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Patho > 21. urinary patho > Flashcards

21. urinary patho Flashcards

1
Q

Horseshoe Kidneys

A

90% lower poles fusion
1 in 500 to 1000 autopsies
Usually has no clinical consequences
Seen in 7% Turner syndrome

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2
Q

Agenesis

Aplasia

Hypoplasia

A

Agenesis is a complete absence of kidney (no anlage present)
Aplasia is failure kidney of to develop beyond its most primitive form (anlage present)
Hypoplasia is partial failure of kidney to develop (usually < 6 renal lobes and pyramids)

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3
Q

In unilateral cases the normal kidney undergoes compensatory hypertrophy at cost of progressive glomerular sclerosis and, in time, chronic kidney disease.

A
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4
Q

Ureteropelvic junction (UPJ) obstruction

A

The most common cause of hydronephrosis in infants and children
In children: boys > girls, 20% bilateral, and associated with other anomalies
In adults: women > men and most often unilateral.

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5
Q

Vesicoureteral reflux (VUR)

A

Congenital: girls > boys and 2% or 3% of preschool-age
Acquired: men&raquo_space; women, urinary obstruction (BPH, bladder atony)

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6
Q

Exstrophy of bladder

A

Developmental failure in the anterior wall of the abdomen and bladder
Bladder communicates directly with the abdominal surface
Chronic cystitis and may undergo colonic glandular metaplasia

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7
Q

Posterior urethral valve(PUV)

A

= congenital obstructive posterior urethral membrane (COPUM)
The most common cause of severe obstructive uropathy
1 in 8,000 boys
Presented with Urinary retention, distended bladder, and weak urinary stream and if severe, oligohydramnios

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8
Q

2 type of polycystic kidney disease

A

AR
AD

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9
Q

Autosomal Recessive (Childhood) Polycystic Kidney Disease (ARPKD)

A

kids
PKHD1 gene on ch 6p12
Encodes fibrocystin
may also have multiple hepatic cysts and congenital hepatic fibrosis.
diffuse cystic dialation of collecting duct perpendicular to capsule

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10
Q

Autosomal dominant (adult) polycystic kidney disease

A

PKD1 gene
polycystin 1 protein defect
present with renal insufficiency, hematuria, and hypertension (bc increased renin)or with abdominal masses

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11
Q

Extrarenal manifestations of ADPK

A

berry aneurism
mitral valve prolapse
liver cysts
diverticulosis of liver

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12
Q

Multicystic renal dysplasia

A

The most common renal cystic disease in children
Causes an enlarged renal mass with cartilage and immature collecting ducts
Renal failure may ultimately result in bilateral

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13
Q

Medullary Sponge Kidney(MSK)

A

Arise from the collecting ducts in the renal papillae
75% are bilateral
By itself does not pose a threat to health
It may predispose to recurrent pyelonephritis, hematuria, and renal stones

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14
Q

Acquired Cystic Kidney Disease

A

Simple Renal Cysts
Long term dialysis associated acquired cystic disease

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15
Q

Simple Renal Cysts

A

50% of elderly above the age 50 Years
Clinically asymptomatic unless they are very large.
May be solitary or multiple and are usually located in the outer cortex
lined by a flat epithelium

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16
Q

Long term dialysis associated acquired cystic disease is a result of

A

result of obstruction with progressive interstitial fibrosis and/or oxalate crystal deposition

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17
Q

Urinary tract infection (UTI)
2 based on location

A

Upper UTI (pyelonephritis) and lower UTI(urethritis, cystitis, and ureteritis)

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18
Q

Classification of UTI

A

Uncomplicated UTI: No structural or functional abnormalities. Mostly in women
Complicated UTI: in individuals with structural or functional abnormalities ( stone, catheter, BPH, neurological deficit etc…). UTI in men are usually complicated.

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19
Q

Acute pyelonephritis

A

gram-negative uropathogens
KEEPS (Klebsiella, E. coli, Enterobacter, Pseudomonas aeruginosa, and Serratia)

Hematogenous infections with gram-positive pyogenic bacteria

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20
Q

Acute pyelonephritis
presents with

A

Presents with fever, flank pain, CVAT and symptoms of cystitis (dysuria, frequency, and urgency).

