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GBA Pathology > PATHOMA12 - Kidney and Urinary Tract Pathology > Flashcards

PATHOMA12 - Kidney and Urinary Tract Pathology Flashcards

1
Q

What is the most common congenital renal anomaly?

A

Horseshoe kidney - Conjoined kidneys usually connected at the lower pole

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2
Q

In horseshoe kidney where is it located?

A

Kidney is abnormally located in the lower abdomen

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3
Q

What happens in horseshoe kidney?

A

The kidney gets caught on the inferior mesenteric artery root during its ascent from the pelvis to the abdomen

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4
Q

What is renal agenesis?

A

Absent kidney formation; may be unilateral or bilateral

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5
Q

What does unilateral renal agenesis lead to?

A

hypertrophy of the existing kidney; hyperfiltration increases risk of renal failure later in life.

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6
Q

What does bilateral agenesis lead to?

A

oligohydramnios with lung hypoplasia, flat face with low set ears, and developmental defects of the extremities (Potter sequence) incompatible with life

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7
Q

What is dysplastic kidney?

A

Non-inherited, congenital malformation of the renal parenchyma characterized by cysts and abnormal tissue (e.g., cartilage)

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8
Q

Is dysplastic kidney unilateral or bilateral?

A

Usually unilateral; when bilateral, must be distinguished from inherited polycystic kidney disease

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9
Q

What is polycystic kidney disease?

A

Inherited defect leading to bilateral enlarged kidneys with cysts in the renal cortex and medulla

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10
Q

How does the autosomal recessive form of polycystic kidney disease present?

A

in infants as worsening renal failure and hypertension; newborns may present with Potter sequence

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11
Q

What is the autosomal recessive form of polycystic kidney disease associated with?

A

congenital hepatic fibrosis (leads to portal hypertension) and hepatic cysts

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12
Q

How does the autosomal dominant form of polycystic kidney disease present?

A

in young adults as hypertension (due to increased renin), hematuria, and worsening renal failure

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13
Q

What is the autosomal dominant form of polycystic kidney disease due to?

A

A mutation in the APKD1 or APKD2 gene; cysts develop over time.

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14
Q

What is the autosomal dominant form of polycystic kidney disease associated with?

A

berry aneurysm, hepatic cysts, and mitral valve prolapse

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15
Q

What is medullary cystic kidney disease?

A

Inherited (autosomal dominant) defect leading to cysts in the medullary collecting ducts

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16
Q

What does parenchymal fibrosis result in?

A

shrunken kidneys and worsening renal failure

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17
Q

What is acute renal failure?

A

Acute, severe decrease in renal function (develops within days)

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18
Q

What is the hallmark of acute renal failure?

A

Azotemia, (increased BUN and creatinine) often with oliguria

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19
Q

What is acute renal failure divided into?

A

Its divided into prerenal, postrenal, and intrarenal azotemia and is based on etiology

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20
Q

What is prerenal azotemia?

A

Due to decreased blood flow to kidneys (e.g., cardiac failure)

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21
Q

Prerenal azotemia is a common cause of what?

A

ARF (acute renal failure)

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22
Q

What does decreased blood flow result in?

A

decreased GFR, azotemia, and oliguria.

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23
Q

In prerenal azotemia what happens to the ability to absorb fluid?

A

reabsorption of fluid and BUN ensues (serum BUN:Cr ratio > 15) tubular function remains intact (fractional excretion of sodium [FENa] < 1% and urine osmolality [osm] > 500 mOsm/kg)

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24
Q

What is postrenal azotemia due to?

A

obstruction of urinary tract downstream from the kidney (e.g., ureters)

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25
Q

In postrenal azotemia what does the decreased outflow result in?

A

decreased GFR, azotemia, and oliguria

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26
Q

In postrenal azotemia, what happens during the early stage of obstruction?

A

There is increased tubular pressure which forces BUN into the blood (serum BUN;Cr ratio > 15); tubular function remains intact (FENa < 1% and urine osm > 500 mOsm/kg).

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27
Q

In postrenal azotemia, what happens with long-standing obstruction?

