Nephrology Insights for Primary Care - PowerPoint Presentation

1. Nephrology Insights for Primary Care- focus on AKI/ CKD/ DialysisKaarlo Hinkkala MD, FRCPCLocum Nephrologist – TBRHSCAssistant Professor - NOSM

2. Conflict of Interest Declaration: Nothing to DisclosePresenter: Dr. Kaarlo HinkkalaTitle of Presentation: Nephrology Insights for Primary Care I have no financial or personal relationship related to this presentation to disclose.

3. ObjectivesBrief survey across the disciplineFocus on CKD, AKI, ESRD, dialysisCover mainly bottom line issuesThings I wish people knew / what grinds my gearsThings you may not have realized we can doWhat we actually do with a variety of problemsAvoid sedating you with clin epi, basic science, guidelines/ minutiaGoing for a common sense approach here (based on evidence)Threw in a few things purely for interest

4. A Cynical Approach to Nephrology…Stop all culprit medsFlip a coin and give either fluids or diureticsIf that fails do the oppositeIf that fails, dialysis will temporarily fix everythingFluids, electrolytes, uremia of courseHyperglycemia, hypo/hyperthermia, HTN, lipids (via plex)Goal of every nephrologist sometimes seems to be to have your patient die with perfect numbersWe often get pressured into temporizing hopeless situations until people man up and put an end to things that need to endWe’re also often asked to manage the decline End stage cardiorenal, hepatorenal, oncology patients

5. AKITreat acute illnessHold ace/arb/ NSAIDS/ diuretics (if not overloaded)U/S and U/AConsider GN and AIN in DDxAIN – PPI, cephalosporin's, septra, NSAIDS, 5-ASAHydrate as much as you think they can reasonably handleIf bicarb is low use instead of NS 3amps/ 1L d5w = “normal bicarb” at same rate you would use NSNS will drive down your bicarb – pH is 5.5Bicarb will drive down K and will make more CO2 (usually not an issue)Write order to change to NS once bicarb >18

6. Then see where they level out and waitHD – lytes / volume reasons or sustained anuriaDon’t dialyze acutely for uremia Unless LOC poor or progressed now to ESRDCardiorenal – sometimes can’t get the fluid off without inc the CrJust push on and accept the Cr will go up with diuresisEither way will get HD if we cant get the fluid off so nothing to lose Dialysis does not heal your kidneys, it just does what they are notNo role to doing it early unless fluid is getting bad

7. K+ 7.7

8. Toxicology / dialysisASA, antifreeze /methanol, LithiumCall poison control and then us as neededOther drugs generally have antidote / too protein bound, not dialyzed well, not toxic enough, etcDecision to HD based on drug level, severity of symptoms, time of ingestion

9. IV ContrastIf important, just do the test and live with the consequences irregardless of GFRStop / hold any meds that will aggravate AKIHydrate as much as you feel comfortableOutpt protocols - bicarb vs NS - use whatever you prefer150ml/hr 1hr prior, then 50 ml/hr x 6hrs is a common outpt protocolAssuming 50 kg (3ml/kg/hr x 1hr, then 1ml/kg/hr x 6hr)If already overloaded, perhaps just hold the lasix/ace

10. Risk from CT is less than cathNAC – homeopathic, but ok to use anywayAKI - see within 48hrs, peaks 5-7dRisk of AKI in 5-10% range Usually mild inc in CrHD - <1% Usually has adv CKD / acute illness / temporaryDialysis not protective against contrastIf ESRD (esp if not on PD), there is nothing to lose by giving dye – kidneys are done

11. LMWH – renal failureWith our current formulary would recommend:Lovenox for everyone with normal GFR Use 30 OD for GFR 15-30 prophylaxis<15 - ?heparin 5000 BIDDalt or tinza would be fine in esrd but not allowed by pharmTinzaparin for therapeutic Tx if GFR <30Dalteparin only in oncology patients for Tx dose

12. Lovenox does bioaccumulateDalteparin does not in esrd at least over 2 weeksTinza is likely even betterI have routinely used regular dose dalteparin for bridging ESRDPractice styles vary widely for lovenoxSome programs use 30 OD even for ESRDLikely fine at least down to gfr 15-20Below that I suspect we are stuck with 5000 BID?

