Day 2 nephrology Flashcards
What are prerenal medications causing kidney disease?
What drugs cause ATN?
What drugs cause AIN?
ACEI’s/ARB’s,NSAIDS,Loop Diuretics,Cyclosporine, Tacrolimus, PTU(propylthiouracil), allopurinol, adalimumab, bevacizumab, methamphetamines, warfarin
Aminoglycosides, Contrast Dye, Cisplatin/Carboplatin, Amphotecerin B, Cidofovir, Zolendronate
All B-lactams, PPI’s, Ciprofloxacin, NSAIDS/Cox-2 inhibitors, Loop Diuretics, Cyclosporine
What drugs cause Glomerular disease?
What drugs cause Postrenal disease?
What are risk factors for ACEI/ARB prerenal nephropathy?
Gold, Pamidronate
Acyclovir, Sulfonamides, Methotrexate, Triamterene
Pre-existing renal insufficiency, prerenal conditions promoting lower blood volume and blood flow.
What is presentation of ACEI/ARB kidney damage?
How to prevent ACEI/ARB kidney damage?
How to treat ACEI/ARB kidney damage?
Rise in SCr up to 30% within 3-5 days of initiation is normal, if higher it’s above 30% you should stop, Hyperkalemia.
Maintain hydration, avoid in patients with risk factors, start low dose and gradually titrate every 2-4 weeks, monitor SCr and K+ every 2-3 days when first initiated.
Discontinue agent, Dose reduce.
What are risk factors for NSAID kidney damage?
What is the least nephrotoxic analgesic? What is the most nephrotoxic?
Treatment for NSAID kidney damage?
Same as ACEI/ARB and Age >60 years.
Aspirin, Indomethacin.
Discontinue agent, recovery is rapid.
What to know about incidence of Calcineurin inhibitors AKI?
Risk factors for Calcineurin inhibitors AKI?
Presentation of AKI from Calcineurin inhibitor?
Acute AKI commonly occurs frequently within the first 6 months of therapy. Chronic kidney disease 5- year risk is 7-21 %.
Drug interaction, concomitant drug use, higher drug doses, >65 years old.
Hypertension, Hyperkalemia, Hypomagnesemia, Renal Tubular Acidosis.
Cyclosporine trough goal? Tacrolimus trough goal?
How to treat immunosuppresant injury?
Risk factors associated with aminoglycoside Kidney disease?
100-350 ng/mL. 3-20 ng/mL.
Bridging to less toxic immunosuppresants. CCB’s–> antagonize vasoconstricter effects.
Large Cumulative doses, prolong therapy, trough levels > 2mg/dL(gentamycin/tobramycin), >10 mg/dL(amikacin). Recurrent previous aminoglycoside therpay, pre-existing renal insufficiency, coadministration of other nephrotoxic agents.
Clinical presentation of aminoglycoside kidney injury?
Highest risk to lowest risk for kidney?
Prevention?
Gradual rise in SCr that is usually seen within 5-10 days. Patients are typically non-oliguric. Hypomagnesemia. Signs and symptom of intrinsic kidney damage.
Neomycin–> Gentamicin–> Tobramycin–> Amikacin
Hydration, avoid nephrotoxins, utilize extended interval dosing(once daily)(achieves undetectable levels, less accumulation). Treat with renal replacement therapy.
Contrast media risk factors?
Presentation of contrast media kidney disease?
Strategy to prevent contrast kidney injury?
Preexisting kidney disease and renal conditions. Contrast volume,dose, and osmolarity. Concomitant nephrotoxins, CI’d with metformin.
SCr increase seen within the first 2 days following contrast administration.
Discontinue nephrotoxic medication at least 24 hours prior to exposure, in high risk patients use nonionic, low-osmolar contrast, limit volume to <100 mL, Initiate and continue water and sodium bicarb. Give N-acetylcysteine.
Cisplatin risk factors?
How does cisplatin present?
Prevent cisplatin kidney injury?
