Renal- FA Flashcards
Explain TWO pathophysiology of renal osteodystrophy
- impaired phosphate excretion -> secondary hyperparathyroidism, also increased phosphate binds to Ca2+, leading to tissue CaPO4 deposition and lowering SERUM Ca2+
- impaired 1-alpha hydroxylase -> impaired vitamin D activation -> impaired intestinal Ca2+ absorption
What happened to Na+ level in renal failure? explain physiology
HIGH
oligouria -> less Na and Cl- in JGA -> more renin -> further retention
Because of this, volume overload state (HF, pulmonary edema, hypertension) will be seen in renal failure
*this is counter intuitive. But think renal failure as inability to concentrate urine and OLIGOURIA
Liddle syndrome
- what kind of mutation on which transporter
- inheritance pattern
- serum Na+
- serum K+
- pH
- aldosterone
- renin
- gain of function on ENac
- Autosomal dominant (gain of function)
- ion balance bottom line: presents as HYPERALDOSTERONISM, but nearly undetectable aldosterone
=> High Na+
=> low K+
=> high pH
=> LOW ALDO
=> low renin (negative feedback, aldo is end product of RAAS)
Why acetazolamide helps pseudomotor cerebri?
by decreasing CSF synthesis
=> very similar for glucoma (in which acetazolamide is used to decrease aqueous humor production)
Urine pH, potassium level, causes for each type of renal tubular acidosis
- type 1
- type 2
- type 4
Type 1: CT can’t reabsorb HCO3-
- basic urine pH (CT can’t excrete H+)
=> increased risk for calcium phosphate stone
- hypokalemia: aldo is working crazy to stimulate acid secretion and HCO3- at CT (but it doesn’t work due to impaired H+ excretion at CT)
- causes: amphotericin B
Type 2: PCT can’t reabsorb HCO3-
- acidic urine pH: aldo try to compensate, more H+ secretion at CT
- hyperkalemia: aldo try to compensate
- causes: Fanconi syndrome (Wilson disease, lead poisoning), acetazolamide
Type 4: hypoaldosteronism, PCT can’t reabsorb HCO3-
- acidic urine pH: hyperkalemia leads to decreased urine NH4+
- hyperkalemia
- causes: TMP/SMX
Wegner vs. Goodpasture
- presentations
- treatment
Goodpasture
- hemoptysis, hematuria
- emergent plasmapheresis
Wegner
- hemoptysis, hematuria PLUS SINUSITIS
- corticosteroid, cyclohexamide
Which kidney diseases (2) present with both nephrotic and nephritic?
- proliferative glomerulonephritis
1. membrenoproliferative
2. diffuse proliferative
Why nephrotic syndrome may result in recurrent infection?
loss of immunoglobulin
How does hyperkalemia leads to acidosis?
All cells have K+/H+ exchanger
hyperkalemia leads to intracellular movement of K+ in exchange of H+, which moves extracellularly
- Same thing in DKA.
In DKA, patient has hyperkalemia: so hyperkalemic state in DKA doesn’t necessarily means real hyperkalemia
List 5 actions of AngII for increasing blood pressure
- induce thirst
- vasoconstriction
- stimulate ADH from post. pituitary
- NHE at PCT
- aldo synthesis
UTI, negative urine culture, what bugs?
N.gonorrhea
Chlamydia
Three renal conditions associated with painless hematuria?
- oncocytoma
- transitional cell carcinoma of bladder
- squamous cell carcinoma of bladder
Oncocytoma- benign or malignant? what cell origin?
benign, originated from collecting duct
- Even though it is benign, It needs to be resected to rule out any possible mass of renal cell carcinoma
Mannitol is contraindicated in what condition? explain physiology (site of action?)
HF. It can also cause pulmonary edema
wherever mannitol goes, it drags water.
Mannitol FIRST goes to BLOOD stream, sucking interstitium water into plasma
- > exacerbation of pulmonary edema or HF
- > After blood circulation, Mannitol then finally enters renal tubule, working primarily at PCT
- > drag water into renal tubule
- > osmotic diuresis
Which two organs synthesize ACE?
lung and kidney
*remember picture for RAAS in FA P.540
Nitrite in urinalysis?
E.coli
- nitrite is specific for gram negative organism
At which part of nephron does K+ and H+ excretion happen in collecting duct?
Cortex
- NOT MEDULLA. This makes sense because interstitial medulla has high concentration gradient. So K+ and H+ (which are not ATP dependent) can not be secreted.
Nephritic vs. Nephrotic: disruption of what structure?
- nephritic: disruption of GBM
=> GBM is both charge and size barrier. RBC (normally RBC is filtered by size) - nephrotic: disruption of podocytes
=> podocytes is only for charge barrier. protein (mostly albumin) loss: albumin can still penetrate fenestrated endothelium
Uremia
- definition
- seen in what renal condition
- complications (4)
- increased BUN ( literally BUN is key)
- chronic renal failure
- complications
1. anion gap metabolic acidosis
2. ARDS
3. pericarditis
4. hyperammoniemia (asterixis, encephalopathy)
5 uses of ACEI
- hypertension
- prevents heart remodeling due to chronic HTN
- slows down progression of diabetic nephropathy
- decreases mortality (no symptomatic relief) in HF
- ADPKD
Simple cyst vs. complex cyst
- key difference on imaging?
- which one is worse? why?
