Flashcards in Renal Deck (250):
What are the three effects of Angiotensin II?
1. systemic vasoconstriction
2. constriction of efferent arteriole
3. Increased aldosterone synthesis
Concentration of tubular fluid in proximal tubule
isotonic with plasma (300 mosm/L)
Concentration of tubular fluid in descending loop of henle
Increasing (water permeable)
Concentration of tubular fluid in ascending loop of henle
Decreasing (salt permeable)
Lowest osmolality site in nephron, assuming low ADH
Distal convoluted tubule. Impermeable, so fluid stays hypotonic with increased reabsorption of solutes
When does ARPKD present?
At birth. In contrast, dominant form comes years later.
Urea acts on which segment of the collecting duct?
medullary segement to increase urea and water reabsorption
When does the pronephros degenerate?
Functions as kidney for the first trimester
Metanephros appears wheN?
5th week of gestation. It becomes the permanent kidney
Ureteric bud comes from
caudal end of mesonephros
Ureteric bud gives rise to:
ureter, pelvises, calyces, collecting ducts
what interaction needed to form normal kidney
ureteric bud pokes the metanephric tissue
--induces metanephric tissue to format glomerulus to distal tubule
most common site of obstruction in fetus
Causes of Potter's
posterior urethral valves
bilateral renal agenesis
IF YOU CAN"T PEE in utero, you get potters
Horseshoe kidney assoc'd with
Nonfunctional kidney with cysts and connective tissue in utero. What caused this?
abnormal interaction btw ureteric bud and metanephros
Describe path of blood into the kidney
Which kidney do you harvest for donation?
Left kidney=it has a longer renal vein
ureters pass over/under the ductus deferens/uterine artery?
60% weight is TBW
measure plasma volume
measure extracellular volume
what gives negative charge in GFR?
V=urine flow rate
how to calc GFR
clearance of inulin or creatinine
When is creatinine clearance not accurate for GFR?
When GFR is very low. will have higher concentration of creatinine in urine
Calculation for effective renal plasma flow (ERPF)
clearance of PAH
PAH=filtered AND secreted into the proximal tubule. all that enters the kidney is excreted
--ERPF underestimates true RPF by 10%
constrict afferent arteriole
dilate efferent arteriole
dilate afferent arteriole
constricts efferent arteriole
increased plasma protein
constriction of ureter
deficiency of tryptophan(neutral amino acid) transporter in proximal tubule. neutral AA excreted in urine.
results in pellagra
blood glucose level when glucosuria starts? max saturation?
which part of nephron generates ammonia?
PTH and ATII on prox tubule
PTH: inhibits Na/Phosphate cotransport
ATII: stimulates Na/H exchange=contraction alkalosis. Holding onto sodium at expense of alkalosis
What % Na absorbed at each nephron segment?
1. Prox tubule=65-80%
2. L of H=10-20
Thick loop of henle
--paracellular resorption of Mg2+ and Ca2+
--dilution of urine as it passes
What allows paracellular resorption in thick ascending limb?
Na/Cl apical cotransporter
--urine becomes hypotonic
PTH effect on DCT
Stimulates Ca/Na Xchange on basolateral surface increasing Ca resorption
Blocks Na/Cl apical cotransporter
-->indirectly blocks Na/Ca2+ exchanger
Mechanism of amiloride/triamterene
Blocks ENaC channel in principal cell of CT
[Tubular Fluid]/[Plasma] ratio
If >1, solute is reabsorbed less quickly than water
If <1, solute reabsorbed more quickly than water
very high TF/P
amino acids and glucose (virtually completely reabsorbed
Tx: hypovolemic hyponatremia
tx: hypervolemic hyponatremia
Salt and fluid restriction, furosemide
free water restriction (NOT hypertonic saline--otherwise will fluid overload them)
do NOT give normal saline! will excrete sodium and retain water. Give convaptan and water restrict
when should you give hypertonic saline?
hyponatremia with NEURO deficits or seizures
Six effects of angiotensin II
1. Vascular smooth muscle
2. constricts efferent arteriole
5. Increased prox tubule Na/H
6. Stimulates hypothalamus
osmolarity (except in extreme low blood volume)
How do beta blockers decrease BP?
inhibiting B1 receptors on the JGA
How much K is reabsorbed along the nephron?
