Transcript Nephrology Pearls

Nephrology Insights for Primary Care
- focus on AKI/ CKD/ Dialysis
Kaarlo Hinkkala
MD, FRCPC
Locum Nephrologist – TBRHSC
Assistant Professor - NOSM
Conflict of Interest
Declaration: Nothing to
Disclose
Presenter: Dr. Kaarlo Hinkkala
Title of Presentation: Nephrology Insights for
Primary Care
I have no financial or personal
relationship related to this
presentation to disclose.
Objectives
• Brief survey across the discipline
– Focus on CKD, AKI, ESRD, dialysis
• Cover mainly bottom line issues
• Things I wish people knew / what grinds my gears
• Things you may not have realized we can do
• What we actually do with a variety of problems
• Avoid sedating you with clin epi, basic science, guidelines/
minutia
– Going for a common sense approach here (based on evidence)
• Threw in a few things purely for interest
A Cynical Approach to Nephrology…
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Stop all culprit meds
Flip a coin and give either fluids or diuretics
If that fails do the opposite
If that fails, dialysis will temporarily fix everything
– Fluids, electrolytes, uremia of course
– Hyperglycemia, hypo/hyperthermia, HTN, lipids (via plex)
• Goal of every nephrologist sometimes seems to be to have your
patient die with perfect numbers
– We often get pressured into temporizing hopeless situations until
people man up and put an end to things that need to end
– We’re also often asked to manage the decline
• End stage cardiorenal, hepatorenal, oncology patients
AKI
• Treat acute illness
• Hold ace/arb/ NSAIDS/ diuretics (if not overloaded)
• U/S and U/A
• Consider GN and AIN in DDx
– AIN – PPI, cephalosporin's, septra, NSAIDS, 5-ASA
• Hydrate as much as you think they can reasonably handle
– If bicarb is low use instead of NS
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3amps/ 1L d5w = “normal bicarb” at same rate you would use NS
NS will drive down your bicarb – pH is 5.5
Bicarb will drive down K and will make more CO2 (usually not an issue)
Write order to change to NS once bicarb >18
• Then see where they level out and wait
• HD – lytes / volume reasons or sustained anuria
– Don’t dialyze acutely for uremia
• Unless LOC poor or progressed now to ESRD
• Cardiorenal – sometimes can’t get the fluid off without
inc the Cr
– Just push on and accept the Cr will go up with diuresis
– Either 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 not
– No role to doing it early unless fluid is getting bad
K+ 7.7
Toxicology / dialysis
• ASA, antifreeze /methanol, Lithium
• Call poison control and then us as needed
• Other drugs generally have antidote / too protein
bound, not dialyzed well, not toxic enough, etc
• Decision to HD based on drug level, severity of
symptoms, time of ingestion
IV Contrast
• If important, just do the test and live with the
consequences irregardless of GFR
• Stop / hold any meds that will aggravate AKI
• Hydrate as much as you feel comfortable
– Outpt protocols - bicarb vs NS - use whatever you prefer
– 150ml/hr 1hr prior, then 50 ml/hr x 6hrs is a common
outpt protocol
• Assuming 50 kg (3ml/kg/hr x 1hr, then 1ml/kg/hr x 6hr)
– If already overloaded, perhaps just hold the lasix/ace
• Risk from CT is less than cath
• NAC – homeopathic, but ok to use anyway
• AKI - see within 48hrs, peaks 5-7d
• Risk of AKI in 5-10% range
– Usually mild inc in Cr
– HD - <1%
• Usually has adv CKD / acute illness / temporary
• Dialysis not protective against contrast
• If ESRD (esp if not on PD), there is nothing to lose by giving
dye – kidneys are done
LMWH – renal failure
• With our current formulary would
recommend:
– Lovenox for everyone with normal GFR
• Use 30 OD for GFR 15-30 prophylaxis
• <15 - ?heparin 5000 BID
– Dalt or tinza would be fine in esrd but not allowed by pharm
– Tinzaparin for therapeutic Tx if GFR <30
– Dalteparin only in oncology patients for Tx dose
• Lovenox does bioaccumulate
– Dalteparin does not in esrd at least over 2 weeks
– Tinza is likely even better
– I have routinely used regular dose dalteparin for
bridging ESRD
• Practice styles vary widely for lovenox
– Some programs use 30 OD even for ESRD
• Likely fine at least down to gfr 15-20
– Below that I suspect we are stuck with 5000 BID?
