Renal DIT Flashcards
3 parts of the embryological kidney
Which gives rise to the ureteric bud?
Which gives rise to the audlut kidney
Pronephros Mesonephros -caudal end -> ureteric bud Metanephros -adult kidney
Ureteric bud arises from? Gives rise to (4)
arises from the caudal end of the mesonephros -> induces metanephric mesenchyme to induce into nephrons and form glomerluli
the bud -> renal calyx, ureters, collection duct, pelvis
Most common site of obstruction in a fetus
ureteropelvic junction -> last to canalize
What does the mesenephros give rise to? (2)
ureteric bud (caudal end)
male genital system (in males)
Potters syndrome presents as?
Due to
Due to oligohydraminos (classically renal a genesis; also ARPKD and posterior urethral valves)
POTTER
Pulmonary hypoplasia Oligohydraminos Twisted face Twisted skin Extremities malfunction Renal agenesis
Horseshoe kidney is associated w/
turners syndrome
Renin is released from what cell under what 3 conditions
Released from Juxtaglomerular cells (next to the afferent artery) in response to
Low afferent BP (JG cells sense)
Low Na concentration in efferent arteriorl (Macula densa sense)
Beta 1 stimulation
Glomeruli filtration barrier is made of (3)
fenestrated endothelium
negatively charged basement membrane
podocytes (viseral layer)
Ureters course in relation to major anatomy?
Retroperitoneal or paritoneal?
retroparitoneal course
Ureters flow under the the uterine arteries in females and vas defer ins in males
% of the body that is water
-EC vs IC
W/in EC
–plasma vs intertitial
60% of the body is water
-1/3 extra cell and 2/3 intracellular
1/4 of extracellular fluid is plasma
3/4 extracellular fluid is interstitial
Renal clearance formula
UV/P
U- urine concent
V - urine flow rate
P - plasma concentration
Clearnance and relation to GFR
Cl< GFR = absorbtion
Cl> GFR = excretion
Cl =GFR = no ∆ ~ inulin
GFR calculation and estimation
calculate using inulin and the Clearance formula
[U(urine concent inulin) V] / (Plasma concent of inulin)
Can estimate w/ creatine which slightly over estimates GFR w/ mild secretion
Normal GFR =
100 mL/min
Effective renal plasma flow concept and formula
Effective renal plasma flow is ALL of the blood flow through the kidney, not just what is measured with clearance
Use PAH (para aminohiipuric acid) to calculate due to active secretion AND filtration at the proximal tubule
RPF~ Cl formula = clearance of PAH
[U (PAH) x V] / P (PAH)
Filtration Fraction formula and concept
filtration fraction is a comparisons of how much is being filtered at a given time compared to total flow
FF = GFR/RPF (or renal plasma flow)
normally 20%
Filtered load formula
GFR x plasma concentration
Excretion rate in renal?
U x V
the top part of the clearance formula ( flow rate x conncentration in the urine)
Prostaglandins and effect on the filtration
dialate afferent arteriole
- Increase GFR
- Increase RPF
- No ∆ in FF
NSAIDs effect on glomeruli filtration
blocks prostaglandins afferent dialation ->
Decrease GFR
Decrease in RPF
-No ∆ in FF
angiotension II role of on glomeruli filtration
preferentially constricts the efferent arteriole
Increases GFR
Decrease in RPF
-> Increase in FF
ACE inhibitors and role on glomeruli filtration
blocks angiotensions II preferential constricion on the efferent arteriole
Decreases GFR
Increases RPR
Decreases FF
explains why creatine increases w/ ACE inhibitors
Ureter stone and effect on glomerlui filtration
blocks the flow downstream -> back pressure
Decreases GFR
No change in RPF
Decrease in FF
Increase in plasma globulin and effect on glomeruli filtration
increase osmotic pressure w/in the blood vessel
Decreases GFR
No change in RPF
Decrease in FF
Glucose clearance minimized due to?
