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(OMS2) CPR II Exam 3 > Chapter 20: The Kidney - Tubular/interstitial Dz/Vascular Dz > Flashcards

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
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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
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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
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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
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5
Q

What are the 2 major processes that play a key pathophysiologic role as diabetic glomerular lesions develop?

A
  1. Metabolic defect linked to hyperglycemia and advanced glycosylation end products produced thickened GBM and increased mesangial matrix
  2. Hemodynamic effects associated w/ glomerular hypertrophy also contribute to the development of glomerulosclerosis
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6
Q

What are the 3 major morphological changes seen in diabetic glomerulosclerosis?

A
  1. Diffuse capillary BM thickening
  2. Diffuse mesangial sclerosis
  3. Nodular glomerulosclerosis****
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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

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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
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9
Q

Pathognomonic feature of Henoch-Schonlein Purpura seen on fluorescence microscopy?

A

Deposition of IgA, sometimes w/ IgG and C3, in mesangial region

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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
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11
Q

Which 4 systemic diseases are associated w/ Nephrotic Syndrome?

A
  1. Diabetic nephropathy
  2. SLE
  3. Hepatitis C - Cryoglobulinemia: Membranoproliferative Type I
  4. HIV nephropathy: FSGS
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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
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13
Q

What are the 3 major renal lesions prototypical of Diabetic Nephropathy?

A
  1. Glomerular lesions
  2. Vascular lesions, principally artriolosclerosis
  3. Pyelonephritis, including necrotizing papillitis
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14
Q

In diffuse proliferative lupus nephritis what will be seen with immunofluorescence?

A

Mesangial and capillary wall (SUBendothelial) IgG localization

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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
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16
Q

What is the most common cause of acute kidney injury (aka ARF)?

A

Acute tubular injury/Necrosis

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17
Q

What are the 2 most common etiologies causing Acute Tubular Injury?

A
  1. Ischemia i.e., hypotension, shock, HUS, TTP, or DIC
  2. Direct toxic injury to the tubules (drugs/toxins)
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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
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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
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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

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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
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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
  1. Initiation - lasts about 36 hrs w/ slight decline in urine output + rise in BUN
  2. Maintenance - salt + H2O overload, rising BUN, and HYPERkalemia, metabolic acidosis, OLIGURIA
  3. Recovery - HYPOkalemiabecomes an issue as well asincreased susceptibility to infection
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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!
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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)
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25
Q

Tubulointerstitial Nephritis is generally characterized by presence of what functional renal abnormality?

A
  • Azotemia –> ↓ GFR
  • Inability to concentrate urine –> polyuria and nocturia
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26
Q

Most common cause of clinical pyelonephritis arises from what?

A

Ascending infection from the bladder

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27
Q

Pyelonephritis is defined as inflammation affecting what anatomical features of the kidney?

A
  • Tubules
  • Interstitium
  • Renal pelvis
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28
Q

What is the second most common cause of acute kidney injury (after pyelonephritis)?

A

Drug and toxin-induced tubulointerstitial nephritis

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29
Q

A small % of pts w/ analgesic nephropathy develop which malignancy?

A

Urothelial carcinoma of the renal pelvis

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30
Q

What are the major clinical signs/sx’s of acute drug-induced interstitial nephritis?

Onset?

A
  • Begins about 15 days after drug exposure
  • With fever, eosinophilia (transient), a rash, and renal abnormalities (i.e., hematuria, mild proteinuria, and leukocyturia)
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31
Q

What is one of the early and reversible results of ischemia associated w/ tubule cell injury?

A
  • Loss of cell polarity
  • Redistribution of Na-K-ATPase from basolateral to luminal surface of tubular cells
  • Increase Na+ delivery to distal tubules
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32
Q

What is the major hemodynamic alteration leading to a reduction in GFR associated with ischemic tubule cell injury?

A
  • Intrarenal vasoconstriction
  • Results in reduced glomerular flow and ↓O2 delivery to functionally important tubules (TAL and PT)
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33
Q

ATI is characterized by what type of cell death and morphological findings?

