Renal Flashcards
1
Q
Pronephros
A
week 4
2
Q
Mesonephros
A
interim kidney in first trimester
becomes male genital system
3
Q
Metanephros
A
permanent kidney
appears in 5th week
4
Q
Ureteric bud gives rise to
A
ureter, pelvises, calyces, collecting ducts, fully canalized by week 10
5
Q
metanephric mesenchyme
A
interacts with ureteric bud
induces differentiation and formation of glomerulus through to distal convoluted tubule
6
Q
Ureteropelvic junction is last to canalize and most common site of ______
A
obstruction
can lead to hydronephrosis
7
Q
Babies who cant pee in utero develop the potter sequence which consists of:
A
pulmonary hypoplasia oligohydramnios twisted face twisted skin extremity defects renal failure (in utero)
oligohydramnios causes the other problems due to compression
caused by aut. recessive polycystic kidney disease, obstructive uropathy, bilateral renal agenesis, chronic placental insufficiency
8
Q
horseshoe kidney
A
inferior poles of both kidneys duse abnormally and get trapped under the inferior mesenteric artery. This results in them remaining low in the abdomen
kidney functions normal
9
Q
Patient is born with only one functioning kidney.
A
congenital solitary functioning kidney
hypertrophy of contralateral kidney
10
Q
unilateral renal agenesis
A
ureteric bud fails to develop and induce differentiation of metanephric mesenchyme
complete absence of kidney and ureter
11
Q
multicystic dysplastic kidney
A
ureteric bud fails to develop and induce differentiation of metanephric mesenchyme
results in nonfunctioning kidney consisting of cysts and connective tissue
unilateral
12
Q
bilateral multicystic dysplastic kidney can result in
A
potters syndrome
13
Q
Duplex collecting system
A
bifurcation of ureteric bud before it enters the metanephric blastema creates a Y shaped bifid ureter
OR
two ureteric buds reaching and interacting with metanephric blastema
strongly associated with vesicoureteral reflux and or ureteral obstruction which increases risk of UTI
14
Q
Posterior urethral valves
A
Membrane remnant in the posterior urethra in males
persistence and lead to urethral obstruction
presents prenatally by hydronephros and dilated or thick walled bladder on ultrasound
15
Q
What is the most common cause of bladder outlet obstruction in male infants
A
Posterior urethral valves
16
Q
What kidney is used for donor transplantation
A
Left kidney because of its longer renal vein
17
Q
Renal blood flow
A
renal artery –> segmental artery –> interlobar artery –> arcuate artery –> interlobular artery–> afferent arteriole –> glomerulus –> efferent arteriole –> vasa recta/peritubular capillaries –> venous outflow
18
Q
Course of ureters
A
renal pelvis –> under gonadal arteries –> over common iliac artery –> under uterine artery/vas deferns (retroperitoneal)
19
Q
Three points of constriction of the ureter
A
ureterovesical junction
ureteropelvic junction
pelvic inlet
20
Q
In a 70 kg person what is the total body water and the ICF and ECF
A
total body water is 60% or 42 kg
ICF is 40% (2/3) or 28 kg
ECF is 20% (1/3) or 14 kg
21
Q
ECF is composed of
A
plasma 25% of ECF
Interstitial fluid 75% of ECF
22
Q
There is a ______ K concentration intracellularly
A
high
23
Q
plasma volume can be measured by radiolabeling ____
A
albumin
24
Q
extracellular volume can be measured by
A
inulin and mannitol
25
The glomerular filtration barrier
composed of
- Fenestrated capillary endothelium
- Basement membrane with type 4 collagen chains and heparan sulfate
- Epithelial layer consisting of podocyte foot processes
26
how does the glomerular filtration barrier work according to size and charge
- all three layers are neg charge and prevent entry of other neg charged molecules like albumin
- fenestrated capillary endothelium prevent entry of >100 nm molecules/blood cells