13. Mild CKDIf etiology assumed to be DM, HTN, vascular disease:Quantify proteinuria (ACR or 24hr) and u/aAlso appreciate with most referrals Ca/PO4/PTH/Alb, Ferritin/ Fe sat, +/- SPEPAn u/s is not a bad ideaSerologies - only if suspect GN (clinical or active urine)ANCA, ANA, anti-GBM, C3, C4, CRP, RF, Hep B/C, IgA/IgM/IgGHIV if clinical suspicionINR/PTT useful in case need biopsyDon’t call a Cr of 150 renal failure as it scares patientsChronic kidney disease – mild/mod/severe

14. If labs other than Cr ok, all I will do is Tx HTN and advise DM/ lifestyle to be optimized, quit smoking, diuretics if edema, avoid nephrotoxic drugs, things you are all competent in alreadyIf Cr bumps up a bit but everything else fine, consider holding meds of concern and just rechecking as it can often fluctuateI don’t know what use a BNP in adv CKD is – they will always be highUseful normally if really high or low – check only onceRefer: Persistent progressionIf its just stuck a bit low, but everything else is optimized I don’t have much else to addDon’t get hung up on a specific GFR85M c chronic GFR 50, the kidneys will outlast himGFR <30 – especially if progressingTrouble managing effects of CKD Worried about etiology

15. Adv CKD – PRI clinicPlan for dialysis / decide modalityCKD care as beforeAnemia / iron managementCa/PO4/ PTHDialysis accessMultidisciplinary teamPharm, dieticians, social work, educators, RN, dialysis access coordinators

16. Anemia / ArenespGiven SC/IV q1-4 weeksStarted usually q2weeks ~1/2 wt in KgSide effects - idiosyncraticMax 100 mcg q 1weekWont do much good beyond thatCauses for resistance chronic inflammation, blood / marrow disorders / cancer, Fe deficiency, ongoing losses, Aluminum, PTH out of controlTend to target HgB 100-110Increase strokes/ thrombotic events if higherEpo shorter half life so less convenientRenal program covers it if has CKD

17. Calcium, Phosphate, PTHIn CKD – can’t activate Vit D and tend to retain PO4 leads to:  Calcium  PO4 PTHPO4, PTH are not an acute problemLead to inc vascular calcificationBone fragility Some people are hopeless as control of this is lifestyle dependant on diet and pill compliance

18. Step 1) fix HypocalcemiaRocaltrol –  Ca,  PO4,  PTHStart 0.25 mcg either 3x/wk to ODAll drugs in the family are equivalentIf Ca normal, don’t use it if PO4 more than 2On HD can increase the Calcium in the bathChronic pts tolerate lower Ca better than you think >2 - don’t care>1.7 – just tweak the meds, ER only if symptomatic (numbness, weakness)1.7-1.5 – MD risk tolerance dependant<1.5 – ER for sureIV Ca gluconate and inc the rocaltrol

19. Step 2) fix PO4 with binders and lifestyleTarget <1.7 anything under 2-2.5 is pretty goodApocal 500 TID c meals, can go to 1000-1500mgCa with foods binds PO4Ca on its own increases serum CaSevelemer 800-1600 TID c mealsCalcium sparing – not as potent of a binderI use as 2nd line add on or if hypercalcemiaAluminum works great, but concerns of toxicity limit its use

20. Step 3) PTHCan deal with PTH only after after PO4 is “reasonable”, ideally <2Main Tx is rocaltrol to suppress it (will inc PO4 and Ca)PTH Target Higher than normal as relatively resistant to itESRD - 30-60 Stage 4 - 15-30 Stage 3 - 7-15PTH that’s too low in adults not really a big deal, just back off rocaltrolParathyroidectomy when refractoryI.e. >100-200 chronically++ hungry bone – Can need mega doses Ca and vit D postSinacalet is like a partial medical parathyroidectomy

21. Nephrocalcinosis~30 F, HD x 5+ years Only shows up 1 hour/run, PO4 ~4, PTH >100Will eventually turn into wounds

22. A few tips about HTN drug choiceConsider which side effect might be an issue in this patientCCB - edema, bradycardiaHCTZ - low NaACE/ ARB - high K, more prone to AKI (chronic diarrhea patients)B blocker - BradycardiaCan I get 2 for 1 with a particular drug?Diuretics - edemaB blockers - HF / AF / tremorHelp with high or low KAlpha blocker - BPHACE, ARB – ProteinuriaHydralazine/ NTG - angina

23. HCTZ ineffective with GFR <25Use lasix if want diureticI often hold ACE/ARB once GFR getting ~15-20Prone to high K?Buy a little time before HD as they physiologically lower GFR Alpha blockers (doxazocin) and spironolactone are often a good drug when asking “what else can I add”No role for dual ACE/ARBAliskerin no clear role/ utility

24. ESRD ParadoxesPatients with excellent BP/ PO4/ lipids, less interdialytic weight gain, not obese, etc actually have increased mortalityConfounded by malnourishment, frailty, poor PO intake, weak heart, chronic disease, etcNever shown benefit to treating lipids in ESRDI don’t bother after GFR <30 with statinsOn enough pills anyway and not doing any goodMultiple other mechanisms of CVD – esp vasc calc

