Chapter 20: The Kidney - Tubular/interstitial Dz/Vascular Dz Flashcards
1
Q
Which stain is used to view Chronic Glomerulonephritis?
What’s seen?
A
- Massone trichrome stain
- Showing complete replacement of all glomeruli by blue-staining collagen
2
Q
90% of what type of glomerulonephritis will progress to chronic GN?
Other forms of GN that may progress?
A
- Crescentic GN (90%)
- Membranous nephropathy
- FSGS
- Membranoproliferative GN
3
Q
As glomeruli progressively become obliterated in chronic GN, what happens to GFR and protein loss?
A
- GFR decreases
- Protein loss in urine diminshes
4
Q
What is the characteristic morphological features of the glomerular lesions associated with SLE (lupus nephritis)?
What is seen on light microscopy and electron microscopy?
A
- SUBendothelial immune complex deposition + mesangial deposition
- GBM shows “wire loops” of capillaries on light microscopy
5
Q
What are the 2 major processes that play a key pathophysiologic role as diabetic glomerular lesions develop?
A
- Metabolic defect linked to hyperglycemia and advanced glycosylation end products produced thickened GBM and increased mesangial matrix
- Hemodynamic effects associated w/ glomerular hypertrophy also contribute to the development of glomerulosclerosis
6
Q
What are the 3 major morphological changes seen in diabetic glomerulosclerosis?
A
- Diffuse capillary BM thickening
- Diffuse mesangial sclerosis
- Nodular glomerulosclerosis****
7
Q
In the US, what is the leading cause of end-stage renal disease, adult-onset blindness and non-traumatic LE amputations?
A
Diabetes
8
Q
What are the major characteristics of Henoch-Schonlein Purpura?
Who does it most typically affect and onset when?
A
- Most common in children btw 3-8 yo, often follows a URI
- Purpuric skin rashes on extensor surfaces of arms and legs
- Abdominal pain and vomiting —> intestinal bleeding
- Arthralgias
- Renal abnormalities - microscopic hematuria, mixed or isolated nephritic/nephrotic syndrome
9
Q
Pathognomonic feature of Henoch-Schonlein Purpura seen on fluorescence microscopy?
A
Deposition of IgA, sometimes w/ IgG and C3, in mesangial region
10
Q
What is the morphology of the skin lesions seen in Henoch-Schonlein Purpura?
A
- Subepidermal hemorrhages and necrotizing vasculitis involving smaller vessels of the dermis
- Deposition of IgA, along w/ IgG and C3 present in the vessels
11
Q
Which 4 systemic diseases are associated w/ Nephrotic Syndrome?
A
- Diabetic nephropathy
- SLE
- Hepatitis C - Cryoglobulinemia: Membranoproliferative Type I
- HIV nephropathy: FSGS
12
Q
Which 4 systemic diseases are associated w/ Nephritic Syndrome?
A
- SLE = 60-70% pts
- Bacterial endocarditis: acute proliferative GN
- Goodpasture Syndrome: RPGN
- Henoch-Schonlein Purpure (HSP): IgA nephropathy
13
Q
What are the 3 major renal lesions prototypical of Diabetic Nephropathy?
A
- Glomerular lesions
- Vascular lesions, principally artriolosclerosis
- Pyelonephritis, including necrotizing papillitis
14
Q
In diffuse proliferative lupus nephritis what will be seen with immunofluorescence?
A
Mesangial and capillary wall (SUBendothelial) IgG localization
15
Q
Out of the 6 patterns of glomerular disease seen in SLE, which is the most common?
Common signs/sx’s in these pts?
A
- Diffuse lupus nephritis (class IV)
- Hematuria and proteinuria.
- HTN and mild to severe renal insufficiency is also common
16
Q
What is the most common cause of acute kidney injury (aka ARF)?
A
Acute tubular injury/Necrosis
17
Q
What are the 2 most common etiologies causing Acute Tubular Injury?