- podocyte foot processes interpose with basement membrane
- slit diaphragm which prevent entry of molecule >50-60 nm
27
Renal clearance formula
Cx=(UxV)/P
Ux= Urine concentration of X
Px= Plasma concentration of X
V=Urine flow rate
Cx=Clearance of X
28
If Cx is ____ than GFR
less than GFR
net reabsorption of X
29
If Cx is ____ than GFR
greater than GFR
net tubular secretion of X
30
If Cx is _____than GFR
equal to GFR
no net secretion or reabsorption
31
____ clearance can be used to measure GFR. Why?
Inulin
because it is freely filtered and is neither reabsorbed nor secreted
32
GFR equation
Uinulin x V/Pinulin = Cinulin
= Kf[(Plasma concentration of glomerular capillary - plasma concentration of bowman space)-(Osmotic concentration of glomerular capillary)]
= (Pcr x Una) / (Ucr x Pna)
V=urine flow rate
33
_____ clearance is an approximate measure of GFR. Why only an estimate?
creatinine
Slightly overestimates the GFR because creatinine is moderately secreted by renal tubules
34
Effective renal plasma flow (eRPF) can be estimated using ______
para-aminohippuric acid (PAH) clearance
100% excretion of all PAH that enters the kidney
35
Effective renal plasma flow equation
eRPF=UpahxV/Ppah=Cpah
underestimates true renal plasma flow slightly
36
renal blood flow =
RPF/(1-Hct)
37
plasma volume
TBVx(1-Hct)
38
Filtration fraction
FF= GFR/RPF
normal filtration fraction is 20%
39
Filtered load
GFR x plasma concentration
40
Prostaglandins _______ afferent arterioles
dilate
"PDA"
This causes increased renal plasma flow and increased GFR. Therefore no change in filtration fraction (GFR/RPF)
41
Angiotensin II ___ efferent arterioles
constrict
"ACE"
This causes a drop in GFR but an increase in GFR, therefore there is an increase in FF (GFR/RPF)
42
Filtered load
GFR x Px
43
Excretion rate
V x Ux
44
Reabsorption rate
filtered-excreted
45
Secretion rate
excreted - filtered
46
Fractional excretion of sodium (Fe na)
Fe Na= Na excreted/Na filtered= (VxUna)/(GFRxPna)
47
At what plasma level does glucosuria begin
~200 mg/dL
48
At what plasma level are transporters fully saturated (Tm)
~375 mg/dL
49
At normal glucose levels (60-120) glucose is ______ reabsorbed in ________ tubule by Na/Glucose cotransport
completely
proximal convoluted tubule (PCT)
50
What part of the nephron do you reabsorb all glucose and amino acids.
early proximal convoluted tubule
51
what part of the nephron is most HCO3-, Na+, Cl-, PO4, K+, H2O, Uric Acid reabsorbed
early proximal convoluted tubule
52
what part of the nephron is there a brush border and isotonic absorption. It generates and secretes NH3 which enables the kidney to secrete more H+
early proximal convoluted tubule
53
Where does PTH act to inhibit Na/PO4 cotransport ? And what does it result in?
early proximal convoluted tubule
PO4 excretion
54
Where does AT II act to stimulate Na/H exchange? and what does it result in
early proximal convoluted tubule
increase Na, H2O, and HCO3 reabsorption
contraction alkalosis
55
Where is 65-80% of Na reabsorbed
early proximal convoluted tubule
56
Where is H20 passively reabsorbed in the nephron and how
Thin descending loop of henle
via medullary hypertonicity
It is impermeable to Na
57
what part of the nephron is the concentrating segment that makes urine hypertonic
Thin descending loop of henle
58
What part of the nephron reabsorbs Na, K , and Cl. Indirectly induces paracellular reabsorption of Mg and Ca through a positive lumen potential generated by K backleak
Thick ascending loop of henle
10-20% of Na reabsorbed
59
What part of the nephron is important for making the urine less concentrated and is impermeable to H20
Thick ascending loop of henle
60
What part of the nephron is important for reabsorbing Na, Cl and is impermeable to H20. It is important for fully diluting (hypotonic) the urine.
