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Rim Halaby (talk | contribs) (Created page with "{{WBRQuestion |QuestionAuthor={{Rim}} |ExamType=USMLE Step 1 |MainCategory=Pathology |SubCategory=Renal |MainCategory=Pathology |SubCategory=Renal |MainCategory=Pathology |Sub...") |
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|MainCategory=Pathology | |MainCategory=Pathology | ||
|SubCategory=Renal | |SubCategory=Renal | ||
|Prompt=A 68 year old Caucasian male patient presents to his physician for his annual check-up. | |Prompt=A 68 year old Caucasian male patient presents to his physician for his annual check-up. The patient’s past medical history is significant for hypertension controlled on lisinopril and advanced diabetes mellitus type II poorly controlled on daily insulin injections. Routine work-up reveals elevated serum creatinine. A renal biopsy under light microscopy similar to the patient’s biopsy is shown in the image below. The following findings could be best explained by which of the following pathologic processes? | ||
[[File:Diabetic_nephropathy.png|300px]] | [[File:Diabetic_nephropathy.png|300px]] | ||
|Explanation=[[Diabetic nephropathy]] is a common microvascular complication in advanced [[diabetes mellitus]]. Renal biopsy under light microscopy would reveal characteristic eosinophilic nodules in the glomerular tuft called “Kimmelsteil-Wilson” lesion. Chronic hyperglycemia leads to accumulation of advanced glycosylation end products (AGEs) that trap extravasated [[immunoglobulin]]s, [[albumin]], [[LDL]], and other proteins via cross-linking to the extra vascular matrix. | |Explanation=[[Diabetic nephropathy]] is a common microvascular complication in advanced [[diabetes mellitus]]. Renal biopsy under light microscopy would reveal characteristic eosinophilic nodules in the glomerular tuft called “Kimmelsteil-Wilson” lesion. Chronic hyperglycemia leads to accumulation of advanced glycosylation end products (AGEs) that trap extravasated [[immunoglobulin]]s, [[albumin]], [[LDL]], and other proteins via cross-linking to the extra vascular matrix. | ||
Educational objective: Diabetic nephropathy is a microvascular complication of uncontrolled [[diabetes mellitus]]. It is characterized by Kimmelsteil-Wilson lesions, which are eosinophilic nodules in glomerular tufts. The pathogenesis of diabetic nephropathy is believed to be due to accumulation of advanced glycosylation end products (AGEs). | Educational objective: Diabetic nephropathy is a microvascular complication of uncontrolled [[diabetes mellitus]]. It is characterized by Kimmelsteil-Wilson lesions, which are eosinophilic nodules in glomerular tufts. The pathogenesis of diabetic nephropathy is believed to be due to accumulation of advanced glycosylation end products (AGEs). | ||
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Kalia K, Sharma S, Mistry K. Non-enzymatic glycosylation of immunoglobulins in diabetic nephropathy. Clin Chim Acta. 2004;347(1-2):169-76. | Kalia K, Sharma S, Mistry K. Non-enzymatic glycosylation of immunoglobulins in diabetic nephropathy. Clin Chim Acta. 2004;347(1-2):169-76. | ||
|AnswerA=Amorphous pink deposits of amyloid in renal cortex | |AnswerA=Amorphous pink deposits of amyloid in renal cortex | ||
|AnswerAExp=Amyloidosis is characterized by [[amyloid]] deposition that is positive for Congo red stain. | |AnswerAExp=Amyloidosis is characterized by [[amyloid]] deposition that is positive for Congo red stain. | ||
|AnswerB=Immune response mediated by CD4 and CD8 lymphocytes | |AnswerB=Immune response mediated by CD4 and CD8 lymphocytes | ||
|AnswerBExp=Immune response mediated by [[CD4]] and [[CD8]] [[lymphocytes]] describes the mechanism of renal rejection following [[transplantation]]. | |AnswerBExp=Immune response mediated by [[CD4]] and [[CD8]] [[lymphocytes]] describes the mechanism of renal rejection following [[transplantation]]. | ||
