CRP-04: Difference between revisions - Pathology Education Instructional Resource

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'''CRP-04'''

==Clinical History==

The patient is a 31 year old male.

BUN 10, creatinine l, urinary protein 1.2 g/24 hr. BP Normal. Intermittent episodes of hematuria. Rule out IgA.

==Gross Description:==

Received in transport media are two cores measuring 12 mm and 6 mm in length and 0.5 nun in diameter. Three 1-mm pieces are taken for EM. A 6-mm piece is submitted for immunofluorescence, and the remainder is submitted for light microscopy.

==Pathology==

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==Microscopic Description:==

===Light Microscopy:===

The specimen consist of three thin fragments of renal cortex that contain twenty-nine glomeruli in the three levels. Nine of these are obsolete, but none show segmental sclerosis. All of the remaining glomeruli demonstrate moderate mesangial expansion and proliferation, and eight of the glomeruli also demonstrate segmental or diffuse endocapillary proliferation with closure of the capillary loops. The silver stain shows focal thickening and spike formation, but this is not widespread. There is no glomerular necrosis, and no crescents are identified. There is minimal interstitial fibrosis and there is only focal mild tubular atrophy, generally association with the obsolete glomeruli. There are no inflammatory infiltrates. The arterioles and small arteries are unremarkable.

===Immunofluorescence:===

There are two to three glomeruli in each section. There is diffuse granular capillary loop staining that is graded 2+ for IgM and IgA and 1+ for IgG, C3 and light chains. There is mesangial granular staining that is graded 2+ for IgM and IgA and l+ for C3 and light chains. There is no mesangial staining for IgG, and there is no mesangial or capillary loop staining for Clq. Tubular epithelium contains albumin droplets, but there is no staining of the tubular basement membranes or vessels.

===Electron Microscopy:===

Three thick sections containing a total of four glomeruli are available. These are similar to those described above and show diffuse mesangial expansion and proliferation, but there is no segmental endocapillary proliferation. Ultrastructural examination reveals occasional small mesangial and paramesangial electron dense deposits. The capillary basement membranes show minimal thickening, and only one definite subepithelial deposit is identified. No subendothelial deposits are noted. There is widespread effacement of the epithelial cell foot processes. Some of the capillary lumina are occluded with mononuclear inflammatory cells.

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Kidney, needle biopsy - lgA nephropathy.

These findings are most consistent with IgA nephropathy. Although lupus nephritis must also considered, the predominant IgA staining, the relatively weak IgG and C3 staining, and the absence of Clq staining are more consistent with IgA nephropathy. The glomerular injury in this biopsy is more severe than typically seen in idiopathic IgA nephropathy and raises the possibility of secondary IgA glomerulonephritis, such as Henoch-Schonlein purpura. However, there is no way to reliably distinguish primary IgA nephropathy from secondary IgA nephropathies based on histology alone.

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 '''CRP-04'''
 ==Clinical History==
+The patient is a 31 year old male.
+BUN 10, creatinine l, urinary protein 1.2 g/24 hr. BP Normal. Intermittent episodes of hematuria. Rule out IgA.
 ==Gross Description:==
+Received in transport media are two cores measuring 12 mm and 6 mm in length and 0.5 nun in diameter. Three 1-mm pieces are taken for EM. A 6-mm piece is submitted for immunofluorescence, and the remainder is submitted for light microscopy.
 ==Pathology==
@@ Line 16: / Line 20: @@
 ==Microscopic Description:==
 ===Light Microscopy:===
+The specimen consist of three thin fragments of renal cortex that contain twenty-nine glomeruli in the three levels.  Nine of these are obsolete, but none show segmental sclerosis. All of the remaining glomeruli demonstrate moderate mesangial expansion and proliferation, and eight of the glomeruli also demonstrate segmental or diffuse endocapillary proliferation with closure of the capillary loops. The silver stain shows focal thickening and spike formation, but this is not widespread. There is no glomerular necrosis, and no crescents are identified. There is minimal interstitial fibrosis and there is only focal mild tubular atrophy, generally association with the obsolete glomeruli. There are no inflammatory infiltrates. The arterioles and small arteries are unremarkable.
 ===Immunofluorescence:===
+There are two to three glomeruli in each section. There is diffuse granular capillary loop staining that is graded 2+ for IgM and IgA and 1+ for IgG, C3 and light chains. There is mesangial granular staining that is graded 2+ for IgM and IgA and l+ for C3 and light chains. There is no mesangial staining for IgG, and there is no mesangial or capillary loop staining for Clq. Tubular epithelium contains albumin droplets, but there is no staining of the tubular basement membranes or vessels.
 ===Electron Microscopy:===
+Three thick sections containing a total of four glomeruli are available. These are similar to those described above and show diffuse mesangial expansion and proliferation, but there is no segmental endocapillary proliferation. Ultrastructural examination reveals occasional small mesangial and paramesangial electron dense deposits. The capillary basement membranes show minimal thickening, and only one definite subepithelial deposit is identified. No subendothelial deposits are noted. There is widespread effacement of the epithelial cell foot processes. Some of the capillary lumina are occluded with mononuclear inflammatory cells.
 </div></div>
 <spoiler text="Diagnosis and Comments">
+Kidney, needle biopsy - lgA nephropathy.
+These findings are most consistent with IgA nephropathy. Although lupus nephritis must also considered, the predominant IgA staining, the relatively weak IgG and C3 staining, and the absence of Clq staining are more consistent with IgA nephropathy. The glomerular injury in this biopsy is more severe than typically seen in idiopathic IgA nephropathy and raises the possibility of secondary IgA glomerulonephritis, such as Henoch-Schonlein purpura. However, there is no way to reliably distinguish primary IgA nephropathy from secondary IgA nephropathies based on histology alone.
 </spoiler>