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Renal Failure Detecting, Averting & Managing
Damian Fogarty BSc MD FRCP @DamianFog
Real, Real, Gone. What Happens when it Fails
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Disclosures & disclaimers Funded research 2000-2014 from Kidney Research
UK, Juvenile Diabetes Foundation, NI HSC Research & Development; NIHR; UK Renal Registry
NICE Anaemia of CKD 2013-2015 GDG Event adjudication for Carmelina Trial (Novartis) Lecture honoraria ~2/year from Boehringer; Baxter-
PD; Pharmacosmos; Novo Nordisk. No private practice
I also struggle with renal tubular acidoses!
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Barn door kidney failure Pressure or volume loss
Trauma Sepsis GI loss Urinary losses Poor oral intake Pressure-Volume toxic medications
ACEi ARBs Diuretics
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Pre-renal AKI leading to ATN
Prerenal disease
Acute tubular necrosis
intact kidney function
renal injury
timeSpectrum accounts for 2/3rd of all AKI
Biggest risk for AKI is CKD
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Perfectly managed AKI
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Who sees AKI?645 cases in NCEPOD report case review
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Importance of AKI-ARF Acute Kidney Injury/Renal Failure
Incidence over last 20 years: 2% 5% of hosp admissions 15-30% preventable 50% had room for improvement Figure fell to ~30% if AKI developed during a hospital admission
rather than being diagnosed at admission 24% did not receive adequate senior review
Quality of care in this group was judged to be less good 85% did not have documented evidence of
critical care outreach involvement
http://www.england.nhs.uk/wp-content/uploads/2013/06/a06-acu-kidney-inj-ad.pdfhttp://www.ncepod.org.uk/2009aki.html
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Hsu R et al Temporal Changes in Incidence of dialysis-requiring Acute Kidney Injury. JASN. 2013;24:37–42.
Post MI
Post surgery
CCF
Sepsis
The growth of acute kidney injury. Siew ED, Davenport A, Kidney International Jan 2015
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Precarious renal circulation in elderly patients
Too wet-CCF risks
Too dry-At risk of AoCKD/AKI
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Mortality risk cc no AKIx2 fold
x6 fold
x9 fold
KDIGO Position Statement on Acute kidney injury. Kidney International 2012
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Kidney disease not as complicated as most think !
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Water and ‘solute’ Coffee
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Approach to renal failure
Medications & OTCs Contrast agents Light chains Glomerular Dx
Assess volumes Pump & Pressure <110mmHg Vasodilation & Sepsis 3rd spacing-Liver Dx, albumin
PRE-RENAL RENAL POST-RENAL
Catheterise Scan kidneys Monitor volumes out
80% 10% 10%
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NCEPOD Top 10 risk factors-usually multiple
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Tools of the trade - very high tech!
Observations Vital ! Fluid balance
+
+Urine
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Fancy & forgotten tests
More of these1. Free light chains (wt loss-back pain)2. CK esp with low GCS; alcohol; drugs3. LDH & blood film (platelets ) 4. Cultures if any hypo-tensive/thermic5. Calcium 6. Anti-cardiolipin/phospholipid7. Bicarbonate & lactate8. Urine for ACR (Alb:Creatinine Ratio)9. UNa<20 mmol/L = volume sensitive
Less of these1. “Renal Screen”2. ANCA for vasculitis
with normal CRP & ESR
3. ANA for lupus in 80 year old men
4. ASO titres5. Urine osmolality6. Serum osmolality
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Top tips More of this
1. Involve critical care earlier2. Review the history from home/relatives3. Postural BP & Pulse changes4. Dry or wet? -CXR and SaO2 help5. Measure output properly- not ”PUT”6. Incontinent-catheterise7. Hold most or all drugs8. Review drug doses on Renal Drug
Handbook https://renaldrugdatabase.com9. In frail elderly-RAAS agents @6pm10. Stage 3 AKI involve renal earlier
Less of this1. Diuretics & fluids together2. Treating K+ <5.5 every 6
hours. 3. 3 x CT scan & contrast in 4
days4. Urgent USS when cause
obvious
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Relieving urological obstruction• Refer all patients with upper tract urological obstruction
to a urologist.
