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Head and Neck Pathology > Kidney Pathology (PAR 8) > Flashcards

Kidney Pathology (PAR 8) Flashcards

1
Q

Azotemia

A

elevation of BUN and creatinine levels
- reflects decreased glomerular filtration rate (GFR)

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2
Q

Prerenal azotemia

A

hypoperfusion of kidneys (reversible)

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3
Q

Postrenal azotemia

A

results when urine outflow is obstructed (reversible)

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4
Q

Uremia

A

when azotemia gives rise to clinical manifestations and systemic biochemical abnormalities

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5
Q

Nephrotic syndrome

A

derangement of the capillary walls of the glomeruli, resulting in increased permeability to plasma proteins

proteinuria
hypoalbuminemia
generalized edema
hyperlipidemia

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6
Q

Nephritic syndrome

A

acute onset caused by inflammatory glomeruli lesions (inflammatory cells get into glomeruli and cause damage)

hematuria
oliguria (low urine output)
proteinuria
azotemia
hypertension

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7
Q

What is the one manifestation nephrotic and nephritic syndrome share?

A

proteinuria

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8
Q

Nephrotic and nephritic syndromes both have a “hyper-“… what are they?

A

NephrOTIC – hyperLIPIDEMIA

NephrITIC– hyperTENSION

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9
Q

Primary Glomerular Disease

A

mostly caused by immune mechanisms (3 ways):

  1. deposition of circulating antigen-antibody complex… activates complement and recruits leukocytes
  2. antibodies reacting in situ within the glomerulus… activate complement and recruit leukocytes
  3. autoantibodies against components of the glomerular basement membrane
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10
Q

Diseases presenting with nephrotic syndrome? (5)

A
  • minimal change disease
  • focal segmental glomerulosclerosis (FSGS)
  • membranous nephropathy
  • membranoproliferative glomerulonephritis (MPGN)
  • dense deposit disease
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11
Q

Minimal Change Disease

A

BENIGN

most frequent cause of nephrotic syndrome in kids 1-7

damage to podocytes (cells in Bowmans capsule that wrap around capillaries of the glomerulus)

ABRUPT nephrotic syndrome in a child that is healthy

ABSENCE OF HYPERTENSION

preserved renal function (usually no permanent damage)

TX: corticosteroids (short course)

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12
Q

Most frequent cause of nephrotic syndrome in kids?

A

Minimal change disease

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13
Q

Focal Segmental Glomerulosclerosis (FSGS)

A

sclerosis of some glomeruli, but only affects part of the glomeruli

primary– idiopathic
- accounts for 20-30% of all nephrotic syndrome

secondary– HIV, heroin abuse, other forms of glomerulonephritis, inherited forms

HYPERTENSION

POOR RESPONSE to corticosteroid therapy

1/2 of patients develop end-stage renal disease within 10 years

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14
Q

Membranous nephropathy

A

most are primary, caused by in situ autoantibodies

sub epithelial immune complex deposits along glomerular basement membrane

diffuse thickening of capillary walls

adults 30-60

SUDDEN ONSET of full-blown nephrotic syndrome

FAILS TO RESPOND TO CORTICOSTEROIDS (similar to FSGS)

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15
Q

Membranoproliferative Glomerulonephritis (MPGN)

A

cause 5-10% of idiopathic nephrotic syndrome in kids and adults

alterations in glomerular basement membrane and mesangium

Cause: deposition of circulating immune complexes or by in situ immune complex formation

POOR PROGNOSIS

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16
Q

Dense Deposit Disease

A

formerly called MPGN type II

RARE

complement dysregulation due to acquired or hereditary abnormalities of alternative pathway of complement activation

POOR PROGNOSIS– tends to recur after transplantation

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17
Q

Disease presenting with nephritic syndrome? (1)

A

acute postinfectious glomerulonephritis

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18
Q

Acute Postinfectious Glomerulonephritis

A

Cause: glomerular deposition of immune complexes
- results in proliferation and damage of glomerular cells
- infiltration of leukocytes, particularly neutrophils

acute nephritic syndrome

children have good prognosis, some adults can develop end stage renal disease within 1-2 decades

Causative infections:
- streptococci
- pneumococcal, staphylococcal
- mumps, measles, chickenpox
- Hep B and C