|AnswerC=Cystic distribution throughout the renal parenchyma | |AnswerC=Cystic distribution throughout the renal parenchyma | ||
|AnswerCExp=[[Polycystic kidney disease]] is characterized by cystic distribution throughout the renal parenchyma. | |AnswerCExp=[[Polycystic kidney disease]] is characterized by cystic distribution throughout the renal parenchyma. | ||
|AnswerD=Immune complex deposition activating the complement pathway | |AnswerD=Immune complex deposition activating the complement pathway | ||
|AnswerDExp=The pathogenesis of several primary glomerulonephritides, including post-infectious glomerulonephritis and membranoproliferative [[glomerulonephritis]], is characterized by immune complex deposition that activates the complement pathway. | |AnswerDExp=The pathogenesis of several primary glomerulonephritides, including post-infectious glomerulonephritis and membranoproliferative [[glomerulonephritis]], is characterized by immune complex deposition that activates the complement pathway. | ||
Revision as of 01:02, 9 September 2013
| Author | [[PageAuthor::Rim Halaby, M.D. [1]]] |
|---|---|
| Exam Type | ExamType::USMLE Step 1 |
| Main Category | MainCategory::Pathology |
| Sub Category | SubCategory::Renal |
| Prompt | [[Prompt::A 68 year old Caucasian male patient presents to his physician for his annual check-up. The patient’s past medical history is significant for hypertension controlled on lisinopril and advanced diabetes mellitus type II poorly controlled on daily insulin injections. Routine work-up reveals elevated serum creatinine. A renal biopsy under light microscopy similar to the patient’s biopsy is shown in the image below. The following findings could be best explained by which of the following pathologic processes?
|
| Answer A | AnswerA::Amorphous pink deposits of amyloid in renal cortex |
| Answer A Explanation | [[AnswerAExp::Amyloidosis is characterized by amyloid deposition that is positive for Congo red stain.]] |
| Answer B | AnswerB::Immune response mediated by CD4 and CD8 lymphocytes |
| Answer B Explanation | [[AnswerBExp::Immune response mediated by CD4 and CD8 lymphocytes describes the mechanism of renal rejection following transplantation.]] |
| Answer C | AnswerC::Cystic distribution throughout the renal parenchyma |
| Answer C Explanation | [[AnswerCExp::Polycystic kidney disease is characterized by cystic distribution throughout the renal parenchyma.]] |
| Answer D | AnswerD::Immune complex deposition activating the complement pathway |
| Answer D Explanation | [[AnswerDExp::The pathogenesis of several primary glomerulonephritides, including post-infectious glomerulonephritis and membranoproliferative glomerulonephritis, is characterized by immune complex deposition that activates the complement pathway.]] |
| Answer E | AnswerE::Non-enzymatic glycosylation of proteins |
| Answer E Explanation | AnswerEExp::Diabetic nephropathy is a common microvascular complication in advanced diabetes mellitus. Renal biopsy under light microscopy would reveal characteristic eosinophilic nodules in the glomerular tuft called “Kimmelsteil-Wilson” lesion. |
| Right Answer | RightAnswer::E |
| Explanation | [[Explanation::Diabetic nephropathy is a common microvascular complication in advanced diabetes mellitus. Renal biopsy under light microscopy would reveal characteristic eosinophilic nodules in the glomerular tuft called “Kimmelsteil-Wilson” lesion. Chronic hyperglycemia leads to accumulation of advanced glycosylation end products (AGEs) that trap extravasated immunoglobulins, albumin, LDL, and other proteins via cross-linking to the extra vascular matrix.
Reference: Kalia K, Sharma S, Mistry K. Non-enzymatic glycosylation of immunoglobulins in diabetic nephropathy. Clin Chim Acta. 2004;347(1-2):169-76. |
| Approved | Approved::No |
| Keyword | |
| Linked Question | Linked:: |
| Order in Linked Questions | LinkedOrder:: |
