renal Flashcards
multicystic dysplastic kidney
hydronephrosis, palpable kidney
usually unilateral with normal function from other kidney but need vcug/renal scan to rule out contralateral anomalies. affected kidney usually atrophies. no treatment, just monitor with renal us and creatinine. no risk of htn or tumor. Will see large cysts by 20w
wilms tumor
most common nephroblastoma, abdominal/flank mass with hematuria, sometimes htn. rarely presents in neonate
renal vein thrombosis
most common blood clot
hematuria, flank mass, thrombocytopenia
some have htn
prune belly syndrome (Eagle Barrett Syndrome)
Usually caused by urethral obstruction, most common in boys.
Increased bladder pressure causes triad of #1 cryptorchidism, #2 poor adbdominal musculature, #3 dilated urinary tract
Can include renal dysplasia, hydroureter. +/- malro, cardiac anomalies, compression of vessels to lower extremities.
oligohydramnios –> pulm insufficiency
should be on uti ppx for poorly functioning bladder
puv
most still progress to ESRD in first 10y. abnormal bladder function –> persistent UTIs –> renal scarring. Dx: VCUG with spinning top deformity (proximal urethra dilated, distal constricted), VU reflux, thickened bladder
autosomal recessive polycystic kidney disease
ARPKD, mc presents in neonatal period. Assc with congenital hepatic fibrosis. Enlarged kidneys and oligo in utero. Urine concentrating defect. B/l flank mass. +/- renal fx impaired. cysts not usually present in neonatal period. may have hptn, hypo Na. 50% develop renal failure in first decade.
vasopressin
released from post pit. Binds to receptors in kidney –> camp –> aquaporins. In premature babies, poor production of camp.
x-linked: v2r mutation, receptor unable to bind AVP
secretion most impacted by intravascular status, then osmolarity
v1 and v2 receptors. v1 in vessels and platelets, v2 only in kidneys
acts on distal tubule and collecting ducts
renal embryology
can see kidney at 9 wks, bladder at 15th wk
loop diuretics
bumetadine and furosemide
act on thick ascending LOH on Na K 2Cl transporter
thiazide diuretics
hydrochlorothiazide
act on distal tubule on Na Cl cotransporter
lead to increased calcium reabsorption
aldosterone
spironolactone
weak diuretic pootassium sparing agent
fena
S(Cr)xU(Na) / S(Na) X U(Cr)
RTA
all non anion gap metabolic acidosis
I: distal: poor secretion of H+, urine is basic around 6-7. Associated with nephrocalcInosis
II: proximal: poor reabsorption of HCO3, can compensate with distal secretion of H+. Urine is normal around 5.5. Assc w fanconi syndrome and many electroylyte abnormaltiies
IV: aldosterone: poor response to aldosterone or decreased production. Hyperkalemia and acidosis.
bladder extrophy
assc with inguinal hernia
cloacal extrophy
anal atresia, omphalocele,
what is a normal urine osmolality? What is pt vs t vs adult concentration ability?
75-300 mOsm/k
Pt: 500
T: 600
Adult: 1500
What is normal urine spec gravity?
1.003 - 1.102
what is osmotic reflection coefficient
(s), a measure of endothelial permeability. The higher ‘s’, the less permeable.s062020
What is the most common cause of congenital hydronephrosis?
#1: Ureteropelvic Junction obstruction (44%) - can be associated with other syndromes #2: Ureterovesical junction obstruction (21%) - dilation of ureter #3: PUV (9%) - thickened bladder wall
most common cause of hypertension
renovascular disease, specifically renal artery thrombosis
what do patients with APCKD usually die of?
respiratory failure from pulm hypoplasia. in utero, little urine production –> oligo. on US, large, sometimes non-dysplastic kidneys. associated with congenital hepatic fibrosis. (VS multicystic dysplastic kidney, usually unilateral and can see large cysts on US)
what is normal renal development?
~9w: first nephron is formed, start making urine
~ 20 w: 5ml/hr of urine, 95% of AF is urine, 1/3 of enphrons present
~36 w: all nephrons are present
~ 40w: 50ml/hr of urine
what is lowe’s syndrome
‘the OCRR is beLOWE the bridge” oculo, cerebral renal syndrome:
cataracts, glaucoma
hypotonia, areflexia, MR
renal tubular dysfunction, proteinuria, aminoacidemia, nephrotic syndrome
cryptoorchidism
dx: elevateed AFP
What is Bartter syndrome
loop of henle abnormality, inability to reabsorb so hypo natremia, hypocalcemia, hypokalemia with dysmorphic features including triangular face. alkalotic.
compare APCKD to MCDK
apckd: don’t see cysts as early on US, usually bilateral, have htn (maybe intrinisic disease or increased ADH), hyponatremic, assc with hepatic fibrosis (65%). 25% die, 25% have poor growth.
mcdk: usually can see multiple large cysts by 20w, unilateral, no assc with malignancy, hepatic fibrosis or htn. Usually doesn’t require intervention
what is urine osm and Na concentration and FENA score in prerenal vs renal failure?
pre-renal: urine osm high, Na low (b/c kidney tries to reabsorb to help with volume status), FeNa <2%
renal: urine osm low (cannot concentrate), Na high, FeNA >2%
What is the formula for free water deficit vs Na deficit?
Free water: change desired x wt x 4ml
Na deficit: change desires x at x 0.6
Where do the different diuretics and adh act on the nephron?
Acetazolamide : PCT Loop diuretics : ascending loop of henle Thiazide : DCT Spironolactone : distal DCT adh: CD
when does nephrogenesis happen?
5-35 weeks.
CO to kidneys drops during birth (think only need to pee once on dol1) and then picks up in the next two months
