Exam 3 - Renal and Uro Part 1 Flashcards
ACUTE KIDNEY INJURY
ACUTE KIDNEY INJURY
2 categories/criteria used for assessing AKI:
- RIFLE category
2. AKIN Criteria
Which type of AKI has the highest incidence, is multifactorial, and accounts for 30-90% of mortality rates?
ICU Acquired
What are the 3 types of etiologies of AKI?
1) Prerenal: decreased perfusion with undamaged parenchymal tissue
2) Intrinsic: structural damage to kidney
3) Postrenal: obstruction of urine flow downstream of kidney
Prerenal AKI is due to what drugs?
ACEI/ARB’s
NSAID’s
Vasopressors
Diuretic/Sepsis
It is REVERSIBLE!
When there is an insult to the kidneys, what happens to GFR and Cr?
GFR drops
Cr raises
How can AKI be prevented?
Adequate fluid intake (2L/day)
Avoid nephrotoxic medications
HYDRATION!
-Crystalloids > Colloids unless pt is low in serum protein
Which Crystalloid is preferred and why? (AKI)
0.9% NaCl = isotonic
D5W is also isotonic but it’s all in free water, vascular to intracellular, NOT used as often
Which type of diuretics were not found to be helpful in the prevention of AKI and are only good for managing fluid overload?
Loop diuretics
Vasodilators are used in the prevention of AKI, which one is used the most?
Dopamine
- Increases blood flow to kidneys
- Increases BP
Which 2 antioxidants are used in the prevention of AKI?
- Vitamin C: Decreases oxidation that is caused by free radicals
- Mucomyst:
- Used as a mucolytic, antidote (APAP poisoning)
- Some benefit in preventing contrast induced nephropathy in some patients
- High sulfur content (rotten egg smell)
Treatment of AKI revolves around what?
Elimination of insult!
Reduce extra-renal complications
Expedite recovery
Name the treatments of AKI, we will then expand:
Dehydration, RRT, Pharmacologic therapy, Diuretics, Diuretic resistance, Electrolyte management
For dehydration, what 2 methods of tx are used?
- Oral therapy
- Isotonic IV fluids (20mL/kg) - smaller amount needed for oliguria/CHF
Goal: MAP > 65, urine output >0.5
Large volumes of NS can cause?
Hyperchloremic acidosis
What is RRT and what are the indications for it?
Renal replacement therapy
A,E,I,O,U: Acid-base abnormalities Electrolyte imbalance Intoxications Overload of fluid Uremia
Pharmacologic Therapy for AKI, dosing considerations are?
Volume of distribution
Volume status of patient
Abx in septic patients
What is the main diuretic used in the tx of AKI?
Mannitol:
- Osmotic diuretic
- Can cause AKI itself, not used often
- Must be filtered (can cause crystallization)
- Used for head trauma, cerebral edema
When is the only time Loop diuretics are indicated for use in AKI?
Only for fluid overload
Loop diuretic resistance is common in AKI, why and what is done for this?
Increased dose doesn’t mean increased efficacy.
Switch oral to parenteral
Increase dose
Use continuous infusions
Use different agents
What are the causes of Diuretic resistance?
- High sodium intake limits natriuretic effect
- Patients with ATN have reduced number of working nephrons
- Heavy proteinuria bind loop diuretics in renal tubule
- Renal compensation at distal convoluted tubule
Which thiazides can be used in the case of loop diuretic resistance?
Chlorothiazide
Metolazone (good for renal pts)
Which agents at the collecting duct can be used for loop diuretic resistance?
Amiloride, Triamterene, Spirinolactone
During electrolyte management, how can hypernatremia and fluid retention be tx?
Limit sodium intake –> loop diuretic failure
During electrolyte management, how is hyperkalemia tx?
RRT
Which two elements are not removed by RRT effectively?
Phosphorus and Magnesium
Avoid calcium!
Pt’s on RRT can develop?
Hypocalcemia secondary to dialysis, need a Ca supplement
CKD
CKD
What are the initating factors of CKD?
DM
HTN
Glomerulonephritis
What happens in Anemia of CKD?
Decreased production of erythropoitetin (made in kidneys)
Iron deficiency common:
-Increased iron demands from erythropoietic stimulating agents (main cause for resistance)
CKD mineral and bone disorders are common in CKD populations due to abnormalities in?
PTH, Calcium, Phosphorus, Ca x P, Vitamin D
Renal osterodystrophy: kidneys can’t make vit. D
What happens in CKD Mineral and Bone disorder?
Decreased renal fxn –> Increased Phosphate –> Decreased Ca –> Increased PTH –> Increased Ca and P reabsorption
Decreased vit. D activation act. in kidney = Increased PTH
Management of CKD
Management of CKD
Management of CKD: Nonpharm therapy
Diet: Limit protein/sodium
Smoking cessation and exercise
Management of CKD: DM with CKD
ACEI or ARB to prevent further progression
-Titrated until GFR drops
Metformin should be continued until GFR < 30
Management of CKD: HTN with CKD
Goal: <140/90
ACEI or ARB if pt with DM too
Thiazides not sufficient
Manage BP per other dz states
Management of CKD: Anemia of CKD
ESA (Erythropoiesis stimulating agent)
Iron supplement
-Use Hgb for monitoring!
When should ESA be discontinued? At what level of Hgb?
Above 10 - STOP!
Increased mortality when Hb is kept above? (Black box warning)
13 g/dL
Still need iron supplements, can’t take ESA alone!
What are the 2 examples of ESA?
