Renal (FA + UWorld) Flashcards
where is PAH concentration the lowest?
Bowman’s capsule.
PAH is relatively low in plasma (= Bowman’s capsule bc freely filtered) PAH is actively secreted in the PCT, increasing its concentration
most common cause of obstructive unilateral hydronephrosis
most common cause of NONobstructive unilat hydronephrosis
most common cause of bilateral hydronephrosis
unilateral: reno-pelvic junction
non-obs: vesico-uretral reflux
bilateral: posterior urethral valves
describe the ureter’s positioning in relation to each:
internal iliac A
uterine vessels
ovarian/testicular vessels
Anterior to IIA
posterior to UA
medial to OA/TA
what does ADH do in the medullary collecting duct?
increase NH3 and water absorption, allowing for max concentrated urine
when in metabolic acidosis, what does the urine do to help?
- it increases excretion of acid (so low urine pH, and presence of more acid buffers)
- it increases bicarb reabsorption (so low bicarb in urine)
what increases as you go along PCT, what decreases?
increase: PAH, Inulin, Urea
decrease: glucose, AA, bicarb
plasma creatinine levels only start to rise after GFR gets how low?
as GFR gets LOWER than 60 Pcreat begins to rise, exponentially
ADH decreases clearance of what substance
UREA
what does metabolic acidosis do to pCO2 levels
compensatory resp alk causes pCO2 to be low
How does diabetes affect incontinence
due to neuropathy pt cant sense bladder is full. this leads to incomplete emptying, as well as overflowincontinence bc detrusor m is poorly innervated
large eosinophilic casts in urine?
MM
pt recieving chemotherapy gets oligouria, what happened?
tumor lysis syndrome– as tumor cells rapidly lyse their K+,PO43-, and uric acidis released into the system. When uric acid is in an acidic area (like the CD) it can precipitate into uric acid kidney stones
what are two common side effects of ACE inhibitors?
cough
hyperkalemia
alpha galactosidase A deficiency is known as
Fabry’s disease
PSGN is what type of HS?
TypeIII
immune complexes
what are the embryological derivatives of the kidney
pro-nephros– degenerates in week
mesonephros– part of genito-urinary tract- gives rise to uretric bud which makes ureters, calcixes, pelvis, CD
metanephros- when stimulated by ureteric bud, it makes the DCT to the glomerulus
what the last part of the kidney to canalize? most common site of obstruction?
ureteropelvic junction – causes hydronephrosis
Potter Sequence
oligohydramnios causes flat face and limb deformities due to compression
- pulmonary hypoplasia is a common cause of death
causes: bilateral renal agenesis, posterior urethral valves, obstructive uropathy, ARPKD
posterior urethral valves
membrane remnant in posterior urethra– hydronephrosis,and dilated/hypertrophy of bladder
what is the relation of ureters to vas deferens?
ureters pass UNDER vas deferens
remember also UNDER uterine artery
whats the breakdown of the body compartments?
60% of wt is TBW
40% of wt is ICF
20% of wt is ECF
in ECF.. 25%ECF is plasma
whats a normal osmolality
285-295 mOSm/kg H2O
whats the charge of the glomerulus?
neg.
so doesn’t let negative molecules in (like albumin)
name the three layers of the glomerulus?
(1) fenestrated capillary
(2) type IV collagen BM
(3) podocyte foot processes (epithelial layer)
renal clearance of X=
C(x)= ( [X in Urine] * rate of urine flow )/ ([X in plasma])
GFR=
( [Inulin in Urine] * rate of urine flow) / ([ Inulin in plasma])
if not Inulin, you can use creatinine, but remember that creatinine slightly overestimates GFR bc it is secreted a little
whats another way to measure GFR?
= ( Pg- Pb) - (Poncg - PoncB)
whats a normal GFR?
100 mL/min
RPF=
( [PAH in Urine] * rate of urine flow) / ([ PAH in plasma])
= (RBF) (1-HCT)
how do you calculate Filtration Fraction (FF)=
GFR/RPF
remember its rPf NOT RBF!!!
whats a normal filtration fraction
20%
how do you calculate filtered load??
Filtered Load of X= GFR * [X in plasma]
what do prostaglandins do at glomerulus?
what does angII do at glomerulus?
PDA, ACE
prostaglandins dilate Afferent arteriole
ang II constricts efferent arteriole
what does dehydration do to GFR, RPF, and FF
decrease GFR
reallllyyy decrease RPF
and b/c FF= GFR/RPF… FF will show an increase
how do you calculate the reabsorption rate of X
how do you calculate the secretion rate of X?
