Renal Flashcards
stimuli that induce renin release
B-adrenergic stimulation (sympathetic tone)
low Na in DCT (macula densa)
low pressure in afferent arteriole
body water
60% body weight
1/3 extracellular, 1/4 of that is plasma
glomerular filtration barrier
fenestrated capillary epithelium
BM with heparan sulfate (- charge)
podocyte foot processes
Renal formulas
CL=UV/P GFR=UV/P (inulin or creatinine) RPF=UP/V (PAH) Filtration fraction=GFR/RPF Filtered load=GFR*Px Excretion rate=V*Ux Reabsorption=filtered-excreted Secretion=excreted-filtered
effect of NSAIDS on kidney
inhibit PG (normally dilate afferent arterioles) so constrict afferent arteriole: decreases RBF and GFR, so FF stays the same
site of excretion of organic anions and cations
PCT
site of isotonic fluid reabsorption
PCT
gout+intellectual disability+lip-biting
Lesch-Nyhan syndrome
Psammoma bodies
Papillary adenocarcinoma of thyroid
serous cystadenocarcinoma of ovary
meningioma
mesothelioma
function of distal tubule
Principal cells: reabsorb H2O and Na
secrete K
Intercalated: secrete H or HCO
reabsorb K
two types of intercalated cells
alpha (a cells): secrete H ions
beta (B cells): secrete HCO3
effect of aldosterone on collecting duct
principal cells: increase reabsorption of Na and secretion of K
intercalated: increases secretion of H
acute pulmonary edema
loop diuretic
idiopathic hypercalciuria (calcium stones)
thiazide avoid loop (increase Ca excretion)
glaucoma
mannitol or acetazolamide
mild to moderate CHF with expanded ECV
loop
conjunction with loop or thiazide to spare K
K sparing
edema associated with nephrotic syndrome
loop
increased intracranial pressure
mannitol
mild to moderate HTN
thiazide
hypercalcemia
loop
hyperaldosteronism
spironolactone or eplerenone (ald antagonists)
heart failure pt with sulfa allergy
ethacrynic acid
peaked t waves
hyperkalemia
tetany
hypocalcemia, hypomagnesia
arrythmias
hypo/hyper K, hypomagnesia
decreased deep tendon reflexes
hypermagnesia
flattened T waves, U waves on EKG
hypokalemia
diagnostic features of DI
polyuria
decreased SG and osmolarity of urine
water deprivation test: no increase in urine osmolarity
desmopressin:
central if urine osmolarity increases
nephrogenic if urine osmolarity stays the same
factors cause hyperkalemia
Digitalis B antagonists acidoses decreased insulin hyperosmolariy cell lysis ACE inhibitors and K sparing
factors cause hypokalemia
increased insulin B agonists alkalosis hyposmolarity cell proliferation loop
emergency treatment of hyperkalemia
B agonist
IV dextrose then IV insulin
IV bicarb
treatment for central DI
desmopressin
treatment for nephrogenic DI
HCTZ, indomethacin, amiloride
treatment for lithium-induced nephrogenic DI
amiloride
high anion gap metabolic acidosis
MUDPILES methanol uremia diabetic ketoacidosis propylene glycol iron tablets or INH lactic acidosis ethylene glycol salicylates (late)
Renal tubular acidosis
type 1 (distal): decreased H excretion, pH>5.5 and increased Ca stones, hypokalemia type 2 (proximal): decreased HCOs reabsorption, pH5.5, decreased aldo response
determining acid base problems
bicarb follows pH in metabolic causes
pCO2 is opposite pH in respiratory causes
CSF changes in Guillain-Barre
albumino-cytologic dissociation
increased protein with normal cell counts
rash on palms and soles
secondary syphilis
rocky mountain spotted fever
coxsackie A virus
kawasaki disease
features of nephrotic syndrome
proteinuria > 3.5 g/day
hypoalbuminemia
peripheral edema
glomerular histology reveals multiple mesangial nodules
diabetic nephropathy
linear patterns of IgG deposition on IF
Goodpasture syndrome
lumpy-bumpy deposits of IgG, IgM, and C3 in the mesangium
poststreptococcal glomerulonephritis
deposits of IgA in the mesangium
IgA nephropathy (Berger’s)
anti-GBM antibodies, hematuria, hemoptysis
Goodpasture syndrome
nephritis, deafness, cataracts
Alport syndrome
crescent formation in glomeuli
rapidly progressive glomerulonephritis
wire-loop appearance on EM
lupus nephritis
most common nephrotic syndrome in children
minimal change disease
most common nephrotic syndrome in adults
focal segmental glomerulosclerosis (FSGS)
Kimmelstiel-Wilson lesions (nodular glomerulosclerosis)
diabetic nephropathy
EM: effacement of epithelial foot processes
minimal change disease
nephrotic syndrome associated with hepatitis B
membrano-proliferative glomerulonephritis (MPGN)
nephrotic syndrome associated with HIV
FSGS
EM: subendothelial humps and tram-track appearance
membrano-proliferative glomerulonephritis (MPGN)
LM: segmental sclerosis and hyalinosis
FSGS
purpura on back of arms and legs, abdominal pain, IgA nephropathy
Henoch-Schonlein purpura
apple-green birefringence with Congo-red stain
Amyloidosis
EM: spiking of the GBM due to electron dense subepithelial deposits
membranous nephropathy
nodular hyaline deposits in the glomeruli
Kimmelstiel-Wilson nodules (diabetic nephropathy)
glomerulonephritis plus pulmonary vasculitis
granulomatosis with polyangitis (Wegener’s)
or Goodpasture Syndrome
WAGR complex
Wilm’s tumor
aniridia (no iris)
genitourinary malformation
mental/motor retardation
risk factors for transitional cell carcinoma
smoking, aniline dyes, cyclophosphamide
classic features of drug-induced acute interstitial nephritis
fever, rash, hematuria, CVA tenderness
eosinophilia
azotemia
what changes will be seen in a BMP in a pt with renal failure
hyperkalemia
hypocalcemia
increased BUN and Cr
most common tumor of the urinary tract
transitional cell carcinoma
most common renal malignancy of early childhood
Wilm’s tumor
fever, rash, hematuria and eosinophilia
acute interstitial nephritis
red cell casts
acute glomerulonephritis
waxy casts
chronic renal failure
thyroid-like appearance of kidney
chronic pyelonephritis
most common renal tumor
renal cell carcinoma
most common type of renal stone
calcium
type of renal stone associated with Proteus vulgaris (also Klebsiella)
struvite stones (staghorn calculi)
drugs that cause acute tubular necrosis
aminoglycosides, cephalosporins, polymyxins
BUN/Cr >20 with decreased RBF
prerenal azotemia
