Renal Pathology 5 Flashcards
what is nephrosclerosis?
sclerosis of the renal arterioles and small arteries
what is nephrosclerosis strongly associated with?
hypertension
how do the kidney appear in cases of nephrosclerosis?
the kidneys are either normal or moderately reduced in size; the cortical surfaces have a fine, even granularity
hypertension secondary to renal artery stenosis is due to what?
increased production of renin from the ischemic kidney
in cases of renal artery stenosis, what class of drug would you use to treat the resultant elevation in renin with?
ARBs- aka drugs that block angiotensin II
what is fibromuscular dysplasia?
a focal irregular thickening in medium and large muscular arteries including renal, carotid arteries
what demographic of patient is FMD more commonly seen?
women in their 3rd-4th decade of life
what can FMD lead to?
aneurysms, which can then rupture
what are the two forms of thrombotic microangiopathy we discussed?
thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS)
what is typical HUS?
most frequently associated with the consumption of food contaminated by e. coli O157:H7
who is most at risk for typical HUS?
children and older adults
what are the signs and symptoms of typical HUS?
following an episode of diarrhea, increased bleeding tendencies, renal failure, microangiopathic hemolytic anemia, thrombocytopenia, and neurologic changes
more than half of those affected with atypical HUS have an inherited deficiency in what?
complement regulatory proteins, such as factor H, factor I, and CD46
if a patient has atypical HUS that is not caused by an inherited deficiency in complement regulatory proteins, what might they have instead?
antiphospholipid syndrome (either primary or secondary to lupus), complications of pregnancy or postpartum, systemic sclerosis, malignant hypertension, chemotherapeutic and immunosuppressive agents, or irradiation of the kidney
what are 5 examples of chemotherapeutic and immunosuppressive drugs that could lead to atypical HUS?
mitomycin, cyclosporine, cisplatin, gemcitabine, and antagonists of VEGF
how is TTP usually manifested?
pentad of symptoms: fever, neurologic symptoms, microangiopathic hemolytic anemia, thrombocytopenia, and renal failure
what is the initiating event of TTP?
platelet aggregation induced by very large multimers of vWF, which accumulate due to a deficiency of ADAMTS13
why might a patient have a deficiency in ADAMTS13?
they may have inhibitory autoantibodies, or they may have inherited an inactivating mutation in ADAMTS13
how do you treat TTP?
plasma exchange, which removes autoantibodies and provides functional ADAMTS13
what is the morphological appearance of the kidney in cases of TTP?
there is diffuse cortical necrosis. the pale ischemic necrotic areas are confined to the cortex
what are the histologic features of a kidney with TTP?
acute ischemic infarction; fibrin stain showing thrombi in the glomerular capillaries
at what vertebral level do the renal arteries arise from the abdominal aorta?
L1
how is bilateral renal artery disease usually diagnosed?
arteriography
what does bilateral renal artery disease usually cause?
chronic ischemia with renal insufficiency in older individuals sometimes in the absence of HTN
why is it so important to recognize and diagnose bilateral renal artery disease?
surgical revascularization can prevent further decline in renal function
what is atheroembolic renal disease?
when there is embolization of fragments of atheromatous plaques from the aorta or renal artery into intrarenal vessels
what demographic of patients is atheroembolic renal disease most likely?
in older adults with severe atherosclerosis, especially after surgery on the abdominal aorta, aortography, or intra-aortic cannulization
what are some other sources/reasons from renal emboli?
mitral stenosis with a fib, MI with mural thrombosis, and vegetative endocarditis
what is sickle cell nephropathy?
when sickle cell disease/trait leads to a variety of alterations in renal morphology and function
what are the most common abnormalities seen in sickle cell nephropathy?
hematuria and a diminished concentrating ability; patchy papillary necrosis; proteinuria