- point of saturation
Na/Glucose cotransporters in the proximal tubule reabsorb ALL glucose up to 160 mg/dL; then have some spill in the urine
Transporters saturated at 350 mg/dL
AA clearance and reabsorbtion
3 cotransporters that use Na absorb : acidic, basic and neutral AA in the proximal tubule
Neutral AA reabsorbtion dysfunciton = Hartnup’s disease
- Tryptophan deficiency -> niacin deficiency -> pellagra
Hartnup’s disease
deficiency in neutral AA/Na co-transporter in the kidney -> excessive loss of reabsorption of tryptophan
Can’t make Niacin (B3) -> pellagra
- diarrhea
- dermatitis
- dementia
- death
Pellegra can be due deficiency of what in the kidney
Presents as?(4)
neutral AA/Na co-transporter (no tryptophan -> B3/niacin)
-Hartnup’s disease
Dementia
Dermatitis
Diarrhea
Death
Part of the nephron responsible for collection of 2/3 of fluids and electrolytes
proximal
First half Proximal tubule collects? (6)
Bicarb (converted -> H2O and CO2 in lumen -> cell and converted back to bicarb)
glucose AA inorganic phosphate lactate electrolytes (isotonically, meaning water follows)
2nd half of proximal tubule collects?
Cl
Where does organic anions and cations get excreted in the nephron?
Due to?
in the proximal tubule
-alpha ketoglutarate gradient set up by Na/K atpase drives out organic anions into the lumen
organic cations are excreted by the electrochemical gradient set up with 3 Na out for every 2 in ATPase
- H is reabsorbed w/ lose of cation
thin ascending loop responsible for
reabsorbing water
impermeable to Na
Thick ascending loop responsible for (2)
actively reabsorbing Na/K/2Cl
->induces Mg and Ca to pass pericellular
Impermeable to water -> dilutes urine
Early distal tubule is responsible for (2)
Na/Cl actively being reabsorbed
Responding to PTH by placing Ca/Na exchangers on the basolateral side to reabsorb Ca
Impermeable to H2O
PTH has 3 functions w/ Ca(3)
Induces Ca reabsorption from bone
Stimulates Vitamin D conversion in the kidney by activating 1 hydroxylase
Places Na/Ca exchanges to reabsorb Ca in the kidney
2 types of cells in the collecting duct and their respectful roles
principle cells -responds to Aldosterone - ENaC and EK channels ADH -V2 and aquaporins
intercalcalated cells
- A cell (alpha) -> secrete H
- B cell (beta) - > secrete HCO3
Aldosterone acts where and has what function (3)
acts on the principle cell in the collecting duct to place Na channels to reabsorb Na and have H2O follow.
-Also places K channels which is thus lost to the lumen
In the alpha intercalated cell -> excretion of H
Epleronone and Spironolactone block
ADH/vasopressin act where and has what function
acts in the collecting duct on V2 and leads to the placement of aquaporins in the lumen to reabsorb water
Interfered w/ by lithium
Uses of mannitol
Drug overdose
elevated intracranial pressure
shock
glaucoma (acute angle closure)
What electrolyte is slightly elevated w/ the use of mannitol
Na in the serum due to the loss of free water
Glaucoma diuretics
Mannitol - acute closed angle
Acetazolamide - chronic
How does acetazolamide help in altitude sickness?