Filtered Load- Excretion rate
Excretion rate- Filtered load
how do you calculate what FRACTION of X was excreted?
Fe(x)= ( [X in urine][P cr]) / ([urine Cr][X in plasma])
at what plasma glucose concentration does glucosuria begin?
200 mg/dL
Fanconi Syndrome
- gen reabsorptive defect of PCT
- metabolic acidosis
- loss of Na+, HCO3-, AA, glucose, PO43-
Bartter Syndrome
- gen reabsorptive defect of TAL (looks like chronic loop dieuretic use)
-metabolic alkalosis - loss of Na/K/Cl and Ca2+
therefore hypokalemia and hypercalciuria
Gitelman Syndrome
- gen reabsorptive defect in DCT (looks like chronic thaizide use_
-metabolic alkalosis - loss of Na/Cl/K/ Mg2+
-hypokalemia, hypomagnesemia
less severe than Bartter
Liddle Syndrome
AD GOF mut of ENAC. presents like hyperaldosteronism (but aldosterone levels are low)
- increase Na+ reabsorption– htt
- hypokalemia
- metabolic alkalosis
Syndrome of Apparent Mineralocorticoid Excess
deficiency of 11Bhydroxysteroid dehydrogenase (often by eating licorice!)
usually this is responsible for inactivating cortisol in cells with Mineralocorticoid receptors. In this deficiency the cortisol binds to the MR and acts like aldosterone
t(x)- corticosteroids to decrease endogenous cortisol production
whats in the juxtoglomerular apparatus
JG cells are modified sm m cells of afferent arteriole macula densa (NaCl sensor, part of DCT)
JG cells secrete renin if MD senses low NaCl at DCT
JGA has B1 receptors, and increase renin release in sympathetic activity
what is Dopamine’s role in the glomeruli?
secreted by PCT
promotes natueresis
low dose- vasodilator
high dose- vasoconstrictor
hypo-osomolality and alkalosis cause what K shift
hyperosmolality and acidosis cause what K shift
- K shift into cells (hypokalemia) with alkalosis and hypo-osmolality
- k shift out of cells (hyperkalemia) with hyperosmolality and acidosis
flat t wave
Uwave
hypokalemia
peaked T wave
wide QRD
hyperkalemia
causes of anion gap metabolic acidosis
Methanol Uremia DKA Propylene Glycol Iron (INH) Lactic acidosis Ethylene glycol Salicylates (late)
causes of non-gap metabolic acidosis
Hyperalimentation Addison's RTA Diarrhea Acetazolamide Spironolactone Saline
what is responsible for the increases acid secretion into urine seen in metabolic acidosis?
- PCT makes glutamine into ammonium
In ATN due to hypovolemia which parts of the kidney are most affected?
medulla: PT and TAL
when are crescents seen on IF?
what are they made of?
RPGN
renal parietal cells, macrophages, monocytes, fibrin
what value is needed to work up Metabolic alkalosis
need to know: urine Chloride levels
if low: then vomiting
if high: then thaizides, loops, or mineralocorticoid excess
RCC arises from?
epithelial cells of PCT
what undergoes hyperplasia in chronic renal A stenosis
Afferent arteriole
- chronic Renal A stenosis= decreased GFR= decreased NaCl to macula densa= stimulation of renin release from JG cells= JG cells undergo hyperplasia
nsaid use can do what to the kidney?
chronic interstitial nephritis
how can you tell TTP-HUS apart from DIC?
DIC involved ovreactive coagulation, causing depletion of coagulation factors and hence increased PT and PTT
however in TTP HUS, only the BT will be increased, not PT or PTT
maintenance phase vs recovery phase whats the [K+] anomaly
hyperkalemia - maintenance
hypokalemia- recovery
what can differentiate pyelonephritis from acute UTI/cystitis
WBC casts
what indicates poor prognosis to PSGN
being an adult
edema + “frothy” urine in kiddo?
Minimal change disease
EM: podocyte foot effacement
where else is type IV collagen found, apart from renal and pulmonary BM?
lens of the eye
what is the blood supply of the renal medulla? what disease can increase the risk of ischemia to here?
Vasa recta
SCD
abdominal mass in child
(1) if crosses the midline it is
(2) if lateral,doesnt cross the midline
(1) neuroblastoma
(2) Wilm’s
increased circulating PLA2 antibodies is assn w/?
