Renal Flashcards
RPF
FF = GFR/RPF PAH = estimate
Filtered load =
FL = GFR * Px
{GFR NOT CLEARANCE!]
AA in urine with vs without proline, hydroxyproline, and arginine
With = Fanconi's anemia (NO AA abs in PCT) without = hartnups (neutral AA only) - pellagra
Fanconi anemia s/s and causes
S/s: prox. renal tubular metabolic ACIDosis
Causes: wilsons, tyrosinemia, glycogen storage diseases, expired tetracyclins, tenofovir, multiple myelomas, ischemia, lead poisoning
order of renal tubule defects:
fanconi barters Gitelman Liddle - GOF; AD S.I. mineralocorticoid excess
Adrenergic R on JG cells
Beta-1
7 effects of Ang-II
Peripheral VC (AT1)
Renal efferent VC
Aldosterone release
ADH release
Thirst
increases PCT Na//H activity (can cause CONTRACTION ALKALOSIS)
Limits reflex bradycardia (via baro-R modulatoin) to maintain BV and BP
macula densa pathway: INCREASED NaCl
high NaCl to macula densa (DCT) –> cells swell –> release adenosine –>
1) A1-R: afferent VC
2) A2-R: efferent VD
3) DECREASED JG release of renin
protaglandins in the kidney
VD afferent
[block with NSAIDs decreases GFR –> ARF]
Hyper vs hypo Mg
HypoMg = tetany, torades, hypokalemia
HyperMg = decreased DTRs, lethargy, hypotension, bradycardia, cardiac arrest, hypocalcemia
Normal anion gap (8−12 mEq/L)
HARD-ASS: Hyperalimentation Addison disease Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion
high anion gap (>12)
MUDPILES: Methanol (formic acid) Uremia Diabetic ketoacidosis Propylene glycol Iron tablets or Isoniazid Lactic acidosis Ethylene glycol (oxalic acid) Salicylates (late)
Type I renal tubular acidosis (distal)
CD, high urine pH
Alpha-intercalated cant secrete H+ → retain H+ and lose K+
high urine pH + increased bone turnover predisposes to stones
Causes:
amphoteraxcin B, analgesic nephropathy, urinary tract obstructions
Proximal/Type 2 renal tubular acidosis
PT, low urine pH
Defective PCT HCO3- absorption @BL → cant resorb Na with it (Na/HCO3 cotransport) → Na gets resorbed at CD, so K+ lost
K+ tries to get resorbed in exchange for H+ @ alpha-intercalated (K//H) → acidifies urine despite metabolic acidosis!
Causes:
Fanconi syndrome, CAH inhibitors (acetazolamide)
Hyperkalemic (type 4) renal tubular acidosis
Hypoaldosteronism, hyper K+, low pH urine
No aldosterone → save K+ → can’t exchange for H+ out acidemia
High cellular K+ also decreases PCT NH3 synthesis decreasing urine NH4+ levels → acidic urine
Causes:
- hypoaldosteronism (ACE-I, ARB, NSAIDS, DM hyporeninism, adrnal insufficiency, heparin, cyclospirin)
- Aldosterone resistance (K+ sparing diuretics, obstructoin nephropathy, TMP/SMX)