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ABIM NEP Drugs & AIN
ABIM NEP Drugs, AIN & CIN
| Question | Answer |
|---|---|
| Explain DRESS Syndrome | Life threatening drug reaction with fever, rash, eosinophilia, LAD, atypical lymphocytes, and and organ damage (granulomatous AIN, hepatitis, pneumonitis). Fever develops 1st then rash. |
| Explain Aristolochic acid nephropathy. | aka Chinese herb slimming regimen associated with GU malignancy. Tends to progress rapidly, assoc w/ fanconi syn, enzymuria, LMW proteinuria, small kidneys with extensive fibrosis and tubular atrophy. Rx-stop drug, steroids may slow progression |
| Cause of Balkan nephropathy? | Aristolochic acid! Seeds of Aristolochia clematitis co-mingled with wheat grain during annual harvest. |
| What is main concern long term for pts w Aristolochic acid nephropathy | lifelong risk of transitional cell carcinoma esp after transplantation, where it may occur in >30% of patients |
| Gold causes ___________. | Nephrotic syndrome from membranous disease and not minimal change lesions |
| Platinum compounds cause ___________. | acute tubular necrosis (ATN) through both apoptosis and necrosis, especially of the proximal tubule |
| Noni juice can cause ______ | hyperK |
| Ephedra (Ma Huang) can cause ______ | HTN and stones |
| Star fruit (carambola) can cause ______ | oxalate nephropathy & neurotoxin accumulates in renal disease |
| Glycerrhizic acid (used as a sweetener) can cause_______. - | “apparent” mineralocorticoid excess (AME) |
| Cadmium exposure can cause? | HTN +CKD from chronic tubulointerstitial nephritis w non-nephritic proteinuria and a bland urine sediment, but not associated with gout. Associations inc working in battery plant, bone disease and stones. |
| Cadmium affects the_____? | proximal tubule |
| Chronic lead toxicity can cause? | triad of gout, HTN, and CKD. Lead is similar to cadmium in causing a chronic tubulointerstitial nephritis with non-nephritic proteinuria and a bland urine sediment |
| Which cancer drugs cause AIN/CIN? | ifosfamide, TKI (tyrosine kinase inh), platins, ipilimumab |
| What AIN associated with urothelial cancers? | Aristolochic acid nephropathy |
| Ascorbic acid (vit C) can cause what type of kidney disease? | oxalate nephropathy |
| Three main causes of AIN? | antibiotics, NSAIDs, PPIs (can develop after yrs) |
| T/F urine eosinophils are specific for AIN. | FALSE. 1/3 of AKI cases have + eos. very nonspecific. Also + eos with UTI, pyelo, etc. |
| T/F WBC casts are common with AIN. | FALSE. 50% of pos have no WBC or RBC casts. many pos have casts, but seldom WBC casts. Can see RBC casts. Think pyelonephritis if see WBC casts. |
| Gallium scan usefulness in AKI? | (based on binding of lactoferrin on WBCs). Gallium scan measures uptake 48-72 hrs after injection. + in normal kidneys, ATN, cancer, pyelo, CIN, atheroembolic dz, GNs, IgAN, MCD, and AIN!!! Not very sensitive or specific. |
| Diagnosis of AIN made using ________. | kidney biopsy. |
| Drug induced AIN associated with what microscopy findings? | >10 eos/20x field + granulomas |
| T/F steroid therapy within a week of AIN diagnosis is associated with improved kidney function. | TRUE. Stop offending agent + SM 1gram pulse + pred 1 mg/kg for ?time. |
| Most common renal manifestation of sarcoidosis? | hypercalciuria 50%. Hypercalcemia seen in 10%. Glomeruli normal. T-cell interstitial infiltrate, sometimes with granulomas or giant cells |
| Renal manifestations of Sjogren Syndrome? | AIN, CIN. Assoc w/ + serologies, bland sediment, ,1 g proteinuria, AKI with tubulopathies (Fanconi, dRTA, NDI, fibrosis). |
| Explain renal manifestations of TINU. | uveitis, AIN, sterile pyuria, tubulopathies (Fanconi, dRTA, NDI, fibrosis). +/- granulomas. |
| What is IgG4 disease? | lymphoplasmacytic (T&B). infiltrate with reactive changes, plasma + for IgG4.. Rx- steroids. 60% have high IgG4 levels. + nodular masses on imaging suspicious for malignancy. |
| “Whorled” or storiform pattern of interstitial fibrosis is seen with ________. | IgG4 disease. Immunoperoxidase stain + IgG4 in plasma cells. |
| Microcystic dilatation of tubules is seen in _____. | lithium induced CIN. Rx CKD care, amiloride, adequate hydration if have NDI. |
| Lead nephropathy findings? | AKI, Fanconi's syndrome, CKD (CIN), HTN |
| Sickle cell nephropathy? | hematuria, AKI, CKD (CIN), FSGS, papillary necrosis. |
| Presentation of papillary necrosis? | asymptomatic hematuria, , Gross hematuria, Pain, UTI. + renal tissue and sediment, imaging shows partial or complete necrosis of papilla (“claw”) |
| Medullary sponge kidney is caused by _____. | Ectasia collecting ducts. Urine stasis, lo citrate, dRTA—> ca containing stones. Asymptomatic hematuria and flank pain. Dx made on CT urogram. Rx citrate. |
| Name immune mediated causes of CIN. | Sjogrens, sarcoidosis, IgG4 disase. |
