- thick ascending limb of Henle
- Na/K/2Cl transporter inhibitor
- ex: furosemide, bumetanide, ethacrynic acid
loop diuretics
- distal tubule
- Na/Cl cotransporter inhibitor
- chlorothiazide, benzothiadiazine, metolazone
thiazide type diuretic
- principal cells of collecting tubule
- spironolactone antagonist of Aldosterone, others Na channel blocker
- ex: spironolactone, amiloride, tramtirene
K+ sparing diuretics
- proximal tubule
- carbonic anhydrase inhibition, bicarb reabsorption reducer
- ex: acetazolamide, methazolamide
carbonic anhydrase inhibitor
- all tubule segments
- create osmotic gradient
- ex: mannitol
osmotic diuretics
sudden decreases in kidney function that lead to fluid imbalance, electrolyte problems, accumulation of nitrogen waste
-complications: pulm edema, hyperkalemia (arrhythmias, metabolic acidosis, confusion)
acute kidney injury
decreased perfusion, no immediate damage, blood shunted away and decreases GFR
-caused by low CO, MI, dehydration, vasodilation
pre-renal acute kidney injury
damage to blood vessels, glomeruli, tubules, intersititum
- large vessels: obstruction due to cholesterol, hypertrophy, tearing, clot in vein
- small vessels: glomerulonephritis, hemturia, vasculitis, HTN, clots
- tubules: acute tubular necrosis, due to nephrotoxins (myoglobin, uric acid crystals, chemo, contrast dyes)
- interstitium: infectious, allergic nephritis common with antibiotics, WBC casts
intra-renal acute kidney injury
obstruction of urine, reversible
- due to stones, tumors, enlarged prostate, seen by renal US
- asymptomatic if unilateral
Post-renal acute kidney injury
hyperkalemia (wide QRS), pulmonary edema unresponsive to diuretics, seizures, aspirin OD, severe metabolic acidosis
indications for hemodialysis
- polyuria, dehydration, hypokalemia, glucosuria, metabolic acidosis
- caused by genetics (glycogen storage, Wilson’s), heavy metals, tetracyclines, toluene
- damage proximal tubule (Na/K/ATPase)
Fanconi syndrome
- defect in chloride transporter
- polyuria, poor muscle tone, heart problems, hypokalemia, alkalosis, hypocalciuria
- overuse of furosemide diuretics, Na/K/2Cl defect
Bartter syndrome
- affects distal tubule, NaCl defect, ECF contraction
- hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria
- thiazide diuretic overuse
Gitelman syndrome
-overaction of Enac, ECF expansion, HTN, decreased renin-ald, metabolic alkalosis
Liddle syndrome
- V2 receptor or aquaporin mutation, non repsonsive to ADH
- excessive water intake –> polyuria, dilute urine, dehydration
- caused by lithium, affects collecting duct
nephrogenic diabetes insipidus
- proximal and collecting duct, decreased pH, muscle weakness, kidney stones, bone resorption, growth retardation
- mutation in Na/H exchanger or proton pumps and carbonic anhydrase
tubular acidosis