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19
Q

Diseases primarily with asymptomatic hematuria? (2)

A

IgA nephropathy (Berger disease) and Hereditary nephritis

** hereditary nephritis is made up of 2 diseases:
- alport syndrome
- thin basement membrane disease

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20
Q

IgA Nephropathy (Berger Disease)

A

most common glomerular disease worldwide

common cause of recurrent hematuria
- gross hematuria after 1-2 days of nonspecific upper respiratory tract infection

some have typical nephritic syndrome

usually, normal renal function is maintained for decades
- 25-50% of patients will have end-stage renal disease in 10-20 years (very slow progression)

KIDS, YOUNG ADULTS

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21
Q

Most common worldwide glomerular disease?

A

IgA nephropathy (Berger disease)

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22
Q

Hereditary Nephritis

A

Group of glomerular disease
- Alport syndrome
- thin basement membrane disease

Cause: mutations in genes encoding glomerular basement membrane proteins

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23
Q

Alport Syndrome

A

nephritis, sensorineural deafness, eye disorders

mutation in type IV collagen gene

most are X-linked (males more affected– more likely to develop end-stage renal disease and deafness)

thinning and splitting of glomerular basement membrane

24
Q

Thin basement membrane disease

A

most common cause of benign familial hematuria, no systemic manifestations

25
Q

Rapidly Progressive Glomerular Disease (Crescentic Glomerulonephritis)

A

acute nephritic syndrome and microscopic glomerular crescents

pronounced oliguria and azotemia

RAPID progression to renal failure (weeks to months)

may be caused by a number of diseases
- Anti-GBM antibody-mediated crescentic GN (goodpasture disease)
- immune complex-mediated crescentic GN
- pauci-immune type crescentic GN

26
Q

Diseases affecting tubules and interstitium?

A

Tubulointerstitial nephritis (TIN)
- acute pyelonephritis
- chronic pyelonephritis
- chronic reflux-associated pyelonephritis
- chronic obstructive pyelonephritis
- drug-induced tubulointerstitial nephritis
- acute tubular injury (ATI)

27
Q

Tubulointerstitial Nephritis

A

group of inflammatory kidney diseases involving interstitum and tubules

TIN caused by bacteria– usually renal PELVIS (pyelonephritis)
TIN that is nonbacterial– interstitial nephritis

TIN can be acute or chronic

28
Q

Acute Pyelonephritis

A

Cause: bacterial infection (gram negative bacilli, E.coli)

majority associated with lower urinary tract infections (ascending infections)
- FEMALES more than males

sudden onset of pain at costovertebral angle
frequent urination
fever, nausea
cloudy urine due to pus

usually UNILATERAL

29
Q

Chronic Pyelonephritis

A

grossly visible scarring and deformity of the pelvicalyceal system in patients with recurrent UTIs

gradual onset, typically discovered late in disease course

2 forms of chronic pyelonephritis:
- chronic reflux associated pyelonephritis (more common)
- chronic obstructive pyelonephritis

30
Q

Chronic Reflex-Associated Pyelonephritis (reflux nephropathy)

A

most common cause of chronic pyelonephritis

results from superimposition of UTIs on congenital vesicoureteral reflux and infrarenal reflux

may be unilateral or bilateral

31
Q

Chronic Obstructive Pyelonephritis

A

obstruction of urinary flow–predisposes to kidney infection

recurrent infections lead to recurrent bouts of renal inflammation and scarring

may be bilateral or unilateral
- unilateral– things like kidney stones
- bilateral– congenital malformations or neoplasia

32
Q

Drug-Induced Tubulointerstitial Nephritis

A

adverse reaction to several different drugs
immune mechanism (type I or type IV hypersensitivity) leading to interstitial inflammation

begins around 15 days after exposure to drug
- fever, eosinophilia, rash, renal abnormalities (hematuria, leukocyturia, oliguria)

stopping the drug that caused it leads to recovers

Common causes:
- penicillin or other abx
- diuretics
- proton pump inhibitors
- NSAIDs

33
Q

Acute Tubular Injury (ATI)

A

most common cause of acute kidney injury

damage to tubular epithelial cells and acute decline in renal function

Decreased GFR, elevation of serum creatinine
- electrolyte abnormalities, acidosis, uremia, fluid overload

