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pathpros > RENAL PATHOLOGY 2 > Flashcards

RENAL PATHOLOGY 2 Flashcards

Covers Vascular Kidney Disorders & Tubulointerstitial disorders,

1
Q

Etiology of chronic pyelonephritis

A

oInadequately treated acute pyelonephritis

orecurrent and persistent bacterial infection due to urinary tract obstruction, urine reflux, or both

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2
Q

What electrolyte imbalance must be watched for in the recovery phase of acute tubular injury?

A

Hypokalemia

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3
Q

Pre renal causes of acute kidney injury due to volume sequestration

A

pancreatitis, peritonitis, rhabdomyolysis

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4
Q

Underlying mechanism for Thrombotic Thrombocytopenic Purpura

A

Deficiency of ADAMTS13–> Very large vWF multimers –> bind platelet surface glycoproteins and activate platelets spontaneously –> microthrombi

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5
Q

Gross morphology of reflux associated chronic pyelonephritis

A

Scars in the upper and lower poles

Irregular, discrete overlying deformed and blunt calyces

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6
Q

Why is there eventual supression of renin synthesis in bilateral RAS/ RAS in a solitary functioning kidney?

A

Lack of pressure natriuresis

(see image for detailed explanantion)

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7
Q

3 causes of Classical Distal Renal Tubule Acidosis (Type 1)

A
  1. Sjogren Syndrome
  2. Rheumatoid arthritis
  3. Drugs- Lithium
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8
Q

Morphology of chronic transplant rejection

A
  • intimal thickening , vascular occlusion
  • interstitial fibrosis, tubular atrophy
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9
Q

Morphology of acute cellular rejection

A
  • extensive interstitial inflammation and tubular inflammation
  • Inflammation of vessels with/without necrosis
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10
Q

definition of oliguria

A

urine output of less than 400 mL/day or less than 20 mL/hr.

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11
Q

In a patient with bilateral functioning kidneys and unilateral RAS, what happens to the renin levels in the non stenotic contralateral kidney?

A

decreased renin secretion

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12
Q

How does typical HUS lead to microthrombi formation?

A

Shiga like toxin(Stx) binds to the globotriasylceramide Gb3 receptor on the renal endothelium –> damage to the endothelium–>platelet activation and vasoconstriction, reduced NO –> microthrombi.

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13
Q

Important renal manifestation of invasive cervical cancer?

A

bilateral hydronephrosis and renal failure

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14
Q

Diagnosis?

fever+ eosinophilia+ rash + hematuria, rising serum creatinine

A

Acute Drug-Induced Interstitial Nephritis

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15
Q

Morphologic feature of analgesic nephropathy

A

Papillary necrosis assoc with dystrophic calcification

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16
Q

Identify this important cause of renal artery stenosis from the clues below:

young to middle aged female hypertensive patients

mid and distal portion of the artery

“string of beads” on angiography

A

Fibromuscular disease

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17
Q

Mechanism of analgesic nephropathy

A

Phenacetin and its metabolites concentrate in the medullary interstitium–> induce generation of reactive metabolites–> direct covalent binding and oxidative damage –>cell injury

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18
Q

Kidney morphology in multiple myeloma

A

Dilated tubules with eosinophilic casts with Tamm-Horsfall protein trapping light chains

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19
Q

Post renal causes of acute kidney injury

A
  • obstruction at the urethra or bladder outlet
  • bilateral ureteral obstruction
  • unilateral obstruction in a patient with a single functioning kidney.
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20
Q

Gross appearance of the kidney in malignant nephrosclerosis

A

fibrinoid necrosis + intraluminal thrombosis and rupture of glomerular capillaries and arterioles –> petechial hemorrhage on the cortical surface –>flea bitten kidney appearance

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21
Q

Morphology of antibody mediated acute rejection

A

inflammation of glomeruli and peritubular capillaries

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22
Q

Two microscopic features of chronic pyelonephritis

A

Thyroidization of tubules – atrophied/dilated tubules with colloid like casts

Chronic interstitial inflammation and fibrosis

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23
Q

Pre renal causes of acute kidney injury due to decreased circulating blood volume

