Renal Flashcards
1
Q
horseshoe kidney
A
most common ceongenital, abnormally in lower abdomen (gets stuck on IMA), conjoined at lower pole
2
Q
renal agenesis
A
can be uni or B/L
3
Q
unilateral renal agenesis
A
hypertrophy of existing kidney, hyperfiltration inc. risk of renal failure in life,
4
Q
B/L renal agenesis
A
oligohydraminos leading to lung hypoplasia, flat face with low set ears, dev. defects of extremities (Potter Sequence); incompatible with life
5
Q
dysplastic kidney
A
non-inheritaed, congenital malformation of renal parenchyma chatacterized by cysts and abnormal tissue especially cartilage; usually unilaterial
6
Q
if dysplastic kidney is kidney then what needs to be done
A
must distinguish it from PKD
7
Q
Polycystic Kidney Disease (PKD) characterisitcs
A
inherited, B/L enlarged kidneys with cysts in renal cortex and medulla,
8
Q
Autosomal recessive PKD (Juvenile form) characteristics
A
presents in infants, worsening renal failure, HTN, potter sequence may be seen, assoc. with congenital hepatic fibrosis (which will show as portal HTN) and hepatic cysts
9
Q
Autosomal dominant PKD (Adult, ADult)
A
presents in young adults, HTN, hematuria, worsening renal failure, due to mutations in APKD1 or APKD2, assoc with berry aneurysm (cause of deaths), hepatic cysts, mitral valve prolapse, pt will have inc. renin causing the HTN
10
Q
family Hx of deaths from intracrainial bleeds from aneuryms and renal disease?
A
think possibly of autosomal dominant PKD
11
Q
Medullary systic kidney disease
A
inherited (autosomal dominant) defect, cysts in medullary collecting ducts, parenchymal fibrosis causing a shrunken kidneys, worsening renal failure
12
Q
Acute renal failure is characterized as
A
azotemia often with oliguria
13
Q
types of acute renal failure
A
prerenal, postrenal, intrarenal azotemia
14
Q
pre-renal acute renal failure
A
dec. blood flow to the kidney; LABS: dec. GFR, azotemia, oliguria, BUN/Cr > 15 (why? low BF causues renin-aldos sequence leading to inc. Na thus inc. H20 thus inc. BUN reabsorption with Cr excretion not chaning), tubulues activity intact
15
Q
post-renal acute renal failure
A
dec. outflow, back P in kidney that lowers GFR; decreased GFR, azotemia, oliguria,
16
Q
intral renal acute renal failure
A
within kidney is a blockage
17
Q
early stage of post renal azotemia
A
inc. back pressure leads to inc. BUN resorpt to increaces BUN: Cr ration, tubular fxn will be intact
18
Q
long standing obstruction of post renal azotemia
A
now decreased resorpt of BUN causing BUN:Cr to decrease, decreased reabsorption of sodium, inability to concentrate urine….long standing blockage starts to damage tubules
19
Q
Intrarenal acute renal failure subtypes
A
ATN, Acute interstitial nephritis, renal papillary necrosis
20
Q
Acute tubular necrosis
A
injury and necrosis of tubular epi. cells, necrotic cells plug tubules causing obstruction and lowering GFR, brown granular casts seen in urine; decrased reabsort of BUN (BUN:Cr <15), decreased reabsort of Na, cant concentrate urine
21
Q
most common cause of ARF
A
ATN
22
Q
etiologies of ATN
A
ischemia and nephrotoxic
23
Q
Ischemic ATN
A
decreased blood supply causing necrosis of tubules, often preceded by prerenal azotemia, prox tubule and medullary segment of thick ascending limb particularly susceptible
24
Q
Nephrotoxic ATN
A
toxic agent causes it, prox tubule is susceptible
25
Nephrotoxic ATN causes
aminoglycosides, heavy metals, myoglobinuria, ethylene glycol (cause oxalate crystals in urine), radiocontrast dye, urate
26
Clinical features of ATN
oliguria with brown granular casts, elevated BUN and creatinine, hyperkalemia with metabolic acidosis
27
oliguria from ATN can last how long
2-3 weeks
28
Acute interstitial nephritis
drug induced hypersensitivity rxn, causes include NSAIDs, PCN, diuretics
29
presentation of acute interstitial nephritis
oliguria, fever, rash days to weeks after starting drug, Eosinophils seen in urine, resolves with drug cessation, can progress to renal papillary necrosis
30
renal papillary necrosis
necrosis of the renal papillae
31
presentation of renal papillary necrosis
gross hematuria, flank pain
32
renal papillary necrosis causes
chronic analgesic use, diabetes mellitus, sickle cell traint or disease, severe acute pyelonephritis
33
