubMed Central PMCID: PMC2762083.