A
- Ischemia i.e., hypotension, shock, HUS, TTP, or DIC
- Direct toxic injury to the tubules (drugs/toxins)
18
Q
How does the pattern of tubular damage in the PCT, PST, and ascending loop of henle seen in acute tubular injury differ between ischemic and toxic sources?
A
- Ischemic = patchy necrosis of these segments
- Toxic = continous necrosis of PCT and PST w/ patchy necrosis of ascending loop of henle
19
Q
Why are tubular epithelial cells particularly vulnerable to ischemia and toxins?
A
- Increased SA for reabsorption
- High rate of metabolism + O2 consumption w/ high energy requirements –> ischemia disrupts this
20
Q
In ATI, what occurs to necrotic tubular epithelial cells over time?
Leads to?
A
Detach and sloughed into tubular lumen –> luminal obstruction by casts
21
Q
What is the histologic findings of acute kindey injury associated w/ ethylene glycol (aka anti-freeze)?
Often find what type of crystals in the tubular lumen?
A
- Marked ballooing and hydropic or vacuolar degeneration of PCT’s
- Calcium oxalate crystals
22
Q
What are the 3 stages of the clinical course of AKI/ARF and major electrolyte/lab findings in each stage?
Which stage is marked by an increases susceptibility to infection?
A
- Initiation - lasts about 36 hrs w/ slight decline in urine output + rise in BUN
- Maintenance - salt + H2O overload, rising BUN, and HYPERkalemia, metabolic acidosis, OLIGURIA
- Recovery - HYPOkalemiabecomes an issue as well asincreased susceptibility to infection
23
Q
What is the prognosis of ATI dependent on?
How likely are these pts to survive?
A
- Depends on magnitude and duration of injury
- With current supportive care, 95% of those who do not succumb to the precipitating cause recover!
24
Q
What are the clinical hallmarks of Tubulointerstitial Nephritis that distinguish it from Glomerular diseases?
A
- Absence of nephritic or nephrotic syndrome
- Defects in tubular function –> defect in concentrating urine = polyuria and nocturia
- Salt wasting
- Dimished ability to excrete acids (metabolic acidosis)
25
Tubulointerstitial Nephritis is generally characterized by presence of what functional renal abnormality?
- **Azotemia** --\> ↓ GFR
- Inability to concentrate urine --\> **polyuria and nocturia**
26
Most common cause of clinical pyelonephritis arises from what?
**Ascending infection** from the bladder
27
Pyelonephritis is defined as inflammation affecting what anatomical features of the kidney?
- Tubules
- Interstitium
- Renal pelvis
28
What is the second most common cause of acute kidney injury (after pyelonephritis)?
**Drug and toxin-induced** tubulointerstitial nephritis
29
A small % of pts w/ analgesic nephropathy develop which malignancy?
**Urothelial carcinoma** of the **renal pelvis**
30
What are the major clinical signs/sx's of acute drug-induced interstitial nephritis?
Onset?
- Begins about **15 days** after drug exposure
- With **fever, eosinophilia** (transient), a **rash**, and **renal abnormalities** (i.e., **hematuria,** mild **proteinuria**, and **leukocyturia**)
31
What is one of the early and reversible results of ischemia associated w/ tubule cell injury?
- **Loss of cell polarity**
- Redistribution of Na-K-ATPase from basolateral to luminal surface of tubular cells
- **Increase Na+ delivery to distal tubules**
32
What is the major hemodynamic alteration leading to a reduction in GFR associated with ischemic tubule cell injury?
- Intrarenal **vasoconstriction**
- Results in reduced glomerular flow and ↓O2 delivery to functionally important tubules (TAL and PT)
33
ATI is characterized by what type of cell death and morphological findings?
- **Focal tubular epithelial necrosis** at multiple points of nephron
- **Occlusion of tubular lumens by casts**
34
What are the eosiniphilic hyaline and pigmented granular casts seen with ATI composed of?
Tamm-Horsfall protein
35
What findings when present can help distinguish acute from chronic interstitial fibrosis?
