Renal Pathology at University Of Nairobi | Flashcards & Summaries

Lernmaterialien für Renal Pathology an der University of Nairobi

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Most common site of toxic injury in AKI
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Proximal convoluted tubules and it is more extensive in toxic ATN than in ischemic ATN
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Subepithelial humps 
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Acute poststreptococcal infection glomerulonephritis
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Mainly in children 
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Minimal change dx, post streptococcal infection glomerulonephritis and IgA nephropathy
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Plasmapheresis can benefit anti gbm GN but not immune complex mediated GN..

Electon microscopy in rpgn shows rupture in gbm..
Electron dense deposits seen in immune mediated but not anti gbm
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True 
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Wire loop lesions
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Active lesions of lupus nephritis.. seen in type 3 and 4 lupus nephritis.. 
Seen in light microscopy due to prominent subendothelial deposits causing thickening of capillary wall
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Transplant glomerulopathy
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Transplant glomerulopathy is defined as reduplication/multilammination of the glomerular basement membrane as observed by light and/or electron microscopy in a kidney allograft in the absence of immune deposits. By this definition, transplant glomerulopathy is a morphologic description of histologic or ultrastructural alterations and not a specific clinicopathologic entity.1 Multiple pathophysiologic mechanisms result in development of this lesion, all related to chronic, repeated endothelial cell injury. Most notable is antibody-mediated rejection. Other reported causes include autoantibodies, cell-mediated rejection, thrombotic microangiopathy, and hepatitis C virus.
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Renal transplant pathology 
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See on slideshare 
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Renal osteodystrophy
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Renal osteodystrophy is a bone disease that occurs when your kidneys fail to maintain the proper levels of calcium and phosphorus in your blood.
  • Symptoms of renal osteodystrophy aren't usually seen in adults until they have been on dialysis for several years. If left untreated, bones thin and weaken, and symptoms include bone and joint pain, and an increased risk of fractures.
  • In a patient with kidney failure, the kidneys stop making calcitriol, a form of vitamin D. The body then can't absorb calcium from food and starts removing it from the bones.
  • Phosphorus, which is found in most foods, also helps regulate calcium levels in the bones. Healthy kidneys remove excess phosphorus from the blood. When the kidneys stop working normally, phosphorus levels in the blood can become too high, leading to lower levels of calcium in the blood and resulting in the loss of calcium from the bones.
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Thrombotic microangiopathy 
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Microvascular thrombosis 
Microangiopathic hemolytic anemia 
Thrombocytopenia 
And sometimes renal failure
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Complement pathways in glomerulopathies
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Immune complex deposits activate complement pathway....

Classical complement pathway which has positive C1q mainly in Lupus nephritis- which has full house IF pattern. Also seen in type 1 MPGN 

Alternative complement pathway which mainly in C3 glomerulopathies and DDD.. activated by contact between certain complement proteins and pathogen.. unlike classical it does not involve antibodies 

Lectin pathway where MBL binds to mannose on bacterial walls and activate C2 and C4.. seen in Primary Membranous nephropathy
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IgA nephropathy 
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Early components of the classical complement pathway usually are absent 

Can have both lectin and alternative complement pathway but absent C1q staining so no classical.. 
Mesangial deposition of IgA and C3.. IgG and C4d can also be there 
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Atypical HUS in thrombotic microangiopathy 
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Caused by acquired or hereditary abnormalities of factors that dampen activation of complement by the alternative pathway
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Q:
Most common site of toxic injury in AKI
A:
Proximal convoluted tubules and it is more extensive in toxic ATN than in ischemic ATN
Q:
Subepithelial humps 
A:
Acute poststreptococcal infection glomerulonephritis
Q:
Mainly in children 
A:
Minimal change dx, post streptococcal infection glomerulonephritis and IgA nephropathy
Q:
Plasmapheresis can benefit anti gbm GN but not immune complex mediated GN..

Electon microscopy in rpgn shows rupture in gbm..
Electron dense deposits seen in immune mediated but not anti gbm
A:
True 
Q:
Wire loop lesions
A:
Active lesions of lupus nephritis.. seen in type 3 and 4 lupus nephritis.. 
Seen in light microscopy due to prominent subendothelial deposits causing thickening of capillary wall
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Q:
Transplant glomerulopathy
A:
Transplant glomerulopathy is defined as reduplication/multilammination of the glomerular basement membrane as observed by light and/or electron microscopy in a kidney allograft in the absence of immune deposits. By this definition, transplant glomerulopathy is a morphologic description of histologic or ultrastructural alterations and not a specific clinicopathologic entity.1 Multiple pathophysiologic mechanisms result in development of this lesion, all related to chronic, repeated endothelial cell injury. Most notable is antibody-mediated rejection. Other reported causes include autoantibodies, cell-mediated rejection, thrombotic microangiopathy, and hepatitis C virus.
Q:
Renal transplant pathology 
A:
See on slideshare 
Q:
Renal osteodystrophy
A:
Renal osteodystrophy is a bone disease that occurs when your kidneys fail to maintain the proper levels of calcium and phosphorus in your blood.
  • Symptoms of renal osteodystrophy aren't usually seen in adults until they have been on dialysis for several years. If left untreated, bones thin and weaken, and symptoms include bone and joint pain, and an increased risk of fractures.
  • In a patient with kidney failure, the kidneys stop making calcitriol, a form of vitamin D. The body then can't absorb calcium from food and starts removing it from the bones.
  • Phosphorus, which is found in most foods, also helps regulate calcium levels in the bones. Healthy kidneys remove excess phosphorus from the blood. When the kidneys stop working normally, phosphorus levels in the blood can become too high, leading to lower levels of calcium in the blood and resulting in the loss of calcium from the bones.
Q:
Thrombotic microangiopathy 
A:
Microvascular thrombosis 
Microangiopathic hemolytic anemia 
Thrombocytopenia 
And sometimes renal failure
Q:
Complement pathways in glomerulopathies
A:
Immune complex deposits activate complement pathway....

Classical complement pathway which has positive C1q mainly in Lupus nephritis- which has full house IF pattern. Also seen in type 1 MPGN 

Alternative complement pathway which mainly in C3 glomerulopathies and DDD.. activated by contact between certain complement proteins and pathogen.. unlike classical it does not involve antibodies 

Lectin pathway where MBL binds to mannose on bacterial walls and activate C2 and C4.. seen in Primary Membranous nephropathy
Q:
IgA nephropathy 
A:
Early components of the classical complement pathway usually are absent 

Can have both lectin and alternative complement pathway but absent C1q staining so no classical.. 
Mesangial deposition of IgA and C3.. IgG and C4d can also be there 
Q:
Atypical HUS in thrombotic microangiopathy 
A:
Caused by acquired or hereditary abnormalities of factors that dampen activation of complement by the alternative pathway
Renal Pathology

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