Blocks carbonic anhydrase in the lumen of the kidney thus leading to excretion instead of reabsorption in proximal tubule
Toxicity associated w. acetazolamide use
hyperchloremic metabolic acidosis
do not use w/ any hypokalemia, hyponatremic or hyper chorolate
Uses of acetazolamide
glaucoma- chronic
urinary alkalization
metabolic alkalosis -> piss away excess bicarb
altitude sickness
Dieuretics to stay away from if sulfa allergy(3)
acetazolamide
Loops
-furosimide
hydrochorothizide
Use ethacrynic acid
Need to use a loop but the patient is allergic to sulfa drugs use
ethacrynic acid
Which diuretics lose Ca and which retain
Loops lose Ca (may exacerbate a kidney stone problem)
Thiazides retain ( maybe use in idiopathic hypercalciuria)
Toxicity w/ loop diuretics(6)
be wary combing w/ what drug class
Ototoxic and nephrotoxic
-aminoglycosides
hypokalemia
dehydration
allergy
gout
Thiazide toxicity (7)
hypokalemic metabolic alkalosis hyponatremia hyperglycemia hyperlipidemia hyperuicemia -> gout hypercalcemia -allergy - sulfa
Drugs used to increased morbidity and mortality in CHF patients (3)
Beta blockers
K sparing dieuretics
ACE inhib/ARBs
Hydrocholorthiazides ex (4)
hydrocholothiazide
chlorothiazide
chorthalidone
metolazone
K sparing dieuretics (4)
SEAT
Spiranolactone
Epleronone
Amiloride
Triamterene
may used in combination w/ Loops or thiazides to retain some K
Toxicity of K sparing diuretics (2)
Hyperkalemia -> arrhythmia
Antiandrogen -> gynectomastia in men / menstural problems in females
diuretics causing acidosis(2)
carbonic anhydrase inhibitor (acetazolamide)
K sparing (spares H excretion as well in the intercalated A cell)
diuretics causing alkalosis (2)
loops and thiazides
the loss of Cl leads to less bicarb being excreted and
anemia in a pateint due to renal failure
lack of erythropoeitin
enzyme in kidney that converts Vit D into its most active form
1 alpha hydroxylase
unregulated by PTH
what does the kidney secrete to vasodialate afferent arterioles to increase GFR
prostaglandins
NSAIDs can precipitate acute renal failure
ANPs action on the kidney
causes increase in GFR and Na filtration w/ no compensatory Na reabsorption in the distal tubule
opposite of aldosterone
SIADH can be caused (5)
Ectopic ADH - small cell lung CA CNS disorder/head truama/ infection Pulmonary disease Drugs - cyclosporine Idiopathic
Presentation of SIADH(3)
Rx?
excessive water retention
hyponatremia w/ continued Na excretion
-low aldosterone due to hypercolemia (net Na loss)
urine osmolarity is low
Need to correct low Na very slowly (central pontine myelinolysis)
Rx -Demeclocycline, flid restricion, conivaptana nd tolvaptan
Central Diabetes insepitis causes (3) and presentation
pituitary tumor
trauma
surgery
intense thirst and polyuria - increased serum osmolarity, low specific gravity of urine (very dilute)
partial - some ADH
complete - No ADH
responds to desmopressin
Nephrogenic diabetes insepitis causes(4) and presentation
hereditary
secondary to hypercalcemia
lithium *
demeclocylcine
intense thirst and polyuria - increased serum osmolarity, low specific gravity of urine (very dilute);
Does not respond to desmopressin
Rx for SIADH (4)
Demopressin if central
Nephrogenic
- Hydrochlorathiazide - induces proximal tube reabsorbstion
- indomethacin - decrease renal blood floe
- amiloride - stops Lithium from getting in the ENaC if causal
Na imbalance
High (4)
Low (3)
Low
- malaise/stupor