- In **acute**, there will be more **rapid** clinical onset w/ **edema**
- Often w/ presence of **neutrophils** and **eosinophils**
36
Which 3 viruses may be responsible for UTI's/renal infection, especially in immunocompromised pts such as those w/ transplants?
1) ***Polyomavirus***
2) CMV
3) Adenovirus
37
What are 2 of the common predisposing medical conditions for Pyelonephritis?
1) Diabetes --\> especially **poorly controlled**
2) Pregnancy
38
Which anatomic defect is an important predisposing factor for ascending infection leading to pyelonephritis?
- **Incompetence** of the **vesicouretal valve**
- Leads to reflux of urine from bladder --\> ureter = **vesicoureteral reflex**
39
How can vesicoureteal reflux be acquired in both children and adults?
- **Children** --\> **congenital defect** (most common) or **acquired by bladder infection**
- **Adults** --\> may be acquired from **persistent bladder atony** due to spinal cord inury
40
How can vesicoureteral reflux by diagnosed?
Voiding cystourethrogram
41
Although ascending infection is the most common route of bacteria entering the kidney, they may also do so hematogenously, which is most often occurs in what clinical setting?
Ongoing sepsis
42
What are the morphological hallmarks of Acute Pyelonephritis?
- Patchy interstitial **suppurative inflammation**
- **Intratubular** aggregates of **neutrophils**
- **Neutrophilic** tubulitis and **tubular necrosis**
43
Acute pyelonephritis usually shows sparing of the glomeruli, but infection by what often destroys glomeruli?
**Fungal** pyelonephritis (i.e., *Candida)* --\> **granulomatous interstitial inflammation**
44
Papillary necrosis is a complication of acute pyelonephritis most often seen in which 4 patients/settings?
1) Diabetics
2) Analgesic Nephropathy
3) Urinary tract obstruction
4) Sickle Cell Disease
45
Is papillar necrosis usually unilateral or bilateral and what type of morphological damage is seen?
- Typically **bilateral** but can be **unilateral**
- Tips/distal 2/3's of pyramids have areas of **gray-white** to **yellow necrosis (ischemic coagulative necrosis)**
46
What is the M:F ratio for papillary necrosis associated with diabetes mellitus?
Time course?
How do the papillae appear and are they calcified?
- **Females 3:1**
- Time course = **10 yrs**
- **Pale grayish necrosis** limited to **papillae**; calcifications = **rare**
47
What is the M:F ratio for papillary necrosis associated with Analgesic Nephropathy?
Time course of abuse?
How does the necrosis appear on the papillae, how diffuse is the necrosis and is there calcification?
- **Females 5:1**
- Time course = **7 years of abuse**
- Almost **ALL** papillae in DIFFERENT stages **red-brown necrosis** w/ **sloughing** into calyces; **calcifications are frequent**
48
Which gender has a higher incidence of papillary necrosis as a result of obstruction?
Are calcifications rare or frequent?
- **Males 9:1**
- **Calcifications** = frequent
49
After the acute phase of pyelonephritis, healing occurs, with scarring commonly seen in which type of pattern?
Pyelonephritic scars are almost always associated w/ inflammation, fibrosis, and deformation of which structures?
- **Patchy, jigsaw pattern** w/ intervening **preserved parenchyma**
- Scar associated w/ underlying **calyx and pelvis**
50
What is the common clinical presentation of acute pyelonephritis (signs/sx's)?
- **Sudden** onset of **pain** at **costovertebral angle** + **fever** and **malaise**
- Often **dysuria, frequency, and urgency** indicating bladder/urethral irritation
51
Which finding in the urine is indicative of renal involvement in a patient presenting w/ signs of acute pyelonephritis?
**Leukocyte casts**, typically rich in **neutrophils** (**pus casts**)
52
What is an emerging viral pathogen causing pyelonephritis in kidney allografts often leading to the development of nephropathy/allograft failure?
Polyomavirus (i.e., JC or BK virus)
53
Only what 2 entities causing renal damage affect the **calyces,** making **pelvocalyceal** damage an important diagnostic clue?