30% ascending L of H
5-100% at DCT
How does ANP work?
Increases Na filtration and GFR at PCT with no compensatory Na resorption distally.
-->Na and H2O loss
PTH effect on kidney
Increased Ca resorption (DCT)
Decreased PO4 resorption (PCT)
Increased activation of vitamin D
Causee of hyperkalemia
Beta adrenergic antagonist
arrhythmias, muscle weakness
-U wave on ECG, flattened T waves
tetany and seizures
--decreases threshold potential
tetany and arrhythmias
How to tell if there is a mixed disorder (acid base)?
pCO2 and HCO3 move in opposite directions
pCO2 predicted is very different
(1.5 HCO3 + 8) +/-2
When do you check anion gap
metabolic acidosis present
Eq for anion gap
--Over 12 is abnormal
Increase anion gap metabolic acidosis
Causes of normal anion gap acidosis
Renal tubular acidosis
Causes of primary metabolic alkalosis
Type 1 RTA
CT cannot excrete H+
Type 2 RTA
Cannot resorb bicarb
Type 4 RTA
lack of aldosterone effect
RTA: pt with urine pH > 5.5 and is hypokalemic
RTA: Pt has a urine pH < 5.5 and is hypokalemic
Type 2 RTA
RTA: hyperkalemic patient with low urine pH and low BP
Type 4 RTA
Increased urine pH puts you at risk for
calcium phosphate stones
Type 2 RTA associated with
fatty casts or oval fat bodies
granular muddy brown casts
acute tubular necrosis
advanced renal disease
Minimal change disease
Focal segmental glomerulosclerosis
Acute poststreptococcal GN
Rapidly progressive GN
Berger's IgA GN
Combined Nephritic and Nephrotic syndromes
Diffuse proliferative GN
Sx of nephrotic syndrome
Why are pts with nephrotic syndrome at risk for thromboembolism and infection?
AT III is lost in urine
Loss of IgG
Most common cause of nephrotic syndrome in adults
LM: segmental sclerosis and hylinosis
EM: effacement of foot proceses
LM: GBM thickening
EM: spike and dome with subepithelial deposits
causes of FSGS
HIV, kidney disease, heroin, obesity, interferon
causes of membranous
SLE< drugs, infection
EM: foot process effacement
Tx of minimal change
cause of minimal change
loss of polyanion in GBM causing ONLY albumin loss
LM: congo red stain with apple-green birefirencence
assoc'd with multiple myeloma, TB, RA
Subendothelial deposits with tram track appearance
type I MPGN
LM: Intramembranous dense deposits
Type I MPGN associated with
Type II MPGN associated with
C3 nephritic factor
proteinuria <3.5 g/day
LM: lumpy bumpy glomeruli
EM: subepithelial immune complexes
IF: granular C3, IgG, IgM
acute post strep GN. occurs a few weeks after infection
LM: crescent shape made of fibrin and C3b proteins
rapidly progressive GN
causes of rapidly progressive GN
1. goodpasture's syndrome
2. Wegener's granulomatosis
3. Microscopic polyangiitis
LM: wire looping of capillaries
EM: subendothelial IgG with C3
Diffuse proliferative glomerulonephritis
LM: mesangial proliferation
EM: mesangial IC deposits
IF: IgA deposits in mesangium
Berger's disease. occurs a few days after infection
Split basement membrane with GN, deafness, and eye problems
What's mutate in alport syndrome?
type IV collagen.
Which kidney stones can you NOT see on an Xray?
Uric acid stones
octahedron kidney stones
which stones precipitate at a high pH?
