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Pathoma Enhanced > CH12 - Kidney and Urinary Tract Pathology > Flashcards

CH12 - 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 reabsorb fluid in the kidneys?

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 b/c allopurinol is a xanthine oxidase inhibitor ->reduces the conversion of nucleic acid byproducts to uric acid

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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 (Type 1 or 4) 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

A sequence of:

1) vascular occlusion
2) vasospasm
3) Infection
4) Obstruction
5) 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

POSTCARDS:

pyelonephritis

Obstruction of the urogenital tract

Sickle cell disease

Tuberculosis

Cirrhosis of the liver

Analgesia/alcohol abuse

Renal vein thrombosis

Diabetes mellitus

Systemic vasculitis.

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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

What clinical presentation is caused by hypoalbuminemia?

A

pitting edema

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64
Q

Hypogammaglobulinemia, secondary to nephrotic syndrome, increases the risk of what?

A

infection

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65
Q

Why does nephrotic syndrome result in a hypercoagulable state?

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’s lymphoma. Reed Sternberg cells can produce tons of cytokines.

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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 (deposition of collagen) on H and 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 b/c it is result of chronic cytokine release. The cytokines cause collagen to be laid down (sclerosis) of glomeruli.

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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

Ultimately due to circulating immune complexes depositing. Usually idiopathic, but associated with hepatitis B or C, solid tumors (advanced stage 4), 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 because the immune deposits are sub-epithelial. The epithelial cells like to sit on BM, so they lay down basement membrane on top of immune complexes - creating a dome. The spikes are where there are no immune complexes.

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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 because immune complex deposition is sub-endothelial or in the basement membrane. Mesangial cells that hold together capillary loops in glomerulus respond by protruding their cytoplasm (proliferative = b/c of their cytoplasm proliferating) and cutting through the immune complex blobs -> 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, with low levels of circulating C3 but high c3a and c3b)

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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 (protein leaks into the wall of the blood vessel).

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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 because hyaline arteriosclerosis is more pronounced in the efferent arterioles. As the wall thickens and lumen narrows, the back pressure increases the 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 -> sclerosis of the mesangium results from this damage -> nephrotic syndrome

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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 (pathomenmonic for diabetes)

99
Q

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

A

ACE inhibitors because they cause decrease in Angiotensin 2, which causes squeezing of efferent arteriole -> decreased back pressure.

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 are the 3 categories of nephrotic syndrome?

A

Cytokine-mediated effacement of podocytes

Minimal change disease

FSGS

Immune complex deposition around Basement Membrane

Membranous Nephropathy

Membranoproliferative Glomerulonephritis

Systemic diseases affecting kidnes (protein deposition)

Diabetes Mellitus

Amyloidosis

104
Q

What is nephritic syndrome?

A

Glomerular disorders characterized by glomerular inflammation and bleeding

105
Q

What is seen in nephritic syndrome?

A
  1. Limited proteinuria (< 3.5 g/day (helps distinguish from nephrotic syndrome))
  2. Oliguria and azotemia because filtration system is damaged
  3. Salt retention (glomerular injury-> inappropriate release of endothelial and/or mesangial vasoactive factors (nephritic syndrome involves mesangial proliferation that damages and constricts the glomerular capillary network)->reduces blood flow to the juxtaglomerular apparatus->activation of renin-angiotensin-aldosterone cascade->increased salt and water retention) -> periorbital edema and hypertension
  4. RBC casts and dysmorphic RBCs in urine
106
Q

In nephritic syndrome what is seen in biopsy?

A

it reveals hypercellular, inflamed glomeruli

107
Q

In nephritic syndrome, what mediates damage?

A

Immune-complex deposition activates complement; C5a attracts neutrophils, which mediate damage. Glomeruli become hypercellular as complement attracts lots of immunce cells.

108
Q

What is poststreptococcal glomerulonephritis (PSGN)?

A

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

109
Q

In PSGN, what does it occur with?

A

nephritogenic strains (which carry the M protein virulence factor)

110
Q

PSGN may occur after infection with what organisms?

A

nonstreptococcal organisms as well as nephritogenic strains

111
Q

How does PSGN present?

A

2-3 weeks after infection as hematuria (cola-colored urine), oliguria, hypertension, and periorbital edema (Neutrophils release vasoconstrictive agents -> Incr aldosterone -> salt retention)

112
Q

PSGN is usually seen in whom?

A

children, but may occur in adults

113
Q

In PSGN what is seen on H&E stain?

A

Its hypercellular, inflamed glomeruli on H&E

114
Q

In PSGN, what is seen on electron microscopy?

A

subepithelial humps on EM, and is mediated by immune complex deposition - granular IF. Immune complexes start sub-endothelialy, move through BM, end up sub epithelial -> and in kids finally move into tubule and be excreted.

115
Q

What is the treatment for PSGN?

A

Treatment is supportive.

116
Q

What is the chance for renal failure in PSGN?