1) Chronic pyelonephritis
2) Analgesic nephropathy
54
What are the 2 major forms of Chronic Pyelonephritis?
Which is most common?
1. **Reflux nephropathy** = MOST common
2. **Chronic obstructive pyelonephritis**
55
What is sterile reflux and what is it caused by?
- Renal damage by vesicoureteral reflux in **absence** of infection
- Due to **severe obstruction**
56
Xanthogranulomatous pyelonephritis is a rare form of chronic pyelonephritis characterized by the accumulation of what?
Associated with what infection?
The large, yellowish orange nodules may be clinically confused with?
- **Foamy** **macrophages** w/ plasma cells, lymphocytes, PMN's, and occasional **giant cells**
- Often w/ *P**roteus*** infections
- **Large, yellowish orange nodules** may be confused w/ **renal cell carcinoma**
57
How does the scarring/symmetry of chronic pyelonephritis differ from that of chronic glomerulonephritis?
- **Chronic pyelonephritis** = irregular scarring w/ **asymmetry** if bilateral
- **Chronic GN** = **diffuse** and **symmetrical** scarring
58
Coarse, discrete, corticomedullary scars overlying dilated, blunted, or deformed calyces w/ flattening of papillae most often in upper and lower poles is the hallmark of what disorder?
Chronic pyelonephritis
59
Dilated tubules w/ flattened epithelium often filled w/ casts resembling **thyroid colloid** (thyroidization) is characteristic of what disorder of the kidney?
Chronic pyelonephritis
60
Reflux nephropathy as a contributor to chronic pyelonephritis is often discovered in kids when?
Late in the disease as renal insufficiency and HTN develop, often as the cause of HTN in a child is being investigated
61
What secondary disorder may develop due to increased scarring in pts w/ chronic pyelonephritis?
Presence of what is a poor prognostic sign in these pts?
- **FSGS**
- Onset of proteinuria + FSGS = **poor prognostic** sign, which may progress to **ESRD**
62
The most likely sequence of events in acute drug-induced interstitial nephritis is that drugs act as what?
Leads to?
- Drugs act as **haptens** binding to components of **tubular cells**
- Become **immunogenic** w/ resulting injury due to **IgE** or **cell-mediated immune rxns** to **tubular cells** or their **BM's**
63
Why is it clinically important to recognize drug-induced acute interstitial nephritis?
Withdrawl of the offending drug is followd by **recovery**, which may take several months
64
On occasaion, necrotic papillae are excreted in the urine and may cause what clinical signs/sx's?
- Gross hematuria
- Renal colic due to ureteric obstruction
65
NSAIDs have been shown to cause what 2 renal syndromes developing concurrently?
- Acute interstitial nephritis
- Minimal change disease
66
Acute uric acid nephropathy often seen in which patients, receiving what therapy?
- Those w/ **leukemias** or **lymphomas** undergoing **chemotherapy** (**tumor lysis syndrome**)
- Released **nuclei acids --\> uric acid** (precipitation favored by **acidic pH** in **collecting tubules**)
67
Nephrolithiasis vs. nephrocalcinosis?
Disorders associated w/ each?
- **Nephrolithiasis =** uric acid stones seen in pts w/ gout and secondary hyperuricemia
- **Nephrocalcinosis** = deposits of calcium in the kidney (**NOT stones**) associated w/ hyperparathyroidism, multiple myeloma, metastatic cancer, and vit D intoxication
68
What is the main cause of renal dysfunction in pts w/ Multiple Myeloma?
Bence-Jones (light-chain) proteinuria
69
What are the 2 mechanism which account for the renal toxicitiy of Bence-Jones (light-chain) proteins in Multiple Myeloma pts?
1) Some **Ig light chains** are **directly toxic** to epithelial cells
2) Combine w/ urinary glycoproteins (**Tamm-Horsfall**) under acidic conditions to form large tubular casts, **obstructing tubular lumens** inducing inflammation = **light-chain cast nephropathy**
70
What are the 4 main ways that renal damage can occur in Multiple Myeloma pts?