Early distal convoluted tubule
5-10% Na reabsorbed
61
PTH effect on early distal convoluted tubule
increases Ca/Na exchange which results in Ca reabsorption
62
What part of the nephron is regulated by aldosterone and it reabsorbs Na in exchange for secreting K+ and H+
Collecting tubule
3-5% Na reabsorbed
63
Effect of aldosterone on the collecting tubule
acts on mineralocorticoid receptor to induce protein synthesis
in principal cells: increase apical K conductance, increase Na/K pump, increase epithelial Na channel (ENaC) activity --> lumen negativity --> increases H+ ATPase activity --> H+ secretion --> increases HCO3/Cl exchanged activity
64
Effect of ADH on the collecting tubule
acts at V2 receptor to insert aquaporin H2O channels on apical side
65
What renal syndrome is due to a defect in the general reabsorption within the PCT
Fanconi syndrome
results in excretion of AA, glucose, HCO3, PO4, and all substances reabsorbed by the PCT
may lead to metabolic acidosis, hypophosphatemia, osteopenia
66
What renal syndrome is due to a resorptive defect in the thick ascending loop of henle that affects Na/K/2Cl cotransporter
Bartter syndrome
results in metabolic alkalosos, hypokalemia, hypercalciuria
increased renin, aldosterone, urine Ca
67
What renal syndrome is due to reabsorption defect of NaCl in DCT
Gitelman syndrome
results in metabolis lakalosis, hypokalemia, hypocalciuria
Increased renin, aldosterone
Decreased serum Mg and Urine ca
68
What renal syndrome is due to gain of function mutation that increases activity of Na channel and thus increased Na reabsorption in collecting tubules
Liddle syndrome
results in metabolic alkalosis, hypokalemia, hypertension, decreased aldosterone
Increased BP
Decreased plasma renin and aldosterone
69
What renal syndrome present similar to hyperaldosteronism ? how do you treat it?
liddle syndrome
treat with amiloride
"it is a liddle like hyperaldosteronism"
70
What renal syndrome is due to a hereditary deficiency of 11beta hydroxysteroid dehydrogenase.
Syndrome of Apparent Mineralocorticoid excess
This results in excess cortisol (usually the enzyme would convert it to cortisone) and ultimately increased mineralocorticoid receptor activity
Metabolic alkalosis, hypokalemia, hypertension, decreased serum aldosterone level
71
Syndrome of Apparent Mineralocorticoid excess can be caused from _____ acid present in licorice which blocks activity of 11beta hydroxysteroid dehydrogenase
glycyrrhetinic acid
72
How can you best treat Syndrome of Apparent Mineralocorticoid excess
treat with K sparing diuretics which decrease mineralocorticoid effects
or treat with corticosteroids which result in decrease of endogenous cortisol production. Ultimately decreasing mineralocorticoid receptor activation
73
TF/P > 1
Tubular fluid concentration/plasma concentration
when solute is reabsorbed less quickly than water or when solute is secreted
74
TF/P = 1
Tubular fluid concentration/plasma concentration
When solute and water are reabsorbed at the same rate
75
TF/P<1
Tubular fluid concentration/plasma concentration
when solute is reabsorbed more quickly than water
76
What cells secrete renin?
juxtaglomerular cells in response to decreased renal blood pressure and increased sympathetic tone (beta 1)
77
What is reaction is renin important for
converting angiotensinogen to angiotensin I
78
What enzyme converts angiotensin I to angiotensin II
ACE
79
Renin
responds to decreased renal perfusion pressure that is detected by renal baroreceptors in the afferent arterioles.
It increases renal sympathetic discharge (beta 1 effect) and decreases NaCl delivery to macula densa cells
80
Angiotensin II
helps maintain blood volume and blood pressure. Net effect of preservation of renal function with increased FF in low volume state with simultaneous Na reabsorption to maintain circulating volume
responds to drop in BP by causing efferent arteriole constriction which increases GFR and increases FF but with compensatory Na reabsorption in proximal and distal nephron
limits reflex bradycardia which would normally accompany its pressor effects
81
ANP/BNP
released from atria (ANP) and ventricles (BNP) in response to increase volume --> relaxes vascular smooth mm via cGMP and increases GFR --> decrease in renin
