Renal Flashcards
Faconi Syndrome
generalized reabsorption defect in PCT
may lead to met acidosis due to increased excretion of hco3 po43 and all substances reabsorbed by the pct
bartter syndrome
reabsorption defect in thick ascending loop of henle affects na+/K+/2cl- cotransporter
gittelmann syndrome
reapsorption defect of nacl in dct
little syndrome
gain function mutation, increases the activity of na+ channels causing met alkalosis, hypokalemia,
Rapid progressive (crescentic) gemerulonephrits
LM? IF? antibodies?
disease associ?
poor prognosis, crescent on LM which contain fibrin and plasma proteins.
Linear IF due to antibodies in the basement membrane and aveolar basement membrane
: goodpastures syndrome: hematuria/ hemoptysis; type 2 hypersensitivity reaction.
Treatment is plasmaphoresis
Negative IF/ pauci- immune: Granolomatosis with polyangiitis (Wegner) PR3-Anca/cAnca
or microscopic polyangitis MPO-ANCA/p-ANCA
Acute poststreptocococal glomerulonephritis
more in children, poststrep (pharynx or skin) type 3 hypersensitivity,
LM: hypercellular enlarged glomeruli
IF: starry sky lumpy bumpy due IgG, IgM, C3 deposition along GBM and mesangium
EM: subepithel IC humps
Nephrotic syndrome
damage GBM, massive proteinurea: >3,5, hypoalbuminemia, edema, hyperlipidemia. Dysruption of glumerolar filtration charge barriar by 1° direct eg slerosis of pedocytes, 2° sytemic process eg diabetes
MCD, minimal chage disease (liopoid nephrosis)
Nephrotic syndrome in children, often triggered by recent infection, vaccination
LM: Normal glomeruli
IF: -
EM:-effacement of podocyte foot processes
FSG, focal segmental glomerulosclerosis
Nephrotic syndrome in african and hispanics. idiopathic, HIV; SS,herion, obesity, does not respond to steroids, progress CKD
LM- segmantal sclerosis and hyanlinosis
IF-often- but may be + for non specific focal deposits like IgM, C3, C1
EM:- effacement of foot processes similar to minimal change disease
Membranous nephropathy
is due to? is most common in? LM, IF, EM?
Nephrotic syndrome, also called membranous glumerolonephritits, Can be 1° eg antibodies to phospholipase A2 receptor or 2° to drugs eg NSAIDS, infections eg HPV, HCV, SLE or sloid tumors, does not repond to steroids
LM: diffuse cap. and GBM thickining
IF:- granular due immune complex IC deposition
EM- “Spike and dome” appearance of subepithelial deposits
Amyloidosis
kidney most commonly involved organ. chronic condition prediposis the deposition.
LM: Congo red stain shows apple green birefringence under polarized light due amoyloid deposition in mesagium
diabetic glomerulonephopathy
most common cause in the US, hyperglycemia, glycation of tissue, mesangial expasion, GBM thickining—-> increase in permeability, GFR increases, HTN—–> glumerolusclerosis
LM: -mesangial expasion, GMB thickining, eosinophilic nodular glomerulosclerosis (kimmelstil-Wilson lesion)
Nephritic syndrome
Inflammatory process. involves glomeruli, leads to hematuria and RBC casts in urine. Associated with Azotemia, oliguria, hypertension (due to salt retention), porteinuria, hypercellular/ inflamed glomeruli on biobsy
diffuse proliferative glomerulonephritis
often SLE. DPGN and MPGN often presnt as nephrotic syndrome and nephritc syndrome concurrently
LM- wire lupes of capillaries
IF granular, EM-subendothlial and sometimes intramembranous IgG based IC often with C3 deposition
alport syndrome
mutation in type 4 collagen, thikining of the GBM—> eye problems etc
membranoproliferative glumeronephrits
MPGN in a nephritic syndrome that often co-presents with nephrotic syndrome.
Type 1 may be 2° to hepatitis B/C, iodiopathic, suendothelial IC deposits with granular IF
Type 2 is assc. with C3 nephritic factor (IgG autoantibody that stabilizes C3 convertase—> persistent complement activation—> decrease in C3
Intramembranous deposits, also called dense deposit disease, mesangial ingrowth—-> GBM splitting—> “tram-track”
BGA ph, co2
ph: acid.<7,4> alca.