Urinalysis shows pyuria and WBC casts

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21
Q

Chronic pyelonephritis due to

A

Due to multiple bouts of acute pyelonephritis

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22
Q

Atrophic tubules containing eosinophilic proteinaceous material resemble

A

thyroid follicles (‘thyroidization’ of the kidney).

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23
Q

Cystitis

A

is inflammation of the bladder.

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24
Q

Causes of Cystitis
ophysical chemical biolog

A

Physical - stone, catheter, radiation
Chemical - cyclophosphamide
Biological - KEEPS, Adenovirus, and
S. haematobium

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25
Q

Adenovirus and cyclophosphamide can cause

A

hemorrhagic cystitis

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26
Q

Urethral caruncle

A

Inflammatory lesion
Typically in older females
Small, red, painful mass about the external

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27
Q

It consists of inflamed granulation tissue covered by

A

an intact but friable mucosa,

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28
Q

Urinary stones = Urinary Calculi (Urolithiasis)
character 3

A

0.5–2% of the general population
Men&raquo_space; women (unknown reasons)
Peak onset of first symptoms is between 20 and 30 years of age

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29
Q

stone Most often found in the

A

renal pelvis or the urinary bladder

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30
Q

stones present with

A

Present with acute ureteral obstruction, ureteral colic (i.e., spasmodic pain caused by the contraction of an obstructed ureter), and hematuria due to mucosal trauma

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31
Q

Passage of a stone into the ureter causes excruciating flank pain, termed

A

renal colic.

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32
Q

normal narrowing of ureter 3 or 5

A

3
traversing the bladder wall
passing iliac vessels
uretropelvic junction

5
passing vas deferens
uretric orific

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33
Q

Urinary stones
size and exception

A

small <3mm except struvite stone

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34
Q

90% are………. (seen on x-ray)
except …….. and ……………. are ……….. (iv urography)

A

radiopaque

pure uric stones and xanthine stones

radiolucent

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35
Q

Risk factors include:
for kidney stone

A

High concentration of solute in the urinary filtrate and low urine volume
Infection cause alkaline urine which favors precipitation of magnesium ammonium phosphate (struvite) and calcium phosphate (apatite)
Vitamin A and citric acid deficiency
High vitamin C intake
Urinary stasis

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36
Q

Types of stones and frequency in adults
male female

A

male
caox
ca and ua
unknown

femsle
caox
struvite
unkn

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37
Q

Calcium oxalate stone is

A

hard and occasionally dark

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38
Q

Calcium phosphate (apatite) stones tend to be

A

softer and paler.

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39
Q

……………….typically form in the bladder because of urine stasis and are composed of calcium oxalate dihydrate

A

Jackstone calculi

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40
Q

Uric acid stone

A

20% chronic gout and 40% acute hyperuricemia

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41
Q

Uric acid stones are

A

smooth, hard, and yellow and are usually less than 2 cm in diameter

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42
Q

Cystine stones

A
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43
Q

cystine 1% of stones overall but represent a significant proportion of ……….. calculi and occur exclusively with……………….

A

childhood

hereditary cystinuria

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44
Q

cause of cysteinuria

A

PCT reabsorbs cystein
but disorder doesnt
so COAL arent absorbed ornithin arginine lysine

cystein being the leasy soluble so stone forms

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44
Q

cystein crystals shape

A

hexagonal

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44
Q

Magnesium ammonium phosphate (struvite) stones
another name
texture

A

Triple stone
Vary from hard to soft and friable

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45
Q

Magnesium ammonium phosphate (struvite) stones arise

A

Arise in alkaline urine due to ammonia formed by urea-splitting bacteria, such as Proteus species

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46
Q

struvite crystals shape

A

cofin lid

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47
Q

Nephrocalcinosis

A

Deposition of calcium in the renal parenchyma
Caused by metastatic or dystrophic calcification

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48
Q

Nephrocalcinosis May cause abnormal renal function, especially tubular defects such as

A

impaired concentrating ability, salt wasting, and renal tubular acidosis.