A

tubular damage ensues, resulting in decreased reabsorption of BUN (serum BUN:Cr ratio < 15), decreased reabsorption of sodium (FENa > 2%), and inability to concentrate urine (urine osm < 500 mOsm/kg)

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28
Q

What is acute tubular necrosis?

A

It is injury and necrosis of tubular epithelial cells

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29
Q

What is the most common cause of acute renal failure?

A

Acute tubular necrosis (intrarenal azotemia)

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30
Q

In acute tubular necrosis, what happens?

A

Necrotic cells plug tubules; obstruction decreases GFR

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31
Q

In acute tubular necrosis, what is seen in the urine?

A

Brown, granular casts are seen in the urine

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32
Q

In acute tubular necrosis what does dysfunctional tubular epithelium result in?

A

decreased reabsorption of BUN (serum BUN:Cr ratio < 15), decreased reabsorption of sodium (FENa > 2%), and inability to concentrate urine (urine osm < 500 mOsm/kg).

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33
Q

What is the etiology for acute tubular necrosis?

A

may be ischemic or nephrotoxic,

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34
Q

What happens with ischemia and acute tubular necrosis?

A

Decreased blood supply results in necrosis of tubules.

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35
Q

With ischemia causing acute tubular necrosis, what is it often preceded by?

A

prerenal azotemia

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36
Q

With ischemia causing acute tubular necrosis, what parts of the nephron are particularly susceptible to ischemic damage?

A

proximal tubule and medullary segment of the thick ascending limb

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37
Q

What is another cause, aside from ischemia that results in acute tubular necrosis?

A

its nephrotoxic and toxic agents result in necrosis of tubules

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38
Q

In nephrotoxic damage leading to acute tubular necrosis, what parts of the nephron are particularly susceptible to damage?

A

Proximal tubule

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39
Q

What is the most common cause of nephrotoxic damage leading to acute tubular necrosis?

A

aminoglycosides

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40
Q

In nephrotoxic damage leading to acute tubular necrosis, what are the causes?

A

They include aminoglycosides, heavy metals, myoglobinuria, ethylene glycol, radiocontrast dye, and urate

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41
Q

What is an example of heavy metals leading to acute tubular necrosis?

A

lead

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42
Q

What causes myoglobinuria leading to acute tubular necrosis?

A

and example is from crush injury to muscle

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43
Q

What is ethylene glycol leading to acute tubular necrosis associated with?

A

oxalate crystals in urine

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44
Q

What is an example of urate leading to acute tubular necrosis?

A

tumor lysis syndrome

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45
Q

In nephrotoxicity leading to acute tubular necrosis what are used prior to initiation of chemotherapy?

A

Hydration and allopurinol

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46
Q

Why is hydration and allopurinol used prior to initiation of chemotherapy?

A

to decrease risk of urate-induced ATN.

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47
Q

What are the clinical features for acute tubular necrosis?

A

1) Oliguria with brown, granular casts 2) Elevated BUN and creatinine 3) Hyperkalemia (due to decreased renal excretion) with metabolic acidosis

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48
Q

Why is there hyperkalemia in acute tubular necrosis?

A

its due to decreased renal excretion

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49
Q

Is acute tubular necrosis reversible?

A

Yes, but often requires supportive dialysis since electrolyte imbalances can be fatal

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50
Q

In acute tubular necrosis, for how long can oliguria persist?

A

for 2 -3 weeks before recovery

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51
Q

In acute tubular necrosis, why is that oliguria can persist for 2-3 weeks?

A

tubular cells (stable cells) take time to reenter the cell cycle and regenerate

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52
Q

What is acute interstitial nephritis?

A

Drug-induced hypersensitivity involving the interstitium and tubules

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53
Q

What does acute interstitial nephritis result in?

A

acute renal failure (intrarenal azotemia)

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54
Q

What are the causes of acute interstitial nephritis?

A

They include NSAIDs, penicillin, and diuretics

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55
Q

What does acute interstitial nephritis present as?

A

oliguria, fever, and rash days to weeks after starting a drug; eosinophils may be seen in urine.

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56
Q

How does acute interstitial nephritis resolve?

A

with cessation of drug

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57
Q

What may acute interstitial nephritis progress to?

A

renal papillary necrosis

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58
Q

What is renal papillary necrosis?