A
  • Focal tubular epithelial necrosis at multiple points of nephron
  • Occlusion of tubular lumens by casts
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34
Q

What are the eosiniphilic hyaline and pigmented granular casts seen with ATI composed of?

A

Tamm-Horsfall protein

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35
Q

What findings when present can help distinguish acute from chronic interstitial fibrosis?

A
  • In acute, there will be more rapid clinical onset w/ edema
  • Often w/ presence of neutrophils and eosinophils
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36
Q

Which 3 viruses may be responsible for UTI’s/renal infection, especially in immunocompromised pts such as those w/ transplants?

A

1) Polyomavirus
2) CMV
3) Adenovirus

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37
Q

What are 2 of the common predisposing medical conditions for Pyelonephritis?

A

1) Diabetes –> especially poorly controlled
2) Pregnancy

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38
Q

Which anatomic defect is an important predisposing factor for ascending infection leading to pyelonephritis?

A
  • Incompetence of the vesicouretal valve
  • Leads to reflux of urine from bladder –> ureter = vesicoureteral reflex
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39
Q

How can vesicoureteal reflux be acquired in both children and adults?

A
  • Children –> congenital defect (most common) or acquired by bladder infection
  • Adults –> may be acquired from persistent bladder atony due to spinal cord inury
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40
Q

How can vesicoureteral reflux by diagnosed?

A

Voiding cystourethrogram

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41
Q

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?

A

Ongoing sepsis

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42
Q

What are the morphological hallmarks of Acute Pyelonephritis?

A
  • Patchy interstitial suppurative inflammation
  • Intratubular aggregates of neutrophils
  • Neutrophilic tubulitis and tubular necrosis
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43
Q

Acute pyelonephritis usually shows sparing of the glomeruli, but infection by what often destroys glomeruli?

A

Fungal pyelonephritis (i.e., Candida) –> granulomatous interstitial inflammation

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44
Q

Papillary necrosis is a complication of acute pyelonephritis most often seen in which 4 patients/settings?

A

1) Diabetics
2) Analgesic Nephropathy
3) Urinary tract obstruction
4) Sickle Cell Disease

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45
Q

Is papillar necrosis usually unilateral or bilateral and what type of morphological damage is seen?

A
  • Typically bilateral but can be unilateral
  • Tips/distal 2/3’s of pyramids have areas of gray-white to yellow necrosis (ischemic coagulative necrosis)
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46
Q

What is the M:F ratio for papillary necrosis associated with diabetes mellitus?

Time course?

How do the papillae appear and are they calcified?

A
  • Females 3:1
  • Time course = 10 yrs
  • Pale grayish necrosis limited to papillae; calcifications = rare
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47
Q

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?

A
  • 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
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48
Q

Which gender has a higher incidence of papillary necrosis as a result of obstruction?

Are calcifications rare or frequent?

A
  • Males 9:1
  • Calcifications = frequent
49
Q

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?

A
  • Patchy, jigsaw pattern w/ intervening preserved parenchyma
  • Scar associated w/ underlying calyx and pelvis
50
Q

What is the common clinical presentation of acute pyelonephritis (signs/sx’s)?

A
  • Sudden onset of pain at costovertebral angle + fever and malaise
  • Often dysuria, frequency, and urgency indicating bladder/urethral irritation
51
Q

Which finding in the urine is indicative of renal involvement in a patient presenting w/ signs of acute pyelonephritis?

A

Leukocyte casts, typically rich in neutrophils (pus casts)

52
Q

What is an emerging viral pathogen causing pyelonephritis in kidney allografts often leading to the development of nephropathy/allograft failure?

A

Polyomavirus (i.e., JC or BK virus)

53
Q

Only what 2 entities causing renal damage affect the calyces, making pelvocalyceal damage an important diagnostic clue?

A

1) Chronic pyelonephritis
2) Analgesic nephropathy

54
Q

What are the 2 major forms of Chronic Pyelonephritis?

Which is most common?