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49
Q

Urate Nephropathy

A

Deposition of urate crystals in the tubules and interstitium

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50
Q

Acute urate nephropathy caused by

A

tumor lysis syndrome and manifests as acute renal injury

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51
Q

Chronic urate nephropathy caused by

A

gout and manifest as chronic renal tubular defects

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52
Q

Tumors of the urinary tract
Tend to have the following characteristics:

A

Tend to have the following characteristics:
- Malignant > benign - Older > younger people
- Men > women

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53
Q

Angiomyolipomas

A

hamartomas composed of fat, smooth muscle, and blood vessels

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54
Q

Angiomyolipomas Present in 25% to 50% of

A

tuberous sclerosis patients (loss-of-function mutations in the TSC1 or TSC2).

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55
Q

Angiomyolipomas
Risk of

A

spontaneous hemorrhage

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56
Q

Oncocytoma

A

~ 5% to 15% of renal neoplasms
From intercalated cells of collecting duct

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57
Q

Oncocytoma Grossly

A

Grossly mahogany brown mass with central scar in one-third of cases

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58
Q

Renal cell carcinoma (RCC)

A

Malignant epithelial tumor arising from kidney tubules

Account for 85% of malignant UUT tumors
Males : Females = 2:1.

59
Q

RCC AKA ‘…………’ due to resemblance to clear cells of adrenal cortex and gross yellow colour

A

hypernephroma

60
Q

in rcc > 95% show a loss of the

A

VHL tumor suppressor gene

61
Q

2 types of RCC

A

hereditary clear cell
sporadic clear cell

62
Q

hereditary

A

5% of RCC
Younger adults, often bilateral and multiple
Associated with VHL syndrome
~ 40% with VHL syndrome develop RCC

63
Q

sporadic clear cell
age
where
risk factors

A

95% of RCC
Arise in adult (average age is 60 years) as a single tumor in the upper pole of the kidney
Predisposing factors: Smoking (major risk factor), obesity, hypertension, unopposed oestrogen therapy, exposure to asbestos, cadmium, petroleum products, heavy metals and dialysis related acquired cystic.

64
Q

Clinical features of RCC

A

33.3% intermittent hematuria
10% triad of painless intermittent haematuria, palpable abdominal mass and costovertebral pain

65
Q

RCC known as in medicine 2

A

“Great mimics in medicine” a significant number of tumors present with nonspecific symptoms, such as weight loss, fever, or hypertension.
“internist’s tumor” as most of these tumors are diagnosed by internists examining patients for, presumably, non renal complaints

66
Q

20%of RCC show paraneoplastic syndromes
like

A

Polycythemia
Hypertension
Cushing syndrome
Hypercalcemia
Feminization or masculinization (gonadotropin release)
May also cause Stauffer syndrome , secondary amyloidosis, a leukemoid reaction, or eosinophilia.

67
Q

type of rcc
80%
15
5

A

clear cell
papillary
chromophobe

68
Q

left kidney RCC known for

A

causing scrotal varicocele

69
Q

Wilms’ tumor (Nephroblastoma)

A

are present at the time of birth but become clinically apparent only between the second and fourth years of life

70
Q

most common of all solid tumors in infants and young children

A

Wilms’ tumor (Nephroblastoma)

71
Q

wilms tumor 2 pathogenesis or 2 syndromes

A

WAGR syndrome

Beckwith-Wiedemann syndrome

72
Q

WAGR syndrome

A

WAGR syndrome-Wilms tumor, aniridia, genital abnormalities, and mental and motor retardation.