Mild CKD
If etiology assumed to be DM, HTN, vascular disease:
• Quantify proteinuria (ACR or 24hr) and u/a
• Also appreciate with most referrals
– Ca/PO4/PTH/Alb, Ferritin/ Fe sat, +/- SPEP
– An u/s is not a bad idea
Serologies - only if suspect GN (clinical or active urine)
– ANCA, ANA, anti-GBM, C3, C4, CRP, RF, Hep B/C, IgA/IgM/IgG
• HIV if clinical suspicion
– INR/PTT useful in case need biopsy
• Don’t call a Cr of 150 renal failure as it scares patients
– Chronic kidney disease – mild/mod/severe
• 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 already
• If Cr bumps up a bit but everything else fine, consider holding meds
of concern and just rechecking as it can often fluctuate
• I don’t know what use a BNP in adv CKD is – they will always be high
– Useful normally if really high or low – check only once
• Refer:
– Persistent progression
• If its just stuck a bit low, but everything else is optimized I don’t have much
else to add
• Don’t get hung up on a specific GFR
– 85M c chronic GFR 50, the kidneys will outlast him
– GFR <30 – especially if progressing
– Trouble managing effects of CKD
– Worried about etiology
Adv CKD – PRI clinic
• Plan for dialysis / decide modality
• CKD care as before
• Anemia / iron management
• Ca/PO4/ PTH
• Dialysis access
• Multidisciplinary team
– Pharm, dieticians, social work, educators, RN,
dialysis access coordinators
Anemia / Arenesp
• Given SC/IV q1-4 weeks
– Started usually q2weeks ~1/2 wt in Kg
– Side effects - idiosyncratic
– Max 100 mcg q 1week
• Wont do much good beyond that
• Causes for resistance
– chronic inflammation, blood / marrow disorders / cancer, Fe deficiency,
ongoing losses, Aluminum, PTH out of control
• Tend to target HgB 100-110
– Increase strokes/ thrombotic events if higher
• Epo shorter half life so less convenient
• Renal program covers it if has CKD
Calcium, Phosphate, PTH
• In CKD – can’t activate Vit D and tend to retain
PO4
– leads to:
•  Calcium
•  PO4
•  PTH
• PO4, PTH are not an acute problem
– Lead to inc vascular calcification
– Bone fragility
– Some people are hopeless as control of this is lifestyle
dependant on diet and pill compliance
Step 1) fix Hypocalcemia
• Rocaltrol –  Ca,  PO4,  PTH
– Start 0.25 mcg either 3x/wk to OD
– All drugs in the family are equivalent
– If Ca normal, don’t use it if PO4 more than 2
• On HD can increase the Calcium in the bath
• Chronic 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 sure
• IV Ca gluconate and inc the rocaltrol
Step 2) fix PO4 with binders and lifestyle
• Target <1.7
– anything under 2-2.5 is pretty good
• Apocal 500 TID c meals, can go to 1000-1500mg
– Ca with foods binds PO4
– Ca on its own increases serum Ca
• Sevelemer 800-1600 TID c meals
– Calcium sparing – not as potent of a binder
– I use as 2nd line add on or if hypercalcemia
• Aluminum works great, but concerns of toxicity
limit its use
Step 3) PTH
• Can deal with PTH only after after PO4 is “reasonable”,
ideally <2
• Main Tx is rocaltrol to suppress it (will inc PO4 and Ca)
• PTH Target
– Higher than normal as relatively resistant to it
• ESRD - 30-60
• Stage 4 - 15-30
• Stage 3 - 7-15
– PTH that’s too low in adults not really a big deal, just back off rocaltrol
• Parathyroidectomy when refractory
– I.e. >100-200 chronically
– ++ hungry bone – Can need mega doses Ca and vit D post
• Sinacalet is like a partial medical parathyroidectomy
Nephrocalcinosis
• ~30 F, HD x 5+ years
• Only shows up 1 hour/run, PO4 ~4, PTH >100
• Will eventually turn into wounds
A few tips about HTN drug choice
• Consider which side effect might be an issue in this patient
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CCB - edema, bradycardia
HCTZ - low Na
ACE/ ARB - high K, more prone to AKI (chronic diarrhea patients)
B blocker - Bradycardia
• Can I get 2 for 1 with a particular drug?