A

Children rarely (1%) progress to renal failure

117
Q

In PSGN, what might some adults develop?

A

25% might develop rapidly progressive glomerulonephritis (RPGN)

118
Q

What is rapidly progressive glomerulonephritis?

A

Nephritic syndrome that progresses to renal failure in weeks to months

119
Q

What is rapidly progressive glomerulonephritis characterized by?

A

crescents in Bowman space (of glomeruli) on H&E stain; Because Acute inflmmation with Neutrophils did not resolve, Chronic inflammation mediated by Macrophages ensued. Crescents are 2/3 of glomerulus that has been replaced by macrophages and the fibrin they have laid down. This is now completely unfunctional (inflammatory debris).

120
Q

For rapidly progressive glomerulonephritis how is the etiology resolved?

A

clinical picture and IF help resolve etiology

121
Q

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

A

Goodpasture syndrome

122
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

123
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

124
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 (most commonly secondary to SLE)

125
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 (Remember that while a lot less common, the most common Nephrotic syndrome in SLE is membranous nephropathy)

126
Q

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

A

Wegener granulomatosis, microscopic polyangiitis, and Churg-Strauss syndrome

127
Q

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

A

Wegener granulomatosis - you will see sinusitis in clinical presentation

128
Q

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

A

microscopic polyangiitis and Churg-Strauss

129
Q

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

A

Granulomatous inflammation, eosinophilia, and asthma are only in Churg-strauss

130
Q

What is IgA nephropathy?

A

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

131
Q

What is the most common nephropathy worldwide?

A

Berger disease ? IgA nephropathy

132
Q

When does Berger disease present?

A

during childhood

133
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)

134
Q

In Berger disease what is increased during infection?

A

IgA production

135
Q

In Berger disease what is seen on IF?

A

IgA immune complex deposition in the mesangium

136
Q

What may Berger disease slowly progress to?

A

renal failure

137
Q

What is alport syndrome?

A

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

138
Q

What does Alport Syndrome result in?

A

the thinning and splitting of the glomerular basement membrane

139
Q

What does Alport syndrome presents as?

A

isolated hematuria, sensory hearing loss, and ocular disturbances

140
Q

What is a urinary tract infection?

A

Infection of urethra, bladder, or kidney

141
Q

A urinary tract infection most commonly arises from what?

A

due to ascending infection; increased incidence in females

142
Q

What are the risk factors for urinary tract infection?

A

they include sexual intercourse, urinary stasis, and catheters,

143
Q

What is cystitis?

A

Inflammation of the bladder

144
Q

What does cystitis present as?

A

1) dysuria - painful urination
2) urinary frequency
3) urgency (gotta go)
4) suprapubic pain

systemic signs (e.g., fever) are usually absent.

145
Q

What are the laboratory tests for cystitis?

A

1) Urinalysis 2) Dipstick 3) Culture

146
Q

What are the laboratory findings for cystitis?

A

1) Urinalysis->cloudy urine with > 10 WBCs/ HPF
2) Dipstick ->Positive leukocyte esterase (due to pyuria = Neutrophils) and nitrites (bacteria convert nitrates to nitrites)
3) Culture > 100,000 colony forming units (gold standard)

147
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

148
Q

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

A

Proteus mirabilis

149
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.

150
Q

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

A

urethritis due to Chlamydia trachomatis or Neisseria gonorrhoeae

151
Q

What is the dominant presenting sign of urethritis?

A

it is dysuria)

152
Q

What is pyelonephritis?

A

Infection of the kidney

153
Q

What is pyelonephritis usually due to?

A

ascending infection; increased risk with vesicoureteral reflux (backward reflux from the bladder up to the ureters)

154
Q

What does pyelonephritis present with?

A

1) fever (systemic signs present)
2) flank pain (inflammation causes sensitization of the nerves of the capsule of the kidney)
3) WBC casts (because infection works its way up the tubule from ureters and WBC’s follow)
4) leukocytosis
5) symptoms of cystitis (because infection ascends from bladder)

155
Q

For pyelonephritis, what are the most common pathogens?

A

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

156
Q

What is chronic pyelonephritis?

A

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

157
Q

What is chronic pyelonephritis due to?

A

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

158
Q

What does chronic pyelonephritis lead to?

A

cortical scarring with blunted calyces (a calyx is so scarred that it almost collapses)

159
Q

In chronic pyelonephritis, what is characteristic of vesicoureteral reflux?

A

cortical scarring at upper and lower poles of the kidney

160
Q

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

A

Atrophic tubules are filled with eosinophilic proteinaceous material resemble thyroid follicles

161
Q

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

A

waxy casts

162
Q

What is nephrolithiasis?

A

Precipitation of a urinary solute as a stone

163
Q

What are the risk factors for nephrolithiasis?

A

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

164
Q

What does nephrolithiasis present as?

A

colicky pain with hematuria and unilateral flank tenderness

165
Q

In nephrolithiasis, what happens to the stone?