A
  1. Reflux nephropathy = MOST common
  2. Chronic obstructive pyelonephritis
55
Q

What is sterile reflux and what is it caused by?

A
  • Renal damage by vesicoureteral reflux in absence of infection
  • Due to severe obstruction
56
Q

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?

A
  • Foamy macrophages w/ plasma cells, lymphocytes, PMN’s, and occasional giant cells
  • Often w/ Proteus infections
  • Large, yellowish orange nodules may be confused w/ renal cell carcinoma
57
Q

How does the scarring/symmetry of chronic pyelonephritis differ from that of chronic glomerulonephritis?

A
  • Chronic pyelonephritis = irregular scarring w/ asymmetry if bilateral
  • Chronic GN = diffuse and symmetrical scarring
58
Q

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?

A

Chronic pyelonephritis

59
Q

Dilated tubules w/ flattened epithelium often filled w/ casts resembling thyroid colloid (thyroidization) is characteristic of what disorder of the kidney?

A

Chronic pyelonephritis

60
Q

Reflux nephropathy as a contributor to chronic pyelonephritis is often discovered in kids when?

A

Late in the disease as renal insufficiency and HTN develop, often as the cause of HTN in a child is being investigated

61
Q

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?

A
  • FSGS
  • Onset of proteinuria + FSGS = poor prognostic sign, which may progress to ESRD
62
Q

The most likely sequence of events in acute drug-induced interstitial nephritis is that drugs act as what?

Leads to?

A
  • 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
Q

Why is it clinically important to recognize drug-induced acute interstitial nephritis?

A

Withdrawl of the offending drug is followd by recovery, which may take several months

64
Q

On occasaion, necrotic papillae are excreted in the urine and may cause what clinical signs/sx’s?

A
  • Gross hematuria
  • Renal colic due to ureteric obstruction
65
Q

NSAIDs have been shown to cause what 2 renal syndromes developing concurrently?

A
  • Acute interstitial nephritis
  • Minimal change disease
66
Q

Acute uric acid nephropathy often seen in which patients, receiving what therapy?

A
  • Those w/ leukemias or lymphomas undergoing chemotherapy (tumor lysis syndrome)
  • Released nuclei acids –> uric acid (precipitation favored by acidic pH in collecting tubules)
67
Q

Nephrolithiasis vs. nephrocalcinosis?

Disorders associated w/ each?

A
  • 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
Q

What is the main cause of renal dysfunction in pts w/ Multiple Myeloma?

A

Bence-Jones (light-chain) proteinuria

69
Q

What are the 2 mechanism which account for the renal toxicitiy of Bence-Jones (light-chain) proteins in Multiple Myeloma pts?

A

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
Q

What are the 4 main ways that renal damage can occur in Multiple Myeloma pts?

A
  1. Bence-Jones proteinuria and cast nephropathy
  2. Amyloidosis
  3. Light-chain deposition disease
  4. Hypercalcemia and Hyperuricemia
71
Q

What is light-chain deposition disease seen in some pts with multiple myeloma?

A
  • Light chains (usually K type) deposit in GBMs and mesangium causing a glomerulopathy
  • Also in tubular BM’s which may cause tubulointerstitial nephritis
72
Q

What is the characteristic tubulointerstitial morphology seen in light-chain cast nephropathy?

A
  • Blue amorphous masses, sometimes concentrically laminated and fractured, filling and distending tubular lumens
  • Some casts surrounded by multinucleate giant cells
73
Q

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?

A
  • AL amyloidosis
  • Light-chain deposition disease
74
Q

Clinically, what is the most common presentation for the renal manifestations associated with light-chain cast nephropathy?

A

1) CKD developing slow and progressively = most common
2) AKI w/ oliguria = less common

75
Q

Hepatorenal syndrome seen in pts w/ acute or chronic liver disease w/ advanced liver failure may cause what type of nephropathy?

A

Bile cast nephropathy

76
Q

Nephroslcerosis is defined as sclerosis of what vessels in the kidney?

Strongly associated with what disease?