25. ESRD – indications to startK, bicarb, volume status that is refractoryUremia most common reasonHad patients feel uremic with Cr 350, others feel fine at 800Start only once feel lousyA bad Cr is not of itself a reason to startIt’s the company that it keeps that mattersGenerally if >1000, I am skeptical if they deny uremia symptomsUremia is insidious Frog in boiling water analogy So slow you get used to it /only when taken away realize how sick you wereChronically weaker, sleeping more, nausea, food not taste the same, dec appetite, itchyjust overall not the person they were 3-6 mo ago as physically declining for no other reason

26. Modality ChoiceIf decision deferred, wont have fistula or PD cath in place at time of startDefault is then HD with line in townOnce decide PD – 0.5-2mo to get catheter, needs 3-4 weeks to heal, then RN time available to trainWe do in IR unless has hernia, large BMI, ++prior surgery2-4 mo from “lets do it” to “ready to go”Fistula – need to see surgeon and often 3 mo to matureMortality benefit, can bath/swim, better clearance, doesn’t get infected, works for years once get it going, no SVC occlusion. Finicky at first and not all will mature

27. PD vs HD - Mortality about the same Individualized choiceProximity to HD center major factor20% die in first year, 35% alive in 5 yearsTend to live ⅓- ¼ of projected remaining life years compared to general populationEnhanced cardiovascular illness is main factorDeath of a thousand cutsPICC lines will destroy the vein Unlikely to ever have a fistula there afterwardIf you need it, so be it, but avoid for softer indications

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30. PDCAPD – continuous ambulatory PDUsually 2 L x 4 exchanges/ day inc qhs long fillCCPD – continuous cycler PDHook up at night to cycler machine 2 L x 4-5 exchanges at night +/- a day fillCycler much more convenientMore alarmsMore drain pain Clearance can be an issue if a slow transporter (slower equilibration)Fast transporter much more commonMostly comes down to pt preference

31. 3 strengths of glucose bagsDetermines how much UF (ultrafiltration)If you can drive a car, no reason you couldn’t do PDIt’s not hard – sterile connection, hang some fluid, push a couple buttons, record BP and weightsMost patients will live with Na 125-135 and Cr 500-800 – that’s okMeasure adequacy by clearance in the fluid not serum creatinineIncrease from baseline may reflect loss RRF, non-compliance

32. PD - advantagesHome always betterSlow / steady-state/ more gentle - HD is more of a short sprintLess acute shifting - not as fatiguing, less hypotensionRetain residual renal Fx longerCosts system half as much as HDEase into ESRD TravelAscites managementSave veins for laterI encourage PD first (or HHD)

33. PD - disadvantages500-800 calories / day extra glucoseHard to get enough clearance for bigger people and more likely to be underdialyzedHernias / Bloating from fluidNeed surgical correction if have before startingCatheter dependant Can get malpositioned / tethered in omentumNot as easy to change as HD lines May need to hold PD/ go on HD while catheter heals as will leakDrain pain

34. More protein wasting than HDLeak – pericatheter, hydrothorax, hydrocelePeritonitis/ tunnel infectionsTreated with IP ABX ceftaz/ancef, and/ or vanc/tobraFYI - 1 dose IP vanco therapeutic for 4-5 daysDon’t give IV vanc if already on IPPatient / family need to have some degree of competence / involvement - BurnoutEncapsulating peritoneal sclerosis - rare

35. HDGenerally 3 x 4 hours/ week4x/week if struggle with fluid gains / removalIf really good residual function - 2x/wkMost have 2-4 L removed per run5L for some heavy gainersCan set different K bathsCan adjust Na, bicarb, Ca, temp also Partially heparinized per run

36. HD – AdvantagesMuch easier to get enough clearanceNot require as competent patient / social situationLess likely to fall through the cracksCan get more fluid off in a shorter timeAvoids PD issues relating to fluid in abdomenLeaks, hernia, infections, caloriesNot need to do the dialysis thing everyday

37. HD - DisadvantagesNot home basedCan leave people feeling wiped out afterCramps, hypotension commonLine infections are usually more severe than peritonitisOccasionally reactions to dialyzerVeins can start to become a scarce commodityNeed for heparin – inc bleeding riskDefault is 1000 bolus, 1000/hr x 3.5 hrs

38. Silver linings of HDNever get poked for outpt labs againEasy to monitor CBC, INR / warfarin, lytes, etcWe can do a bit of minor wound careCaptive audience for a consultant to see Can pre-schedule a visitHD/ PD records all in meditech now