| Xanthogranulomatous CIN distinguished by _______. | lipid laden macrophages. Usually infected with gram negative bacteria. Form staghorn calculi. |
| Michaels Guttman bodies seen in _______. | renal malacoplakia. |
| Nl physiologic fcns of prostaglandins? | maintain renal blood flow& GFR: inc Na reabsorption, inc aldo secretion (results in inc K secretion), lowers water reabsorption, causes vasodilation |
| List NSAID induced renal problems/diseases. | edema, exa HTN, CHF, hyperK, RTA IV, hypoNa, pre renal AKI, ischemic ATN, AIN, NS (MCD, membranous), analgesic nephropathy, papillary necrosis, renal cancer. |
| Describe drug induced small vessel vasculitis | classic leukocytoclastic skin lesion & necrotizing and prolif GN with 2+ IgG stain in mesangium . Often Low complements +MPO & PR3 & human neutrophil elastase. Assoc w levamisole used to cut cocaine (potentiates euphoria) |
| Gemcytabine causes ____. | AKI from TMA. low plt, low haptoglobin, , hi LDH, |
| Drugs reported to cause TMA | bevacizumab, CNI, gemcitobine, mitomycinC, clopidrogel, ticlopidine, opana (oxy morphone), quinine |
| Drugs reported to cause vasculitis | cocaine, PTU, infliximab |
| Interferon reported to cause? | NS from min change dz MCD |
| Anabolic steroids reported to cause? | FSGS |
| Zolendronate reported to cause? | ATN |
| Tenofivir reported to cause? | AKI/ATI/ATN, CKD, fanconi like tubulopathy (RTAII) , rarely NDI (mitochondrial toxin) |
| Aminoglycosides reported to cause? | tubular injury starts 3+days, AKI seen after 7-10 days, usually recovers. EM—> abnl mitochondria, myelin bodies d/t liposomal injury. Causes Bartter like (Na, K, Mg, Ca wasting +, met alk), fanconi syn |
| Polymyxin B or E reported to cause? | ATI/ATN, most common w high dose and long duration of rx + other nephrotoxin |
| Vancomycin reported to cause? | ATI/ATN. AIN. NOT metabolized & excreted by kidney. Dose related. Suspected mech: mitochondrial inj, complement activation & inflammation, oxidative stress. |
| Amphotericin B reported to cause? | ATI/ATN, dRTAI, NDI, hypoK, hypoMg. Constricts off arteriole, creates pores—> permeability cause K & Mg leak out of cells and H+ to leak back in (hypoMg, hypoK, RTAI distal) |
| Hydroxymethyl starch (Hextend) reported to cause? | osmotic nephropathy |
| Atazanavir reported to cause? | crystal nephropathy (rod like crystals) w granulomas + (radioopaque) stones |
| Indinavir reported to cause? | crystal nephropathy (rod like crystals) + (radioopaque) stones |
| Quinolones reported to cause? | AIN (+/-granulomatous), necrotizing vasculitis, ATN, crystal nephropathy (rod like crystals). AIN is most commonly seen on biopsy. No stones. |
| Methotrexate reported to cause? | crystalline nephropathy, most common ppt in acid urine pH <7. Avoid with IVF + alkalinization. |
| Rx methotrexate nephrotoxicity? | leucovorin, hi flux dialysis but see rebound, glucarbidase (cleaves MTX to nontoxic metabolite) |
| Acyclovir reported to cause? | crystalline nephropathy, no stones. Note usu IV high dose, not oral. |
| Sulfadiazine reported to cause? | crystalline nephropathy, +/- (radioluscent) stones. Rx alkalinize urine. |
| Ascorbic acid reported to cause? | crystalline nephropathy |
| Orlistat reported to cause? | crystalline (oxalate) nephropathy |
| Topiramate reported to cause? | (weak CA inh) met acidosis + CaPhos stones, RTAIII |
| Lithium reported to cause? | NDI (hyperNa w dilute urine), ATI/ATN, CIN, renal cysts, FSGS |
| ARBs and ACEIs reported to cause? | hemodynamic AKI, ATI/ATN, hyperK, NAGMA (hi renin, low aldo) |
| Alendronate reported to cause? | no renal effects |
| Pamidronate reported to cause? | NS, AKI from collapsing FSGS or MCD |
| Zolendronic acid reported to cause? | AKI from toxic ATI/ATN |
| PPIs to cause? | AIN, rarely hypoNa, hypoMg or CKD |
| reported to cause? | |
| Medication causes of crystal nephropathy | atazanavir/indinavir, quinolones, acyclovir, sulfonamides, MTX, ascorbic acid, orlistat, triamterene, |
| Medication causes of nephrolithiasis | atazanavir/indinavir (radioopaque), topiramate, carbonic anhydrase inh, sulfadiazine, triamterene,ephedrine |
| Explain osmotic nephropathy & list causes. | Cause AKI/ATI. IVIG/sucrose, hydroxyethyl starch, dextran, mannitol, radiocontrast. drug taken into cell by pinocytosis and cannot be metabolized—> swell |
| Tyrosine kinase inhibitors (sunitinib and sorafenib) reported to cause? | TMA & preeclampsia-like state. Also, acute & chronic interstitial nephritis, CKD, hypophosphatemia. Have anti-VGEF effect |
| Anti-VEGF agents like bevacizumab reported to cause? | preeclampsia-like state w/ HTN and proteinuria. Dose dependent denovo HTN or worsened preexisting HTN.. |
| SGLT2 inhibitors (canagliflozin) renal effects? | cause the kidneys to remove sugar from the body through the urine—>UTIs + euglycemic diabetic ketoacidosis |
Created by:
ka1usg
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