A
  • Renal arterioles and small arteries
  • Strong association w/ HTN

*Benign nephrosclerosis is a general process, NOT a specific Dx

77
Q

Nephrosclerosis is associated with what factors?

A
  • Advancing age
  • Blacks > whites
  • Strongly associated w/ HTN and DM; may be seen in absence of HTN too
78
Q

What are the 2 processes occuring in the pathogenesis of Benign Nephrosclerosis?

A
  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
Q

What is the gross morphology (i.e., cortical surface) of the kidneys in Benign Nephrosclerosis?

A
  • 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
Q

Benign nephrosclerosis is NOT usually associated w/ renal insufficiency except in which 3 groups of pts w/ HTN?

A
  1. Pts of African descent
  2. Pts w/ severe BP elevations
  3. Pts w/ 2nd underlying dz, especially diabetes
81
Q

What are histological features of the kidneys seen in Benign Nephrosclerosis?

A
  • Hyaline arteriolsclerosis
  • Fibroelastic hyperplasia
  • Patchy ischemic atrophy of tubules and glomeruli
82
Q

Malignant Nephrosclerosis typically occurs most often in whom?

A
  • Younger pts
  • More often in men and in blacks
83
Q

What are the 2 histologic alterations that characterize blood vessels in malignant HTN (Nephrosclerosis)?

Which of these changes correlates w/ renal failure?

A
  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
Q

Explain the pathogenesis of the lesions in Malignant Nephrosclerosis after the initial vascular damage.

A
  • 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
Q

How does the cortical surface of the kidney appear in Malignant Nephrosclerosis?

A

Small, pinpoint petechial hemorrhages = “flea-bitten” appearance

86
Q

Patients w/ malignant HTN have markedly elevated levels of?

Leads to what type of cycle?

A
  • Renin
  • Self-perpetuating cycle of damage and HTN
87
Q

The full-blown syndrome of Malignant HTN is characterized by what BP, and other serious clinical manifestations?

A
  • BP = >200 / >120 mmHg
  • Papilledema
  • Retinal hemorrhages
  • Encephalopathy
  • CV abnormalities
  • Renal failure
88
Q

Most often the early symptoms of Malignant HTN include what?

What renal findings?

A
  • Sx’s related to ↑ ICP –> HA, N/V, and visual impairments (i.e., scotomas or seeing spots)
  • Marked proteinuria and micro/macroscopic hematuria
89
Q

What is the importance clinically in recognizing Renal Artery Stenosis in regards to treatment?

A
  • Potentially curable form of HTN = 70-80% cure rate
90
Q

Renal artery stenosis leads to what pathophysiologic changes?

A
  • Increased prod. of renin from ischemic kidney –> HTN
  • Sodium retention may occur and perpetuate the HTN
91
Q

What is the most common cause of renal artery stenosis (70%)?

Who is most at risk?

A
  • Narrowing at origin of renal artery by atheromatous plaque
  • More frequent in men, ↑ with advanced age, and diabetes
92
Q

Which cause of renal artery stenosis is more often seen in younger age groups (3rd-4th decades) and is more common in woman?

A

Fibromuscular dysplasia of renal artery

93
Q

What is the classic appearance on arteriography of renal artery stenosis due to fibromuscular dysplasia?

A

“String of beads” appearance

94
Q

In general pts w/ renal artery stenosis present clinically similar to what other disorder?

How can it be diagnosed?

A
  • 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
Q

What is the arteriolosclerosis like in the ischemic kidney in renal artery stenosis vs. non-ischemic (functional) kidney?

A
  • 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
Q

The primary cause/inciting event of HUS differs from TTP how as far as pathogenesis?

A
  • HUS = caused by endothelialinjuryandactivation
  • TTP = inciting event is platelet activation –> aggregation
97
Q

What is the trigger for endothelial injury in typical HUS vs. atypical HUS?

A
  • Typical HUS - trigger is Shiga-like toxin (EHEC > Shigella)
  • Atypical HUS - trigger is excessive activation of complement
98
Q

What are the 3 major findings in the Thrombotic Microangiopathies (HUS and TTP)?