A

Hemorrhage

Burns

Diarrhea

Diuretics

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24
Q

Gross appearance of the kidney in benign nephrosclerosis

A

Finely granular cortical surface (grain leather)

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25
Q

Diagnosis

Glycosuria, aminoaciduria, hypercitraturia, and phosphaturia

Hypokalemia

Urine ph<5.5

Bicarbonate 15-18mEq/L

A

Fanconi Syndrome assoc with proximal (Type 2) RTA

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26
Q

Causes for renal dysfunction in multiple myeloma

A
  1. Bence Jones proteinuria
  2. Amyloidosis of AL type, formed from free light chains (usually of λ type).
  3. Light-chain deposition disease - light chains (usually of κ type) deposit in GBMs and mesangium in nonfibrillar forms
  4. Hypercalcemia and hyperuricemia
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27
Q

Morphology of acute tubular necrosis

A

casts in tubular lumen

Flattened dilated lumina with sloughing off of apical cytoplasm

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28
Q

Which important complication of acute pyelonephritis is shown in the attached image?

A

Papillary necrosis

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29
Q

Mechanism of drug induced acute interstitial nephritis

A

Drugs act as haptens–>covalently bind to some plasma membrane /extracellular component of tubular cells –>immunogenic–> IgE or cell-mediated immune reactions directed against the tubular cells or the BM.

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30
Q
  1. Term that best describes the morphology shown in the attached image
  2. What is the underlying cause?
A
  1. Onion skinning seen in hyperplastic arteriolosclerosis
  2. Severe hypertension
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31
Q

What is the most likely etiology responsible for the finding shown?

A

Atherosclerotic Renal Disease

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32
Q

Radiologic finding assoc with acute pyelonephritis

A

CT scan with contrast - striated nephrogram

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33
Q

2 conditions associated with nephrosclerosis

A

hypertension

diabetes

34
Q

How does hypertension lead to hyaline arteriolosclerosis?

A

Increased intraluminal arteriolar pressure–> damaged vessel wall–>leakage of plasma proteins.

35
Q

Why do RBCs in the vasa recta sickle?

A

The low oxygen tension or relatively hypoxic, hypertonic, and acidotic environment of the inner medulla predisposes red blood cells in the vasa recta to sickle

36
Q

How does diabetes mellitus lead to hyaline arteriolosclerosis?

A

glucose combines with proteins in the basement membrane of arterioles–>a process called nonenzymatic glycosylation (NEG) –>causes the basement membrane to leak proteins from the plasma into the vessel wall.

37
Q

What will be the gross morphology of the kidney in the condition described below?

sudden onset of pain at the costovertebral angle, fever, malaise

Dysuria, frequency, urgency

A

Condition : Acute pyelonephritis

Gross morphology: grayish whiote focal abscesses

38
Q

How do NSAIDs cause acute kidney injury?

A

decreased synthesis of vasodilatory prostaglandins–> ischemia.

39
Q

Pre renal causes of acute kidney injury due to reduction in effective arterial blood volume

A

Cardiogenic shock

Sepsis

40
Q

Morpholgic change in wall of blood vessels in response to hypertension

A

Hyaline arteriolosclerosis

41
Q

List some causes for a non anion gap acidosis

A

a. Loss of bicarbonate from the gastrointestinal tract- diarrhea
b. Loss of bicarbonate from the kidney- proximal renal tubular acidosis
c. inappropriately low renal acid excretion - classical distal RTA [cDRTA], generalized distal RTA [type 4 RTA]
d. Progressive CKD

42
Q

2 important causes for renal artery stenosis

A
  1. Atherosclerosis
  2. Fibromuscular dysplasia
43
Q

2 main causes for acute tubular necrosis

A
  1. Ischemia
  2. Direct toxic injury to tubules
44
Q

How does an individual contract typical HUS?