Nephrotic syndrome def
proteinuria (>3.5 g/day); hypoalbuminemia (cause edema), hypogammaglobulinemia (inc risk of infection), hypercoaguable state (lose ATIII), hyperlipidemia and hypercholesterolemia
34
Nephrotic Syndromes
minimal change disease, FSGS, Membranous nephropathy, membranoproliferative glomerulonephritis, diabetes mellitus cause, Systemic amyloidosis
35
minimal change disease
most common nephrotic in children, usually idiopathic, may be assoc with hodgkin lymphoma
36
Most common nephrotic syndrome in children
minimal change disease
37
minimal change disease pathogenesis
effacement of the foot processes, due to cytokines
38
MCD histology
normal glomeruli on HnE stain, effacement of processes on EM, no Ig complex deposits (negative IF)
39
MCD proteinuria characterisitc
selective; loss of albumin but not Ig
40
MCD Tx
steroids
41
Focal segmental glomerular sclerosis
most common cause of nephrotic syndrome in hispanics and african americans, usually idiopathic; may be assoc. with HIV, heroin use, sickle cell disease
42
most common cause of nephrotic syndrome in Hispanics and African Americans
FSGS
43
FSGS histology
focal and segmental sclerosis on HnE, effacement of foot process on EM, negative IF
44
what does focal refer to
only 1 glomeruli or small number of them
45
what does segmental mean
only portion of the affected glomeruli is affected
46
if MCD does not respond of steroids and progress it becomes what
FSGS
47
FSGS respnce to steroids
poor response and progresses to chronic renal failure
48
membranous nephropathy
usually idiopathic; assoc. with Hep B, Hep C, SOlid tumors, SLE, Drugs...most common cause of nephrotic in caucasian adults
49
most common nephrotic syndrome in caucasian adults
membranous nephropathy
50
membranous nephropathy histology
thick glomerular basement membrane on HnE, granular IF, sub-epi deposits with spike and dome appearance on EM
51
nephrotic syndrome assoc with SLE
membranous nephropathy
52
if the membrane in glomeruli is thickened then...
its membranous nepohropahty or membranoproliferative due to the Ig depot
53
membranous nephropathy pathogenesis
the Ig deposits sub-endothelial and then the podocyte lays down more basement membrane leading to the spike and done appearance
54
membranoproliferative glomerular nephritis (MPGN)
thick capillary membraines on HnE, often with tram track appearance, granular IF
55
MPGN pathogensis
Ig deposits, mesangium proliferates thru the deposit to create tram track
56
MPGN subtypes
Type I: subendothelial, Type II: intramembranous
57
TYpe I MPGN
subendothelial, assoc. with HBV, HCV; mor eoften with tram track look
58
Type II MPGN
intramembranous; assoc. with C3 nephritic factor (an auto antibody that stabalized C3 convertase)
59
MPGN causes nephrotic or nephritic?
can cause either or BOTH
60
membranous and MPGN distribution in glomeruli
membranous type = right under podocytes (epithelial), MPGN I = under endothelial, MPGN = intramembrane
61
Nephrotic syndrome caused by DM
high glucose cauises non-enzyme glycosylation of vascular basement membrane resulting in hyaline arteriolosclerosis, efferent artiole more affected than afferent leadin to inc. glomerular pressure
62
DM nephrotic syndrome pathogenesis
the NEG cuases back pressure leading to sclerosis of the glomerulus,
63
Tx to slow the DM neptjrotic syndrome progression
ACE inhibitor due to angiotensin II acts on efferent vessel
64
Kimmelstiel-wilson noldules
seen in the DM nephrotic syndrome from the sclerosis and is patho-neumonic
65
Systemic Amyloidosis
kidney most common involved, amyloid deposits in mesangium resulting in nephrotic syndrome, apple green birefringence under polarized light
66
Nephritic syndrome
limited proteinuria, oliguria, azotemia, salt retention with periorbital edema and HTN, RBC casts and dysmorphic RBC in urine...glomerular inflammation and bleeding
67
Bx of nephritic syndomr glomeruli
hypercellular, inflamed glomeruli; immune complex deposition activates complement, C5a is a chemoattractant for neutros
68
nephritic syndrome subtypes
Post. Strept. glomerular nephritis, RPGN, IgA nephropathy, Alport syndrome
69
PSGN
nephritic syndrome that arises after group A Beta hemolytic strep infection of skin or pharynx
70
more often PSGN strept need what virulence factor?
