IPLab:Lab 6:Glomerulonephritis - Revision history

Peter Anderson: /* Autopsy Findings */

2020-07-08T23:40:43Z

Autopsy Findings

← Older revision		Revision as of 18:40, 8 July 2020
Line 3:		Line 3:

	On examination the kidneys were similar in appearance. Cortices were pale, diffusely granular with a few 1-2 mm cysts. On being sectioned, the cortex of each kidney was thin (4-5 mm) and pale. Renal medullae were pale yellow-tan in color and there was abundant peripelvic fat. The ureters, pelvis, calyces and hilar vessels showed no abnormalities.		On examination the kidneys were similar in appearance. Cortices were pale, diffusely granular with a few 1-2 mm cysts. On being sectioned, the cortex of each kidney was thin (4-5 mm) and pale. Renal medullae were pale yellow-tan in color and there was abundant peripelvic fat. The ureters, pelvis, calyces and hilar vessels showed no abnormalities.

	~~== Autopsy Findings ==~~
	The left (97 grams) and right (88 grams) kidneys were of similar appearance. Cortices were pale, diffusely granular with a few 1-2 mm cysts. On being sectioned, the cortex of each kidney was thin (4-5 mm) and pale. Renal medullae were pale yellow-tan in color and there was abundant peripelvic fat. The ureters, pelvis, calyces and hilar vessels showed no abnormalities.

	== Images ==		== Images ==

Peter Anderson: /* Clinical Summary */

2020-07-08T23:40:35Z

Clinical Summary

← Older revision		Revision as of 18:40, 8 July 2020
Line 1:		Line 1:
	== Clinical Summary ==		== Clinical Summary ==
	This 17-year-old ~~white~~ male had end-stage renal disease requiring hemodialysis for 10 years. For the previous four years he had hypertension which slowly increased to about 180/120 mm Hg. Laboratory findings included a ~~greatly~~ elevated BUN and creatinine. He ~~was admitted for~~ bilateral nephrectomy and ~~discharged in satisfactory condition~~ on the ~~10th postoperative day~~. He was ~~to be contacted~~ in ~~the future for transplantation~~.		This 27-year-old male had end-stage renal disease requiring hemodialysis for 10 years. For the previous four years he had hypertension which slowly increased to about 180/120 mm Hg. Laboratory findings included a markedly elevated BUN and creatinine. He underwent bilateral nephrectomy and was placed on the transplant list.

			On examination the kidneys were similar in appearance. Cortices were pale, diffusely granular with a few 1-2 mm cysts. On being sectioned, the cortex of each kidney was thin (4-5 mm) and pale. Renal medullae were pale yellow-tan in color and there was abundant peripelvic fat. The ureters, pelvis, calyces and hilar vessels showed no abnormalities.

	== Autopsy Findings ==		== Autopsy Findings ==

Seung Park at 16:19, 3 January 2014

2014-01-03T16:19:35Z

← Older revision		Revision as of 11:19, 3 January 2014
Line 18:		Line 18:
	File:IPLab6GN10.jpg\|For comparison this is an immunofluorescent photomicrograph of a glomerulus from a patient with Goodpasture's syndrome. The linear (arrows) immunofluorescence is characteristic of Goodpasture's syndrome.		File:IPLab6GN10.jpg\|For comparison this is an immunofluorescent photomicrograph of a glomerulus from a patient with Goodpasture's syndrome. The linear (arrows) immunofluorescence is characteristic of Goodpasture's syndrome.
	</gallery>		</gallery>

			== Virtual Microscopy ==
			<peir-vm>IPLab6GN</peir-vm>

	== Study Questions ==		== Study Questions ==

Seung Park: /* Images */

2013-08-30T01:36:05Z

Images

← Older revision		Revision as of 20:36, 29 August 2013
Line 37:		Line 37:

	=== Images ===		=== Images ===
	* [~~http://peir.path.uab.edu~~/library/index.php?/tags/226-glomerulonephritis PEIR Digital Library: Glomerulonephritis Images]		* [{{SERVER}}/library/index.php?/tags/226-glomerulonephritis PEIR Digital Library: Glomerulonephritis Images]
	* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html#8 WebPath: Glomerulonephritis]		* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html#8 WebPath: Glomerulonephritis]

Seung Park: /* Related IPLab Cases */

2013-08-23T00:48:15Z

Related IPLab Cases

← Older revision		Revision as of 19:48, 22 August 2013
Line 41:		Line 41:

	== Related IPLab Cases ==		== Related IPLab Cases ==
			* [[IPLab:Lab 1:Kidney Infarction\|Lab 1: Kidney: Infarction (Coagulative Necrosis)]]