A

Necrosis of renal papillae

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59
Q

What does renal papillary necrosis present with?

A

gross hematuria and flank pain

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60
Q

What are the causes for renal papillary necrosis?

A
  1. Chronic analgesic abuse (e.g., long-term phenacetin or aspirin use) 2. Diabetes mellitus 3. Sickle cell trait or disease 4. Severe acute pyelonephritis
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61
Q

What is nephrotic syndrome?

A

Glomerular disorders characterized by proteinuria (> 3.5 g/day)

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62
Q

What does nephrotic syndrome result in?

A
  1. Hypoalbuminemia 2. Hypogammaglobulinemia 3. Hypercoagulable state 4. Hvperlipidemia and hypercholesterolemia
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63
Q

In nephrotic syndrome, what is involved with hypoalbuminemia being the cause?

A

pitting edema

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64
Q

In nephrotic syndrome caused y hypogammaglobulinemia, what is there an increased risk of?

A

infection

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65
Q

In nephrotic syndrome caused by a hypercoagulable state, what is that state due to?

A

loss of antithrombin III

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66
Q

With hyperlipidemia and hypercholesterolemia causing nephrotic syndrome, what may result?

A

This may result in fatty casts in urine

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67
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease (MCD)

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68
Q

What is the etiology for MCD?

A

For minimal change disease, it is usually idiopathic and may be associated with Hodgkin lymphoma

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69
Q

How does MCD appear on H&E stain?

A

Normal glomeruli on H&E stain, lipid may be seen in proximal tubule cells

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70
Q

In MCD, what is seen on electron microscopy?

A

effacement of foot processes

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71
Q

In MCD what is seen on immunofluorescence and why?

A

negative immunofluorescence (IF) because there are no immune complex deposits

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72
Q

In MCD, what happens in terms of proteinuria?

A

There is selective proteinuria where there is loss of albumin, but not immunoglobulin

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73
Q

What is the treatment for MCD?

A

It has an excellent response to steroids

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74
Q

How is the damage in MCD mediated?

A

damage is mediated by cytokines from T cells

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75
Q

What is the most common cause of nephrotic syndrome in Hispanics and African Americans?

A

Focal segmental glomerulosclerosis (FSGS)

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76
Q

What is the etiology for focal segmental glomerulosclerosis?

A

It is usually idiopathic, maybe associated with HIV, heroin use, and sickle cell disease

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77
Q

What is focal segmental glomerulosclerosis?

A

Focal (some glomeruli) and segmental (involving only part of the glomerulus) sclerosis on H&E stain

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78
Q

What is seen on electron microscopy in FSGS?

A

In focal segmental glomerulosclerosis, there is effacement of foot processes on EM

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79
Q

For focal segmental glomerulosclerosis, what is seen on IF?

A

Negative immunofluorescence due to no immune complex deposits

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80
Q

How does FSGS respond to steroids and what may it progress to?

A

Poor response to steroids and may progress to chronic renal failure

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81
Q

What is the most common cause of nephrotic syndrome in Caucasian adults?

A

Membranous nephropathy

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82
Q

What is the etiology for membranous nephropathy?

A

It is usually idiopathic, it may be associated with hepatitis B or C, solid tumors, SLE, or drugs (e.g., NSAIDs and penicillamine)

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83
Q

For membranous nephropathy, what is seen on H&E stain?

A

Thick glomerular basement membrane

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84
Q

What is the appearance of membranous nephropathy on electron microscopy?

A

subepithelial deposits with spike and dome appearance on EM

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85
Q

For membranous nephropathy, what is its appearance on EM due to?

A

immune complex deposition

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86
Q

How does membranous nephropathy respond to steroids and what might it progress to?

A

Poor response to steroids; progresses to chronic renal failure

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87
Q

What is membranoproliferative glomerulonephritis?

A

Thick glomerular basement membrane on H&E stain, often with tram-track appearance

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88
Q

What is membranoproliferative glomerulonephritis due to?

A

immune complex deposition (granular IF)

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89
Q

What is membranoproliferative glomerulonephritis divided into?

A

two types based on location of deposits

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90
Q

What is membranoproliferative glomerulonephritis - Type I?