Quite common, dose-limiting toxicity(20-30%), Carboplatin has a lower risk and is preferred agent in high-risk patients. Elderly, dehydrated, other nephrotoxic, large cumulative doses, alcohol use(more susceptible to hypomagnesia).
electrolyte abnormalities(hypomagnesia is hallmark), decreased urinary concentration.
Hydration, Give Amifostine(pre-treatment) chelates cisplatin and reduces ROS, consider use in high risk patient).
Amphotericin B risk factors?
Amphotericin B presentation?
What to know about acute interstitial nephritis?
Rate of injury is higher with conventional formulation and is potentially permanent. Risk factors are pre-existing renal disease, large doses, rapid infusion and volume depletion, hypokalemia, increased age, concomitant nephrotoxins.
1-2 weeks from initiation, SCr peaks 10-12 days after initiation, imparied ability to concentrate urine(non oliguria), hypomagnesia and hypokalemia.
See a lot of white and red blood cells in pee, NSAIDS show after 6 months, allergic hypersensitive response, treat by stopping and giving corticosteroids.
Lithium presentation?
Treat lithium how?
What causes post renal nephropathy?
develop over years, usually identified as a rising BUN/SCr or the onset of hypertension. Polydipsia and Polyuria.
Amiloride, renal replacements
Precipitation of drug crystals in tubules can lead to tubular obstruction. Indirect causes are chemotherapy agents(uric agent crystals)(Direct causes are bactrim, acyclovir, sulfa, methotrexate, etc.), Rhabdomyolysis(statin’s, daptomycin–> precipitation of myoglobin).
Risk factors for acyclovir?
How to treat acyclovir?
Volume depletion, preexisting renal impairment, excessive drug dosing. Develops within 48 hours, typically asymptomatic but can cause significant flank pain. Red and white blood cells in urine, crystal sediment in urine.
Avoid rapid/high doses(infuse over at least 1 hour), adjust for renal dysfunction, hydration with high urine flow.
What are the stage criteria for KDOQI?
Complications of CKD?
Etiology of CKD?
> 90 stage 1, 60-89 stage 2, 30-59 stage 3, 15-29 stage 4, <15 stage 5.
Anemia, CKD related bone disorders, Altered sodium and water balance, Hyperkalemia, Metabolic Acidosis, Uremia, Cardiovascular disease.
Managing diabetes, hypertension, glomerulonephritis, sociodemographic, low kidney mass, low birth weight, family history of CKD, Proteinuria, Diabetes, Hypertension, Smoking, Hyperlipidemia.
Pathophysiology of anemia of CKD?
What causes Phosphorus-calcium- PTH loop in CKD?
How is vitamin D affected by CKD?
Primary cause is decreased production of erythropoeitin. Iron deficiency is common in stage 5 renal disease–> decreased GI absorption, inflammation, frequent blood testing, blood loss from hemodialysis, increased iron demands from erythropoietin stimulating agent therapy.
Declining kidney function–> decreased phosphorus elimination–> hyperphosphatemia and a recipricol decrease in calcium. PTH tries to compensate for all this and increases calcium absorption of bone.
Decreased renal blood flow leads to decreased delivery of 25OHD and loss of 1-alpha-hydroxylase leads to vitamin d deficiency. This leads to PTH stimulation.
Treatment of Diabetes in CKD?
Treatment of Hypertension in CKD?
Treatment of Anemia in CKD?
Diabetic patients have 40-50% of developing CKD. Control glucose. Control with ACEI’s or ARB’s.
ACEI’s/ARB’s.
Erythropoeitin stimulating agents. Epoeitin Alfa, Darbepoeitin Alfa.
MOA of erythrypoeitin stimulating agents?
Adverse effects of ESA’s?
What to monitor with ESA’s? Desired rate of Hb increase?
Bind to erythropoetin receptor
Hypertension(most common), seizures, black box warnings(1 pertaining to oncology, surgical, CKD patient’s).
Monitor Hb every 2-4 weeks to adjust the dose. 1-2 g/dL/month. Target should be 10-11 g/dL(FDA). >13g/dL can cause stroke, worsening hypertension, vascular thrombosis, possible increased mortality and CV events.