	{{IPLab 6}}		{{IPLab 6}}

	[[Category: IPLab:Lab 6]]		[[Category: IPLab:Lab 6]]

Seung Park: /* Images */

2013-08-23T00:47:49Z

Images

← Older revision		Revision as of 19:47, 22 August 2013
Line 38:		Line 38:
	=== Images ===		=== Images ===
	* [http://peir.path.uab.edu/library/index.php?/tags/226-glomerulonephritis PEIR Digital Library: Glomerulonephritis Images]		* [http://peir.path.uab.edu/library/index.php?/tags/226-glomerulonephritis PEIR Digital Library: Glomerulonephritis Images]
			* [http://library.med.utah.edu/WebPath/RENAHTML/RENALIDX.html#8 WebPath: Glomerulonephritis]

	== Related IPLab Cases ==		== Related IPLab Cases ==

Seung Park: /* Images */

2013-08-23T00:47:15Z

Images

← Older revision		Revision as of 19:47, 22 August 2013
Line 37:		Line 37:

	=== Images ===		=== Images ===
			* [http://peir.path.uab.edu/library/index.php?/tags/226-glomerulonephritis PEIR Digital Library: Glomerulonephritis Images]

	== Related IPLab Cases ==		== Related IPLab Cases ==

Seung Park: /* Journal Articles */

2013-08-23T00:44:25Z

Journal Articles

← Older revision		Revision as of 19:44, 22 August 2013
Line 34:		Line 34:

	=== Journal Articles ===		=== Journal Articles ===
			* Lan HY, Yang N, Nikolic-Paterson DJ, Yu XQ, Mu W, Isbel NM, Metz CN, Bucala R, Atkins RC. [http://www.ncbi.nlm.nih.gov/pubmed/10652026 Expression of macrophage migration inhibitory factor in human glomerulonephritis]. ''Kidney Int'' 2000 Feb;57(2):499-509.

	=== Images ===		=== Images ===

Seung Park at 00:43, 23 August 2013

2013-08-23T00:43:31Z

@@ Line 23: / Line 23: @@
 * <spoiler text="What is the pathogenetic mechanism of poststreptococcal glomerulonephritis?">Patients have elevated antibody titers to streptococcal antigens, decreased complement levels, and accumulations of immune complexes and complement in the glomeruli suggesting immune complex mediated glomerular injury. Some streptococcal antigens (endostreptosin and several cationic antigens) have been demonstrated on the glomerular basement membrane. Thus, it is not known for sure if the glomerular damage is caused by circulating antigen antibody complexes, antibodies attacking streptococcal antigens that are attached to the basement membrane, or a combination of both processes. In any event, antibodies bind to antigens, activate complement, and cause damage to the glomeruli.
 </spoiler>
 {{IPLab 6}}
 [[Category: IPLab:Lab 6]]

Peter Anderson at 15:36, 21 August 2013

2013-08-21T15:36:52Z

← Older revision		Revision as of 10:36, 21 August 2013
Line 18:		Line 18:
	File:IPLab6GN10.jpg\|For comparison this is an immunofluorescent photomicrograph of a glomerulus from a patient with Goodpasture's syndrome. The linear (arrows) immunofluorescence is characteristic of Goodpasture's syndrome.		File:IPLab6GN10.jpg\|For comparison this is an immunofluorescent photomicrograph of a glomerulus from a patient with Goodpasture's syndrome. The linear (arrows) immunofluorescence is characteristic of Goodpasture's syndrome.
	</gallery>		</gallery>

			== Study Questions ==
			* <spoiler text="What is the usual clinical course of poststreptococcal glomerulonephritis?">One to two weeks after infection (usually sore throat or skin infection) by certain types of group A beta-hemolytic streptococci, patients develop malaise, fever, nausea, oliguria, and hematuria. Most patients recover with conservative treatment aimed at maintaining sodium and water balance. The renal injury usually resolves with no loss of function.</spoiler>
			* <spoiler text="What is the pathogenetic mechanism of poststreptococcal glomerulonephritis?">Patients have elevated antibody titers to streptococcal antigens, decreased complement levels, and accumulations of immune complexes and complement in the glomeruli suggesting immune complex mediated glomerular injury. Some streptococcal antigens (endostreptosin and several cationic antigens) have been demonstrated on the glomerular basement membrane. Thus, it is not known for sure if the glomerular damage is caused by circulating antigen antibody complexes, antibodies attacking streptococcal antigens that are attached to the basement membrane, or a combination of both processes. In any event, antibodies bind to antigens, activate complement, and cause damage to the glomeruli.
			</spoiler>

	{{IPLab 6}}		{{IPLab 6}}

	[[Category: IPLab:Lab 6]]		[[Category: IPLab:Lab 6]]