A

subendothelial associated with HBV and HCV

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91
Q

What is membranoproliferative glomerulonephritis - Type II?

A

(dense deposit disease) intramembranous; associated with C3 nephritic factor (autoantibody that stabilizes C3 convertase, leading to overactivation of complement, inflammation, and low levels of circulating C3)

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92
Q

How does membranoproliferative glomerulonephritis respond to steroids and what might it progress to?

A

Poor response to steroids; progresses to chronic renal failure

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93
Q

How is diabetes mellitus related to nephrotic syndrome?

A

high serum glucose leads to nonenzymatic glycosylation of the vascular basement membrane resulting in hyaline arteriolosclerosis.

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94
Q

With diabetes mellitus leading to nephrotic syndrome what happens to the glomerular filtration pressure?

A

There is high glomerular filtration pressure

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95
Q

With diabetes mellitus leading to nephrotic syndrome why is there high glomerular filtration pressure?

A

glomerular efferent arteriole is more affected than the afferent arteriole

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96
Q

With diabetes mellitus leading to nephrotic syndrome resulting in high glomerular filtration pressure, what does this lead to?

A

Leads to hyperfiltration injury leading to microalbuminuria

97
Q

What does diabetes mellitus relating to kidney?s eventually progress to?

A

nephrotic syndrome

98
Q

What is diabetes mellitus leading to nephrotic syndrome characterized by?

A

sclerosis of the mesangium with formation of Kimmelstiel-Wilson nodules

99
Q

In diabetes mellitus leading to nephrotic syndrome what slows the progression of hyperfiltration-induced damage?

A

ACE inhibitors

100
Q

What is the most commonly involved organ in systemic amyloidosis?

A

The kidney

101
Q

How does systemic amyloidosis lead to nephrotic syndrome?

A

Amyloid deposits in the mesangium, resulting in nephrotic syndrome

102
Q

How is systemic amyloidosis characterized?

A

by apple-green birefringence under polarized light after staining with Congo red

103
Q

What is nephritic syndrome?

A

Glomerular disorders characterized by glomerular inflammation and bleeding

104
Q

What is seen in nephritic syndrome?

A
  1. Limited proteinuria (< 3.5 g/day) 2. Oliguria and azotemia 3. Salt retention with periorbital edema and hypertension 4. RBC casts and dysmorphic RBCs in urine
105
Q

In nephritic syndrome what is seen in biopsy?

A

it reveals hypercellular, inflamed glomeruli

106
Q

In nephritic syndrome, what mediates damage?

A

Immune-complex deposition activates complement; C5a attracts neutrophils, which mediate damage,

107
Q

What is poststreptococcal glomerulonephritis (PSGN)?

A

Nephritic syndrome that arises alter group A beta-hemolytic streptococcal infection of the skin (impetigo) or pharynx

108
Q

In PSGN, what does it occur with?

A

nephritogenic strains (which carry the M protein virulence factor)

109
Q

PSGN may occur after infection with what organisms?

A

nonstreptococcal organisms as well as nephritogenic strains

110
Q

How does PSGN present?

A

2-3 weeks after infection as hematuria (cola-colored urine), oliguria, hypertension, and periorbital edema

111
Q

PSGN is usually seen in whom?

A

children, but may occur in adults

112
Q

In PSGN what is seen on H&E stain?

A

Its hypercellular, inflamed glomeruli on H&E

113
Q

In PSGN, what is seen on electron microscopy?

A

subepithelial humps on EM, and is mediated by immune complex deposition - granular IF

114
Q

What is the treatment for PSGN?

A

Treatment is supportive.

115
Q

What is the chance for renal failure in PSGN?

A

Children rarely (1%) progress to renal failure

116
Q

In PSGN, what might some adults develop?

A

25% might develop rapidly progressive glomerulonephritis (RPGN)

117
Q

What is rapidly progressive glomerulonephritis?

A

Nephritic syndrome that progresses to renal failure in weeks to months

118
Q

What is rapidly progressive glomerulonephritis characterized by?

A

crescents in Bowman space (of glomeruli) on H&E stain; crescents are comprised of fibrin and macrophages

119
Q

For rapidly progressive glomerulonephritis how is the etiology resolved?

