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Renal Failure Detecting, Averting & Managing
Damian Fogarty BSc MD FRCP @DamianFog
Real, Real, Gone. What Happens when it Fails
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!
Barn door kidney failure Pressure or volume loss
Trauma Sepsis GI loss Urinary losses Poor oral intake Pressure-Volume toxic medications
ACEi ARBs Diuretics
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
Perfectly managed AKI
7
Who sees AKI?645 cases in NCEPOD report case review
8
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
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
Precarious renal circulation in elderly patients
Too wet-CCF risks
Too dry-At risk of AoCKD/AKI
Mortality risk cc no AKIx2 fold
x6 fold
x9 fold
KDIGO Position Statement on Acute kidney injury. Kidney International 2012
Kidney disease not as complicated as most think !
Water and ‘solute’ Coffee
15
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%
16
NCEPOD Top 10 risk factors-usually multiple
Tools of the trade - very high tech!
Observations Vital ! Fluid balance
+
+Urine
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
18
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
21
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
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
23
Perfectly managed AKI
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
25
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
27Age
Diabetes
Obesity
Age
High Blood
Pressure
Smoking
1990
Per million population205+ (260)125 to <20557 to <12549 to <57below 49 (44)
Chronic dialysis incidence rates due to diabetes
2000
29
1
10 at clinics
100 in primary care
Chronic Kidney DiseasePopulation prevalence
0.5 %
5 %
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
Non linear relationship between real GFR and serum creatinine
Creat = 60 µmol/l
Creat = 120 µmol/l
If creatinine doubles GFR halves
♂
32
5 10 15 20years
Elevated BPRising creatinine
Albuminuria can occur many years before other features of CKD
Albumin in urine
100
30
3
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
Prevention of progressive kidney and vascular disease
34
Hypertension
BP control slows DN progression
35Parving et al, BMJ 1987
The lower the BP The lower the BP the better the renal outcome….in these the better the renal outcome….in these studies!studies!
36
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
Don’t be too quick to stop RAAS inhibitors with stable rises in creatinine/potassium & patient under close follow up
38
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?
CKD management a marathon not a sprint!Take time to lower the BP
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.
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
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