ANP : secreted in response to increased atrial pressure which causes increased GFR and increased Na filtration with no compensatory Na reabsorption in distal nephron. Net effect: Na loss and volume loss
"check" on the renin-angiotensin-aldosterone system
82
What is the effect of ANP/BNP on the afferent and efferent arterioles
```
Afferent dilates
Efferent constriction
Promotes natriuresis (excretion of Na in urine)
```
83
ADH
responds to increased plasma osmolality and responds to low blood volume states
stimulates reabsorption of water in collecting ducts
Also stimulates reabsorption of urea in collecting ducts to maintain corticopapillary osmotic gradient
84
Aldosterone
primarily regulated ECF volume and Na content
responds to low blood volume states and increased plasma [K]
Causes increased Na reabsorption, K secretion, H secretion
85
What responds to hyperkalemia by increasing K excretion
Aldosterone
86
Angiotensin II effects
vasoconstriction --> increased BP
Constrict efferent arteriole --> Filtration fraction increase --> preserves GFR when RBF is low
Increase kidney Na/H activity at the PCT cell --> Na, HCO3, H20 reabsorption --> contraction alkalosis
Causes aldosterone secretion which causes the alpha intercalated cells to secrete H+ by increase in H+ ATPASE activity
Aldosterone secretion also causes principal cells to reabsorb Na nd secrete K
ADH release from posterior pituitary causes principal cells to reabsorb H20 by increasing aquaporins
87
Juxtaglomerular apparatus
consists of mesengial cells, juxtaglomerular cells, and macula densa
maintains the GFR via renin-angiotensin aldosterone system
88
Juxtaglmerular cells
modified smooth muscle of afferent arteriole
89
Macula densa
NaCl sensor
Located at distal end of loop of Henle
sense decrease NaCl delivery to DCT and increase renin release --> efferent arteriole vasoconstriction --> increases GFR
90
How can beta blockers impact the juxtaglomerular apparatus
they decrease BP by inhibiting Beta 1 receptors of the JGA and thus decreasing renin release
91
Released by interstitial cells in peritubular capillary bed in response to hypoxia
erythropoietin
this is why it is supplemented in patients with chronic kidney disease
92
_____ cells convert 25-OH vitamin D3 to 1,25-(OH)2 vitamin D3 (calcitriol, active form). What enzyme is important for this?
PCT cells
via 1alpha hydroxylase ( + by PTH)
93
Paracrine secretion of ______ vasodilates the afferent arterioles to increase RBF
prostaglandins
94
NSAIDs block ________and thus constriction of afferent arterioles and decreased GFR. This may result in acute renal failure in low renal blood flow states
prostaglandins
95
______ is secreted by PCT cells and promotes natriuresis. At low doses it ______ the interlobular arteries, afferent arterioles, efferent arterioles and thus increases RBF (little or no change to GFR). At higher doses it acts as a _______
Dopamine
Dilates
Vasoconstrictor
96
Parathyroid hormone effect on kidney
Secreted in response to a drop in plasma Calcium concentrations, increase in PO4, or decrease in plasma 1,25-(OH)2D3
Causes increase in Ca reabsorption (DCT), decrease in PO4 reabsorption (PCT), and increase 1,25(OH)2D3 production
increased Ca and PO4 absorption from gut via vitamin D
97
Insulin shifts K out or into cells?
INsulin therefore INto cells --> hypokalemia
98
What causes hypokalemia due to shift of K into cells
Hypoosmolarity
Alkalosis
Beta adrenergic agonist ( increase Na/K ATPase)
Insulin (increase Na/K ATPase)
99
What causes hyperkalemia due to shift of K out of cells?
```
Digitalis (blocks Na/K ATPase)
Hyperosmolarity
Lysis of cells
Acidosis
Beta blockers
High blood sugar
Succinylcholine
```
"DO LABSSS"
100
Hypokalemia effects
U waves and flattened T waves on ECG
| Arrhythmias, mm cramps, spasm, weakness
101
Hyperkalemia effects
Wide QRS, peaked T waves, arrhythmias, mm weakness
102
Hypocalemia effects
Tetany, seizures, QT prolongation, twitching (Chvostek sign), spasm (trousseau sign)
103
Hypercalemia effects
```
Stones --> renal stones
Bones --> Bone pain
Groans --> abdominal pain
Thrones --> increased urinary frequency
Psychiatric overtones --> anxiety, altered mental status