Associated with deletion of WT1 tumor suppressor gene

73
Q

Beckwith-Wiedemann syndrome

A

associated with mutations in WT2 gene cluster (imprinted genes) and increased IGF-2

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

74
Q

clinical of wilms and histologically looks like

A

Unilateral flank mass with hematuria and hypertension

Looks like a developing fetal kidney

75
Q

Tumors of the renal pelvis

A

Urothelial carcinoma of the renal pelvis account for 8% of malignant UUT tumors

76
Q

Tumors of the renal pelvis
present with

A

Present with hematuria or urinary obstruction and colic

77
Q

Tumors of urinary bladder
age
sex

A

Peaks in 60 to 80 years of age
M:F= 3:1
2X more common than RCCs with the same mortality rate

78
Q

Carcinoma of ……….represents the most common urinary tract neoplasm

A

the urinary bladder

79
Q

Tumors of urinary bladder
present with

A

painless hematuria, but it may also cause dysuria, urgency, frequency, hydronephrosis, and pyelonephritis

80
Q

Risk factors
for bladder tumors

also specifically squamous cell carcinoma and adebocarcinoma

A

Cigarette smoking

Azodyes and chemicals used in the rubber industry and textile printing (2-naphthylamine)

Chronic bladder infection (S. haemotobium and stone) for squamous cell carcinoma

Bladder exstrophy, cystitis glandularis and urachal remnant for adenocarcinoma

81
Q

bladder tumor location common

A

post. and lateral wall

82
Q

pathogenesis

A

RAS and FGFR3 mutations papillary

TP53 and RB mutations in situ

83
Q

90% of bladder tumors are
10% are

A

90% are urothelial carcinomas
10% are squamous cell carcinomas, adenocarcinomas (at dome), and some very rare forms, including metastases

84
Q

Many cases urothelial carcinomas are actually multifocal and recur and phenomenen called

A

(“field defect”)

85
Q

70% are low-grade exophytic tumors that have a favorable prognosis
Low-grade tumors tend to recur for many years, and occasionally they may progress to a higher-grade invasive carcinoma, so lifelong urologic follow-up is mandatory

A
86
Q

treatment of bladder tumor

A

Advanced diseases managed by cystectomy ± radio and chemotherapy

Immunopotentiators, such as bacille Calmette-GuÄrin (BCG)

weakened tb

87
Q

Anatomic changes of urinary system caused by obstruction
Includes

A

hydronephrosis, hydroureter and hypertrophy of the bladder

88
Q

2 causes of obstruction

A

intrinsic and extrinsic

89
Q

intrinsic cause of obstruction include

A

calculi
stricture
tumor
clotneurogenic

90
Q

extrinsic cause of obstruction include

A

pregnancy
periurethral inflam.
tumor

91
Q

Hydronephrosis

plus associated with

A

Dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney.

92
Q

Compartment base disease of the kidney

A

Traditionally, diseases of the kidneys are divided into 4 major groups
1. Glomerular diseases
2. Tubular diseases
3. Interstitial diseases: often involve interstitium and tubules (tubulo-interstitial diseases).
4. Vascular diseases

93
Q

Compartment base disease of the kidney usually results in the evolution of one of the two major pathological syndromes:

A

acute renal injury and chronic renal injury

94
Q

Acute kidney injury (AKI)
plus urine output

A

Characterized by azotemia (increased blood urea nitrogen [BUN] and creatinine [Cr]) often with oliguria (reduced urine output < 400 mL/day)

95
Q

Types of AKI

A

perirenal
intrarenal
post renal

96
Q

Prerenal AK

A

The commonest type
Due to decreased blood flow to kidneys  ↓ GFR, azotemia, and oliguria

97
Q

pre renal diagnostic
BUN;creatinine level

osmolality

A

Reabsorption of fluid and BUN ensues (serum BUN:Cr ratio > 20); tubular function remains intact (urine osmolality [osm] > 500 mOsm/kg).

98
Q

Intrarenal AKI
plus
BUN and osmolality

A

Dysfunctional tubular epithelium results in decreased reabsorption of BUN (serum BUN:Cr ratio < 10) and inability to concentrate urine (urine osm < 500 mOsm/kg)

99
Q

causes of Intrarenal AKI

A

acute tubular necrosis and interstitial nephritis

100
Q

Postrenal AKI

A

Due to obstruction of urinary tract

101
Q

During early stage of obstruction, in postrenal
bun and osmolality

A

increased tubular pressure “forces” BUN into the blood (serum BUN:Cr ratio > 20); tubular function remains intact and urine osm > 500 mOsm/ kg).