2 forms:
- ischemic ATI– due to inadequate blood flow (trauma, blood loss, acute pancreatitis, septicemia)
- nephrotoxic ATI– caused by variety of poisons (heavy metals, organic solvents, drugs, radiographic contrast agents)

34
Q

Diseases affecting blood vessels? (3)

A
  1. nephrosclerosis
  2. malignant hypertension
  3. thrombotic microangiopathies (TMA)
    - shiga toxin mediated HUS
    - atypical HUS
    - thrombotic thrombocytopenia purpura (TTP)
35
Q

Nephrosclerosis

A

sclerosis of small renal arteries and arterioles

strong association with hypertension

arterial medial and intimal thickening

hyalinization of arteriolar walls (caused by extravasation of plasma proteins through injured endothelium and increased deposition of basement membrane matrix)

usually NOT bad enough to cause renal failure

36
Q

Malignant Hypertension

A

BP greater than 200/120

may arise de novo or suddenly in patients with mild hypertension (occurs in 5% of hypertensive individuals in the US)

may present with severe acute kidney injury and renal failure
- arteries and arterioles– fibrinoid necrosis and hyperplasia of smooth muscle cells
- petechial hemorrhages on renal cortical surface

MEDICAL EMERGENCY– requires prompt and aggressive anti-hypertensive therapy

1/2 of patients survive at least 5 years

37
Q

Thrombotic microangiopathies (TMA)

A

microvascular thrombosis with microangiopathic hemolytic anemia, thrombocytopenia, and sometimes renal failure

Primary forms:
- shiga toxin mediated hemolytic uremic syndrome (HUS)
- atypical HUS
- thrombotic thrombocytopenic purpura (TTP)
- drug-mediated TMAs

38
Q

Shiga Toxin-Mediated HUS

A

up to 75% follow intestinal infection with shiga-toxin producing E. coli or shigella dysenteriae type I

prodromal GI upset (diarrhea, etc.)/flu-like symptoms

sudden onset of bleeding (hematemesis and melena), severe oliguria, hematuria, microangiopathic hemolytic anemia, neurologic changes

one of the main causes of ACUTE kidney injury in CHILDREN

most patients recover in a few weeks when managed properly… around 25% of kids eventually get renal insufficiency (happens over 15-25 years)

39
Q

Atypical HUS

A

hereditary (common) or acquired (rare)

Cause: abnormalities in complement proteins that dampen activation of the alternative pathway

excessive activation of complement with ensuing microvascular injury and microvascular thrombosis

sudden onset WITHOUT prodromal diarrhea

POOR PROGNOSIS compared to shiga-toxin mediated HUS

40
Q

Thrombotic Thrombocytopenic Purpura (TTP)

A

Acquired (common) or inherited (rare)

deficiencies in ADAMTS13 (plasma protein that cleaves von Willebrand factor multimer into smaller sizes)

abnormally large vWF multimers activate platelets spontaneously leading to thrombosis in multiple organs

sudden onset, RAPIDLY FATAL WITHOUT THERAPY

41
Q

Chronic Kidney Disease

A

broad term describing final common pathway of progressive nephron loss resulting from any type of kidney disease

alterations in function of remaining intact nephrons are MALADAPTIVE and cause further scarring

eventual end-stage disease with sclerosed glomeruli, tubules, interstitium, and vessels

POOR PROGNOSIS without treatment, rate of progression highly variable

42
Q

Simple Cysts

A

generally innocuous lesions

multiple/single cystic spaces of variable size (1-5cm)

microscopically: single layer of cuboidal epithelium

usually confined to the CORTEX

common postmortem finding without clinical significance

43
Q

Autosomal Dominant (Adult) Polycystic Kidney Disease

A

relatively common– accounts for 10% of cases of end-stage renal disease

defective PKD1 gene (some cases are PKD2)

multiple, expanding cysts affecting BOTH KIDNEYS
- kidneys may reach ENORMOUS SIZE

no symptoms until 4th decade of life
- flank pain
- intermittent gross hematuria
- hypertension
- urinary infection

slow progression but ULTIMATELY FATAL WITHOUT TRANSPLANT

44
Q

Autosomal Recessive Polycystic Kidney Disease

A

CHILDHOOD FORM of polycystic disease

RARE

mutations in PKHD1 (whereas adult form is PKD1)

numerous small cysts completely replace the medulla and cortex of kidney bilaterally, accompanied by LIVER ABNORMALITIES

serious manifestations at birth; infants may die quickly from hepatic or renal failure