```
104
Hypomagnesia effects
Tetany
Torsades de pointes
hypokalemia
hypocalcemia
105
Hypermagnesia effects
```
Decreased DTRs
Lethargy
Bradycardia
Hypotension
Cardiac Arrest
Hypocalcemia
```
106
hypophosphatemia effects
Bone loss
osteomalacia in adults
rickets in children
107
Hyperphosphatemia effects
renal stones
metastatic calcifications
hypocalcemia
108
SIADH effects on BP, Renin, aldosterone
normal or increased BP
Decreased Plasma renin
decreased aldosterone
109
Primary hyperaldosteronosim (Conn syndrome)
Increased BP and aldosterone
| Decreased plasma renin
110
Renin secreting tumor
Increased BP, increased plasma renin, increased aldosterone
111
Metabolic acidosis
decreased pH due to decreased [HCO3] or <20
compensate by decreasing PCO2 by hyperventiation
immediate compensation
112
Metabolic alkalosis
increased pH due to increased [HCO3] or >28
immediate compensation by increasing PCO2 by hypoventiation
113
Respiratory acidosis
Decreased pH due to increased PCO2 or >44
delayed compensation by increasing [HCO3] reabsorption
114
Respiratory alkalosis
Increased pH due to decreased PCO2 or < 36
delayed compensation by decreasing [HCO3] reabsorption
115
Winters formula
PCO2=1.5[HCO3]+8 +/- 2
predicted respiratory compensation for a simple metabolic acidosis
if predicted< measured PCO2 respiratory acidosis
if predicted> measured PCO2 respiratory alkalosis
116
Henderson Hasselbach equation
pH= 6.1 + log((HCO3)/(0.03PCO2))
117
Check the anion gap when there is
metabolic acidosis
118
anion gap formula
Na- (Cl+HCO3)
if >12 anion gap
if 8-12 normal anion gap
119
anion gap metabolic acidosis (AGMA)
MUDPILES
```
Methanol (formic acid)
Uremia
Diabetic Ketoacidosis
Propylene Glycol
Iron tablets or INH
Lactic Acidosis
Ethylene glycol (oxalic acid)
Salicylates (late)
```
120
Normal anion gap metabolic acidosis (NAGMA)
```
HARDASS
Hyperalimentation
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
```
121
Metabolic alkalosis caused by
Loop diuretics
Vomiting
Antacid Use
Hyperaldosteronism
122
Distal renal rubular acidosis
Type 1
NAGMA
inability of alpha intercalated cells tos ecrete H+ --> no new HCO3 is generated --> metabolic acidosis
urine ph >5.5 and low serum K
increased risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover)
123
Proximal renal tubular acidosis
Type 2
NAGMA
defect in PCT HCO3 reabsorption which increases excretion of HCO3- in urine resulting in metabolic acidosis
urine pH <5.5 and decreased serum K
Increased risk for hypophosphatemic rickets (in fanconi syndrome)
124
Hyperkalemic tubular acidosis
type 4
NAGMA
hypoaldosteronism or aldosterone resistance; hyperkalemia --> drop in NH3 synthesis in PCT --> decrease in NH4 excretion
125
Amphotericin B toxicity can cause what type of renal tubular acidosis
Distal renal tubular acidosis
| type 1
126
Fanconi syndrome, multiple myeloma, carbonic anhydrase inhibitors can cause what type of renal tubular acidosis
Proximal renal tubular acidosis
type 2
127
Decreased aldosterone production or increased aldosterone resistance can cause what type of renal tubular acidosis
Hyperkalemic tubular acidosis
type 4
128
Hematuria with no casts
bladder cancer or kidney stones
129
Pyuria with no casts
Acute cytitis
130
RBC casts
Glomerulonephritis, hypertensive emergency
131
WBC casts
Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
132
Fatty casts (oval fat bodies)
Nephrotic syndrome. Associated with Maltese cross sign)
133
Granular muddy brown casts
acute tubular necrosis
134
Waxy casts
end stage renal disease/chronic renal failure
135
Hyaline casts
nonspecific, can be a normal finding, often seen in concentrated urine samples
136
Nephrotic syndrome
Massive proteinuria (>3.5 g/day), with hypoalbuminemia. hyperlipidemia, edema, frothy urine with fatty casts
podocyte disruption results in impaired charge barrier
associated with hypercoagulable state due to antithrombin (AT) III loss in urine and increased risk of infection (loss of immunoglobulins in urine and soft tissue compromise by edema)
137
Nephritic syndrome
Inflammatory
RBC casts in urine and hematuria if glomeruli involved
due to GBM disruption
can see hypertension (due to salt retention), increased BUN and creatinine, oliguria, hematuria, azotemia