1. **Bence-Jones proteinuria** and **cast nephropathy**
2. **Amyloidosis**
3. **Light-chain deposition disease**
4. **Hypercalcemia** and **Hyperuricemia**
71
What is light-chain deposition disease seen in some pts with multiple myeloma?
- Light chains (usually K type) deposit in **GBMs and mesangium** causing a **glomerulopathy**
- Also in tubular BM's which may cause **tubulointerstitial nephritis**
72
What is the characteristic tubulointerstitial morphology seen in light-chain cast nephropathy?
- **Blue amorphous** masses, sometimes **concentrically laminated** and **fractured,** filling and distending tubular lumens
- Some casts surrounded by **multinucleate giant cells**
73
If a patient with multiple myeloma presents w/ **significant non-light chain proteinuria** (i.e., albuminuria) what type of nephrotic disease process may this suggest?
- AL amyloidosis
- Light-chain deposition disease
74
Clinically, what is the most common presentation for the renal manifestations associated with light-chain cast nephropathy?
1) **CKD** developing slow and progressively = **most common**
2) **AKI** w/ oliguria = less common
75
Hepatorenal syndrome seen in pts w/ acute or chronic liver disease w/ advanced liver failure may cause what type of nephropathy?
Bile cast nephropathy
76
Nephroslcerosis is defined as sclerosis of what vessels in the kidney?
Strongly associated with what disease?
- **Renal arterioles** and **small arteries**
- Strong association w/ **HTN**
**\*Benign nephrosclerosis** is a general process, NOT a specific Dx
77
Nephrosclerosis is associated with what factors?
- Advancing age
- Blacks \> whites
- Strongly associated w/ HTN and DM; may be seen in absence of HTN too
78
What are the 2 processes occuring in the pathogenesis of Benign Nephrosclerosis?
1. **Medial** and **intimal thickening** due to hemodynamic changes, aging, etc
2. **Hyalinization** of **arteriolar walls** --\> extravasation of plasma protein thru injured endothelium and increased deposition in BM's
79
What is the gross morphology (i.e., cortical surface) of the kidneys in Benign Nephrosclerosis?
- Cortical surface is **fine** w/ **granularity** ("resembles **leather**") due to **cortical scarring and shrinking**
- Will be of normal size or **moderately reduced** in size
80
Benign nephrosclerosis is NOT usually associated w/ renal insufficiency except in which 3 groups of pts w/ HTN?
1. Pts of **African descent**
2. Pts w/ **severe BP elevations**
3. Pts w/ 2nd underlying dz, especially **diabetes**
81
What are histological features of the kidneys seen in Benign Nephrosclerosis?
- **Hyaline arteriolsclerosis**
- **Fibroelastic hyperplasia**
- **Patchy** ischemic atrophy of **tubules** and **glomeruli**
82
Malignant Nephrosclerosis typically occurs most often in whom?
- **Younger** pts
- More often in **men** and in **blacks**
83
What are the 2 histologic alterations that characterize blood vessels in malignant HTN (Nephrosclerosis)?
Which of these changes correlates w/ renal failure?
1. **Fibrinoid necrosis** of arterioles
2. **Hyperplastic arteriolosclerosis** (AKA "**Onion skinning**") = proliferation of smooth m. cells of the interlobular arteries --\> **correlates w/ renal failure**
84
Explain the pathogenesis of the lesions in Malignant Nephrosclerosis after the initial vascular damage.
- Injured endothelium = ↑ permeability to fibrinogen + plasma proteins
- Focal cell death + platelet deposition --\> **fibrinoid necrosis** of arterioles and small arteries
- Activation of platelets + coagulation factors --\> **intravascular thrombosis**
- **Hyperplastic arteriolosclerosis** --\> marked **ischemia** of kidneys
85
How does the cortical surface of the kidney appear in Malignant Nephrosclerosis?
**Small, pinpoint** petechial hemorrhages = **"flea-bitten" appearance**
86
Patients w/ malignant HTN have markedly elevated levels of?
Leads to what type of cycle?