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Diuretics - edema
B blockers - HF / AF / tremor
Help with high or low K
Alpha blocker - BPH
ACE, ARB – Proteinuria
Hydralazine/ NTG - angina
• HCTZ ineffective with GFR <25
– Use lasix if want diuretic
• I often hold ACE/ARB once GFR getting ~15-20
– Prone 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/ARB
• Aliskerin no clear role/ utility
ESRD Paradoxes
• Patients with excellent BP/ PO4/ lipids, less
interdialytic weight gain, not obese, etc
actually have increased mortality
– Confounded by malnourishment, frailty, poor PO
intake, weak heart, chronic disease, etc
• Never shown benefit to treating lipids in ESRD
– I don’t bother after GFR <30 with statins
• On enough pills anyway and not doing any good
– Multiple other mechanisms of CVD – esp vasc calc
ESRD – indications to start
• K, bicarb, volume status that is refractory
• Uremia most common reason
– Had patients feel uremic with Cr 350, others feel fine at 800
• Start only once feel lousy
– A bad Cr is not of itself a reason to start
• It’s the company that it keeps that matters
• Generally if >1000, I am skeptical if they deny uremia symptoms
• Uremia is insidious
– Frog in boiling water analogy
• So slow you get used to it /only when taken away realize how sick you were
– Chronically weaker, sleeping more, nausea, food not taste the same,
dec appetite, itchy
• just overall not the person they were 3-6 mo ago as physically declining for
no other reason
Modality Choice
• If decision deferred, wont have fistula or PD cath in
place at time of start
– Default is then HD with line in town
• Once decide PD – 0.5-2mo to get catheter, needs 3-4
weeks to heal, then RN time available to train
– We do in IR unless has hernia, large BMI, ++prior surgery
– 2-4 mo from “lets do it” to “ready to go”
• Fistula – need to see surgeon and often 3 mo to
mature
– Mortality 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
• PD vs HD - Mortality about the same
– Individualized choice
– Proximity to HD center major factor
• 20% die in first year, 35% alive in 5 years
– Tend to live ⅓- ¼ of projected remaining life years
compared to general population
– Enhanced cardiovascular illness is main factor
• Death of a thousand cuts
• PICC lines will destroy the vein
– Unlikely to ever have a fistula there afterward
– If you need it, so be it, but avoid for softer indications
PD
• CAPD – continuous ambulatory PD
– Usually 2 L x 4 exchanges/ day inc qhs long fill
• CCPD – continuous cycler PD
– Hook up at night to cycler machine 2 L x 4-5 exchanges at night +/- a day
fill
• Cycler much more convenient
– More alarms
– More drain pain
– Clearance can be an issue if a slow transporter (slower equilibration)
• Fast transporter much more common
• Mostly comes down to pt preference
• 3 strengths of glucose bags
– Determines how much UF (ultrafiltration)
• If you can drive a car, no reason you couldn’t do
PD
– It’s not hard – sterile connection, hang some fluid,
push a couple buttons, record BP and weights
• Most patients will live with Na 125-135 and Cr
500-800 – that’s ok
– Measure adequacy by clearance in the fluid not serum
creatinine
• Increase from baseline may reflect loss RRF, non-compliance