138
Nephrotic-Nephritic syndrome
severe nephritic syndrome with profound GBM damage that damages the glomerular filtration charge barrier causing nephrotic range proteinuria (>3.5) and concomitant features of nephrotic syndrome
139
What nephritic syndromes are commonly seen in nephrotic-nephritic syndrome
Diffuse proliferative glomerulonephritis
| Membranoproliferative glomerulonephritis
140
Most common cause of nephrotic syndrome in children
Minimal change disease (lipoid nephrosis)
mostly primary and is triggered by recent infection, immunization, immune stimulus. --> excellent response to steroids
light microscopy - normal
Immunofluorescence - negative
Electron microscopy - effacement of podocyte foot processes
141
Most common cause of nephrotic syndrome in AF and Hispanics
Focal segmental glomerulosclerosis (nephropathy)
primary or secondary
primary has inconsistent response to steroids and make progress to chronic kidney disease
light microscopy- Segmental sclerosis and hyalinosis
Immunofluorescence- often negative but may be + for nonspecific focal deposits of IgM, C3, C1
Electron microscopy - effacement of foot processes similar to minimal change disease
142
Membranous nephropathy/ membranous glomerulonephritis
can be primary or secondary
primary has poor response to steroids and can progress to CKD
Light microscopy- diffuse capillary and GBM thickening
Immunofluorescence- granular due to IC deposition
Electron microscopy- spike and dome" appearance of subepithelial deposits
143
Most common organ to be affected by amyloidosis
Kidney!
light microscopy - congo red stain shows apple green birefringence under polarized light due to amyloid deposition in the mesangium
Nephropathy
144
Most common cause of end stage renal disease in the united states
Diabetic glomerulonephropathy
Hyperglycemia --> nonenzymatic glycation of tissue proteins --> mesangial expansion
GBM thickening and increased permeability
Hyperfiltration due to glomerular HTN and increased GFR --> glomerular hypertrophy and glomerular scarring (glomerulosclerosis) leading to further progression of nephropathy
Light microscopy- Mesengial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (kimmelstiel-wilson lesions)
145
Acute poststreptococcal glomerulonephritis
seen in children 2-4 weeks after a group A strep infection of pharynx or skin.
resolves in children
Adults can get renal insufficiency
sx: peripheral, periorbital edema, cola colored urine, HTN. + strep titers/serologies, decrease complement levels (C3) due to consumption
LM: glomeruli enlarged and hypercellular
IF: starry sky granular appearance. Lumpy bumpy. Due to IgG, IgM, C3 deposition along GBM and mesangium
EM: subepithelial immune complex humps
146
Acute poststreptococcal glomerulonephritis is what type of hypersensitivity reaction
type III
147
This nephritis results in a crescent moon shape on light microscopy
rapidly progressive (crescentic) glomerulonephritis
cresent consists of fibrin and plasma proteins with glomerular parietal cells, monocytes, and macrophages
148
What conditions can result in rapidly progressive glomerulonephritis
1) good pastures
2) Granulomatosis with polyangitis (wegners)
3) Microscopic polyangitis
149
This nephritic syndrome is mostly due to SLE
Diffuse proliferative glomerulonephritis
Light microscopy: wire looping of capillaries
IF: granular
EM: subendothelial and sometimes intramembranous IgG based ICs often with C3 deposition
150
IgA nephropathy (Berger disease)
episodic hematuria that occurs concurrently with resp or GI tract infections (IgA is secreted by mucosal linings)
Renal pathology of IgA vasculitis or HSP
LM: mesengial proliferation
IF: IgA based IC deposits in mesangium
EM: mesengial IC deposition
151
Alport syndrome is due to a mutation in
type IV collagen
152
Alport syndrome
mutation in type IV collagen results in thining and splitting of glomerular basement membrane
153
Triad of eye problems, glomerulonephritis, sensorineural deafness
cant see, cant pee, cant hear a bee
Alport syndrome
EM: basket weave
154
Type I membranoproliferative glomerulonephritis may be secondary to _____ or _____ infection
hep B or hep C
155