- Renin
- Self-perpetuating cycle of damage and HTN
87
The full-blown syndrome of Malignant HTN is characterized by what BP, and other serious clinical manifestations?
- **BP = \>200 / \>120 mmHg**
- Papilledema
- Retinal hemorrhages
- Encephalopathy
- CV abnormalities
- Renal failure
88
Most often the early symptoms of Malignant HTN include what?
What renal findings?
- **Sx's related to ↑ ICP** --\> HA, N/V, and visual impairments (i.e., scotomas or seeing spots)
- Marked proteinuria and micro/macroscopic hematuria
89
What is the importance clinically in recognizing Renal Artery Stenosis in regards to treatment?
- Potentially **curable** form of HTN = **70-80% cure rate**
90
Renal artery stenosis leads to what pathophysiologic changes?
- Increased prod. of **renin** from ischemic kidney --\> **HTN**
- **Sodium retention** may occur and perpetuate the HTN
91
What is the most common cause of renal artery stenosis (70%)?
Who is most at risk?
- Narrowing at origin of renal artery by **atheromatous plaque**
- More frequent in **men**, ↑ with advanced age, and diabetes
92
Which cause of renal artery stenosis is more often seen in younger age groups (3rd-4th decades) and is more common in woman?
**Fibromuscular dysplasia** of renal artery
93
What is the classic appearance on arteriography of renal artery stenosis due to fibromuscular dysplasia?
**"String of beads" appearance**
94
In general pts w/ renal artery stenosis present clinically similar to what other disorder?
How can it be diagnosed?
- Resemble those w/ **essential HTN**
- Occasionally **bruit** can be heard over kidney on ausculation (rare)
- Elevated renin levels, response to ACE inhibitors, renal scans, and IV pyelography may all **aid in Dx**
- Need **arteriography** to localize stenotic lesion
95
What is the arteriolosclerosis like in the ischemic kidney in renal artery stenosis vs. non-ischemic (functional) kidney?
- Ischemic kidney will be reduced in size and show signs of **diffuse ischemic necrosis**
- **Contralateral kidney** may show **more severe** arteriolosclerosis, depending on severity of the HTN!
\*Think the ischemic kidney w/ stenosis is essentially shut off from the blood supply, while the functional kidney is getting rocked by extremely high/persistent BP
96
The primary cause/inciting event of HUS differs from TTP how as far as pathogenesis?
- **HUS** = caused by **e****ndothelial****injury**and**activation**
- **TTP** = inciting event is **platelet activation** --\> **aggregation**
97
What is the trigger for endothelial injury in typical HUS vs. atypical HUS?
- **Typical HUS** - trigger is **Shiga-like toxin** (EHEC \> Shigella)
- **Atypical HUS** - trigger is **excessive activation of complement**
98
What are the 3 major findings in the Thrombotic Microangiopathies (HUS and TTP)?
- **Thrombi** in capillaries and arterioles
- **Microangiopathic hemolytic anemia**
- **Thrombocytopenia\*\*\*\*** (big clue in a question stem!)
99
Who is most often affected by Typical HUS?
How is this form treated/managed and prognosis?
- Mainly **children**
- Renal failure is managed w/ **dialysis** and most pts recover normal renal function within weeks
- **Long-term prognosis** is variable due to **renal damage**
100
What are the 2 common inherited deficiencies which cause Atypical HUS?
- Deficiencies in **complement regulatory proteins**
- Most common = **Factor H** (breaks down alternative path)
- Some are deficient in **Factor I** and **CD46**
101
Other than inherited deficiencies of complement, what are some of the other causes of Atypical HUS?
- **Antiphospholipid syndrome**, either 1° or 2° to SLE
- Pregnancy --\> **postpartum renal failure**
- **Vascular diseases of kidney:** systemic sclerosis and malignant HTN
- Chemotherapeutic and immunosuppressive drugs
- **Irradiation** of kidney
102
What is the prognosis of Atypical HUS?
Generally not as well as typical due to underlying conditions
103
Thrombotic Thrombocytopenic Purpura (TTP) is classically manifested by what pentad, what is the **dominant** feature?