PD - advantages
• Home always better
• Slow / steady-state/ more gentle - HD is more of a short
sprint
– Less acute shifting - not as fatiguing, less hypotension
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Retain residual renal Fx longer
Costs system half as much as HD
Ease into ESRD
Travel
Ascites management
Save veins for later
I encourage PD first (or HHD)
PD - disadvantages
• 500-800 calories / day extra glucose
• Hard to get enough clearance for bigger people and
more likely to be underdialyzed
• Hernias / Bloating from fluid
– Need surgical correction if have before starting
• Catheter dependant
– Can get malpositioned / tethered in omentum
– Not as easy to change as HD lines
• May need to hold PD/ go on HD while catheter heals as will leak
• Drain pain
• More protein wasting than HD
• Leak – pericatheter, hydrothorax, hydrocele
• Peritonitis/ tunnel infections
– Treated with IP ABX
• ceftaz/ancef, and/ or vanc/tobra
• FYI - 1 dose IP vanco therapeutic for 4-5 days
• Don’t give IV vanc if already on IP
• Patient / family need to have some degree of
competence / involvement - Burnout
• Encapsulating peritoneal sclerosis - rare
HD
• Generally 3 x 4 hours/ week
– 4x/week if struggle with fluid gains / removal
– If really good residual function - 2x/wk
• Most have 2-4 L removed per run
– 5L for some heavy gainers
• Can set different K baths
– Can adjust Na, bicarb, Ca, temp also
• Partially heparinized per run
HD – Advantages
• Much easier to get enough clearance
• Not require as competent patient / social
situation
– Less likely to fall through the cracks
• Can get more fluid off in a shorter time
• Avoids PD issues relating to fluid in abdomen
– Leaks, hernia, infections, calories
• Not need to do the dialysis thing everyday
HD - Disadvantages
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Not home based
Can leave people feeling wiped out after
Cramps, hypotension common
Line infections are usually more severe than
peritonitis
• Occasionally reactions to dialyzer
• Veins can start to become a scarce commodity
• Need for heparin – inc bleeding risk
– Default is 1000 bolus, 1000/hr x 3.5 hrs
Silver linings of HD
• Never get poked for outpt labs again
– Easy to monitor CBC, INR / warfarin, lytes, etc
• We can do a bit of minor wound care
• Captive audience for a consultant to see
– Can pre-schedule a visit
• HD/ PD records all in meditech now
• Already coming to an IV infusion center 3x/week
anyway – no need for CCAC/ PICC
– We can dose many IV ABX q HD as GFR low enough
• Ancef, vanco, tobra, ceftaz, PO cipro, etc covers a lot
– PRBC support easy to do on HD
• Blood given on HD is volume neutral
• Arenesp also given in HD IV
• IV iron routinely used
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PO poorly absorbed and causes gut grief
On going losses in circuit
On enough pills anyway
I use IV Fe a lot for GIB in non renal patients too
• Venofer 500mg x 2 doses and you’re all topped up
Home HD
• QOL better
– At home and more likely to be able to work
• Amount varies, but clearance about double
– Nocturnal – 8hrs x 3-5days / week
• Fluid and dietary restrictions markedly relaxed
– Some patients need PO4 added to their dialysate!