Type II membranoproliferative glomerulonephritis is associated with _____ nephritic factor
C3
IgG antibody that stabilizes C3 convertase which results in persistent complement activation --> drop in C3 levels
intramembranous deposits also called dense deposit disease
156
Type I and II membranoproliferative glomerulonephritis have this appearance on H&E and PAS stains
mesangial ingrowth --> GBM splitting --> tram track appearance on H&E and PAS stains
157
Most common kidney stone presentation
calcium oxalate stone in patient with hypercalciuria and normocalcemia
158
Calcium oxalate
hypocitraturia, low pH, radioopaque on xray and CT, shaped like an envelope or dumbbell
can result from ethylene glycol (antifreeze), vitamin c abuse, malabsorption
treat with thiazides, citrate, low sodium diet
159
Calcium phosphate
increased pH, radioopaque on xray and CT, wedge shaped prism
tx with low sodium diet and thiazides
160
Ammonium magnesium phosphate (struvite)
increased pH, radiopaque on xray and CT, coffin lid appearance
Usually due to urease + bugs that hydrolyze urea to ammonia --> urea alkalinization
forms staghorn calculi
tx: eradication of underlying infection, surgical removal of stone
161
Uric acid
decreased pH, radiolUcent on xray, minimally visible on MRI, rhomboid or rosettes
hyperuricemia. Often seen in diseases with increased cell turnover
treat with alkalinization of urine, allopurinol
162
cystine
decreased pH, radioopaque on xray and CT, hexagonal
cystine reabsorbing PCT transporter loses function, causes cystinuria
results in COLA - cysteine, Ornithine, lysine, arginine poor reabsorption
staghorn calculi
+ sodium nitroprusside test
treat with low sodium diet, alkalinization of urine, chelating agents if refractor
163
serum _____ becomes elevated if obstruction is bilateral or if patient has obstructed solitary kidney
creatinine
164
Most common primary renal maligancy. Most common in men 50-70 yo. Increased incidence with smoking and obesity
Renal cell carcinoma (RCC=3 letters= chromosome 3 gene deletion)
polygonal clear cells that accumulate lipids and carbs. Often golder yellow due to increased lipid content
originate from the PCT __> invades renal vein (may develop varicocele if left sided) __ IVC --> hematogenous spread --> metastasis to lung
pt can also present with hematuria and polycythemia
rarely curative
165
Benign epithelial cell tumor arising from collecting ducts and results in a well circumscribed mass with central scar. Patient has painless hematuria and large eosinophilic cells with abundant mitochondria without perinuclear clearing
Renal oncocytoma
166
Most common renal malignancy of early childhood between 2-4 yo
Nephroblastoma (wilms tumor)
167
Nephroblastoma (wilms tumor)
presents with large palpable unilateral flank mass and or hematuria. Contains embryonic glomerular structures
168
Nephroblastoma (wilms tumor) results from what kind of mutation
LOF mutations of tumor suppressor genes WT1 and WT2 on chromosome 11
169
Denys drash syndrome
- Wilms tumor
- Diffuse mesangial sclerosis (Early onset nephrotic syndrome)
- Dysgenesis of gonads (male pseudohermaphroditism), WT1 mutation
170
WAGR complex
wilms tumor
Aniridia (absence of iris)
Genitourinary malformation
Mental retardation/intellectual disability (WT1 deletion)
171
Beckwith-wiedemann syndrome
wilms tumor, macroglossia, organomegaly, hemihyperplasia (WT2 mutation)
172
Transitional cell carcinoma
urothelial carcinoma
most common tumor of urinary tract system
painless hematuria without casts
risk: Phenacetin, Smoking, Aniline dyes, and cyclophosphamide
173
Squamous cell carcinoma of the bladder
chronic irritation of urinary bladder can result in squamous metaplasia --> dysplasia and squamous cell carcinoma
risk: schistosoma haematobium infection, chronic cystitis, smoking, chronic nephrolithiasis.
present with painless hematuria
174
Patient leaks with urge to void immediately due to overactive bladder (detrusor instability)
related to UTI
urgency incontinence
175
Overflow incontinence
imcomplete emptying (detrusor underactivity or outlet obstruction) --> leak with overfilling
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What is the most common cause of UTI? what are the other causes?