Goals per KDOQI for iron supplementation?
Should you start on oral or IV iron?
What are the types of iron?
TSat>20%. >100 ng/mL(non-dialysis). >200ng/mL(dialysis). 200 mg is what you want to hit.
Try oral at first then switch to IV unless patient is receiving dialysis then you want IV dialysis.
Ferrous sulfate, fumarate, gluconate, and polysaccharide iron complex are the oral products. 200 mg iron is what you want to hit.
How much elemental iron comes in a 325 mg ferrous sulfate tablet? Ferrous fumarate? Gluconate? Polysaccharide iron complex?
Adverse effects of iron? Counseling for iron? Drug interactions?
A/E’s of IV iron? Which one to test for anaphylaxis?
20% elemental iron. 12%. 33%. 100%.
GI disturbances, black stool, constipation. Take with food, take iron with vitamin C(increases absorption). High interaction with fluroquinolones.
BBW of anaphylaxis(iron dextran–> must give patient small test dose first). Hypotension, nausea, headache, muscle cramping.
What don’t you want your Ca x Phos to get higher than?
Treatment of hyperphosphatemia?
What to know about calcium acetate?
55.
dietary restriction, prevent GI absorption(phosphate binders), dialysis does not remove phosphorus, parathyroidectomy.
PhosLo is brand name. Do nut crush/chew
What to know about Calcium Carbonate?
What to know about Sevelamer?
Lanthanum carbonate?
Tums, needs acidic environment to work.
Renagel, Revela. 1st line in patients with hyper calcemia, Hcl(gel)(give non acl if acidosis) may cause mild acidosis, do not crush/chew
Fosrenol, calcium and aluminum free(can chew)
Aluminum hydroxide?
Ferric citrate?
How to treat elevated PTH?
algernagel, used with phos> 7mg/ dL and undergoing HD
calcium and aluminum free, risk of iron overload.
Cinacalet(Sensipar), Vitamin D supplementation
What vitamin D product needs liver conversion? In liver and kidney?
Active version of vitamin D?
3 options for people with end stage renal disease?
Doxercalciferol. Ergocalciferol, cholecalciferol.
Calcitriol, Paricalcitol.
Hemodialysis, Peritonealdialysis, Transplant
What are the 3 ways substances move in hemodialysis?
Does hemodialysis require an AV fistula? What is 2nd and 3rd line?
Complications of HD?
passive diffusion, ultrafiltration, convection.
Yes. Advantages are it is long lasting, lowest rate of complication, increased survival, lower hospitalization, most cost effective however requires 1-2 months to mature to use. 2nd line is AV graft, 3rd line is venous catheters
Hypotension–> control by avoiding food or during HD, lower dialsylate temperature, Management by placing patient in Trendelenberg position, decrease ultrafiltration rate, Give bolus of IV fluids, Midodrine(alpha 1 adregernic agonist)
Is muscle cramps a complication of HD?
Is thrombosis a complication of HD? Infection?
Yes, Prevent by accurately assessing dry weight, stretching,massage, flexing. Manage by giving IV fluids, Vitamin E.
Yes, manage with saline flush, referral to vascular surgeon, possibly use t-PA. Yes, can treat via antibiotics.
Important factors for drug dosing in HD?
Advantages to HD?
Disadvantages to HD?
Molecular size and weight, amount of protein binding, volume of distribution.
high solute clearance, easy to measure, technique failure is low, takes place in HD center.
loss of independence, others mentioned, vascular access is commonly associated with thrombosis, declined in renal function is more prominent than with PD.
Advantages of PD?
Disadvantages of PD?
What to know about CRRT?
Hemodynamic stability, higher clearance of larger solutes, better preservation of residual renal function, suitable for elderly and pediatric patients, patient independence.
risk of peritonitis, malnutrition secondary to proteins and amino acids, risk of catheter malfunction, inadequate ultrafiltration, patient burnout, no convenient IV access.
solutes slower removed, high potential for clots(need anticoagulation), lower mortality in critical care, High drug cost, high training and such, extremely low study on drug dosing.