• Immediate referral if one or more of following present:• Pyonephrosis i.e. sepsis & obstruction• Obstructed single kidney• Bilateral upper urinary tract obstruction
• When nephrostomy or stenting required – undertake as soon as possible and within 12 hours of diagnosis
NICE CG169
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Drug issues Drugs interfering with renal perfusion/volume
ACE inhibitors and angiotensin receptor blockers NSAIDs All antihypertensives/Nitrates /Nicorandil Diuretics (loop and thiazide)
Drugs requiring dose reduction or cessation Low molecular weight heparins Opiates Metformin (associated lactic acidosis) Sulphonylurea-based hypoglycaemic agents Aciclovir
Interstitial nephritis (± rash, eosinophilia) Omeprazole and other PPIs Penicillin based antibiotics HAART
Drugs requiring close monitoring Warfarin Aminoglycosides-longer courses more injurious
Drugs aggravating hyperkalaemia Digoxin Beta blockers Trimethoprim Potassium sparing diuretics e.g. spironolactone, amiloride
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Indications for AKI Referral to a Nephrology or ICU Team
If AKI is part of multi organ failure more appropriate to refer to ICU. Patients likely to need dialysis or specialist renal treatment:
1. Hyperkalaemia (> 6.5 mmol/L) refractory to medical management2. Pulmonary oedema refractory to medical management3. Severe metabolic acidaemia pH ≤ 7.2 due to kidney failure; HCO3 <124. Uraemic complications (pericarditis or uraemic encephalopathy)A. Renal transplantB. Chronic kidney disease (stage 4 or 5)C. Patients suspected of intrinsic renal disease (vasculitis, primary GN, interstitial
nephritis) Nephrology – Conservative Care Interface
AKI may be part of a terminal illness in a hospitalized patient. Severity of the clinical event/progression of advanced untreatable co-morbidity
critical. Senior medical & nursing staff should identify early in the course of their deterioration Decide on ceilings of care & appropriateness of referral to ICU/renal team. If in doubt discuss
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Perfectly managed AKI
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My first e-alert (aka phone an old friend) Male age 56, T2DM x 20 years, lifelong asthma IHD-CABG 22nd Feb 2011 Fri 25th Feb ICU to ward.
Text from his brother (friend of mine) that his creatinine was 100 post op and now 188.
Sitting in bed- thought SOB normal; cough Apyrexic, tachycardic ~100/min SR Dull left base.
Metformin and ACEi stopped Started on Taz Euvolaemic
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Creat 70umol/l in the year 2000; Drifted slowly to 100-120 prior to CABG. Does he need follow up?
NICE says yes based on: ~3-5% of pure AKI patients develop CKD in next year
versus 1-2% of any hospitalised patient (~RR 3; absolute risk small)
Much higher if dialysis requiring: follow up these
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27Age
Diabetes
Obesity
Age
High Blood
Pressure
Smoking
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1990
Per million population205+ (260)125 to <20557 to <12549 to <57below 49 (44)
Chronic dialysis incidence rates due to diabetes
2000
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1
10 at clinics
100 in primary care
Chronic Kidney DiseasePopulation prevalence
0.5 %
5 %
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40 80 120
number
weegranny body-builder
serum creatinine is normally distributed according to muscle bulk
umol/l
Interpreting serum creatinine‘normal range’ 40-110 umol/l
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Non linear relationship between real GFR and serum creatinine
Creat = 60 µmol/l
Creat = 120 µmol/l
If creatinine doubles GFR halves
♂
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5 10 15 20years
Elevated BPRising creatinine
Albuminuria can occur many years before other features of CKD
Albumin in urine
100
30
3
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EstimatedGFR
(mls/min)
100
50
Years
Dialysis
4321 5
Progression of CKD
Rapid progressionSlow progression
Stable
10
Markers of rapid progression?•High blood pressure •Proteinuria•AKI events
If CKD stage 3 (GFR 30-60)•25% will have a vascular event in next 5 years•1% will be on dialysis
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Prevention of progressive kidney and vascular disease
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Hypertension
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BP control slows DN progression
35Parving et al, BMJ 1987
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The lower the BP The lower the BP the better the renal outcome….in these the better the renal outcome….in these studies!studies!