102
Q

Long standing obstruction, tubular damage ensues,
in post renal aki

A

resulting in decreased reabsorption of BUN (serum BUN:Cr ratio < 10) and inability to concentrate urine (urine osm < 500 mOsm/kg).

103
Q

to say Chronic Kidney Disease (CKD)

A

GFR persistently less than 60 mL/min/1.73 m2 for at least 3 months

104
Q

Common causes of CKD

A

HTN, DM, glomerulonephritis, polycystic kidney disease and obstructive uropathy

105
Q

End stage renal disease (ESRD) –

A

eGFR being < 15ml/min where dialysis or kidney transplantation is necessary for reasonable quality of life and survival

106
Q

CKD patients presents with

A

no vit D metabolism

bleeding

blood urea creat. phosphate K increases
PH and Ca decrease

anemia encephalopathy pericarditis

secondary hyperparathyroidism

uremic frost on skin

casts and proteinuria

107
Q

role of BMP7 acidosis RANK-L

A

BMP7 activate osteoblasts and is produced by kidney
CKDless BMP7 so osteopenia

acidosis increases RANK-L and this causes osteopenia

108
Q

Vascular diseases
2

A

Renal artery stenosis
nephroscelerosis

109
Q

nephrosclerosis

A

Renal pathology associated with sclerosis of renal arterioles and small arteries
Strongly associated with hypertension, which can be both a cause and a consequence of nephrosclerosis.

110
Q

types of nephroclerosis

A
111
Q

benign

A
112
Q

malignant

A
113
Q

Diseases of tubules and Interstitium no.

A

3
acute tubular necrosis
acute intertsitial nephritis
renal papillary necrosis

114
Q

; most common cause of AKI

A

Acute tubular necrosis

115
Q

Acute tubular necrosis
pathogenesis
histology in urinalasis
type based on etiology

A

Injury and necrosis of tubular epithelial cells; most common cause of AKI
Necrotic cells plug tubules, obstruction decreases GFR
Muddy brown granular casts in urinalysis
Reversible (2-3 weeks) , but often requires supportive dialysis
Etiology may be ischemic or nephrotoxic

116
Q

Ischemic ATN
where location
and why there

A

Often preceded by prerenal azotemia
Proximal tubule and medullary segment of the thick ascending limb are particularly susceptible
However, in severe hypotensive shock, the entire cortex may undergo necrosis (renal cortical necrosis).

Tubular epithelial cells, with their high rate of energy-consuming metabolic activity and numerous organelles,
are particularly sensitive to hypoxia and anoxia.

117
Q

Nephrotoxic ATN
where
causes

A

Proximal tubule is particularly susceptible
Causes include aminoglycosides (most common), heavy metals (e.g., lead), myoglobinuria (e.g., from crush injury to muscle), ethylene glycol (associated with oxalate crystals in urine), radiocontrast dye, and urate (tumor lysis syndrome)

118
Q

Acute interstitial nephritis (AIN)
cause mnemonic
present as
progress to
marker in urinalysis

A

Drug-induced hypersensitivity involving the Interstitium and tubules;
SMART CAN

results in intra renal AKI

Presents as oliguria, azotemia, fever, and rash days to weeks after starting a drug
Resolves with cessation of drug
May progress to renal papillary necrosis
Eosinophils and eosinophilic casts may be seen in urine.

119
Q

Renal papillary necrosis
present with
causes mnemonic

A

Necrosis of renal papillae
Presents with gross hematuria and flank pain (ureteral colic)
SODA
sickle cell
obstructive pyelonephritis
diabetes
analgesics

120
Q

Glomerular disease (Glomerulopathies)
types
clinical presentation

A

Important cause of AKI and 15% of ESRD

Can be inflammatory (glomerulonephritis) or non inflammatory.
Acute or chronic glomerulonephritis
Can be caused by primary glomerular injury or Secondary glomerular injury (systemic diseases)
Clinically present with feature of nephrotic and/or nephritic syndrome

121
Q

Approach on diagnosis of glomerulopathies

A

Two steps
1st is the glomerular disease nephrotic and/or nephritic syndrome?
2nd is biopsy
Light microscope/LM: H&E, silver stain, PAS, Congo red or Masson’s trichrome
Immunofluorescence /IF: granular vs linear Ab
Electron microscopy/EM: foot process and Ab