• HTN better controlled
• People feel better on it and almost as good as
transplant patients feel
– Less shifting / day-to-day fluctuations
• 6 week training program
– Only do if patient motivated or will burn out
– Not prohibitive to learn but is more involved than PD
• If I had ESRD, I’d start with PD and transition to
HHD in a couple years as my residual Fx burnt out
Withdrawal off Dialysis
• Good way to die (if not in CHF)
– Painlessly drift into uremic coma
– Sudden cardiac arrest
• Takes 1/2-2 weeks if anuric
– Much longer if still peeing plenty
• Feel free to use their HD line PRN once they are palliative
– Also may use line in resuscitation
• Need to aspirate out heparin prior to use
• Saline flush then 2 cc of citrate or heparin (1000 U/mL) afterward
– Or just leave it TKVO until HD RN can lock it off for you
– Reluctant allow use line in general
• If not locked properly – will need to be changed
– Needs to aspirate 300-400 mL/min or it’s useless for HD
Transplant Patient Advice
• Usually on tacrolimus (or cyclosporine) and MMF
– Most on low dose prednisone (occ steroid free protocol)
• Never acutely stop prednisone
– Best way to precipitate acute rejection
• Never stop the Tacrolimus / cyclosporine even if septic
• Tac has an NSAID-like vasoconstrictive effect on kidney so
minimize other nephrotoxins
• Prone to high K; PO4/ mg wasting
• Inc risk of lymphoma, cervical and skin cancer
• Living donor – last 15 years, deceased - 10yr
• CVS disease still very high (better than HD/PD)
• Non-ATN increase in Cr needs a Bx
– DDx – Ab rejection, cellular rejection,
reoccurrence of prior disease, BK nephropathy,
drug level too high
• Tx varies from plex/IVIG, thymo/steroids, dec overall
immunosuppression, adjusting drug dose
Transplant Drugs
• Tacrolimus
– Dm, HTN, drug-drug interactions, tremors, gout,
chronic fibrosis of graft, lipids, alopecia
• MMF
– Diarrhea, teratogenic, cytopenia, transaminitis
– MMF is not a big deal to be off for a week PRN
CRRT – Continuous Renal Replacement
• Used in ICU
– Regular HD 0.5-1L per hour x 4 hours, 3x/week
• UF not tolerated well on pressors
• Easy to get behind with fluid - easily become +10-20L in a week
– Instead, how about we take off net 50-200 cc/hr but do it
around the clock
• 50cc/hr x 7d is 8.4L, 200cc/hr x 7d is 34L in a week
– Intentionally made not as efficient as would otherwise deplete
lytes too much as continuous
• Not as good for toxicology, acute emergencies
• Rapid shifting of urea/ lytes decreases osmotic pressure
– Would make more prone to hypotension otherwise
– Continuous exposure to heparin
• Can use citrate to anticoagulate the circuit, not the patient
Aphaeresis
• CRRT machines have a different filter that leaks protein /
albumin so can do plasmaphersis
• Allows temporization of acute crisis by removing immune
antibodies, it does not stop production
– Vasculitis, anti-GBM, GBS, MG, antibody mediated transplant
rejection, APLA, waldenstroms / hyperviscosity, lipid disorders
– TTP – supplies the deficient protein and removes Ab
• Need special machine to do other cell lines
– Stem cell harvest, sickle cell, blast crisis, Plt
• No clear role in toxicology for pharmacokinetic reasons
Meditech
• FYI – all dialysis records are in meditech
• You can print out HD/PD/ Transplant patient
med lists as a ready to sign order
To End with A few Random Images Purely for Interest
-Audience participation requested
-Some renal, others not
What is happening on this EKG?
•45M Fulminent Pancreatitis, 3 pressers maxed and
dying
•Familial hyper triglyceridemia – on 3 drugs prior
•Triglycerides at 35
•Lab techs could recognize his blood by the tube
•Asked if could remove it
•Advised not sure if clinically relevant to decrease it
but nothing to lose so tried
•FFP cooled him so came down on pressers briefly
•Died with triglyceride of 5 and effluent cleared
•Probably not of utility in acute illness according to
metabolic specialist later spoke with in spite of UTD
suggestion – case report / publication bias
Questions?