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EstimatedGFRas %
100%
50%
Years
Dialysis4321 5
Progression of proteinuric CKD best controlled by Renin Angiotensin Aldosterone (RAAS) blocking drugs
Rapid progression
Slow progression with ACEi or ARB
10%
ACE or ARB started: Creat 130 before, 150 after BUT slower decline in GFR fall
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Don’t be too quick to stop RAAS inhibitors with stable rises in creatinine/potassium & patient under close follow up
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Before stopping RAAS inhibitors check patient not dehydrated; stop diuretics; stop NSAIDs.
Check BP
Post AKI-does the patient need to restart RAAS drug for proteinuria?
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CKD management a marathon not a sprint!Take time to lower the BP
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Creat 70umol/l in the year 2000; drifted to 100-120 with no ACR rise (2mg/mmol).
? DKD due to interstitial and or arterial aetiology not pure diabetic nephropathy.
Remote follow up from renal ACR now rising so will be seen now 5 years later.
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Assess AKI risks & volume (early & often) Pre, intra & post renal causes; Pre, intra & post renal monitoring & management CKD common but higher risks from vascular
outcomes Proteinuric are most progressive/preventable Stop more volume/pressure toxic drugs in AKI Start & restart them in the proteinuric CKD patient41
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References1. NICE Acute Kidney Injury clinical guidance (CG169) (2013) http://guidance.nice.org.uk/CG1692. National Confidential Enquiry into Patient Outcome and Death (NCEPOD) “Acute Kidney Injury:
Adding Insult to Injury (2009) http://www.ncepod.org.uk/2009aki.htm 3. Elective and Emergency Surgery in the Elderly: An Age Old Problem (2010)
http://www.ncepod.org.uk/reports2.htm 4. Renal Association Clinical Practice Guidelines: Acute Kidney Injury (2011)
http://www.renal.org/Clinical/GuidelinesSection/AcuteKidneyInjury.aspx5. British Consensus Guidelines on Intravenous Fluid Therapy for Adult Surgical Patients (2011)
http://www.bapen.org.uk/pdfs/bapen_pubs/giftasup.pdf6. NICE Intravenous Fluid Therapy clinical guidance (2013) http://guidance.nice.org.uk/CG/Wave25/5
Perioperative acute kidney injury: risk factors, recognition, management, and outcomes. Clinical Review. Borthwick E, Ferguson A. BMJ 2010 Jul 5;341:c3365. doi: 10.1136/bmj.c3365.
7. GAIN Northern Ireland Guidelines for Management of Chronic Kidney Disease (2010) http://www.gain-ni.org/images/Uploads/Guidelines/Chronic%20Kidney%20Disease.pdf
8. GAIN Guidelines for the Treatment of Hyperkalaemia in Adults (2009)http://www.gain-ni.org/images/Uploads/Guidelines/hyperkalaemia_guidelines.pdf
9. Surviving Sepsis Campaign http://www.survivingsepsis.org/bundles/Pages/default.aspx10. NICE CKD Guidelines 2014. https://www.nice.org.uk/guidance/cg18211. KDIGO guidelines: http://kdigo.org/home/guidelines/
@DamianFogdamian.fogarty@belfasttrus
t.hscni.net