A

Intestinal infection by Escherichia coli strain O157:H7 through ingestion of _contaminated ground meat (_as in hamburgers)

45
Q

Types of RTA

A
  1. Proximal RTA (type 2)
  2. Classical distal RTA (type 1)
  3. Hyperkalemic RTA (type 4)
46
Q

Idenitfy the morphologic feature shown in the attached image and list conditions associated with it

A
  1. Fibrinoid necrosis + concentric, laminated (“onion-skin”) thickening of the walls
  2. Malignant hypertension
47
Q

Identify the pattern of transplant rejection whose mechanism has been described below:

preformed antibodies specific for antigens on graft endothelial cell

Occurs within hours, immediately after the graft is implanted and blood flow is restored

A

Hyperacute rejection

48
Q

Is this pre renal acute kidney injury OR acute tubular necrosis?

BUN/ Cr ratio >20:1

Urine sodium <25mEq/L

FeNa <1%

Urine osmolality >500mOsm/kg

A

Favors pre-renal disease

49
Q

Type of RTA described below:

urine pH <5.5

a positive urinary anion gap

Low aldosterone

Hyperkalemia

A

Type 4 RTA

50
Q

Pre renal causes of acute kidney injury due to reduction in cardiac output because of profound vasoconstriction

A

NSAIDs

Hepatorenal syndrome

Severe heart failure

51
Q

Deficiency of which enzyme necessary for breaking down bone within osteoclasts presents with renal tubular acidosis ?

A

Carbonic anhydrase II is an enzyme that generates carbonic acid from water and carbon dioxide to help create the acidic milieu necessary to break bone down within the osteoclasts.

Carbonic anhydrase II deficiency syndrome manifests as the following triad:

  1. Osteopetrosis
  2. Renal tubular acidosis
  3. Cerebral calcification
52
Q

Conditions associated with the renal morphology shown

A

Image shows Urate nephropathy

Condition assoc is Gout

53
Q

Characteristic finding of acute tubular necrosis on urinalysis

A

Muddy brown granular casts

54
Q

What type of infarct is seen in the kidney- pale or red?

A

Wedge shaped pale infarcts

55
Q

Identify the pattern of transplant rejection whose mechanism has been described below:

CD8+ CTLs activated by alloantigens within the graft may directly destroy graft cells, or CD4+ cells secrete cytokines and induce inflammation, which damages the graft

Within days-weeks

A

Acute cellular rejection

56
Q

Most common cause of acute kidney injury?

A

Acute tubular necrosis

57
Q

What pattern of pathologic calcification is assoc with nephrocalcinosis- Dystrophic/ metastatic?

A

Metastatic calcification

58
Q

Complications of acute pyelonephritis

A
  1. Papillary necrosis
  2. Pyonephrosis
  3. Perinephric abscess
  4. Chronic pyelonephritis
  5. Septicemia with endotoxic shock
59
Q

Identify the pattern of transplant rejection whose mechanism has been described below:

antibodies bind to vascular endothelium and activate complement via the classical pathway –>inflammation –> endothelial damage–>graft failure

A

Antiobody mediated acute rejection

60
Q

Light microscopic morphology of hyperacute transplant rejection

A

oArteries - acute fibrinoid necrosis

oGlomeruli- thrombotic occlusion of capillaries

61
Q

Type of RTA described below:

Positive UAG

Urine pH >5.5

Hypokalemia

defect in acid secretion by type A intercalated cells in the distal nephron

A

Classical Distal Renal Tubule Acidosis (Type 1)

62
Q

Is this pre renal acute kidney injury OR acute tubular necrosis?

BUN/ Cr ratio < 15:1

Urine sodium >40mEq/L

FeNa >2%

Urine osmolality 300-350mOsm/kg

A

Favors acute tubular necrosis

63
Q

Diagnosis?

recurrent fever, flank pain, dysuria

Gross: large, yellowish orange nodule

LM: accumulation of foamy macrophages intermingled with plasma cells, lymphocytes, polymorphonuclear leukocytes, and occasional giant cells.

A

Xanthogranulomatous pyelonephritis

64
Q

What are some clinical clues to suspect renovascular hypertension?

A

Sudden-onset hypertension prior to 30 years of age or after 55 years of age.