1) Fever
2) **Neurological sx's** = **Dominant feature**
3) Microangiopathic hemolytic anemia
4) Thrombocytopenia
5) Renal failure
104
TTP and Atypical HUS both appear more commonly in adults, occassionally having similar sx's. How are they distinguished from one another?
Presence of **normal ADAMTS13** in plasma = **Atypical HUS**
105
TTP is associated with inherited or acquired deficiencies in what?
The most common cause is due to what?
**- ADAMTS13** = plasma metalloprotease which regulates vWF
- **Inhibitory autoantibodies** against **ADAMTS13 = MOST COMMON!**
106
Who is most often affected by TTP and it typically presents before what age?
- Woman
- Presents **before** 40 yo
107
What is the standard of treatment of TTP?
**Plasma exchange** to remove autoantibodies + **provide functional ADAMTS13**
108
In TTP, deficiencies of ADAMTS13, a negative regulator of vWF, permits the formation of what?
Abnormally large multimers of vWF that activate platelets
109
Light microscopy of **chronic** disease associated with **atypical HUS/TTP** will show what?
- Mildy **HYPER****cellular** glomeruli
- Thickened capillary walls
- **Splitting/reduplication** of BM ("**tram-tracks**")
- **"Onion-skinning"** of arterial walls
110
What are the morphological characteristics seen on micrcoscopy in both HUS/TTP?
Which arteries will show necrosis? (quiz question!)
- In acute, active dz, the kidney shows **patchy or diffuse CORTICAL necrosis** and **subscapular petechiae**
- **Thrombi occluded** glomerular capillaries
- **Mesangiolysis**
- **Interlobular arteries** w/ **fibrinoid necrosis** of wall and **occlusive thrombi**
111
Bilateral renal artery disease (aka atherosclerotic ischemic renal disease) is a common cause of what in older individuals?
**Chronic ischemia w/ renal insufficiency**, sometimes w/o HTN
112
How is bilateral renal artery disease definitively diagnosed?
Treatment?
- Arteriography
- Surgical revascularization
113
Atheroembolic renal disease is caused by what?
Most often seen in whom and when?
- Fragments of atheromatous plaques from **aorta** or **renal artery** embolize into intrarenal vessels
- Most commonly in **older adults** w/ **severe atherosclerosis**, esp. following surgery on AA, aortography, or intra-aortic cannulization
114
The emboli of Atheroembolic Renal Disease can be identified in the lumens of arcuate and interlobular arteries due to what appearance?
Content of **cholesterol crystals**, which appear as **rhomboid clefts**
115
Sickle-cell disease (homozygous) or trait (heterozygous) may lead to sickle-cell nephropathy, which is most commonly manifested how?
On occasion can develop into what serious disorder?
- Commonly, **hematuria** and **hyposthenuria** (inability to concentrate)
- **Patchy papillary necrosis** may also occur
- **Proteinuria** is also common, sub-nephrotic range (\<3.5 g)
- On occasions, overt **nephrotic syndrome** arises --\> **FSGS**
116
Diffuse Cortical Necrosis is an uncommon condition occuring most frequently after what?
Appears how morphologically?
- **Obstetric emergencies**, septic shock, or extensive surgeries
- **Coagulative necrosis** of both glomeruli and tubules, with necrosis confined to **cortex**
117
Why are the kidneys a common site for the development of infarcts?
Most infarcts are due to?
- Receive 1/4 of the cardiac output, "end-organ" vascular supply, and lack of collateral circulation
- Most infarcts are due to **embolism**
118
What are the most common source of emboli leading to renal infarcts?
- Mural thrombosis from left atrium/ventricle due to MI
- Vegetative endocarditis
- Aortic aneurysms
- Aortic atherosclerosis
119
Due to the lack of collateral blood supply, how do renal infarcts appear morphologically?
Shape?
- **S****harply demarcated**,**pale, yellow-white**areas of**coagulative necrosis**
- **Wedge-shaped**