- Siezures
- coma
- mental status change
High
- irritability
- stupor
- coma
K imbalance
High (4)
Low(5)
High
- Wide QRS
- Peaked t waves
- muscle weakness
- arrhythmia - v tach
Low
- flat T waves
- maybe U waves
- arrhythmia - v tach
- torsades
- muscle weakness
K and Mg run together
Ca imbalance
High (4)
Low (2)
High
- Stones - kidney
- Bones - pain
- Groans - ab pain
- psychiatric overtones - anxiet change in mental status confusion
Low
- Tetany
- siezure
Mg inbalance
High (3)
Low(2)
High
- decreased DTRs,
- lethargy,
- bradycardia
Low
- arrythmia - torsasdes
- tetany
Shifts K out of the cell causing hyperkalemia (5)
Digitalis Cell Lysis insulin deficiency beta blockers acidosis
Drugs that may cause
- k sparing
- Ace inhibitors
Shifts K into the cell causing hypokalemia (4)
Insulin (increase Na/K ATPase)
alkalosis
Beta agonists ( increase Na/K ATPase)
Drugs that may cause
- thiazides and loops
Rx for acute hyperkalemia (3)
beta agonists
induced alkalosis
insulin - give dextrose 1st
Causes of respiratory acidosis
Hypoventilation respiratory muscle weakness Lung obstruction Air trapping Opiods -> resp depression Acute/chronic lung disease
Causes of metabolic acidosis
-increased anion gap (9)
MUDPILES - gaining H
Methanol Uremia DKA Propylene glycol Iron tablets/ Isoniazid Lactic acidosis - coding and not perfusing Ethylene glycol Saliclates -late
Calculate anion gap
Na - (Cl - HCO3)
Respiratory alkalosis causes (3)
Hyperventilation
- high altitude
- psychogenetic
Salicylates - early
Acute hypoxemia - PE
metabolic alkalosis causes (4)
loop dieuretics
vomiting
antacid use
hyperaldosterone (hypokalemia, hypertension also)
Metabolic acidosis w/o anion gap(4)
losing bicarb
Renal tubule acidosis (3 types)
Diarrhea
acetazolamide
spironolactone
hypealimentation
addisons
saline infusion as well
Renal tubular acidosis Type I - defect and presentation?
urine pH?
defect in H secretion by alpha inceralated cells in the collecting tubule
urine pH of 5.5
hypokalemia w/ increased risk of CaPhosphate stones due to neutralization
metabolic acidosis w/out anion gap
Renal tubular acidosis type 4 - defect and presentation ?
urine pH
defect in the hypoaldosterone or perceived hypoaldosterone -> hyperkalemia
hyperkalemia impairs collecting tubules from generating NH4 and excretion -> metabolic acidosis
urine pH <5.5 normal
Renal tubular acidosis type 2 - defect and presentation?
urine pH?
Defect in proximal tubule HCO3 reabsorbtion (maybe falcon’s syndrome).
leads to hypokalemia and risk of hypophatemia
-> metabolic acidosis w/out anion gap
Urine pH <5.5
henderson haselbalch equation essentially for metabolic disorders
pH =
Normal pCO2 and HCO3
HCO3/pCO2
pCO2 ~ 40 (35-45mmHg)
HCO3 ~22 (22-28 mEq/L)
what do you have when you have a normal pH and off HCO3 and pCO2
you have mixed metabolic presentation, you should never have complete correction of metabolic disorder w/ compensation
What value change cues you into a metabolic acidosis?
HCO3 decreased below 22 mEq/L
-pCO2 may decrease as patient tries to correct by breathing faster
What metabolic value cues you into a metabolic alkalosis
HCO3 greater than 22 mEq/L normal pCO2
-pCO2 may increase as the patient breathes slower to correct
what metabolic value clues you into a respiratory alkalosis
pCO2 less than 40 mmHg
HCO3 may decrease if kidneys are trying to correct
what metabolic value clues you into respiratory acidosis?