M protein, defines it as a nephritic strain
71
PSGN presentation
2-3 weeks after infection, hematuria (coca cola urine), oliguria, HTN, periorbital edema, more often seen in children but adults can be affected
72
PSGN histology
hypercellular, inflames glomeruli on HnE, Ig deposition (granular IF), subepithelial humps on EM
73
PSGN Tx
supportive due to the deposits go to sub-epi layer and then eventually disappear; children rarely progress to renal failure; adults could dev. RPGN
74
RPGN
nephritic syndrome that progresses to renal failure in weeks to months
75
RPGN Bx
crescents in bowens space and the cresencts are made of fibrin and macrophages
76
RPGN IF subtypes
linear = Goodpasture syndrome; granular = PSGN, diffuse proliferative glomerularnephritis; Negative IF = wegener granulomatosis, polyangiitis, churg strauss syndrome
77
Goodpasture syndrome
Ab againts collagen in glomerular and alveolar basement membranse; presents as hematuria hemoptysis, classically young adult males
78
SLE most common type of renal disease
diffuse proliferative golerulonephroitis type, SLE usuallly causes this instead of the nephrotic one mentioned, granular immune complex deposition
79
after a negative IF (pauci immune) then
ANCA test is performed; c-ANCA = wegeners granulomatosis (kidney disease is RPGN along with lung invokvement and nasopharynx involvement); p-ANCA is microscopic polyangiitis or churg strauss....to distinguish CS has granulomatous inflammation, eosinophils, asthma
80
IgA nephropathy
mose common nephropathy world wide, IgA depot in mesangium
81
IgA nephropathy presentation
episodic gross or microscope hematuria with RBC casts following usually a mucosal infection; granular IF; may slowly progress to renal failure
82
ALport syndrome
inheritated defect in type IV collagen; most commonly X-linked; results in thinning and splitting of glomerular basement membrane
83
ALport syndrome presentation
isolated hematuria, sensory hearing loss, ocular disturbances
84
UTI usually caused by
ascending infections
85
cystitis
bladder inflammation; presents with dysuria, urinary frequency, urinary urgency, supra-pubic pain; systemic signs are usually absent
86
risk factors for UTI
sexual intercourse, urinary stasis, catheters
87
Labs for cystitis
UA: cloudy urine with >WBC
Dipstick: + leukocyte esterase and nitrites
CUlture >100,000 CFU
88
etiologies of cystits
E. COli (80%), staph. saprophyticus (young sexually active women), kleb. pneumoniae, proteus mirabilis (alkaline urine), enterococcus faecalis
89
sterile pyuria
pyuria with - urine culture; suggests urethritis from chlamydia, trachomatis, neisseria gonorrhoeae
90
pyelonephritis
kidney infection; usually ascending infection
91
pyelonephritis inc. risk factor
vesicoureteral reflux
92
pyelonephritis presentation
fever, flank pain, WBC casts, leukocytosis along with the Sx of cystitis ( dysuria, urinary frequency, urinary urgency, supra-pubic pain)
93
pyelonephritis etiologies
E. COli (90%), klebsiella species, enterococcus faecalis
94
Chronic pyelonephritis
interstiail fibrosis and atrophy of tubules due to multiple bouts of acute form; due to vesicoureteral reflux (children) or obstruction
95
chronic pyelonephritis Bx
cortical scarring with blunted calyces; if scarring at upper and lower poles then it is characteristic for vesicoureteral reflux
96
chronic pyelonephritis histology
thyroidization of kidney (atrophic tubules contain eosinophilic peoteinaceous material reminiscent of thyroid follicles)
97
chronic pyelopnephritis UA
waxy casts seen
98
nepholithiasis
urinary solute as a stone; risk factors include high conc. of solute in urinary filtrae and low urine volume
99
nephrolitiasis presentation
colicky pain with hematuria and unilateral flank tenderness; stone will pass in hours or else sugery may be required
100
calcium oxalate or calcium phosphate stones
most common seen in adults
101
causes of Ca-oxalate or Ca-Pi stones
idiopathic calciuria; hypercalcemia causes must be ruled out; may be seen in crohns
102
Tx of Ca-oxalate or Ca-Pi stones
thiazides (Ca sparring diuretucs)
103
ammonium, Mg, Pi
2nd most common type
104
ammonium, Mg, Pi causes
infection with urease + organisms (proteus vulgaris, klebsiella); alkaline the urine causing stone; stag horn stones; usually requires surgery
105
ammonium, Mg, Pi stone Tx
staghorn stones thus need surgery, Ab for the offending agent
106
Uric acid stones
3rd most common; radiolucent
107
Uric stone causes
risks: hot, arid climate, low urine volume, acidic pH; stones seen in gout pt, hyperuricemia or myeloproliferative disorders inc. risk
108
uric stone Tx
HYDRATION AND ALKALIZATION OF URINE; allopurinaol can help in gout pt