A

clinical picture and IF help resolve etiology

120
Q

In rapidly progressive glomerulonephritis, the immunofluorescence pattern of linear (anti-basement membrane antibody) refers to what disease?

A

Goodpasture syndrome

121
Q

In rapidly progressive glomerulonephritis, the immunofluorescence pattern of linear (anti-basement membrane antibody), the antibody is against what?

A

Antibody against collagen in glomerular and alveolar basement membranes

122
Q

In rapidly progressive glomerulonephritis, the immunofluorescence pattern of linear (anti-basement membrane antibody), how does is present?

A

as hematuria and hemoptysis, classically in young, adult males

123
Q

In rapidly progressive glomerulonephritis, the immunofluorescence pattern of granular (immune complex deposition) refers to what disease?

A

PSGN (most common) or diffuse proliferative glomerulonephritis

124
Q

What is diffuse proliterative glomerulonephritis due to?

A

diffuse antigen - antibody complex deposition, usually sub-endothelial; most common type of renal disease in SLE

125
Q

In rapidly progressive glomerulonephritis, the immunofluorescence pattern of negative IF (pauci-immune) refers to what disease?

A

Wegener granulomatosis, microscopic polyangiitis, and Churg-Strauss syndrome

126
Q

For the immunofluorescence pattern of negative IF (pacui-immune) what disease is associated with c-ANCA?

A

Wegener granulomatosis

127
Q

For the immunofluorescence pattern of negative IF (pacui-immune) what disease is associated with p-ANCA?

A

microscopic polyangiitis and Churg-Strauss

128
Q

For the immunofluorescence pattern of negative IF (pacui-immune) what distinguishes Churg-Strauss from microscopic polyangiitis?

A

Granulomatous inflammation, eosinophilia, and asthma

129
Q

What is IgA nephropathy?

A

Berger disease - IgA immune complex deposition in mesangium of glomeruli; most common nephropathy worldwide

130
Q

What is the most common nephropathy worldwide?

A

Berger disease ? IgA nephropathy

131
Q

When does Berger disease present?

A

during childhood

132
Q

In childhood what does Berger disease present as?

A

Presents as episodic gross or microscopic hematuria with RBC casts, usually following mucosal infections (eg. gastroenteritis)

133
Q

In Berger disease what is increased during infection?

A

IgA production

134
Q

In Berger disease what is seen on IF?

A

IgA immune complex deposition in the mesangium

135
Q

What may Berger disease slowly progress to?

A

renal failure

136
Q

What is alport syndrome?

A

Its an inherited defect in type IV collagen; most commonly X-linked

137
Q

What does Alport Syndrome result in?

A

the thinning and splitting of the glomerular basement membrane

138
Q

What does Alport syndrome presents as?

A

isolated hematuria, sensory hearing loss, and ocular disturbances

139
Q

What is a urinary tract infection?

A

Infection of urethra, bladder, or kidney

140
Q

A urinary tract infection most commonly arises from what?

A

due to ascending infection; increased incidence in females

141
Q

What are the risk factors for urinary tract infection?

A

they include sexual intercourse, urinary stasis, and catheters,

142
Q

What is cystitis?

A

Infection of the bladder

143
Q

What does cystitis present as?

A

dysuria, urinary frequency, urgency, and suprapubic pain; systemic signs (e.g., fever) are usually absent.

144
Q

What are the laboratory tests for cystitis?

A

1) Urinalysis 2) Dipstick 3) Culture

145
Q

What are the laboratory findings for cystitis?

A

1) Urinalysis?cloudy urine with > 10 WBCs/high power field (hpf) 2) Dipstick?Positive leukocyte esterase (due to pyuria) and nitrites (bacteria convert nitrates to nitrites) 3) Culture?greater than 100,000 colony forming units (gold standard)

146
Q

What is the etiology for cystitis?

A

1) E. coli (80%) 2) Staphylococcus saprophytics increased incidence in young, sexually active women (but E. coli is still more common in this population) 3) Klebsiella pneumoniae 4) Proteus mirabilis 5) Enterococcus faecalis

147
Q

In cystitis, if there is alkaline urine with ammonia scent, what is the etiology?