E coli is most common overall
Staph sapro (sexually active)
Klebsiella
Proteus mirabilis (urine has ammonia scent)
177
UTI lab findings
+ leukocyte esterase
+ nitrites (indicated gram -)
Sterile pyuria and - urine cultures suggest urethritis by N gonorrhoeae or chlamydia trachomatis
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Acute pyelonephritis
neutrophils infiltrate renal interstitium
affect cortex with sparing of glomeruli/vessels
WBC in urine ( +/- WBC cast)
CT shows striated parenchymal enhancement
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Chronic pyelonephritis
due to recurrent acute pyelonephritis
coarse asymmetric corticomedullary scarring , blunted calyx
Tubules contain eosinophilic casts resembling thyroid tissue (thyroidization of kidney)
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Xanthogranulomatous pyelonephritis
seen with chronic pyelonephritis
grossly orange nodules that can mimic tumor nodules; characterized by widespread kidney damage due to granulomatous tissue containing foamy macrophages
associated with proteus infection
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Acute kidney injury -abrupt decline in renal function as measured by increase of _____ and ____
creatinine and BUN
or by oliguria/anuria
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Prerenal azotemia
due to decreased RBF --> decreased GFR
Na/H20 and urea retained by kidney in an attempt to conserve volume
this increases BUN/creatinine ratio (urea is reabsorbed, creatinine is not) and decrease FEna
higher urine osmolality compared to intrinsic renal and postrenal injury
183
Intrinsic renal failure
due to acute tubular necrosis : patchy necrosis --> debris obstructing tubule and fluid backflow across necrotic tubule --> decrease GFR
Urine has epithelial/granular casts
Urea reabsorption is impaired
decrease BUN/creatinine ratio and increase FE sodium
184
Postrenal azotemia
due to outflow obstruction. develops only with bilateral obstruction or in a solitary kidney
185
Chronic renal failure
usualyl due to HTN, DM, congenital anomalies
186
Hypocalcemia, hyperphosphatemia, and failure of vitamin D hydroxylation associated with chronic renal disease and leads to
Secondary hyperparathyroidism
High serum PO4 can bing Ca and result in tissue deposits. This causes a drop in Ca
Decrease 1,25 OH2D3 results in decreased intestinal Ca absorption
results in subperiosteal thinning of bones
187
Acute interstitial nephritis (tubulointerstitial nephritis)
Acute interstitial renal inflammation
pyuria (classically eosinophils) and azotemia occuring after administration of drugs that act as haptens, inducing hypersensitivity
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Pee (diuretics)
Pain free (NSAIDs)
Penicillins and cephalosporins
Proton pump inhibitors
rifamPIN
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188
Most common cause of acute kidney injury in hospitalized patients
Acute tubular necrosis
189
Acute tubular necrosis
can be fatal during the oliguric phase
increases FE sodium
granular "muddy brown" casts
can also be caused by ischemic - secondary to decreased renal blood flow which results in death of tubular cells that may slough into tubular lumen
Can also be caused by nephrotoxic due to secondary injury resulting from toxic substances
proximaly tubules are especially susceptible to nephrotoxic injury
190
Acute tubular necrosis stages
1) inciting event
2) maintenance phase -oliguric. Risk of hyperkalemia, metabolic acidosis, uremia
3) recovery phase-polyuric, BUN and serum creatinine fall, risk of hypokalemia and renal wasting of other electrolytes minerals
191
Vasospasms + DIC can result in generalized cortical infarction of both kidneys
Diffuse cortical necrosis
associated with obstetric catastrophes and septic shock
192
Renal papillary necrosis
sloughing of necrotic renal papillae --> gross hematuria and proteinuria
may be triggered by recent injection or immune stimulus
associated with sickle cell disease or trait, acute pyelonephritis, NSAIDs, diabetes mellitus
193
Numourous cysts in cortex and medulla. The kidneys are enlarged B/L. Eventually leads to destruction of parenchyma and progressive renal failure
autosomal dominant polycystic kidney disease
194
Cystic dilation of colelcting ducts that presents in infancy.
Autosomal revessive polycystic kidney disease
associated with congenital hepatic fibrosis
significant oliguric renal failure in utero can lead to potter sequence.
195
Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine
Autosomal dominant tubulointerstitial kidney disease
or medullary cystic kidney disease
medullary cysts usually not visualized and there are smaller kidneys on ultrasound
poor prognosis
196
mutation in PKD1 on chromosome 16 is common in what renal cyst disorder
Autosomal dominant polycystic kidney disease
also PKD2 on chromosome 4
associated with berry aneurysms, mitral valve prolapse, benign hepatic cysts, diverticulosis
197
Ureter is immediately anterior to
internal iliac artery