45
Q

Nephronophthisis-Medullary Cystic Kidney Disease Complex

A

usually begins in childhood

Four variants:
- infantile
- juvenile
- adolescent
- adult

15-20% have extra renal manifestations
- RETINAL ABNORMALITIES
- intellectual disability
- cerebellar malformations
- liver fibrosis

initial manifestations: polyuria and polydipsia

progression to end stage renal disease over 5-10 years

46
Q

Renal Stones (Urolithiasis)

A

calculus formation at any level of urinary collecting system (usually in kidney)

symptomatic urolithiasis more common in WOMEN

80% composed of either calcium oxalate or calcium oxalate + calcium phosphate
- cause for stone formation of calcium-containing stones is often unclear

10% composed of struvite (magnesium ammonium phosphate) in individuals with persistently alkaline urine from UTIs

able to obstruct urine outflow or produce trauma resulting in ulceration and bleeding

47
Q

Hydronephrosis

A

dilation of renal pelvis and calyces with atrophy of parenchyma caused by urinary outflow obstruction

bilateral complete obstruction produces ANURIA (no urine), bilateral incomplete obstruction causes POLYURIA

unilateral obstruction may remain silent for long periods

possible causes of hydronephrosis:
- congenital malformation
- foreign bodies (calculi)
- proliferative lesions (hyperplasia, malignant/benign tumors)
- inflammatory lesions (prostatitis, uretriti, urethritis)
- neurogenic (paralysis of bladder)
- normal pregnancy (reversible)

removal of obstruction usually allows for complete return of function within a few weeks
- extended time of obstruction may produce irreversible changes

48
Q

Congenital/Developmental Kidney Patho

A

most common cause of end-stage renal disease in patients YOUNGER THAN 21

may be isolated or part of syndrome… most are from sporadic developmental defects

49
Q

Multicystic Dysplastic Kidney (MCDK)

A

most common form of renal cystic disease in KIDS

kidney is grossly distorted

bilateral involvement results in SPONTANEOUS ABORTION

50
Q

Renal Agenesis

A

bilateral agenesis is INCOMPATIBLE WITH LIFE

often associated with other congenital disorders (limb defects, hypoplastic lungs)

unilateral agenesis is uncommon, but compatible with life

51
Q

Hypoplasia

A

most commonly unilateral

reduced number of renal lobes and pyramids

52
Q

Oncocytoma

A

BENIGN

intercalated cells of collecting ducts representing 10% of renal neoplasms

plethora of mitochondria– finely granular eosinophilic cytoplasm

53
Q

Wilms Tumor

A

children younger than 10 usually
- rare in adults

mesoderm derived

may arise sporadically or inherited (autosomal dominant)

54
Q

Renal Cell Carcinoma

A

derived from renal tubular epithelium

80-85% of all primary MALIGNANT neoplasms of kidney

MALES 60s and 70s

40% of patients DIE

RISKS greater in:
- smokers
- hypertensive patients
- obese patient
- occupational exposure to cadmium

Most common forms:
- clear cell carcinoma (most common)
- papillary renal cell carcinoma
- chromophobe renal carcinoma (least common)

55
Q

Clear Cell Carcinomas

A

most common renal cell carcinoma

most are SPORADIC, may be familial or associated with von Hippel-Lindau (VHL) disease

associated with homozygous loss or inactivation of the VHL tumor suppressor protein

frequently invade the RENAL VEIN

56
Q

Papillary Renal Cell Carcinoma

A

frequently multifocal and bilateral

familial or sporadic

associated with increased expression and activating mutations of the MET oncogene

57
Q

Chromophobe Renal Carcinoma

A

LEAST COMMON renal cell carcinoma

arise from intercalated cells of collecting ducts (like oncocytoma)

tumor stains more DARKLY (less clear than clear cell carcinoma)

characterized by multiple losses of entire chromosomes

generally GOOD PROGNOSIS

Head and Neck Pathology (3 decks)

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