Membranous Glomerulonephritis
in Membranous Glomerulonephritis, what is often seen elevated in the blood?
LDL, chol, TGs
Renal Tubular Acidosis Type I
at the CD, alpha intercalated cells can’t secrete H+ so no new HCO3- made
only RTA with urine pH>5.5
Renal Tubular Acidosis Type II
at the PCT, defect in HCO3- reabsorption
urine pH <5.5
Renal Tubular Acidosis Type IV
at the CD, hypoaldosteronism
only RTA with hyperkalemia
urine pH <5.5
whats the “cutoff” between nephritic and nephrotic syndrome?
nephritic is when the urine protein <3.5 g/day
nephrotic is when the urine protein> 3.5 g/day
LM: hypercellular
IF: starry sky , granular ,lumps and bumps
EM: humps
whats it called?
whats the deposit?
Post Strep Glomerulonephritis
Type III HS- immune complex deposition sub-epithelial of IgG, IgM, and C3
LM: crescenteric shape
IF: linear deposits along GBM (if Goodpasture’s)
whats it called?
what the deposit?
Rapidly Progressive Glomerulonephritis: which includes Goodpasture’s, Wegener’s (c-ANCA), Microscopic Polyangiitis (p-ANCA)
crescent= macrophages, monocytes, c3b and FIBRIN
what type of HS is Goodpastures’s?
Type II HS
antibodies against GBM (type IV collagen)
LM: “wire looping”
EM: subendothelial immunecomplexes of IgG (also C3)
IF: granular
Diffuse Proliferative Glomerulonephritis
- SLE
- membranoproliferative GN
LM: mesangial proliferation
EM/IF : mesangial IgA immune complex deposits
IgA nephropathy (Berger's) often caused by HSP (= abdominal pain + arthralgia+palpable purpura on legs and butt)
LM: thin and splitting GBM
EM: basket weave
Alport Syndrome- XD mut in type IV Collagen
“ can’t see, can’t pee, can’t hear a bee”
LM: “tram track” on PAS/H&E stain due to GBM splitting by subendothelial immune complex growth
Membranoproliferative Glomerulonephritis
causes: idiopathic, hep B/C; antibodies against C3 which decrease C3 levels
LM; normal
EM: podocyte foot effacement
in a child
Minimal Change disease , kiddo w frothy urine + edema
usually idiopathic, can be following infection, can be due to lymphoma
LM: thickening of GBM segmentally and hyalinosis
EM: podocyte effacement
Focal Segmental Glomerulosclerosis
in AA/hispanics
LM: DIFFUSE capillary and GBM thickening
EM: “spike and dome”
IF; granular
Membranous Glomerulonephritis (nephropathy)
most common in caucasians (also seen in SLE)
can be due to PLA2 antibodies, drugs, infections solid tumors
LM: congo red stain shows apple green bifringence in mesangium
Amyloidosis
LM: Kimmelsteil-Wilson lesions (big ovoid eosinophilic), mesangial and GBM thickening
Diabetic Glomerulonephropathy
caused by non-enzymatic glycosylation
most common type of kidney stone?
cause
looks like
treat with
Calcium Oxalate - normocalcemic, hypercalcuria - hypocitraturia, decreased urine pH - other causes: ehtylene glycol, Vit C overdose, malabsorption looks like: envelope or dumbbell treat: thiazides,citrate, low Na diet
what is the less common type of calcium stone?
cause
looks like
treat with
calcium phospate
cause: increase pH
wedge-shaped prism
tx: low sodium and thiazides
your kidney stone looks like a coffin?
whats it made of
whats the cause
what do you treat with
Ammonium Magnesium Phosphate aka struvite making staghorn caliculi
cause: P mirabilis, S. saprophyticus, Klebsiella which are urease (+) so make ammonia causing high pH
t(x): get rid of infection! remove staghorn caliculi
your kidney stone is clear and rhomboid shaped?
whats it made of
whats the cause
what you treat with
Uric A stone
caused by excess uric acid (TLS or Lesch Nyhan) or more commonly decreased urine PH
treat: alkalinize urine (acetazolamide) or allopurinol
what if your kidney stone looks like a hexagon and your Na nitroprusside test is +
whats it made of
whats the cause
what you treat with
- Cystine
cause is a AR mut in the Cystine PCT transporter (note this transporter also reabsorbs COLA: cysteine, ornithine, lysine, arginine)
presents in childhood
treatment: low Na, alk urine