122
Q

Nephrotic characters
plus urine as
clinical presentation
histology

A

Characterized by proteinuria (> 3.5 g/day) resulting in hypoalbuminemia(<3g/dl), hypogammaglobulinemia, hypercoagulable state, hyperlipidemia and hypercholesterolemia

foamy urine

pitting edema
infections

fatty casts

123
Q

nephritic characters
present with
biopsy reveals

A

Characterized by glomerular inflammation and bleeding
Presented with limited proteinuria, oliguria and azotemia, Salt retention with periorbital edema and hypertension
Biopsy reveals hypercellular, inflamed glomeruli
Immune-complex deposition activates complement; C5a attracts neutrophils, which mediate damage

124
Q

glomerular lesion classification

A

diffuse or focal
global or segmental

125
Q

causes of nephrotic syndrome 2 and list each

A

primary glomerular diseases
membranous nephropathy Focal segmental glomerulosclerosis (FSGS)
Minimal change disease(MCD)
Membranoproliferative glomerulonephritis (MPGN)

systemic diseases
diabetes
amyloidosis
lupus
drugs
infection

126
Q

Minimal change disease(MCD)
aka and why
associated with
LM EM IF
treatment

A

lipoid nephrosis or nil disease
lipoid bc lipid seen in urine
nil bc only seen in EM

Usually idiopathic may be associated with Hodgkin lymphoma.
Selective proteinuria
LM - Normal glomeruli.
EM - Effacement of foot processes.
IF - Negative.
Excellent response to steroids (damage is mediated by cytokines from T cells)

127
Q

Most common cause of nephrotic syndrome in children.

A

Minimal change disease(MCD)

128
Q

pathogenesis of MCNS if systemic and glomerular

A

systemic
T and B cell dysfunction
inflammation
damage to BM

Glomerular
podocyte dysfunction
damaged BM

129
Q

Focal segmental glomerulosclerosis (FSGS)
cause or association
LM EM IF
treatment

A

Usually idiopathic; may be associated with HIV, heroin use, and sickle cell disease
LM - Focal and segmental sclerosis.
EM - Effacement of foot processes.
IF – Negative
Poor response to steroids; progresses to chronic renal failure.

130
Q

Most common cause of nephrotic syndrome in adult.

A

Focal segmental glomerulosclerosis (FSGS)

131
Q

Membranous nephropathy
cause
LM EM* IF

A

85% considered idiopathic but recent studies show autoimmune reaction against podocyte antigen (type-M phospholipase A2 receptor (PLA2R)).
Poor response to steroids; progresses to chronic renal failure.

LM- Thick glomerular basement membrane.
IF - Granular immune complex deposition.
EM- Subepithelial IC deposits with ‘spike and dome’ appearance.

132
Q

The 2nd common cause of nephrotic syndrome adults

A

Membranous nephropathy

133
Q

Membranoproliferative glomerulonephritis (MPGN)
TYPES based on cause
treatment
LM* EM IF

A

Type I - subendothelial; associated with HBV and HCV
Type II (dense deposit disease) - intramembranous; associated with C3 nephritic factor (autoantibody that stabilizes C3 convertase)
Type III is rare and shows features of type I MPGN and membranous nephropathy in association with systemic diseases or drugs.
Poor response to steroids; progresses to chronic renal failure

LM- Thick glomerular basement membrane often with ‘tram-track’ appearance.
IF – granular IC deposition.
EM – duplicated (split) basement membranes and IC deposition.

134
Q

Diabetic nephropathy
cause
pathogenesis
and can cause

A

Includes renal artery atherosclerosis and hyaline arteriolosclerosis of afferent and efferent arterioles.
Efferent arteriole&raquo_space; afferent arteriole
Hyperfiltration injury leads to microalbuminuria(≤ 300 mg/day) which eventually progresses to nephrotic syndrome.

can cause diffuse glomerulosclerosis and nodular glomerulosclerosis (Kimmelstiel Wilson disease).

