ABIM NEP Drugs in Renal Failure
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| FDA requires use of ___ for drug dosing. | Creat clearance. GFR not validated!
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| ______ determines loading dose of medication. | Volume of distribution
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| ______ determines maintenance dose of medication. | creatinine clearance, half life.
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| T/F uremia decreases plasma protein binding of mycophenolic acid, thereby increasing free drug concentration. | TRUE. Those patients with poor CrCl more likely to have diarrhea
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| Rx acute dabigatran ingestion? | Activated charcoal. Hemodialysis is effective, removing 50-60% of dabigatran over a 2- to 4-hour dialysis session. However, lg vol of distribution (50-70 L) results in "rebound" levels after HD. May consider CVVH.
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| Renal effects of dasatinib, a protein-tyrosine kinase inhibitors? | nephrotic-range proteinuria from dasatinib but not imatinib (Gleevec) or nilotinib (Tasigna). Poss mech of action? disruption of the VEGF signaling pathway. dasatinib also assoc w pulm HTN, pleural effusions, myelosuppression.
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| Acidosis from NSAIDS caused by? | blockade of prostaglandins and is usually hyperchloremic w/o anion gap.
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| nucleoside reverse transcriptase inhibitors (NRTI) adjustments for dialysis? | give after dialysis, may cause of lactic acidosis.
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| Non-nucleoside reverse transcriptase inhibitors (NNRRTI) adjustments for dialysis? | no adjustments needed for renal failure. have P450 3A4 interactions
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| T/F Venlafaxine (Effexor) overdose has been associated with seizures, serotonin syndrome, neuroleptic malignant syndrome, and rhabdomyolysis. | TRUE
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| Sodium thiosulfate is used for? | calcific uremic arteriolopathy. The drug is a strong acid, & causes +AGMA. In rare circumstances, the metabolic acidosis can be severe, requiring a dosage reduction.
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| How does acetaminophen toxicity causes AG? | when there’s depletion of glutathione, pyroglutamic acid is overproduced in the presence of large amounts of acetaminophen
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| Renal effects of tenofovir? | AKI and proximal tubular injury (fanconi syn) via mitochondrial toxicity.
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| Renal effects of indinavir? | no adjustment needed. May cause Stones and interstitial nephritis
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| Renal effects of ritonavir? | no adjustments needed. May cause AKI.
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| Renal effects of gentamicin? | AKI, Fanconi syndrome, and Bartter-like syndrome.
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| Renal effects of Rosiglitazone (thiazolidinedione) | increased renal salt retention and the development of edema.
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| Renal effects of Cisplatin? | causes AKI, tubulopathies, Fanconi syndrome, salt wasting, and magnesium wasting, NDI, CKD
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| Renal effects of Amphotericin B? | AKI and a distal renal tubular acidosis (RTA).
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| Renal effects of Mitomycin C? | causes a thrombotic microangiopathy.
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| Renal effects of bevacizumab | Anti-VGEF: anti-angiogenic agents that inhibit vascular endothelial growth factor (VEGF) signaling pathways regularly produce a rise in arterial pressure, often associated with HTN, proteinuria and renal dysfunction
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| Renal effects of IVIG | AKI, hypoNa, pseudohypnatremia, + osm gap from maltose accumulation
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| Renal effects of Ifosfamide? | Fanconi syndrome, proximal phosphate wasting, AKI, and nephrogenic diabetes insipidus. Renal tubular dysfunction can develop months after completing chemotherapy.
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| Renal effects of Paclitaxel? | NONE! Not associated with any significant renal toxicity.
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| Renal effects of ciprofloxacin? | - crystalline nephropathy d/t crystal precipitation in the renal tubules. Risk factors: excessive dose, alkaline urine, underlying kidney injury, and old age.
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| Renal effects of HES ? | AKI, sometimes requiring dialysis, is more common when this drug is used in critically ill patients with sepsis and acute lung injury/acute respiratory distress syndrome (ARDS)
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| Renal effects of NSAIDS? | HTN, edema, AKI (esp w/ vol depletion, lower renal blood flow or hyperCa), nephropathy (MCD or MGN), hyperK, hypoNa, AIN.
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| Mechanism of action of NSAIDs in kidney? | Lower renin production through inh of PGs. Cause HYPORENIN/HYPOALDO (RTAIV)+ hyperK. Also, enhance [urine] ability via PGE2 that usu attenuates ADH effect—>counteract diuretic effect via lower RBF, inc UNa reabsorption in PCT,
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| Renal effects of Pentamidine? | like amiloride, triamterene, and trimethoprim, pentam is associated with hyperkalemia by blocking the epithelial sodium channel in the principal cell in the cortical collecting duct.
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| Renal effects of linezolid therapy? | lactic acidosis by disrupting mitochondrial function.
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| Renal effects of Acetaminophen? | oxoproline acidosis in alcoholics and patients with poor nutrition due to the underlying glutathione and deficiencies these patient maintain.
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| Renal effects of Interferon? | nephrotic syndrome (usu MCD) and AKI from AIN. Other glomerular lesions include FSGS and MGN.
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| The drugs most often noted in the published literature as causing AIN? | antimicrobial agent. PPIs are likely the overall leading cause of drug-induced AIN, based on their massive use.
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| pts with HIV starting cART can develop ___. | IRIS: restoring protective immune responses —> pathological inflammatory response (AIN)
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| Describe Acute phosphate nephropathy. | Intense ppt of CaPhos in medulla>>cortex. The serum phosphate levels likely >7, resulting in phosphaturia. Recall crystals are needle-like. CaPhos stained using von Kossa stain, which will not stain calcium oxalate.
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| Hormonal effects of ACEIs ? | raise plasma renin activity and renin levels, but lower AII and aldosterone
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| Hormonal effects of ARBs ? | raise plasma renin activity, renin levels and AII levels, but lower aldosterone.
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| Hormonal effects of Aldosterone antagonists ? | raise the levels of all of the hormones, but antagonize the mineral corticoid receptor.
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| Metformin requires adjustment and what stage of renal function? | CKD4. Usual dosing acceptable in CKD 3/4 w/o increased incidence of lactic acidosis
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| Lithium nephrotoxicity may be prevented or treated by the use of ___. | Amiloride is Rx of choice for NDI. (no hypoK & no need Na restrict thus less vol depletion). Also reduce Li uptake into cells. NOTE Li dosage may be affected by amiloride.
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| T/F Administration of activated charcoal is useful for lithium OD. | FALSE because charcoal does not bind lithium ions. Consider polyethylene glycol
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| Preferred agent to bind lithium in G.I. tract? | polyethylene glycol. especially important for patients who ingest a sustained-release lithium. Charcoal does not work.
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| Conventional hemodialysis can reduce plasma lithium by ___. | 1 mEq/L per 4 h of treatment. High flux likely more effective, but unproven. HD does not clear intracellular lithium effectively, expect rebound.
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| Hemodialysis should be performed for lithium OD for what scenarios? | coma, convulsions, respiratory failure, deteriorating mental status, or renal failure… or if lithium level fails to fall. Also strongly consider HD if level > 4 mEq/L, or levels 2.5-4 w CV or CNS symptoms. Seldom needed if lvl<2.5
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