IPLab:Lab 5:Nodular Intercapillary Glomerulosclerosis: Difference between revisions

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== Clinical Summary ==
== Clinical Summary ==
This 57-year-old white male with a 25-year history of Type I diabetes mellitus (insulin-dependent ) developed an acute myocardial infarction followed by cerebral infarction, pulmonary dysfunction, and renal failure. There was a history of hypertension and proteinuria. Laboratory findings included a BUN and creatinine of 69 mg/dL and 3.3 mg/dL which subsequently rose to 113 and 4.8, respectively. He subsequently died of multisystem failure.
This 57-year-old white male with a 25-year history of Type 1 diabetes mellitus developed an acute myocardial infarction followed by cerebral infarction, pulmonary dysfunction, and renal failure. There was a history of hypertension,  proteinuria, and elevations in BUN and creatinine. He subsequently died of multisystem failure.


== Autopsy Findings ==
The autopsy showed concentric left ventricular hypertrophy, an acute myocardial infarction, and a right cerebral infarction. The pancreas showed amyloidosis of the islets. There was extensive atherosclerosis and arteriolosclerosis. The kidneys were large, weighing 220 and 240 grams respectively, and had a rough surface, a few cortical scars, and blurring of the corticomedullary junctions.
The autopsy showed the expected left ventricular hypertrophy, a large acute myocardial infarction, and a large right cerebral infarction. The pancreas showed amyloidosis of the islets. There was extensive atherosclerosis and arteriolosclerosis. The kidneys were slightly enlarged, weighing 220 and 240 grams respectively, and had rough surfaces, a few cortical scars, and blurring of the corticomedullary junctions.  


== Images ==
== Images ==
<gallery heights="250px" widths="250px">
<gallery heights="250px" widths="250px">
File:IPLab5DM1.jpg|This is a gross photograph of the kidneys from this case. Note that there are multiple shrunken regions (old infarcts) (arrows) and the kidneys have a rough granular appearance on the surface, which is caused by multiple small infarcts of small vessels throughout the cortex.  
File:IPLab5DM1.jpg|This is a gross photograph of the kidneys from this case. Note that there are multiple shrunken regions (old infarcts) (arrows) and the kidneys have a rough granular appearance on the surface, which is caused by multiple small infarcts of small vessels throughout the cortex.  
File:IPLab5DM2.jpg|This is a low-power photomicrograph of the kidney from this patient. The section extends from cortex (1) to the medulla (2).  
File:IPLab5DM2b.jpg|This is a low-power photomicrograph of the kidney from this patient. The section extends from cortex (1) to the medulla (2).  
File:IPLab5DM3.jpg|This is a higher-power photomicrograph of the cortical region. In this region there is ischemic obsolescence of glomeruli and one glomerulus with nodular glomerulosclerosis (1). Also note the thickened walls of the blood vessels (2).  
File:IPLab5DM3b.jpg|This is a higher-power photomicrograph of the cortical region. In this region there is ischemic obsolescence of glomeruli and one glomerulus with nodular glomerulosclerosis (1). Also note the thickened walls of the blood vessels (2).  
File:IPLab5DM4.jpg|This is a high-power photomicrograph of two glomeruli with intercapillary glomerulosclerosis (arrows).  
File:IPLab5DM4b.jpg|This is a high-power photomicrograph of two glomeruli with intercapillary glomerulosclerosis (arrows).  
File:IPLab5DM5.jpg|This is a photomicrograph of a glomerulus with nodular glomerulosclerosis (1). Also note the intertubular fibrosis and the changes in the blood vessels (2).  
File:IPLab5DM5b.jpg|This is a photomicrograph of a glomerulus with nodular glomerulosclerosis (1). Also note the intertubular fibrosis and the changes in the blood vessels (2).  
File:IPLab5DM6.jpg|This is a higher-power photomicrograph of a glomerulus with nodular glomerulosclerosis (arrows). These are the classic Kimmelstiel-Wilson lesions ("K-W lesions") seen in diabetics with nodular glomerulosclerosis.  
File:IPLab5DM6b.JPG|This is a higher-power photomicrograph of a glomerulus with nodular glomerulosclerosis (arrows). These are the classic Kimmelstiel-Wilson lesions ("K-W lesions") seen in diabetics with nodular glomerulosclerosis.  
File:IPLab5DM7.jpg|This is a photomicrograph of kidney with a focal exudative lesion in a glomerulus (arrow) and sclerosis, interstitial fibrosis, and congestion.  
File:IPLab5DM7b.jpg|This is a photomicrograph of kidney with a focal exudative lesion in a glomerulus (arrow) and sclerosis, interstitial fibrosis, and congestion.  
</gallery>
</gallery>


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=== Journal Articles ===
=== Journal Articles ===
* Herzenberg AM, Holden JK, Singh S, Magil AB.  [http://www.ncbi.nlm.nih.gov/pubmed/10469869 Idiopathic nodular glomerulosclerosis].  ''Am J Kidney Dis'' 1999 Sep;34(3):560-4.
* Herzenberg AM, Holden JK, Singh S, Magil AB.  [http://www.ncbi.nlm.nih.gov/pubmed/10469869 Idiopathic nodular glomerulosclerosis].  ''Am J Kidney Dis'' 1999 Sep;34(3):560-4.
* Vinik AI.  [http://www.nejm.org/doi/full/10.1056/NEJMcp1503948 Diabetic Sensory and Motor Neuropathy].  ''N Engl J Med" 2016 April 14; 374:1455-1464.
* Kamel KS and Halperin ML.  [http://www.nejm.org/doi/full/10.1056/NEJMra1207788 Acid–Base Problems in Diabetic Ketoacidosis].  ''N Engl J Med" 2015 Feb 5;372:546-554.


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

Latest revision as of 15:03, 8 July 2020

Clinical Summary

This 57-year-old white male with a 25-year history of Type 1 diabetes mellitus developed an acute myocardial infarction followed by cerebral infarction, pulmonary dysfunction, and renal failure. There was a history of hypertension, proteinuria, and elevations in BUN and creatinine. He subsequently died of multisystem failure.

The autopsy showed concentric left ventricular hypertrophy, an acute myocardial infarction, and a right cerebral infarction. The pancreas showed amyloidosis of the islets. There was extensive atherosclerosis and arteriolosclerosis. The kidneys were large, weighing 220 and 240 grams respectively, and had a rough surface, a few cortical scars, and blurring of the corticomedullary junctions.

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