Co2: “< 40>”
when we have met. alkalosis we need to look at?
Anion GAP: AG acidosis>12< NON Gap
Def of Anion GAP: Na-CL-CO2
What causes an AG acidosis?
MUD PILES
Methanol, Uremia, DKA, Pro, Isopropyl, Lactic acid, Ethylene salicylates
what needs to be checked if there is a NON GAP?
Urine Anion Gap
If UAG is negative, it will be due to dirrhea: loss of bicarbs and volume
what is the UAG?
Urine Anion Gap: Na+-K-CL
if it is positive, it means there is RTA (renal tubular acidosis)
what needs to be checked if you have met. acidosis
UCL >10<
>10 not volume resposive—->HTN in present—> hyperaldosteron, if no HTN then barter or gittleman
if <10 it is due to dehydration
RBC casts
glomerulonephritis
WBC casts
pyelonephritis, transplant rejection, tubulointeristial inflammation
Fatty casts
nephrotic syndrome
granular casts
acute tubular necrosis “muddy casts”
waxy casts
end-stage renal disease/chronic kidney disease
hyline casts
nonspecific
acute tubular necrosis
3 stages: inciting, maintenance: oligiuric, recovery: polyuric, electrolyte wasting
divided by into: ischemic and nephrotoxic
renal papillary necrosis
SS and gross hematuria
acute interstitial necrosis
also called tubulointerstial nephritis. AIT inflammation. Pyruria: eosinophils and azotmia 2° eg Sjörgen, SLE
remember the Pś Pee: diurecis Pain: NSAIDS Penicillins and cephalosporins PPI RifamPin
Polycystic kidney d.
dominant: above 45, recessive in infancy
supply of the ureter
prox. -renal artery,
middle-gonadel artery, aorta,common internal iliac
distal- internal iliac and sup.vesical
horseshoe kidney
trapped under the inferior mesenteric
renal oncytoma
Benign epithelial tumor arises from the collecting duct, large eosinophilic cells with abundant mitochondria
renal cell carcinoma
originates from th PCT, polygonal clear calls, lipids and carbohydrate accumulation- flank pain, painless hematuria, VHL, RCC Chromosome3 delition
PEAR= PTHrP, Ectopic EPO, ACTH, Renin
Nephroblastoma
aka Wilms tumor, children2-4, flank mass, hematuria and poss. HTN. WT1 or WT2 gene on chromosome 11
Denys-Drash and Bechwith-Wiedemann syndrme
Oxybutynin
for the overactve bladder
overflow incontinence
incomplete emtying, outlow obtrction alpha-blocker for prostate
Mannitol
pulmonary edema, containdicated in HF and anuria
Acetazomide= ACIDazolamide
CA inhibitor, decreases HCO3. Use: glaucome, metabolic alkalosis, altitude sickness
works on PCT
Loop diuretis
Sulf. diuretics inhibit cotransport sytem NA+/K+/CL-, of the thick acending limb of loop of H.
Ethacrynic acid
Non-sulf. inhibitor of co.trans. sys. NA+/K+/CL-thick acending limb
Thiazid
inhibit Nacl reaption in DCT and decresase the Ca excretion
postassium sparing -one
SEAT, Spiro-, Elpranone, Amiloride, Triamtere work on the cortical collecting tubule
ACEI
-pril, decreases ATll, dereases GFR
ARBs
-sartan, blocks ATll rezeptor, can cause hyperkalimia, decrease GFR
Alikiren
Alikiren kills renin, therefor blos angiotensinogen to ATl conversion, use is hypertension
FF=
GFR/RBF
calcium stones shape
calcium oxalat: hypocitraturia, shaped like a dumbbell or envelope, Crohn, treat with thiazides
Ammonium magnesium phosphate stones
looks like a coffin, caused urease producing bacteria: proteus, staph sapro. and kelbsiella
Uric acid stones
rhomboid or resettes, assoc. with hyperuricemia, tret with allopurinol
Cystine stone
hexagonal, auto. ress. cystine-reab. PCT transporter defect, causing cytinuria causing and COLA urine= Orinitine, Lysine, Arginine
the vessel palpable in the pelvis next to the ureter?
is the internal pelvic artery
clearence is calculate by?
c=urine concentration X urine flow I/ plasma concentration
C= UC X I/ PC
what is a derivative of methanephric blastoma
PCT