A

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

166
Q

What is chronic renal failure?

A

End-stage kidney failure

167
Q

What may chronic renal failure result from?

A

glomerular, tubular, inflammatory, or vascular insults

168
Q

What are the most common causes of chronic renal failure?

A

diabetes mellitus, hypertension, and glomerular disease,

169
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

170
Q

What is asterixis?

A

Tremor of the hand when wrist is extended

171
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,

172
Q

In chronic renal failure, what is anemia due to?

A

decreased erythropoietin production by renal peritubular interstitial cells

173
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

174
Q

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

A

secondary hyperparathyroidism, osteomalacia, and osteoporosis

175
Q

In chronic renal failure, what is the treatment?

A

involves dialysis or renal transplant.

176
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.

177
Q

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

A

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

178
Q

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

A

It is idiopathic hypercaliuria (calcium channel malfunction -> Calcium inappropriately dumped into tubules)

179
Q

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

A

with Crohn disease (small bowel damage ->Increased resorption of oxolate) -> Calcium oxalate stones

180
Q

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

A

Hydrochlorothiazide (caicium-sparing diuretic). -> decreased Calcium going into renal tubules-> decreased urine calcium

181
Q

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

A

Ammonium magnesium phosphate (AMP STONE)

182
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);

183
Q

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

A

PROTEUS vulgaris and Klebsiella cause alkalinization of urine

184
Q

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

A

staghorn calculi in renal calyces, which act as a nidus (focus of infection where bacteria multiply) for urinary tract infections

185
Q

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

A

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

186
Q

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

A

Uric acid (5%)

187
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)

188
Q

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

A

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

189
Q

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

A

Nephrolithiasis composed of uric acid

190
Q

For nephrolithiasis composed of uric acid what increases the risk?

A

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

191
Q

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

A

hydration and alkalinization of urine (potassium bicarbonate);

192
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)

193
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

194
Q

What is associated with nephrolithiasis caused by cysteine?

A

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

195
Q

Nephrolithiasis composed of cysteine may form what?

A

staghorn calculi in children. (Remember mcc of staghorn calculi in adults was AMP stone)

196
Q

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

A

It involves hydration and alkalinization of urine

197
Q

What are the types of renal neoplasia?

A

Angiomylipoma, renal cell carcinoma and wilms tumor

198
Q

What is angiomyolipoma?

A

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

199
Q

In what is there an increased frequency of angiomyolipoma?

A

in tuberous sclerosis

200
Q

What is renal cell carcinoma?

A

Malignant epithelial tumor arising from kidney tubules

201
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

202
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.

203
Q

For renal cell carcinoma what is the most common symptom?

A

Hematuria

204
Q

What may renal cell carcinoma rarely present with?

A

left-sided varicocele

205
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

206
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.

207
Q

For renal cell carcinoma what does gross exam reveal?

A

a yellow mass,

208
Q

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

A

It exhibits clear cytoplasm

209
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).

210
Q

For renal cell carcinoma are the tumors hereditary or sporadic?

A

May be either

211
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

212
Q

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

A

cigarette smoke

213
Q

For renal cell carcinoma when do hereditary tumors arise?

A

in younger adults and are often bilateral,

214
Q

What is Von Hippel-Lindau disease?

A

It is an autosomal dominant disorder

215
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.

216
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

217
Q

What is Wilms tumor?

A

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

218
Q

What is the most common malignant renal tumor in children?

A

Wilms tumor with an average age of 3 years

219
Q

How does Wilm?s tumor present?

A

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

220
Q

What is Wilm?s tumor associated with?

A

WT1 mutation, especially in syndromic cases

221
Q

What is WAGR syndrome?

A

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

222
Q

What is Beckwith-Wiedemann syndrome?

A

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

223
Q

What are the lower urinary tract carcinomas?

A

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

224
Q

What is urothelial (transitional cell) carcinoma?

A

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

225
Q

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

A

Urothelial (transitional cell) carcinoma

226
Q

Where does urothelial (transitional cell) carcinoma?

A

it usually arises in the bladder

227
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

228
Q

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

A

in older adults

229
Q

How does urothelial (transitional cell) carcinoma classically present?

A

with painless hematuria

230
Q

How does urothelial (transitional cell) carcinoma arise?

A

via two distinct pathways; flat and papillary

231
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

232
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

233
Q

Describe the tumors for urothelial (transitional cell) carcinoma?

A

Tumors are often multifocal and recur (field defect)

234
Q

What is squamous cell carcinoma?

A

Malignant proliferation of squamous cells, usually involving the bladder

235
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)

236
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.

237
Q

What is adenocarcinoma?

A

Malignant proliferation of glands, usually involving bladder

238
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)

239
Q

What is exstrophy related to adenocarcinoma?

A

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

240
Q

If a patient has a calcium stone, what must be ruled out first?

A

hypercalcemia (not most common cause)

Pathoma Enhanced (19 decks)

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