pCO2 greater than 40 mmHg
HCO3 may increase if kidneys are trying to correct
focal vs diffuse renal pathology
whether or not 50% of the glomeruli are affected
proliferative renal pathology
hypercellular glomeruli
membranous renal pathology
thickening of the glomerular basement membrant
Strictly Nephrotic syndrome renal path (5)
Focal segmental glomerulosclerosis membranous nephropathy minimal change disease amyloidosis diabetic glomerulonephropathy
overlap
-diffuse proliferative glomerulonephritis - SLE loops
membranoproliferative glomrulonephritis - Hep B,C lupes, endocarditis (subacute)
strictly nephritic syndrome renal path (4)
Post streptoglomerulonephritis
Rapidly progressive glomerulonephritis
Bergers IgA glomerulonephropathy
Alport syndrome
Overlap
- diffuse proliferative glomerulonephritis - SLE loops
- membranoproliferatve glomerulonephritis - Hep B, C, Lupes and endocardits (subacute)
Defining nephritic syndrome
Pathology and presentation
inflammation of the glomeruli
-> hematuria and RBC casts in the urine (tea/brown urine)
(azotemia, oliguria, HTN (Na retention), maybe proteinuria <3.5g/day
Acute post streptococcal glomerulonephritis
timeline
presentation on
Light microscope
EM
IF
nephritic
Post pharyngitis or strep pyrogens impetigo about 1-3 wks after - Type III hypersensitivity
LM see lumpy bumpy deposits sub epithelial
IF - granular appearance w/ IgG, IgM and C3 deposition in the GBM and mesangium
-> depletion of complement C3
anti DnAse B in blood and low C3 w/ dark urine
Poststreptococcal glomerulonephritis
Rapidly progressive (cresentic) glomerluonephritis
presentation?
Types (3)
nephritic
See proliferation of fibrin, plasma proteins and parietal cells and debris in the glomeruli
Due to
- Goodpastures - Type II hypersen w/ linear IF (anti GBM Ig)
- Granulomatosis w/ polyangitis (wegeners) - cANCA
- Microscopic polyangitis - pANCA
Diffuse proliferative glomerulonephritis
presentation
LM
EM
IF
Wire loopus - most common cause of death in SLE; nephritic but also nephrotic
LM shows anti DNA complexes depositing between the endothelium dBM -> thickening (wire loops)**
EM - sub endothelial and maybe intramembranous IgG based immune complex w/ 3 ( NOT as KEY)
Bergers disease (IgA nephropathy)
associated w?
LM
EM
IF
nephritic
related to henoch schonlein purport (part of vasculitis w/ palpable purport on arms/legs/butt and GI changes w/ ab pain, vomitting and interstitial bleeding)
seen after URI or gastroenteritis like w/ HP above
IF - IgA based immune complexes (from the vasculitis) deposits in the mesangium
thus LM -> mesangium proliferation and EM -> mesangium deposits
Alport syndrome nephropathy due to
See on histology?
Presentation (3)
nephritic
X linked mutation of Type iV collagen
-> split basement membrane
glomerulonephritis
deafness
cataracts (eye problems)
Presentation of nephrotic syndrome (5 issues)
proteinuria >3.5 g/day*
hypoalbunemia* -> peripheral edema *
Also
- decreased Anti thrombin III -> thromboembolism
- increased risk of infection (loss of Ig)
- hyperlipidemia (liver wants to make vascular osmolar somehow)
Focal Segmental Glomerulonephritis
LM
EM
Associated w?
nephrotic
most common cause of nephrotic syndrome in the US
LM -> semental sclerosis and hyalinosis
EM - effacement of the foot process as a result
Associated w/ HIV
-Higher rate in AA and latinos
Membranous nephropathy
LM
EM
Due to?