A
  • Thrombi in capillaries and arterioles
  • Microangiopathic hemolytic anemia
  • Thrombocytopenia**** (big clue in a question stem!)
99
Q

Who is most often affected by Typical HUS?

How is this form treated/managed and prognosis?

A
  • 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
Q

What are the 2 common inherited deficiencies which cause Atypical HUS?

A
  • Deficiencies in complement regulatory proteins
  • Most common = Factor H (breaks down alternative path)
  • Some are deficient in Factor I and CD46
101
Q

Other than inherited deficiencies of complement, what are some of the other causes of Atypical HUS?

A
  • 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
Q

What is the prognosis of Atypical HUS?

A

Generally not as well as typical due to underlying conditions

103
Q

Thrombotic Thrombocytopenic Purpura (TTP) is classically manifested by what pentad, what is the dominant feature?

A

1) Fever
2) Neurological sx’s = Dominant feature
3) Microangiopathic hemolytic anemia
4) Thrombocytopenia
5) Renal failure

104
Q

TTP and Atypical HUS both appear more commonly in adults, occassionally having similar sx’s. How are they distinguished from one another?

A

Presence of normal ADAMTS13 in plasma = Atypical HUS

105
Q

TTP is associated with inherited or acquired deficiencies in what?

The most common cause is due to what?

A

- ADAMTS13 = plasma metalloprotease which regulates vWF

  • Inhibitory autoantibodies against ADAMTS13 = MOST COMMON!
106
Q

Who is most often affected by TTP and it typically presents before what age?

A
  • Woman
  • Presents before 40 yo
107
Q

What is the standard of treatment of TTP?

A

Plasma exchange to remove autoantibodies + provide functional ADAMTS13

108
Q

In TTP, deficiencies of ADAMTS13, a negative regulator of vWF, permits the formation of what?

A

Abnormally large multimers of vWF that activate platelets

109
Q

Light microscopy of chronic disease associated with atypical HUS/TTP will show what?

A
  • Mildy HYPERcellular glomeruli
  • Thickened capillary walls
  • Splitting/reduplication of BM (“tram-tracks”)
  • “Onion-skinning” of arterial walls
110
Q

What are the morphological characteristics seen on micrcoscopy in both HUS/TTP?

Which arteries will show necrosis? (quiz question!)

A
  • 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
Q

Bilateral renal artery disease (aka atherosclerotic ischemic renal disease) is a common cause of what in older individuals?

A

Chronic ischemia w/ renal insufficiency, sometimes w/o HTN

112
Q

How is bilateral renal artery disease definitively diagnosed?

Treatment?

A
  • Arteriography
  • Surgical revascularization
113
Q

Atheroembolic renal disease is caused by what?

Most often seen in whom and when?

A
  • 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
Q

The emboli of Atheroembolic Renal Disease can be identified in the lumens of arcuate and interlobular arteries due to what appearance?

A

Content of cholesterol crystals, which appear as rhomboid clefts

115
Q

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?

A
  • 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
Q

Diffuse Cortical Necrosis is an uncommon condition occuring most frequently after what?

Appears how morphologically?

A
  • Obstetric emergencies, septic shock, or extensive surgeries
  • Coagulative necrosis of both glomeruli and tubules, with necrosis confined to cortex
117
Q

Why are the kidneys a common site for the development of infarcts?

Most infarcts are due to?

A
  • Receive 1/4 of the cardiac output, “end-organ” vascular supply, and lack of collateral circulation
  • Most infarcts are due to embolism
118
Q

What are the most common source of emboli leading to renal infarcts?

A
  • Mural thrombosis from left atrium/ventricle due to MI
  • Vegetative endocarditis
  • Aortic aneurysms
  • Aortic atherosclerosis
119
Q

Due to the lack of collateral blood supply, how do renal infarcts appear morphologically?

Shape?

A
  • Sharply demarcated,pale, yellow-whiteareas ofcoagulative necrosis
  • Wedge-shaped

(OMS2) CPR II Exam 3 (17 decks)

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