109
cysteine stones
rare, more commonly in children
110
cysteine stones causes
cysteinuria (due to genetic defect in tubles)
111
cysteine stone Tx
may form stag horns, hydration and alkalization of urine
112
end sdtage kidney failure
result from glomerular, tubular, inflammatory, vascularf insults to kidney; most common causes HTN, DM, glomerular disease
113
Uremia
azotemia; nausea, anorexia, pericarditis, platelet dysfxn, encepalopathy with asterixis, urea deposition in skin
114
clinical features seen in end stage kidney failure
Uremia, salt/water retention (with resultant HTN), hyperkalemia with metabolic acidosis, anemia, hypocalcemia, renal osteodystrophy (damage to bone due to failure; components osteitis fibrosa cystica, osteomalacia, osteoporosis)
115
renal peritubular interstitial cells
secrete EPO
116
osteitis fibrosa cystica
hypocalcemia...PTH rise....resportion of calcium from bone leading to cysts and fibrosis
117
osteomalacia
cannout mineralize the osteoid created
118
end stage renal failure Tx
kidneys shrink and due to dialysis they create cysts, increased risk for renal cell carcinoma (pt on dialysis)
119
Angiomyolipoma
hamartoma comprised of BV, Smooth Muscle, Adipose tissue; increased frequency in tuberous sclerosis
120
Renal cell carcinoma
malignant epithelial tumor arising kidney tubules
121
renal cell carcinoma presentation
classic triad: hematuria, palpable mass, flank pain; other Sx: fever, lbs loss, paraneoplastic syndrome (EPO, renin, PTHrP, ACTH)
122
renal cell carcinoma extra things
rarely may present with left sided varicocele (only occurs on LEFT side including only L-kidney)
123
most common cell variant for renal cell carcinoma
cells with clear cytoplasm
124
renal cell carcinoma pathogenesis
loss of VHL tumor suppressor; causes increse inculin growth factor-1, inc. HIF transcription factor that increase VEGF, PDGF
125
sporadic pathway of RCC
single tumor, upper pole, adult smoker, assoc. with VHL loss
126
hereditary pathway of RCC
younger, multiple and B/L, assoc. with VHL loss
127
Von Hippel-Lindau disease
autosomal dom disorder assoc. with inactivation of VHL; increases risk for hemangioblastoma of cerebellum and RCC
128
RCC loves to go where..
renal vein
129
Wilms tumor
most common to arise in children (avg age is 3), malignant renal tumor comprised of blastema (primitive cells for kidney dev.), primitive glomeruli, tubules, stromal cells
130
Wilms tumor presentation
large, unilateral flank mass, hematuria, HTN
131
Wilms tumor gene mutation
WT1
132
WAGR syndrome
WIlms tumor, Aniridia, Genital abnormalities, Retardation
133
Beckwith-Wiedemann syndrome
Wilms tumor, neonatal hypoglycemia, muscular hemihypertrophy, organomegaly (including tongue)
134
urothelial carcinoma
malignant tumor from urothelial lining of renal pelvis, ureter, bladder, urethra
135
most common type of lower urinary tract cancer
urothelial carcinoma; usually arise in bladder
136
number 1 major risk factor for urothelial carcinoma
cigarettes because of the polycyclic aromatic hydrocarbons
137
risk factors for urothelial carcinoma
smoking, naphthylamine, azo dyes (coloring including hair), long term cyclophosamide or phenacetin use
138
urothelial carcinoma presentation
usually older adults with painless hematuria
139
2 pathways for causation of urothelial carcinoma
flat and papillary; papillary growth being a vascularized growth with epi cells (progress from LG to HG then INVADES); flat pathyway is a flat lesion that starts has HG and then invades ,assoc. with earl;y p53 mutations
140
urothelial carcinoma are often multifocal and recur due to
the entire urothelial field are exposed to the carfinogens so eventually they are all cancerous or become cancerous
141
squamous cell carcinoma
malignant proliferation of squamous cells; usually involves bladder; arises in a background of squamous metaplasia
142
squamnous cell carcinoma risk factors
chronic cystitis, schistosoma hematobium (middle eastern usually), long standing nephrolithiasis
143
urothelial cells become what during irriation
becomes squamous metaplasia and then allows for squamous cell carcinomas
144
adenocarcinoma
malignant proliferation of glands, usually involve bladder
145
adenocarcinoma arise frm
urachal remnant, cystitis glandularis, exstrophy
146
urachal remnant
from a tube that drains bladder to yolk sac and has glands in it, thus allow for production of adenocarfcinoma; the adenocarcinoma will be at dome of bladder
147
cystits glandularis
chronic inflammation leading to a columnar metaplasia to allow for creation of adenocarcinoma of bladder
148
exstrophy
congenital defect to form caudal portion of bladder wall and anterior abdom wall
