Flashcards in Renal Deck (90):
What happens to : Pronephros, Mesonephros, Metanephros
Pronephros: degenerates at week 4
Mesonephros: degerates and creates ureteric bud (ureter, pelvises, calyces, collecting duct) and male genital sytem
Most common site of fetal renal obstruction
What is Potters sequence/syndrome?
oligohydramnios -> compression of fetus -> limb deformities, facial deformities, and pulmonary hypoplasia
What etiology of Potters?
babies can't Pee (potters). ARPKD, posterior urethral valves, renal agenesis
What is horseshoe kidney?
bottom of kidneys fuse while in pelvis. when they ascend from the pelvis they get stuck on the inferior mesenteric artery but work just fine.
What is horseshoe kidney associated with?
turners syndrome (a single x chromosome)
What causes multicystic dysplastic kidney ?
abnormal interaction between ureteric bud and metanephric mesenchyme
water under the bridge. ureters under uterine artery/ductus deferens. all retroperitoneal
tells you GFR cause it is filtered out but not secreted or resorbed at all
Glomerulous filter components
fenestrated capillary endothelium (size), heparan sulfate basement membrane (negative charge barrier), epithelial podocyte foot processes
both filtered out and entirely secreted so it measures total glomerulous flow rate
normal filtration fraction
effect of prostaglandins on filtratin
(paracrine) dialate afferent ateriole -> more RPF and GFR but FF static
effect of Angiotensin II on filtration
constricts efferent arteriole. decrease RPF, increase GFR and FF
where and how is glucose resporbed? exceptions?
Na cotransport in PCT 100%. uncontrolled diabetes and normal pregnancy
nephrogenic cause of pellagra and symptoms
deficient sodium-tryptophan transporter -> low W -> cant make niacin -> dermatitis, diarrhea, disturbed (mental)
PTH effect on nephron
inhibit na/phosphate coreuptake in PCT, enhance calcium/sodium coreuptake in DCT
AT II effect on PCT
stimulates Na/H antiport -> acidify urine, more CO2/bicarb uptake, Na uptake, water uptake
loop diuretics hit?
triporter (Na/K/2Cl) of Thick ascending loop
What does aldosterone modulate in nephron?
Aldosterone inserts mineralocorticoid Na-channel on lumin of collecting duct. Na goes in exchanged for H and K.
what does ADH do to the nephron?
inserts aquaporin in collecting tubule
describe renin-angiotensin-aldosteron system
(liver) angiotensinogen --(renin/kidney)--> angiotensin I --(ACE/kidney/lung)--> Angiotensin II --> Aldosterone release (adrenal) and ADH (posterior pituitary)
effects of Angiotensin II
vasoconstriction (up BP), constrict efferent arteriole, Aldosterone release from adrenal, ADH release from posterior pituitary, PCT Na/H antiport (absorb Na/bicarb/water), stimulate thirst, limits reflex bradycardia
what inhibits bradykinin?
what upregulates renin?
low BP (JG cells), low sodium (macula densa), high sympathetic tone
released from atria due to high volume to relax smooth mucles via cGMP and increase GFR and lower renin. No compensatory Na reabsoption
afferent arteriole release renin
macula densa cells
distal convoluted tube sense NaCl
kidney effects RBCs by
kidney processing of vitamin D
converts 2,5-oh vit D ---(1alpha-hydroxylase)--> 1,2,5 oh which is active form. parathyroid hormone activates
What shifts K out of cells?
DO Insulin LAB(eta): digitalis, hyperOsmolarity, Insulin deficency, Lysis of cells, Acidosis, Beta adrenergic antagonist
Serum Na high/low symptoms
low: nausea, malaise, stupor, coma.
high: irritability, stupor, coma
Serum K high/low symptoms
low: U waves on ECG, flattened T waves, arrhythmias, muscle weakness
high: wide qrs, peaked T waves, arrhythmias, muscle weakness
Serum Ca high/low symptoms
low: tetany, seizures
high: Stones, bones (pain), groans (ab pain), psyc overtones (anxiety, odd)
Serum Mg high/low symptoms
low: tetany, arrhythmias
high: decreased reflexes, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
Serum Phosphate high/low
low: bone loss, osteomalacia
high: renal stones, metastatic calcifications, hypocalcemia
Metabolic acidosis labs
pH low, pCO2 low, HCO3 low (hyperventalation response immediate)
pH high, pCO2 high, HCO3 high (hypoventalation response immediate)
pH low, pCO2 high, HCO3 high (bicarb renal retention delayed)
pH high, pCO2 low, HCO3 low (renal response)
What is anion gap and what is abnormal?
