-
Molecules transported from blood into urine via capillaries at the glomerulus
Filtration
-
Molecules transported from urine back into blood
Reabsorption
-
Molecules transported from blood into urine via capillaries along the tubule
Secretion
-
Role of the Kidney
- Excretion of waste products and foreign substances
- Fluid and electrolyte balance
- Arterial blood pressure control
- Acid-base balance
- Erythropoietin and vitamin D production
-
Proximal tubule action site for what meds
- Carbonic anhydrase inhibitors (acetazolamide)
- Osmotic diuretics (mannitol)
-
proximal tubule reabsorption of
- Water and sodium primarily
- 67% of sodium reabsorption occurs here
- Glucose
- Bicarbonate
- Chloride
- Potassium
- Amino acids
- Urea
- Phosphorus
-
proximal tubule secretion of
- Diuretics
- antibiotics
- creatinine
- uric acid
-
descending loop of henle reabsorption of
- Water alone
- Impermeable to sodium and chloride
-
descending loop of henle secretion of
urea
-
descending loop of henle action site for what medications
none
-
ascending loop of henle reabsorption of what
- Na+/K+/2Cl- cotransport
- Sodium (25% reabsorbed here)
- Potassium, chloride
- Calcium, magnesium, bicarbonate
- Impermeable to water
-
ascending loop of henle secretion of
nothing
-
ascending loop of henle action site for what meds
- Loop diuretics
- Furosemide
- torsemide
- bumetanide
- ethacrynic acid
-
distal convoluted tubule reabsorption of
- Na+/Cl- cotranpsport
- Sodium (5% reabsorbed here)
- Water- Follows sodium out of tubule
- Chloride
- Na+/Ca2+ cotransport
- Calcium
-
distal convoluted tubule secretion of
none
-
distal convoluted tubule action site for what meds
- Thiazide diuretics
- Hydrochlorothiazide
- chlorthalidone
- indapamide
- metolazone
- chlorothiazide
-
loop vs. thiazide diuretics
- Thiazide
- Ineffective if CrCl<30
- Exception: Metolazone
- Na+ excretion > H2O
- Best for HTN > edema
- Loop
- Effective if CrCl <30
- H20 excretion > Na+
- Best for edema > HTN
-
collecting duct reabsorption of
- Sodium (30% reabsorbed here)
- Water
- Bicarbonate, urea
-
collecting duct secretion of
- Potassium via Na+/K+-ATPase pump
- Major site for potassium secretion
-
collecting duct action site for what meds
- Potassium-sparing diuretics: Triamterene, amiloride
- Aldosterone antagonists: Spironolactone, eplerenone
- Vasopressin (ADH, AVP): Stimulates water reabsorption
- Vasopressin-2 antagonists: Tolvaptan, conivaptan: Opposes water reabsorption
-
3 negative effects of the RAAS
- Indirect vasoconstriction via sympathethic stimulation
- Increased contractility of the heart
- Vascular and myocardial hypertrophy
-
2 positive effects of RAAS
- Increased aldosterone
- Potent and direct arteriole constriction
-
2 strategies for diuretic resistance
Change to continuous IV infusion of loop diuretic
- Add-on diuretic that acts at later stage of nephron
- Thiazide diuretic
- Metolazone very potent
- Aldosterone antagonist
- Spironolactone
- Triamterene or amiloride
-
renal function test used in obese population
salazar-corcoran
-
renal function test used in pediatric pts
schwartz
-
normal BUN SCR ratio
15:1
-
guidelines on which weight to use
- Less than their ideal body weight
- Use actual (total) body weight
- 100-130% of their ideal body weight
- Use ideal body weight
- >130% of their ideal body weight
- Use adjusted body weight
- Adjusted body weight = ((Actual weight – IBW) x0.4) + IBW
-
anuric
less than 50 mL in the past 24 hours
-
oliguric
50-500 mL in the past 24 hrs
-
non-oliguric
>500 mL in the past 24 hrs
-
3 cases where cockroft-gault is overestimating
- Rapidly rising SCr
- If SCr rises by 0.5 mg/dl or more in a 24-hour period, assume that CrCl is less than 10 ml/min
- Malnourished
- Elderly
-
3 cases where cockcroft-gault is underestimating
- Rapidly falling SCr
- High protein diet or use of creatine supplements
- High muscle mass (bodybuilders
-
Acute Kidney Injury (AKI)
- Rapid deterioration in renal function over a short time-frame
- Often see abrupt changes over 48 hours or less
- Usually reversible
-
Chronic kidney disease
- Prolonged kidney damage that occurs for more than 3 months
- Often progressive in nature and irreversible
-
4 risk factors for acute kidney injury
- Pre-existing chronic kidney disease
- Volume depletion
- Decreased fluid intake, vomiting, diarrhea, diuretic use
- Effective volume depletion
- Congestive heart failure, cirrhosis with ascites
- Use of nephrotoxic medications
- More details to come
-
RIFLE criteria
Risk - 1)increase in SCr to 1.5 times higher than baseline. 2)GFR decreased by greater than 25%. 3)<0.5 ml/kg/hr output for 6 hrs
Injury - 1)increase in SCr to 2 times higher than baseline. 2) GFR decreased by greater than 50%. 3) <0.5 ml/kg/hr output for 12 hours
Failure - 1)increase in SCr to 3 times higher than baseline OR rise to >4mg/dL OR >0.5 mg/dl rise in a 24-hour period. 2) GFR decreased by greater than 75% 3) <0.3 ml/kg/hr output for 24 hrs or no uring production for 12 hrs
Loss - Failure for >4wks
End-stage kidney disease - failure for >3 months
-
Most common cause of acute kidney injury
Pre-renal AKI
-
Results from decreased perfusion of blood to the kidney
pre-renal AKI
-
Pre-renal AKI Causes
- true decrease in blood volume
- relative decrease in blood volume
- renal ischemia
-
Treatment of Pre-renal AKI
- Usual goal is to increase intravascular volume
- Hydration with IV fluids
- Crystalloids (NS, D5W) or colloids (albumin, hetastarches)
- Example: Normal saline 75-125 ml/hr.
- Blood products if bleeding
- Packed red blood cells (PRBC)
- Usually reversible with rapid improvement if caught early
-
which drugs dilate the efferent arterioles
-
which drugs constrict the afferent arterioles
- NSAIDS
- cyclosporine
- tacrolimus
-
Acute kidney injury accompanied by structural damage to the kidney
intrinsic AKI
-
Drug-Induced ATN Prevention
- aminoglycosides
- amphotericin B
- cisplatin, carboplatin
-
Contrast-induced nephropathy prevention
- intravenous hydration
- hold nephrotoxic agents and diuretics
- use iso-osmolar or low-osmolar contrast and use the lowest volume necessary
-
Interstitial edema secondary to inflammation without involvement of the glomerulus or tubules
Acute Interstitial Nephritis (AIN)
-
hallmarks of acute interstitial nephritis
- UA often with protein, WBCs, RBCs, and WBC casts
- Classic triad is rash, fever, and eosinophiluria
- Eosinophils in urine (>1%) has a high specificity (negative predictive value)
-
causes of acute interstitial nephritis
- Drug-induced (>75%) of cases
- Infection
-
Drug-induced AIN
- Antibiotics
- All beta-lactams, but especially nafcillin, oxacillin, ampicillin, and penicillin
- Sulfonamides and rifampin
- NSAIDs, PPIs, allopurinol, cimetidine, phenytoin, furosemide
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