A

Proteus mirabilis

148
Q

In cystitis, what is sterile pyuria?

A

it is the presence of pyuria (> 10 WBCs/hpf and leukocyte esterase) with a negative urine culture.

149
Q

In cystitis, what does sterile pyuria suggest and what is it due to?

A

urethritis due to Chlamydia trachomatis or Neisseria gonorrhoeae

150
Q

What is the dominant presenting sign of urethritis?

A

it is dysuria)

151
Q

What is pyelonephritis?

A

Infection of the kidney

152
Q

What is pyelonephritis usually due to?

A

ascending infection; increased risk with vesicoureteral reflux

153
Q

What does pyelonephritis present with?

A

fever, flank pain, WBC casts, and leukocytosis in addition to symptoms of cystitis

154
Q

For pyelonephritis, what are the most common pathogens?

A

1) E coli (90%) 2) Klebsiella species 3) Enterococcus faecalis

155
Q

What is chronic pyelonephritis?

A

Interstitial fibrosis and atrophy of tubules due to multiple bouts of acute pyelonephritis

156
Q

What is chronic pyelonephritis due to?

A

vesicoureteral reflux (children) or obstruction (e.g., BPH or cervical carcinoma)

157
Q

What does chronic pyelonephritis lead to?

A

cortical scarring with blunted calyces

158
Q

In chronic pyelonephritis, what is characteristic of vesicoureteral reflux?

A

scarring at upper and lower poles

159
Q

In chronic pyelonephritis, what is thyroidization of the kidney?s?

A

Atrophic tubules containing eosinophilic proteinaceous material resemble thyroid follicles

160
Q

In chronic pyelonephritis, what may be seen in urine for thyroidization of the kidney?s?

A

waxy casts

161
Q

What is nephrolithiasis?

A

Precipitation of a urinary solute as a stone

162
Q

What are the risk factors for nephrolithiasis?

A

they include high concentration of solute in the urinary filtrate and low urine volume

163
Q

What does nephrolithiasis present as?

A

colicky pain with hematuria and unilateral flank tenderness

164
Q

In nephrolithiasis, what happens to the stone?

A

it is usually passed within hours; if not, surgical intervention may be required.

165
Q

What is chronic renal failure?

A

End-stage kidney failure

166
Q

What may chronic renal failure result from?

A

glomerular, tubular, inflammatory, or vascular insults

167
Q

What are the most common causes of chronic renal failure?

A

diabetes mellitus, hypertension, and glomerular disease,

168
Q

What are the clinical features for chronic renal failure?

A

1) uremia 2) salt and water retention with resultant hypertension 3) hyperkalemia with metabolic acidosis 4) anemia 5) hypocalcemia 6) renal osteodystrophy

169
Q

What is asterixis?

A

Tremor of the hand when wrist is extended

170
Q

In chronic renal failure, what happens in uremia?

A

increased nitrogenous waste products in blood (azotemia) result in nausea, anorexia, pericarditis, platelet dysfunction, encephalopathy with asterixis, and deposition of urea crystals in skin,

171
Q

In chronic renal failure, what is anemia due to?

A

decreased erythropoietin production by renal peritubular interstitial cells

172
Q

In chronic renal failure, what is hypocalcemia due to?

A

decreased l-alpha-hydroxylation of vitamin D by proximal renal tubule cells and hyperphosphatemia

173
Q

In chronic renal failure, what is renal osteodystrophy due to?

A

secondary hyperparathyroidism, osteomalacia, and osteoporosis

174
Q

In chronic renal failure, what is the treatment?

A

involves dialysis or renal transplant.

175
Q

In chronic renal failure, what often develops during dialysis and what does this increase the risk for?

A

cysts within shrunken end-stage kidneys during dialysis increasing risk for renal cell carcinoma.

176
Q

What is the composition for the most common type of nephrolithiasis?

A

Calcium oxalate and/ or calcium phosphate, usually seen in adults

177
Q

What is the most common cause for the most common type of nephrolithiasis?

A

It is idiopathic

178
Q

In what disease might the most common cause of nephrolithiasis be seen?

A

with Crohn disease

179
Q

For the most common type of nephrolithiasis what is the treatment?

A

Hydrochlorothiazide (caicium-sparing diuretic).