- simple cyst: liquid (anaechoic on ultrasound)
- complex cyst: septated, enhancing (solid mass)
complex cyst has potential to progress to renal cell carcinoma (again, it is MASS)
Which infection is associated with membranoproliferative glomerulonephritis? which subtype of MPGN?
Hep B and C
Type 1 MPGN is associated with HepB and C
Urine crystal shape of each type of kidney stone
- Calcium oxalate
- struvite
- uric acid
- cystine
- calcium oxalate: dumbbell
- struvite: coffin lid
- uric acid: RHOMBOID (didn’t know this)
- cystine: hexagone
Serum level which substances (4) go up with thiazide?
- Glucose
- Lipid
- Uric acid
- Calcium
- GLUC
- sketchy: glucose candy jar and butter on top of diving,
kid doing yellow knitting, calcium on top of diving
*thiazide is contraindicated in diabetes, gout
Afferent arteriole constriction vs. dehydration: what happens to
- GFR
- RPF
- FF
BOTH decreases GFR and RPF
BUT,
Afferent arteriole constriction
- no change in FF: same degree of reduction of GFR and RPF
Dehydration
- increased FF: GFR lesser degree of reduction
=> This makes sense:
With afferent arteriole constriction, entry of blood is limited. So reduction in GFR and RPF will be in same degree
But with dehydration, you still wanna filter more so that you can get rid of toxic stuffs. Thus GFR reduction is lesser degree compared to RPF reduction
At which two nephron segments do PTH work? how does it work?
- PCT: PTH inhibits phosphate absorption
(Na+/PO4 cotransporter) - DCT: PTH stimulates Ca2+ reabosoprtion
( Ca2+/Na+ exchanger) - overall Ca2+/phosphate go opposite in PTH
vs. vitamin D, which increases BOTH Ca2+ and phosphate
Congenital diseases associated with horseshoe kidney?
- Turner
- All trisomies (21, 18, 13)
Systemic infection signs in UTI?
UTI usually do NOT give systemic signs (fever, chills)
- Think like this, UTI is so specific and focused
ACEI results in acute kidney injury? What pre-existing renal condition patient may have?
bilateral renal artery stenosis
- with bilateral renal artery stenosis, patient can maintain GFR and appropriate renal perfusion by AngII (efferent constriction makes higher amount of blood hanging out in glomeruli)
=> ACEI will lead to loss of efferent constriction, resulting in loss of appropriate maintenance of GFR and renal perfusion
Acidosis vs. Alkalosis: What does each do to potassium level?
Acidosis => K+ move out of cell => hyperkalemia
Alklaosis => K+ move into cell => hypokalemia
- Note: H+/K+ channel is everywhere in cell, and it is BIDIRECTIONAL. It is NOT ATP-DEPENDENT, but rather GRADIENT DEPENDENT.
So depending on gradient, K+ can either enter the cell or exit the cell (vice versa for H+)
What does B-blocker to on potassium level?
hyperkalemia
B-blocker blocks Na+/K+-ATPase
What is associated with hyaline cast?
Hyaline cast is not specific
What is associated with Waxy cast?
chronic renal failure or end stage renal failure
Hep B and HepC are associated with what two renal conditions?
- type 1 membrnoproliferative glomerluonephritis
- membranous nephropathy
- membrano-
Both will also show issue at GBM in LM - Type1: membrane splitting
- membranous nephropathy: GBM thickening
Which two substances can cause calcium oxalate kidney stone?
ethylene glycol
vitamin C
BOTH can get metabolized to oxalate
Inheritance pattern of Alport syndrome?
x-linked dominant
Struvite kidney stone: radiolucent? or radiopaque?
radiopaque
uric acid and cystine stones are radiolucent
Increased serum creatinine: what should I think?
decreased GFR: renal failure
Sore throat. red urine. Two differential diagnosis? how to differentiate these two based on patient history?
- IgA nephropathy
- PSGN
- IgA nephropathy occurs CONCURRENTLY with sore throat. That is patient is having sore throat NOW. While PSGN occurs 3-6 WEEKS AFTER sore throat. Patient HAD sore throat BEFORE.
- DO NOT AUTOMATICALLY PICK PSGN just by reading sore throat. Pay attention to exact history of sore throat
What is complication of renal artery stenosis?
hypertension
ischemic kidney secrets renin consistently (due to decreased Na+ delivery at DCT), leading to peripheral vasoconstriction and over retention of Na+/H2O from the kidney on the other side
Does ACEI cause hyperkalemia?
ACEI alone does NOT COMMONLY cause hyperkalemia.
COMBINATION with OTHER POTASSIUM SAVING DRUGS (SPIRONLACTONE) can cause hyperkalemia
Which two blood BP drugs (that work on kidney) are teratogenic?
ACEI
ARB
Explain how NSAIDs or aspirin cause acute interstitial nerphritis. Are symptoms nephrotic? or nephritic?
vasoconstriction -> ischemic damage
-> nephrotic symptoms
: loss of GBM negative charges due to ischemic damage
Which drugs (6) can cause acute interstitial nephritis
Rembmer 6 Ps
- Pee : diuretics- BOTH loop and thiazide
- Pain: NSAIDs
- rifamPin
- Penicillin
- PPI
- high yields are NSAIDs, diuretics, and penicillin
What accounts for pyuria in acute interstitial nephritis?
what abnormality will be found in urinalysis?
eosinophilia
willms tumor: what gene? what chromosome?
WT-1 or WT-2
- both are on chromosome 11
- Don’t confuse with ADPKD1 (chromosome 16) or ADPKD2 (chromosome 4)