39. Already coming to an IV infusion center 3x/week anyway – no need for CCAC/ PICCWe can dose many IV ABX q HD as GFR low enoughAncef, vanco, tobra, ceftaz, PO cipro, etc covers a lotPRBC support easy to do on HDBlood given on HD is volume neutralArenesp also given in HD IVIV iron routinely usedPO poorly absorbed and causes gut griefOn going losses in circuitOn enough pills anywayI use IV Fe a lot for GIB in non renal patients tooVenofer 500mg x 2 doses and you’re all topped up

40. Home HDQOL better At home and more likely to be able to workAmount varies, but clearance about doubleNocturnal – 8hrs x 3-5days / weekFluid and dietary restrictions markedly relaxedSome patients need PO4 added to their dialysate!HTN better controlled

41. People feel better on it and almost as good as transplant patients feelLess shifting / day-to-day fluctuations6 week training programOnly do if patient motivated or will burn outNot prohibitive to learn but is more involved than PDIf I had ESRD, I’d start with PD and transition to HHD in a couple years as my residual Fx burnt out

42. Withdrawal off Dialysis Good way to die (if not in CHF)Painlessly drift into uremic coma Sudden cardiac arrestTakes 1/2-2 weeks if anuricMuch longer if still peeing plentyFeel free to use their HD line PRN once they are palliativeAlso may use line in resuscitation Need to aspirate out heparin prior to useSaline flush then 2 cc of citrate or heparin (1000 U/mL) afterwardOr just leave it TKVO until HD RN can lock it off for youReluctant allow use line in generalIf not locked properly – will need to be changedNeeds to aspirate 300-400 mL/min or it’s useless for HD

43. Transplant Patient AdviceUsually on tacrolimus (or cyclosporine) and MMFMost on low dose prednisone (occ steroid free protocol)Never acutely stop prednisoneBest way to precipitate acute rejectionNever stop the Tacrolimus / cyclosporine even if septicTac has an NSAID-like vasoconstrictive effect on kidney so minimize other nephrotoxinsProne to high K; PO4/ mg wasting

44. Inc risk of lymphoma, cervical and skin cancerLiving donor – last 15 years, deceased - 10yrCVS disease still very high (better than HD/PD)Non-ATN increase in Cr needs a BxDDx – Ab rejection, cellular rejection, reoccurrence of prior disease, BK nephropathy, drug level too highTx varies from plex/IVIG, thymo/steroids, dec overall immunosuppression, adjusting drug dose

45. Transplant DrugsTacrolimusDm, HTN, drug-drug interactions, tremors, gout, chronic fibrosis of graft, lipids, alopecia MMFDiarrhea, teratogenic, cytopenia, transaminitisMMF is not a big deal to be off for a week PRN

46. CRRT – Continuous Renal ReplacementUsed in ICU Regular HD 0.5-1L per hour x 4 hours, 3x/weekUF not tolerated well on pressorsEasy to get behind with fluid - easily become +10-20L in a weekInstead, how about we take off net 50-200 cc/hr but do it around the clock50cc/hr x 7d is 8.4L, 200cc/hr x 7d is 34L in a weekIntentionally made not as efficient as would otherwise deplete lytes too much as continuousNot as good for toxicology, acute emergenciesRapid shifting of urea/ lytes decreases osmotic pressure Would make more prone to hypotension otherwiseContinuous exposure to heparinCan use citrate to anticoagulate the circuit, not the patient

47. AphaeresisCRRT machines have a different filter that leaks protein / albumin so can do plasmaphersisAllows temporization of acute crisis by removing immune antibodies, it does not stop productionVasculitis, anti-GBM, GBS, MG, antibody mediated transplant rejection, APLA, waldenstroms / hyperviscosity, lipid disordersTTP – supplies the deficient protein and removes AbNeed special machine to do other cell linesStem cell harvest, sickle cell, blast crisis, PltNo clear role in toxicology for pharmacokinetic reasons

48. MeditechFYI – all dialysis records are in meditechYou can print out HD/PD/ Transplant patient med lists as a ready to sign order

49. To End with A few Random Images Purely for Interest -Audience participation requested-Some renal, others notWhat is happening on this EKG?

50. 45M Fulminent Pancreatitis, 3 pressers maxed and dyingFamilial hyper triglyceridemia – on 3 drugs priorTriglycerides at 35Lab techs could recognize his blood by the tubeAsked if could remove itAdvised not sure if clinically relevant to decrease it but nothing to lose so triedFFP cooled him so came down on pressers brieflyDied with triglyceride of 5 and effluent clearedProbably not of utility in acute illness according to metabolic specialist later spoke with in spite of UTD suggestion – case report / publication bias

51. Questions?

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