180
Q

For the second most common type of nephrolithiasis what is the composition?

A

Ammonium magnesium phosphate

181
Q

What is the most common cause for the second most common type of nephrolithiasis?

A

Infection with urease-positive organisms (e.g Proteus vulgaris or Klebsiella);

182
Q

For the second most common type of nephrolithiasis what leads to the formation of the stone?

A

alkaline urine

183
Q

What does the second most common type of nephrolithiasis classically result in?

A

staghorn calculi in renal calyces, which act as a nidus for urinary tract infections

184
Q

For the second most common type of nephrolithiasis what does treatment involve?

A

surgical removal of stone (due to size) and eradication of pathogen (to prevent recurrence)

185
Q

What is the composition for the third most common type of nephrolithiasis?

A

Uric acid (5%)

186
Q

How is the nephrolithiasis that is comoposed of uric acid different from the other stones?

A

Its radiolucent (as opposed to other types of stones which are radiopaque)

187
Q

What are the risk factors for nephrolithisasis composed of uric acid?

A

they include hot, arid climates, low urine volume, and acidic pH.

188
Q

What is the most common stone seen in patients with gout?

A

Nephrolithiasis composed of uric acid

189
Q

For nephrolithiasis composed of uric acid what increases the risk?

A

hyperuricemia (e.g., in leukemia or myeloproliferative disorders)

190
Q

For nephrolithisasis composed of uric acid, what does the treatment involve?

A

hydration and alkalinization of urine (potassium bicarbonate);

191
Q

For the treatment of nephrolithiasis composed of uric acid, what is also given to patients with gout?

A

allopurinol is also administered in patients with gout (in addition to hydration and alkalinization of urine with potassium bicarbonate)

192
Q

What form of nephrolithiasis is most commonly seen in children?

A

Cysteine, it is a rare cause of nephrolithiasis and is most commonly seen in children

193
Q

What is associated with nephrolithiasis caused by cysteine?

A

cystinuria (a genetic defect of tubules that results in decreased reabsorption of cysteine)

194
Q

Nephrolithiasis composed of cysteine may form what?

A

staghorn calculi

195
Q

For nephrolithiasis composed of cysteine, what is involved in the treatment?

A

It involves hydration and alkalinization of urine

196
Q

What are the types of renal neoplasia?

A

Angiomylipoma, renal cell carcinoma and wilms tumor

197
Q

What is angiomyolipoma?

A

Hamartoma comprised of blood vessels, smooth muscle, and adipose tissue

198
Q

In what is there an increased frequency of angiomyolipoma?

A

in tuberous sclerosis

199
Q

What is renal cell carcinoma?

A

Malignant epithelial tumor arising from kidney tubules

200
Q

How does renal cell carcinoma present?

A

with classic triad of hematuria, palpable mass, and flank pain, Fever, weight loss, or paraneoplastic syndrome (e.g EPO, renin, PTHrP, or ACTH) may also be present

201
Q

For renal cell carcinoma what is the frequency of the symptoms?

A

All three symptoms rarely occur together; hematuria is the most common symptom.

202
Q

For renal cell carcinoma what is the most common symptom?

A

Hematuria

203
Q

What may renal cell carcinoma rarely present with?

A

left-sided varicocele

204
Q

How might renal cell carcinoma lead to left sided varicocele?

A

Involvement of the left renal vein by carcinoma blocks drainage of the left spermatic vein leading to varicocele

205
Q

For renal cell carcinoma why is right sided varicocele not seen?

A

Right spermatic vein drains directly into the IVC; hence, right-sided varicocele is not seen.

206
Q

For renal cell carcinoma what does gross exam reveal?

A

a yellow mass,

207
Q

For renal cell carcinoma what is seen microscopically for the most common variant?

A

It exhibits clear cytoplasm

208
Q

For renal cell carcinoma what does the pathogenesis involve?

A

loss of VHL (3p) tumor suppressor gene, which leads to increased IGF-l (promotes growth) and increased HIF transcription factor (increases VEGF and PDGF).

209
Q

For renal cell carcinoma are the tumors hereditary or sporadic?

A

May be either

210
Q

For renal cell carcinoma when do sporadic tumors classically arise?

