renal block 2

what makes someone high risk for AKI?

1. critical illness

2. nephrotoxic drugs

3. radiocontrast agents (IV contrast)

whats an angiogram?

radio contrast

how do you limit nephrotoxin exposure?

1. stop taking aminoglycosides, amphotericin B (if possible)

2. use a low osmolar IV contrast dye

prevention dose for IV volume expansion and who should receive it?

critically ill, non-hemorrhagic shock patients

• 0.9% NaCl 1.0-1.5 mL/kg/hr for 3-12 hours before and 6-12 hours after contrast exposure

• sodium bicarbonate 3 mL/kg/hr 1 hr prior and then 1 mL/kg/hr for 6 hours after

what is n-acetylcysteine used and dosage?

• used for prevention alongside IV isotonic crystalloids

• 600-1200 mg bid day before and day of

carbonic anhydrase inhibitor drug example

acetazolamide and diamox

where is carbonic anhydrase found?

in the luminal/basolateral membranes and cytoplasm

common molecular moiety of carbonic anhydrase inhibitor?

sulfonamide

carbonic anhydrase inhibitor moa

• no Na/H exchange → increases Na, H2o, and bicarbonate in urine

• Block carbonic anhydrase in the proximal tubule → ↓ NaHCO₃ reabsorption → ↑ sodium, bicarbonate, and water excretion.

carbonic anhydrase inhibitor uses

altitude sickness and secondary glaucoma

osmotic moa

• creates an osmotic driving force inside the tubular lumen, keeping the water from leaving

• increases excretion of all electrolytes (Na, K, Ca, Mg, Cl, HCO)

osmotic drugs

mannitol and urea

osmotic drug uses

• dialysis equilibrium (mannitol)

• glaucoma

• reduction of cerebral edema pre/post neurosurgery

loop diuretic moa

blocks Na/K/Cl cotransporter in the thick ascending limb in loop of henle

common side effect of loops?

hypokalemia

therapeutic uses of loops?

pulmonary edema, heart failure, and hypertension

thiazide moa

• inhibits the na/cl cotransporter

• Na remains in tubular fluid along with water

thiazide side effect?

hypokalemia

thiazide structure

sulfonamide and benzothiadiazine

thiazide effect on urinary excretion

• increases excretion of Na and Cl

• weak CA inhibitors and increase HCO3 excretion

potassium sparing moa spironolactone

• synthetic aldosterone antagonist competing with aldosterone

• cant induce luminal production of NA/K exchangers in late distal tubule and CD

amiloride and triamterene moa

blocks Na transport chains in late distal and CD

negative of furosemide?

variable oral bioavailability and ototoxicity

causes of diuretic resistance

• excessive sodium intake

• inadequate dosing

• reduced oral bioavailability

• nephrotic syndrome

• reduced renal blood flow

oliguria

50-500 ml/day

HMG Co-A reductase for AKI prevention

not really beneficial unless pt is already on a statin

theophylline

• not suggested

• adenosine antagonist causes vasodilation and improves renal blood flow

dopamine

• not recommended

• increases urine output but no benefit over properly hydrating

fenoldopam

• not recommended

• hypotension risk

diuretic prophylaxis

• don’t use HARMFUL

• overcompensates flow

insulin prophylaxis

• can have a direct protective effect

• 110-149 mg/dl

TREATMENT hypovolemic volume management

0.9% NaCl 250-500 mL IV over 15-30 min

TREATMENT hypervolemic volume management

• reduce IV fluids (20-50 mL/h)

• consider diuresis

TREATMENT furosemide

40-80 mg IV/PO and increase by 20-40 q 6-8 h

TREATMENT torsemide

10-20 mg IV/PO, double dose q2 h

most common cause of CKD

DIABETES then hypertension

uremia

final stage of CKD

• waste products accumulate in blood due to kidney failure

stage 1 gfr

90+

stage 2 gfr

60-89

stage 3 gfr

30-59

stage 4 gfr

15-29

stage 5 gfr

<15 (uremic syndrome)

as GFR decreases what is the effect on PTH, FGF-23, and vit D?

• PTH and FGF increase

• vit d decreases

does phosphate increase or decrease with gfr?

excretion decreases so there is a retention of phosphate

fgf-23 function

to get rid of phosphate (the more fgf → increase in phosphate excretion)

PTH function

raises blood calcium

• increases CA reabsorption

which drugs can impact renal blood flow?

NSAIDs, ACEi, SGLT2i, cyclosporine, and tacrolimus

if CrCl is <20 mL/min, how does it effect diuretics?

thiazides will lose effectiveness (except metolazone (zaroxolyn))

indications for acute renal replacement therapy?

• acid base abnorm → acidosis

• electrolyte imbalance

• intoxication

• fluid overload (edema)

• uremia, pericarditis

uacr range?

less than 30

t/f anemia is side effect of stage 3/4

true

carbonic anyhdrase site of action

PCT

which calcium based binder is more effective?

calcium acetate

sevalemer carbonate

lowers LDL

• use in extraskeletal calcification

• risk of metabolic acidosis

• cipro and mycophenlate interaction possibly

calcium carbonate is more soluble in __

acidic environments

which iron based binder in better long term?

sucroferric oxyhydroxide