Severe or refractory hypertension

Severe hypertension with heart failure/flash pulmonary edema

Sudden onset of worsening azotemia after the institution of an ACE inhibitor or ARB

Epigastric abdominal bruit in the setting of increased BP

65
Q

Why is the medulla spared in diffuse cortical necrosis?

A

Vasa recta that supply arterial blood to the medulla arise from juxtamedullary efferent arterioles, proximal to vessels supplying the outer cortex. Thus, occlusion of outer cortical vessels (e.g., by vasospasm, thrombi or thrombotic microangiopathy) leads to cortical necrosis and spares the medulla.

66
Q

3 thrombotic microangiopathies assoc with renal manifestations

A

Typical Hemolytic uremic syndrome (HUS)

Atypical Hemolytic uremic Syndrome (HUS)

Thrombotic thrombocytopenic purpura (TTP)

67
Q

Gross morphology of obstruction associated chronic pyelonephritis

A

Diffuse scarring with thinned out cortex.

68
Q

4 manifestations of sickle cell nephropathy

A

Renal Infarction

Hematuria

Hyposthenuria

Papillary necrosis

69
Q

In which clinical scenario would you be likley to encounter the finding shown ?

A

Finding shown: Diffuse cortical necrosis

Clinical scenario: Any condition associated with hypovolemic or endotoxic shock

70
Q

Intrinsic causes of acute kidney injury

A
  1. Acute tubular injury
  2. Drug induced interstitial nephritis
  3. Intratubular obstruction
  4. Glomerular diseases
  5. Occlusion of large renal vessles
71
Q

most common cause of tubulointerstitial nephritis in the United States

A

Medications

72
Q

List 3 conditions in which papillary necrosis is seen?

A

diabetics, sickle cell disease, obstructive uropathy

73
Q

Recap the 3 major categories of acute kidney injury and how they are distinguished based on FeNa, BUN/Cr, UNa, UOsm, Urinalysis

A
74
Q

key distinguishing feature between renal papillary necrosis due to diabetes versus analgesic nephropathy

A

DM: All of the affected papillae are at the same stage Analgesic nephropathy: several papillae are at different stages of necrosis

75
Q

Why is the left kidney affected more than the right kidney in sickle cell nephropathy?

A

longer left renal vein is compressed between the aorta and the superior mesenteric artery —> increased venous pressure a “nutcracker phenomenon.”—> leads to increased relative hypoxia in the renal medull –> sickling.

76
Q

2 drugs assoc with proximal RTA

A

Acetazolamide, Ifosfamide

77
Q

Identify the condition described

Neurologic symptoms
Fever
Thrombocytopenia
Hemolysis –microangiopathic hemolytic anemia
Kidney Failure

A

Thrombotic Thrombocytopenic Purpura

78
Q

List drugs causing acute drug induced interstitial nephritis

A
  • Mnemonic: SMART CAN*
  • *S**= SULFONAMIDES
  • *M**=METHICILLIN
  • *A**=AMPICILLIN
  • *R**=RIFAMPICIN
  • *T**=THIAZIDES
  • *C**=CIMETIDINE
  • *A**=ALLOPURINOL
  • *N**=NSAIDS
79
Q

Mechanism of atypical HUS

A

Impaired function of complement regulatory proteins - Factor H, complement Factor I and CD46 OR Autoantibodies against complement regulatory proteins

80
Q

Identify the pattern of transplant rejection described below:

T cells –>react against graft alloantigens–>

cytokines–> stimulate the proliferation and activities of fibroblasts and vascular smooth muscle cells in the graft –>intimal thickening and vascular occlusion

A

Chronic transplant rejection

81
Q

In a patient with bilateral functioning kidneys and unilateral RAS, what happens to the renin levels in the stenotic ischemic kidney?

A

Renin in the ischemic kidney is elevated

82
Q

6 causes for renal infarction

A
  1. AFib–> Left atrial thrombus formation → systemic circulation
  2. Mural thrombi overlying myocardial infarcts in the LV
  3. Atherosclerotic emboli from the abdominal aorta or renal artery
  4. Thrombosis superimposed on underlying atherosclerosis
  5. Infected valves in bacterial endocarditis
  6. Sickle cell nephropathy

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