Anion gap = Na - (Cl+HCO3). normal is 8-12
anion gap metabolic acidosis etiology
MUDPILES: Methanol, Uremia, Diabetic Keto, Propylene glycol, Iron tablets, Lactic acidosis, Ethylene glycol, Salicylates
non-anion gap metabolic acidosis etiology
HARD ASS: Hyperalimentation, Addisons Disease, Renal tubular acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion
Renal tubular acidosis type 1
distal: collecting duct can't excrete H. hypokalemia. calcium phosphate kidney stones. urine pH > 5.5
Renal tubular acidosis type 2
proximal: PCT cant reabsorb HCO3. Seen in fanconi syndrome. urine pH
Renal tubular acidosis type 4
hyperkalemic: hypoaldosterone or response of collecting tubule -> can't secrete K. high K = can't release ammonia to buffer -> acidic pee
casts in urine
means is from the kidney
glomerulonephritis, ischemia, malignant hypertension
tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
fatty casts "oval fat bodies"
granular casts "muddy brown"
acute tubular necrosis
advanced renal disease/kidney failure
nonspecific, even normal
Focal segmental glomerulosclerosis. type, LM, EM
#1 nephrotic. LM: segmental sclerosis/hyalinosis. EM: foot process effacement (same as minimal change).
Focal segmental glomerulosclerosis associations
HIV, heroin, massive obesity, interferon
Membranos nephropathy type, LM, EM, IF
#2 Nephrotic. LM: diffuse capillary and GBM thickening. EM: "spike and dome" subendothelial deposits. IF: granular. This is SLE nephrotic (also idopathic or drug-induced)
Minimal Change disease
Children Nephrotic. LM: normal. EM: foot process effacement. Loss of albumin not globulins cause GBM anions gone.
Nephrotic LM: congo red shws apple-green birefringence. associated with chronic conditions.
Type I: subendothelial immunocomplex deposits. granular IF "tram-track". associated HBV, HCV
Type II: intramembranous IC "dense deposits". Associated C3 nephritic factor
Nephrotic. Nonenzymatic glycosylation of GBM and efferent arteriole. LM: mesangial expansion/gbm thickening/glomerulous eosinophilic nodules (Kimmelstel-wilson)
Acute poststreptococcal glomerulonephritis: LM, EM, IF, epidemiology
Nephritic. LM: large gloms, neutrophils, "lumpy-bumpy". EM: subepithelial IC. IF: granular. seen in kids w/ periorbital edema, dark urine.
Rapidly progressive glomerulonephritis causes
Nephritic or Nephrotic. Goodpastures, wegeners, microscopic polyangiitis
goodpastures hypersensitiveity type, IF, antibody targets
type II, kidney and lung basement menbrane antibodies, linear IF
Wegeners vs microscopic polyangitits
Both RPGN. Wegeners (c-ANCA) vs Microscopic Poly Angitis (p-ANCA)
IgA nephritic syndrome. Purpura, URI, GI-itis. LM: mesangial proliferation. EM: mesangial IC. IF: IgA IC deposites
Nephritic. Mutation in type IV collagen(x linked) -> BM splitting. Nephritis/deafness/eye problems
Kidney stone types
calcium, ammonium/magnesium phosphate, uric acid, cystine
which kidney stones are opaque vs lucent
opaque: calcium, ammonium magnesium phsphate, cystine
lucent: uric acid
vitamin c cause what kinda stones
ethelene glycol (anti freeze) stones type
urease-positive bugs cause what kinda stones?
staghorn calculi stones?
ammonia stones. serve as plateform for uti
#1 renal cancer?
Renal cell carcinoma
genetic association with renal cell carcinoma?
Chrom 3 deletion (VHL syndrome)
renal cell carcinoma presentating symp
hematuria, mass, pain. paraneoplastic syndrome cause EPO (polycythemia), ACTH, PTHrp. often presents with mets cause retroperotoneal
renal cell carcinoma histology and age group
PCT cells: polygonal, lots of lipids (clear). Men 50-70 with smoking and obesity
renal cell carcinoma treatment
resection, resistant to chemo and radio
Wilms tumor (nephroblastoma)
childhood renal cancer. embryonic glomeruli. due to deletion of WT1 gene on Ch 11.
WAGR complex (brandon your a warg!)
Wilms tumor, aniridia (no iris), genitourinary malformation, retardation
Transitional cell carcinoma
urinary tract cancer. painless bloody pee.
Pee SAC: Phenacetin, Smoking, Aniline dyes, Cyclophosphamide
thyroidization of the kidney
Drug induced interstitial nephritis
occurs a week or two later with eosinophile urine, azotemia.
diffuse cortical necrosis
bilateral widespread infarction. associated with obstetric catastrophes (abruptio placentae)
High urine bun and low serum creatinine
Urine osmolality > 500 (normal)
Urine Na 20% (high)
Kidney is working to conserve volume
Intrinsic renal failure
BUN is high cause kidneys are fucked
Urine osmolality 40 (normal)
FeNa >2% (high)
BUN is high cause cant excrete
can't make activated vitamin D, hypocalemia, and hyperphosphatemia so bones thin. also has secondary compensatory hyperparathyroidism
cysts destroy kidney. PKD1 or PKD2 genes. Associations: berry aneurysms, mitral valve prolapse, benign hepatic cysts