135
Q

Renal amyloidosis (Amyloid nephropathy)
histology

A

Kidney is the most commonly involved organ in systemic amyloidosis(both 1ᵒ and 2ᵒ)
Amyloid deposits in the mesangium, resulting in nephrotic syndrome.

H&E cotton candy

136
Q

causes of nephritic syndrome

A

Acute poststreptococcal glomerulonephritis (APSGN)

Rapidly progressive glomerulonephritis(RPGN)

Goodpasture syndrome (anti-GBM disease)

IgA nephropathy (Berger disease)

Alport syndrome

137
Q

Acute poststreptococcal glomerulonephritis (APSGN)
plus present with
LM EM* IF

A

= Acute proliferative (post-infectious) glomerulonephritis.
Mainly 2-4 weeks after infection
Children&raquo_space; adults

hematuria
HTN
periorbital edema

LM: Hypercellular glomeruli with neutrophils and monocytes.

IF: Granular deposits of IgG, IgM, and C3 throughout the glomerulus.

EM: Subepithelial immune complex deposits (humps)

138
Q

Rapidly progressive glomerulonephritis(RPGN)
AKA
prognosis

A

= Crescentic Glomerulonephritis
Characterized by rapid and progressive loss of renal function
Leads to death from renal failure within weeks to months of onset
Most patients never recover, and their survival depends on continuous dialysis or kidney transplantation.

139
Q

Rapidly progressive glomerulonephritis(RPGN)
types

A

1 anti GBM AB
2 immune complex
3 pauci immune

140
Q

Goodpasture syndrome (anti-GBM disease)
cause
m;f
also wht other organ
LM IF* EM

A

Small vessel vasculitis
Due to antibodies against Goodpasture antigen
Male > female, peak age is 20-30.
Results in damage of the lungs and the kidneys.
Pulmonary involvement typically precedes the renal disease
Most patients will develop type I RPGN.

LM shows hypercellularity, crescents, and fibrin depostion in glomeruli.
IF shows a smooth and linear pattern of IgG and C3 in the glomerular basement membrane (GBM).
EM there are no deposits, but there is glomerular basement membrane disruption.

141
Q

IgA nephropathy (Berger disease)
Affected age and sex
present with
associated with
prognosis
LM EM IF

A

It affects children and young adults (mostly males).
Characterized by recurrent gross hematuria (a predominately nephritic presentation), usually following mucosaI infections (e.g., gastroenteritis).
Associated with celiac sprue and Henoch-Schonlein purpura (HSP).
Prognosis many cases slowly progress to renal failure over 25 years.

LM show normal glomeruli or mesangial proliferation.
IF shows mesangial deposits of IgA and C3.
EM shows mesangial immune complex deposits.

142
Q

The most common cause of glomerulonephritis in the world.

A

IgA nephropathy (Berger disease)

143
Q

Alport syndrome
CAUSE
present
EM

A

In 85% the mutation is in the COL4A5 gene coding for the alpha-5 chain of type 4 collagen.
Present with gross or microscopic hematuria begins in childhood, hearing loss and various ocular abnormalities of the lens and cornea can occur.
Electron microscopy shows alternating thickening and thinning of basement with splitting of the lamina densa.

144
Q

Chronic glomerulonephritis
present with
urinalasys

A

(Synonym: End-Stage Kidney)
Not a specific entity but an end stage of numerous acute or chronic glomerular diseases which result in irreversible impairment of renal function.
Clinical features include anemia, anorexia, and malaise, proteinuria, hypertension, and azotemia.
Urinalysis shows broad waxy casts.
Treatment is with dialysis and renal transplantation.

145
Q

Conditions which may progress to chronic GN

A

Rapidly progressive GN (90%) > Membranous GN (50%) > Membranoproliferative GN (50%) > Focal segmental glomerulosclerosis (50%) > IgA nephropathy (40%) >Acute post-streptococcal GN (1%).

146
Q

chronic GN and CPN difference

A

The kidneys are diffusely and symmetrically scarred (small and shrunken) unlike chronic pyelonephritis if bilateral, the involvement is asymmetric.

Patho (33 decks)

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