A

Classically in adult males (average age is 60 years) as a single tumor in the upper pole of the kidney

211
Q

For renal cell carcinoma what is the major risk factor for sporadic tumors?

A

cigarette smoke

212
Q

For renal cell carcinoma when do hereditary tumors arise?

A

in younger adults and are often bilateral,

213
Q

What is Von Hippel-Lindau disease?

A

It is an autosomal dominant disorder

214
Q

What is Von Hippel-Lindau disease associated with?

A

inactivation of the VHL gene leading to increased risk for hemangioblastoma of the cerebellum and renal cell carcinoma.

215
Q

What is the staging for renal cell carcinoma?

A

1) T - based on size and involvement of the renal vein (occurs commonly and increases risk of hematogenous spread to the lungs and bone) 2) N - spread to retroperitoneal lymph nodes

216
Q

What is Wilms tumor?

A

Malignant kidney tumor comprised of blastema (immature kidney mesenchyme) primitive glomeruli and tubules, and stromal cells

217
Q

What is the most common malignant renal tumor in children?

A

Wilms tumor with an average age of 3 years

218
Q

How does Wilm?s tumor present?

A

as a large, unilateral flank mass with hematuria and hypertension (due to renin secretion)

219
Q

What is Wilm?s tumor associated with?

A

WT1 mutation, especially in syndromic cases

220
Q

What is WAGR syndrome?

A

Wilms tumor, Aniridia, Genital abnormalities, and mental and motor Retardation

221
Q

What is Beckwith-Wiedemann syndrome?

A

Wilms tumor, neonatal hypoglycemia, muscular hemihypertrophy, and organomegaly (including tongue)

222
Q

What are the lower urinary tract carcinomas?

A

1) Urothelial (transitional cell) carcinoma 2) squamous cell carcinoma 3) adenocarcinoma

223
Q

What is urothelial (transitional cell) carcinoma?

A

Malignant tumor arising from the urothelial lining of the renal pelvis, ureter, bladder, or urethra

224
Q

What is the most common type of lower urinary tract cancer?

A

Urothelial (transitional cell) carcinoma

225
Q

Where does urothelial (transitional cell) carcinoma?

A

it usually arises in the bladder

226
Q

For urothelial (transitional cell) carcinoma what are the major risk factors?

A

it is cigarette smoke; additional risk factors are naphthylamine, azo dyes, and long-term cyclophosphamide or phenacetin use

227
Q

In whom is urothelial (transitional cell) carcinoma generally seen?

A

in older adults

228
Q

How does urothelial (transitional cell) carcinoma classically present?

A

with painless hematuria

229
Q

How does urothelial (transitional cell) carcinoma arise?

A

via two distinct pathways; flat and papillary

230
Q

How does flat urothelial (transitional cell) carcinoma develop and what is it associated with?

A

as a high-grade flat tumor and then invades; associated with early p53 mutations

231
Q

How does papillary urothelial (transitional cell) carcinoma develop?

A

as a low-grade papillary tumor that progresses to a high grade papillary tumor and then invades; not associated with early p53 mutations

232
Q

Describe the tumors for urothelial (transitional cell) carcinoma?

A

Tumors are often multifocal and recur (field defect)

233
Q

What is squamous cell carcinoma?

A

Malignant proliferation of squamous cells, usually involving the bladder

234
Q

When does squamous cell carcinoma arise?

A

It arises in a background of squamous metaplasia (normal bladder surface is not lined by squamous epithelium)

235
Q

What are the risk factors for squamous cell carcinoma?

A

They include chronic cystitis (older woman). Schistosoma hematobium infection (Egyptian male), and long-standing nephrolithiasis.

236
Q

What is adenocarcinoma?

A

Malignant proliferation of glands, usually involving bladder

237
Q

What does adenocarcinoma arise from?

A

a urachal remnant (tumor develops at the dome of the bladder), cystitis glandularis, or exstrophy (congenital failure to form the caudal portion of the anterior abdominal and bladder walls)

238
Q

What is exstrophy related to adenocarcinoma?

A

congenital failure to form the caudal portion of the anterior abdominal and bladder walls

GBA Pathology (20 decks)

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