Most common kidney stone presentation
calcium oxalate stone in a pt with hypercalciuria and normalcalcemia
Treatment for calcium stones
thiazides and citrate
Causes of oxalate stones
ethylene glycol and vitamin C overdose
struvite stones (ammonium magnesium phosphate)
Tx for calcium stones
thiazides and citrate
Cause of struvite stones
urease positive bugs:
coffin lid stones
rhombus red brown stones
renal cell carcinoma histology
clear limid filled cells
RCC associated with a gene deletion on
PPresentation of RCC
Resection. Resistant to conventional chemo and radiation
WWilm's tumor (nephroblastoma) histology
embryonic glomerular structures. Child 2-4 has flank mass and hematuria
Wilm's tumor deltion
WT1 tumor suppressor on chromosome 11
biopsy of kidney: papillary growth lined by transitional epithelium with mild nuclear atypia
transitional cell carcinoma
Transitional cell carcinoma associated with
ppainless hematuria suggests
Where can transitional cell carcinoma occur?
calyces, pelvis, ureters, bladder
acute pyelonephritis affects which part of kidneys?
Cortex. glomeruli and vessels are spared
Cause of chronic pyelonephritis
vesicoureteral reflux or chronic kidney stones. Normal person shouldn't get recurrent UTIs-->chronic pyelonephritis
WWhich parts affected in chronic pyelonephritis?
Corticomedullary scarring with blunted calyces. Tubules have eosinophilic casts
HIstology of chronic pyelonephritis
Lymphocytic invasion with fibrosis
presentation of drug induced interstitial nephritis
How long after drug will drug TIN happenn?
After 1-2 weeks..
Can be months with NSAIDs
Which drugs cause TIN (allergic reaction to drug)
Diffuse cortical necrosis caused by
Vasospasm and DIC. Associated with obstetric catastrophes and septic shock
maintenance phase of acute tubular necrosis
oliguric for 1-3 weeks. Risk of hyperkalemia
Recovery phase of acute tubular necrosis
polyuric. Risk of hypokalemiia
Causes of toxic ATN
ethylene glycol-->oxalate crystals
Renal papillary necrosis caused by
chronic phenacetin (acetaminophen)
Difference in handling of BUN vs creatinine
BUN is reabsorbed
Creatinine is NOT reabsorbed
Acute renal failure: prerenal azotemia
BUN: Cr is increased >20
-urea retained by kidney to conserve volume
Intrinnsic renal failure
BUN: Cr ratio decreased <15
-caused by ATN/ischemia/toxins/crescentic GN
-Tubules filled with debris
-decreased BUN reabsorption
BUN: Cr >15
-Caused by outflow obstruction (bilateral)
Urine osm: >500
Urine Na < 1%
Urine osm: 40
Intrinsic or post-renal. Differentiate these by looking at the BUN: Cr ratio
Consequences of renal failure
Fluid/sodium retention (CHF)
Side effect of increased BUN and Cr
Failure of vitamin D hydroxylation
-->2ndary hyper PTH
WWHy does hyperphosphatemia worsen renal osteodystrophy?
Tissue calcifications occur within tissues-->calcium phosphate instead of being excreted
Why do pts with ADPKD get hypertension?
Increased renin production
ADPKD associated with
mitral valve prolapse
benign hepatic cysts
presents in infant, often as potter's syndrome
AARPKD associated with
congenital hepatic fibrosis. After birth, will have HTN, portal HTN, progressive renal insufficiency
Medullary cystic disease
tubulointerstitial fibrosis and renal insufficiency-->cannot concentrate urine.
Inherited with shrunken kidneys seen on ultrasound
where does mannitol affect the nephron?
The thin descending limb
where does acetazolamide work its effect?
when is mannitol contraindicated
CHF and anuria
calcium wasting diuretic
CHF, cirrhosis, nephrotic syndrome, pulmonary edema (too much fluid)
Toxicity of loops
Non sulfonamide loop diuretic. Virtually the same, can also cause gout
indications for hCTZ
nephrogenic diabetes insipidus
Name the K sparing diuretics
Mehcanism: spironolactone and eplerenone
Competitive aldosterone antagonists.
mmechanism triamterene and amiloride
Block ENaC at cortical collecting duct
IIndications for spironolactone
side effects of spironolactone
Antiandrogenic effects--man boobs
WWhich diuretics cause acidemia?
carbonic anhydrase inhibitors--decrease HCO3 reabsorption
aldosterone--blocks K/H secretion. Also, hyperkalemia increases H leak from cells
Which diuretics cause alkalemia?
loop and thiazide diuretics
--hypokalemia worsens alkalosis
Urine calcium increases with
Why are ARBs better than ACE-Is?
they don't increase bradykinin
-->no cough or angioedema. ACE is still able to break down bradykinin
What do ACEI do to GFR?