Epoetin alfa (Epogen, Procrit) Darbepoetin alfa (Aranesp)
Black box warnings of ESA:
Death, MI, Stroke, Cancer
Management of CKD: Iron status
Required by CKD pt’s taking ESA’s
Should maintain adequate intake of Iron, B12, and folate
Oral preps of Iron:
Ferrous sulfate
Ferrous gluconate
Ferrous fumarate
Most common IV prep of iron:
Iron Sucrose (Venofer)
Adverse effects of Iron:
Constipation
BLACKENED DISCOLORATION OF STOOL
IV forms:
Allergic rxns
Limited by slower infusions
Management of CKD: Selecting an iron prep
Oral therapy 1st line if possible, fewer SE’s
IV for RRT pt’s
Iron status while on ESA therapy monitored every?
3 months
Tx goals for CKD Mineral and Bone disorder?
Keep calcium and phosphate in normal ranges
Ca x P < 55, otherwise indicative of dz
Monitor PTH
CKD mineral and bone disorder: Non-pharm therapy?
Dietary phosphate reduction unless dialysis pt
Dialysis not sufficient enough
Parathyroidectomy if non-responsive to pharm tx’s
CKD mineral and bone disorder: Phosphate binders
Binds to phosphate so it’s not absorbed
Tums Calcium carbonate Calcium acetate Sevelamer Alum hydroxide
CKD mineral and bone disorder: What type of phosphate binder is better in early CKD? Why?
Calcium based are better in early CKD (pts are hypocalcemic)
Calcium carb soluble in acid, given before meals to bind Phosphate
What is a nonabsorbable hydrogel that also lowers LDL and raises HDL?
Sevelamer
AE’s of Phosphate binders:
Hypercalcemia, Aluminum toxicity
Drug-food, drug-drug interactions!
Calcium salts bind to oral meds (Iron, zinc, FQ’s)
separate agents
Aluminum toxicity will worsen anemia and can lead to CNS toxicity
CKD mineral and bone disorder: Vitamin D therapy
Caclitriol is active 1,25 - D3
Suppresses PTH secretion, stimulates Ca absorption
Paricalcitol activate PTH receptors but don’t increase Ca and P absorption
What does Cinacalcet (Sensipar) do?
Sensitizes PTH receptors to effects of Ca
Decreases PTH
DRUG INDUCED KIDNEY INJURY
DRUG INDUCED KIDNEY INJURY
Most common manifestation of DIKD?
Decreased GFR
DIKD in 60% of hospital AKI?
Abx, NSAIDs, ACEIs, Anti-virals, chemo
Signs of DIKD:
Decrease in GFR
Rise in Sir and BUN
“Dumb kidneys” not filtering effectively
Decreased urine output with HTN progression
Proximal tubular injury:
metabolic acidosis
Distal tubular injury:
Polyuria
Metabolic acidosis
Hyperkalemia
DIKD structural/fxnal alterations: What drugs cause ATN?
aminoglycosides
Cisplatin, carboplatin
Cyclosporine, Tacrolimus
DIKD structural/fxnal alterations: What drugs cause osmotic nephrosis?
Mannitol, IV immunoglobulin
Temporary injury
DIKD structural/fxnal alterations: What drugs cause hemodynamically mediated kidney injury?
ACEI and ARB
NSAID
Changes in afferent/efferent arterioles
DIKD structural/fxnal alterations: What drugs cause obstructive nephropathy?
Intratubular obstruction?
Nephrolithiasis?
Intratubular obstruction: Acyclovir, Methotrexate
Nephrolithiasis:
Sulfonamides
Anti-virals
DIKD structural/fxnal alterations: What drugs cause Glomerular disease?
Lithium
NSAIDs
DIKD structural/fxnal alterations: Vasculitis and thrombosis
Hydralazine
Allopurinol
Methamphetamines
Cyclosporine
DIKD structural/fxnal alterations: Cholesterol emboli
Rare
Warfarin
Thrombolytics
ATN
ATN
Most common agents in ATN:
Aminoglycosides Contrast media Cisplatin Amphotericin B Foscarnet Osmotically active agents (Colloids, Manitol)
ATN: Aminoglycosides
Gradually (5-10 days after therapy) progressive increase in BUN/SCr
Completely reversible
Damages cells
ATN: Aminoglycosides Risk Factors
Large total dose
Prolonged therapy
Trough conc > 2
Concurrent nephrotoxins
ATN: Aminoglycosides prevention
Alt. abx use
Limit concurrent nephrotoxin usage
Pharmacokinetic monitoring (change doses based on lvls)
Once daily dosing
ATN: Radiographic Contrast Media Nephrotoxicity
Up to 50% of CKD pt’s
Oliguria in high-risk pts
Renal ischemia and direct cellular toxicity
High osmolarity
ATN: Radiographic Contrast Media Nephrotoxicity Prevention
Contrast:
- Minimize dose
- Use non-iodinated contrast
- Use low or iso-osmolar contrast
Avoid concurrent nephrotoxins
Sodium Bicarb (not really helpful) and Mucomyst
ATN: Cisplatin Nephrotoxicity
Used for tumors
Major dose limiting toxicity: Nephrotoxicity
ATN: Cisplatin Nephrotoxicity Prevention
Vigorous hydration with NS
Amifostine (Ethyol)
-Chelates cisplatin in cells
ATN: Cisplatin Nephrotoxicity Tx
Partially reversible
Supportive care
ATN: Amphotericin B Nephrotoxicity
Antifungal agent
Not common
Direct tubular cell damage
Prevention: Liposomal formulation (AmBisome)
Taking bilayer, embed in drug in bilayer –> no kidney damage inside
Tx: Supportive
Intratubular Obstruction: Tumor lysis syndrome
Prevented by hydration and allopurinol
Intratubular Obstruction: Rhabdo
HMG-CoA reductase inhibitors and CYP3A4 inhibitors
Drugs that lead to AKI due to drug precipitation
Acyclovir, Foscarnet, Methotrexate