Nephrotic
Used to be #1 more common in caucasion
EM spike and dome appearance
- w/ sub epithelial deposits (between the thick BM and podocytes)
- BM spikes between thick deposits
->LM - diffuse capillary and GBM thickening (membranous basement membrane)
Can be SLE’s nephrotic presentation (DPGM more common)
Minimal Change disease
LM
EM
nephrotic disease -> selective loss of albumin in kids ages 2-7
LM shows NORMAL glomeruli
EM shows foot process effacement
responds to corticosteriods
Amyloidosis nephropathy
LM
nephrotic syndrome
LM w/ congo red stain shows apple green birefringence under polarized light -> expansion of the mesangium w/ amyloid deposits
Kidney is the most commonly affected
Membrano-proliferative glomerulonephritis (MPGN)
LM
Associated w? (4)
Nephrotic syndrome or can present nephritic
Membrane proliferates -> tram track
SUBENDOthelial deposits of IgG
2 types
- type I Tram track appearance of GBM due to mesangial ingrowth
-Type II intermembranous immune complex deposits -> dense deposits
HBV; HCV; SLE; Subacute endocarditis
Diabetic glomerulonephropathy
LM(2)
Nephrotic syndrome
Nonenzymatic glycosylation of basement membrane -> increase permeability
also glycosylation of efferent arterioles -> increase in GFR
mesangial expansion
See esoisinophilic nodular glomerulosclerosis - Kimmerlstiel Wilson lesions
Kimmelseil wilson lesions
eosinophilic nodular glomerulosclerosis in diabetic glomerulonephropathy
lumpy bumby deposits of IgG, IgM and C3
post streptococcal glomerulonephritis
Deposits of IgA in the mesangium
Bergers Disesae
Nephritis, deafness and cataracts
Alport
Crescent formation in the glomeruli
4 types of rapidly progressive glomerulonephritis
- goodpastures
- Wegeners
- Microscopic polyangitis
- SLE
Wire loop appearance on the LM
SLE loopus - diffuse proliferative glomerulonephritis
Most common nephrotic syndrome in adults
Focal segmental glomerulosclerosis
EM shows effacement of the epithelial foot processes
minimal change disease
nephrotic syndrome associated w/ HBV
Membranoproliferative glomerulonephritis
Nephrotic syndrome associated w/ HIV
Focal segmental glomerulosclerosis
Pupura on back of arms and legs, abdominal pain and IgA nephropathy
Henoch schonlein
EM shows spiking of the GBM due to dense sub epithelial deposits
Membranous glomerulopathy
RBC casts indicate
glomerular damage - like infarction or acute glomerulonephritis
WBC casts indicate
acute pyelonephritis
Bacterial casts indicate
pyelonephritis
epithelial cell cast indicates
Acute tubular necrosis
Toxic ingestions- ethylene glycol or mercury
waxy casts indicate
chronic renal failure
hyaline casts indicate
benign pathology, maybe dehydration
fatty casts indicate
nephrotic syndrome - hylaine casts w/ extensive fat infiltration
Granular casts indicate
chronic renal disease, ATN
muddy brown
Causes of calcium stones(4)
hypercalcemia
- CA
- PTH
- Vitamine C excess >2000
- ethylene glycol
What can you give to prevent recurrent Calcium stones?
thiazide diuretics
Which bugs are associated w/ kidney stones and what kind of stones do they cause (3)
Urease containing bugs
- Proteous mirabilis
- Staphylococci
- Klebsiella
Urea split -> Ammonia and H2O
Form ammonium magnesium phosphate stones (struvite)
Which kidney stone is invisible on plain film?
How might you visualize the stones
uric acid stones
visualize on CT and US
Hyperuricemia due to CA may lead to this type of renal pathology
Uric kidney stones
See a younger kid with recurrent kidney stones suspect
Rx?
cystine stones
- secondary to cystiuria
treat with alkalization
polygonal clear cell tumor filled with lipids and carbohydrates see in the men 50 -70 who may be overweight and smoked
Renal cell carcinoma
Renal cell carcinoma paraneoplastic syndromes (4)
ACTH
PTHrP
EPO
prolactin
Most common renal malignancy in malignancy in kids?
Most common malignancy in adults?
- METS where?
Most common tumor?
Wilms
Renal cell carcinoma
- hematogenous spread to bones and lung
Transitional cell carcinoma
inhereted renal cell carcinoma is due to ?
Hippel lindau syndrome
Can be sporadic deletion on chromosome 3 as well
Presentation of Wilms tumor
kid that is 2-4 that has hematuria and palpable flank mass
Deletion of tumor suppressor gene WT1 -> ?
What chromosome?