Decrease GFR, b/c efferent arterioles are opened
Why is ACE good for CHF?
When are ACE inhibitors contraindicated?
bilateral renal artery stenosis
dysplastic kidney--how is it inherited?
Not inherited. COngenital malformation of renal parenchyma characterized by cysts and abnormal tissue, especially CARTILAGE. NOT BILATERAL LIKE ADPKD
baby with portal htn
ADPKD. cysts in the liver, kidney, and brain.
mitral valve prolapse
how is medullary cystic kidney disease inherited?
autosomal dominant with SHRUNKEN kidneys
IF Fena is <1% this tells you
tubular function is intact=can resorb sodium. this happens in prerenal ATN
why is BUN:cr <15 in intrarenal renal failure
epithelial cells are not working, cannot resorb BUN, so it is excreted through the kidneys
Why is BUN:Cr>20 in pre-renal failure?
Kidneys reabsorb as much fluid as possible and BUN follows
Why is BUN:Cr>15 in post-renal failure?
High pressure in ureters "pushes" BUN and fluid back into the body from tubular fluid
If pre-renal failure doesn't resolve...
becomes ischemic acute tubular necrosis. Prox tubule and medullary thick ascending limb are susceptible
What are consequences of ATN?
hyperkalemia with metabolic acidosis. Can't excrete potassium or organic anions (lactic acid)
hyperlipidemia seen in
minimal change associated with
most common cause of nephrotic syndrome in hispanics and A-As
FSGS associated with
Minimal change and FSGS immunofluorexcence
None. Also poor response to tx/steroids. will progress to renal failure
Pt with lupus gets nephrotic syndrome
Membranous nephropathy also associated with
nephritic syndrome in lupus pt
DIffuse proliferative GN
immune complex deposition
type I membranoproliferative
more likely to have tram track
what determines if GAS can cause nephritic syndrome?
presence of M proteins
In adults with post-strep GN
more likely to present to crescent rapidly progressive GN
lupus patient with rapidly progressive glomerulonephritis
diffuse proliferative GN
Negative IF rapidly progressive nephritis
pt with rapidly progressive GN, hemoptysis, hematuria, and sinus infections
Perform cANCA--could be wegeners not goodpasteur's (classic)
most common cause of nephritis world wide
Berger's igA. Usually after mucosal infection, episodic.
churg strauss features not present in microscopic polyangiitis
tests for UTI
leukocyte esterase and nitrites
culture: >100K CFU
chlamydia and n. gonorrhea
Most common pathogens for pyelonephritis
"thyroidization" of kidney
problem with staghorn calculi
can serve as a nidus for additional UTIs
what produces EPO
renal peritubular interstitial cells
why are crohn's pts more likely to make calcium oxalate stones?
Not able to absorb calcium necessary to bind oxalate
shrunken kidneys with cysts
Dialysis patients. Pts at increased risk for RCC
Triad of RCC
Cause of RCC
loss of VHL
-Increased HIF=VEGF PDGF
wilms tumor cell
Serum lab levels of calcium, phoshorus, and PTH in chronic kidney disease
1. Phosphate retention
2. Low calcium from low vitamin D
3. Increased PTH
loop diuretics act on
thick ascending loop of henle. Decrease medullary concentration gradient
osmotic diuretics act on
thin descending loop
when do you see states of hypercalcemia and hypercalciuria?
Hyper PTH and sarcoidosis
Situations with hyperoxaluria
low calcium diets (less calcium in gut to bind oxalate for excretion)
Upper part of ureter is supplied by
The renal artery
Explain what happens with hypoaldosteronism to Na, K, HCO3 and Cl
acidosis=Low bicarb (H+ATP pump)
High chloride to balance out HCO3-
Hypokalemia and hypotension