Wilms tumor
Chromosome 11
Beckwith wiedmann syndrome or WAGR complex
Wilms tumor
Aniridia - absence of iris
Genitalurinary malformation
Retardation - mental/motor
painless hematuria in a patient that has a history of smoking?
Other risk factors (2)
transitional cell carcinoma
aniline dyes
cyclophosphamide
Cyclophosphamide renal risks (2)
HUS
Transitional cell carcinoma
thyroidization of the kidney
chronic pylonephritis
dilated tubules look like colloid
Acute interstitial nephritis most commonly due to?(8)
timeline?
Drugs taken 1-2 weeks prior
NSAIDs PCN/cephalosporins ciprofloxin cimetidine PPIs allopurinol indinovir mesalamine
Presentation of acute interstitial nephritis?(6)
fever rash pyuria - eosinophilia* azotemia* hematuria CVA
Diffuse cortical necrosis is?
Due to?
acute generalized cortical infarction of BOTH kidneys
Due to vasospasm and DIC most commonly
associated w/ obstetric catatstrophy, ARDS, multi organ failure
Acute tubular necrosis
due to (3)
most common cause of intrinsic renal failure
Drugs
- aminoglycosides
- cephalosporins
- polymyxins
Radiograph contrast dye
-pretreat with NaHCO3 and fluids
Rhabdomyalisis and myoglobinuria
- crush injury
- statin
- seizure
- cocaine use
Drugs causing acute tubular necrosis(3)
aminoglycosides
cephalosporins
polymixins
Key findings w/ acute tubular necrosis
muddy brown casts
renal failure
if due to rhadomyalisis/myoglobinuria
-renal failure
elevated CPK
4+ blood in urine w/out RBC in urine cell count
Renal papillary necrosis is ?
Presentation? (2)
sloughing of the renal papillae due to ischemic triggers
gross hematuria and proteinuria
Casuses of renal papillary necrosis (4)
DM
Sickle cell
acute pyelonephritis
chronic phenacetin (acetomenophen) and ASA
prerenal azotemia is due to
BUN : Cr
dehydration or hypotension -> decreased GFR
Na/H2O and urea is retained by the kidney in attempt to conserve
20>1
Na is resorbed so FeNa 500)
Intrinsic azotremia due to?
BUN:Cr
Intrinsic renal damage, acute tubular necrosis or ischemia or toxins
less common glomerulonephritis
Patchy necrosis -> debris obstructing the tubules so DECREASE in GFR
BUN reabsorbtion is impaired so 2% due to tubular damage
postrenal azotremia due to?
BUN:Cr
outflow obstruction
- BPH
- Stone
- neoplasia
- congenital anomalies
develops only if bilateral obstruction
BUN:Cr >15:1; no problem reabsorbing but depending on the block need back pressure
FeNa > 2% due to backpressure -> tube damage
Consequences of renal failure (6)
Na/H20 retention
-CHF, pulmonary edema HTN
Hyperkalemia
-not able to put out
Metabolic acidosis
-same line as K
Uremia
-high BUN/Cr
Anemia
-less EPO
Renal osteodystrophy
- Vitamin D failure
Uremia symptoms seen in renal failure (5)
Nausea vomitting pericarditis Asterixis (liver flap) encephalopathy platelet dysfunction
Renal osteodystrophy cause and consequence
seen in renal failure
Vitamin D hydroxylation failure leads to decreased activated vitamin D around to reabsorb Calcium in the kidney and also in the gut
PTH is activated w/ low serum Ca
subperiosteal thinning of bones
RX- Vitamin D Supplementation
Presentation of ADPKD
multiple large bilateral cysts
flank pain hematuria HTN urinary infection progressive renal failure
Due to mutation in PKD1 or PKD2
Dialysis patients may have
cysts
ARPKD presentation
significant renal failure in utero (can be imaged)
oligohydraminos
-> can lead to potter syndrome
medullary cystic disease
inherited disease causing tubulointerstitial fibrosis and progressive renal failure
poor prognosis
