Category Archives: Renal

EuAsia Day 2: AKI

Epidemiology of AKI and outcome (YS Guh)

AKI characterised by rapid decrease in renal excretory function

Continuum of injury as it develops which corresponds to worsening prognosis

Multiple definitions with limitations e.g. all depend on urine output and creatinine

Most common cause of AKI – SEPSIS

Increase mortality and morbidity in AKI

CKD is a major risk factor for AKI

The quicker pts recover from the AKI, the better the outcome

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RIFLE criteria for AKI

AKIN criteria for AKI 

KDIGO definitions

Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study.

Recovery after Acute Kidney Injury (2017)


Biomarkers for AKI: what, why, how (@erichoste)

Multiple biomarkers available and indicate different things

May be improve the diagnosis of AKI

Not a single delegate in the room uses biomarkers in clinical practice

Interesting but how does it translate to clinical outcomes/management is currently unknown

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Interactions of AKI with other organs (K Chan)

Affects all organ systems

5 types of cardiorenal syndromes

Relationship with AKI and brain is 2 way

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Acute kidney injury: short-term and long-term effects 

Cardiorenal syndromes

Initiation Strategies for Renal-Replacement Therapy in the Intensive Care Unit 


Contrast-associated AKI: an issue? (M Ostermann)

Incidence depends on pt groups and criteria for AKI

Most of work done in cardiac patients

Most contrast agents have iodine, high isomolarity compared to plasma and have high viscosity

Impact of contrast – contrast-induced AKI associated with poor short and long term outcomes after PCI for STEMI (HORIZONS-AMI) BUT significant limitations

Newer evidence suggest the risk is for pts who had poor renal function prior OR no risk at all

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Contrast-induced acute kidney injury after primary percutaneous coronary intervention: results from the HORIZONS-AMI substudy.

Acute kidney injury in the critically ill: is iodinated contrast medium really harmful?

Post-contrast acute kidney injury in intensive care unit patients: a propensity score-adjusted study.

Contrast-associated acute kidney injury in the critically ill: systematic review and Bayesian meta-analysis.

Prophylactic hydration to protect renal function from intravascular iodinated contrast material in patients at high risk of contrast-induced nephropathy (AMACING): a prospective, randomised, phase 3, controlled, open-label, non-inferiority trial

ICM year in review: respiratory, cardiodynamics and renal

This first session of the day in room Lisbon was a rapid run through of the journals’ most important papers of the last year  – a bumper year as the journals impact factor has soared.

Some notes below:

Respiratory papers

IC-GLOSSARI, the Intensive Care Global Study on Severe Acute Respiratory Infection which was a great ESICM project led by Yasser Sakr and is described as “a multicenter, multinational, 14-day inception cohort study”, in which I admit a COI in that i was involved on one of the sites, but a good paper in that it crossed continents and showed that admission to the ICU for severe lung infection is not only common but also associated with high morbidity and mortality rates.

ECMO epidemiology, this German study showed an increase in ECMO use especially amongst more elderly patients, since 2007.  VV ECMO seems to have reached a “plateau” in use. Mortality has decreased over time – the authors attribute this to experience – but is still stunningly high –  58 and 66 % for vv-ECMO and va-ECMO respectively.

ARDS rehabilitation – Pfoh and colleagues examined “physical declines occurring after hospital discharge” in people who survive ARDS and followed up patients for 5 years.  The headline is that most people decline, and older people and those with co-morbidities decline more.

Lung US training – This paper followed 11 respiratory therapists who had never used ultrasound before over 9 months and claims that 12 scans is the magic number to attain competence.  The jury is out…

The TRACHUS trial looked at ultrasound for tracheostomy – a good idea surely.  Anyway the paper says that it is safe and useful.  As @PhilMcglone said in his review for The Bottom Line – Why choose between bronchoscopy and ultrasound when we can use both?

Finally in the respiratory section this directions-type paper from Jeremy Beitler and the ARDSnet group (now ARDSne(x)t – see what they did there…) on personalising ARDS treatment. The research agenda is going to ask simultaneously both “whether a treatment affords clinically meaningful benefit and for whom.” Watch this space. Or read the paper:

Cardiodynamics and Ultrasound

Antoine Vieillard-Baron discussed the most important papers from this excitingly titled topic.

The FENICE trial was another landmark “global inception cohort study” and looked at fluid management and fluid boluses ( et al).  It showed massive variation in what a fluid bolus is and how it is used.  The question posed by AVL was why did only 2% of physicians use echo to manage fluid? Not enough trainers? Too difficult? Maurizio himself weighed in on the twitter chat below:

Then a study from 3 countries on point of care ultrasound use was presented.  Adrian has reviewed it nicely here for the NEXT journal club – or read the paper.  POCUS is underused generally, and only half the CVC insertions were performed under US guidance.

Finally a nice review article (authored by the presenter) on how to use ultrasound in ventilation management – 4 key areas:

  1. Assessment of cardiac function
  2. Assessment of diaphragmatic function
  3. Assessment of lung function
  4. Identification of pleural effusion


Matt wrote a nice blog on this yesterday, so briefly some of the papers discussed today were:

Statins in heart valve surgery

The kidney injury epidemiology study (AKI-EPI)

And the Truche study – looking again at continuous vs intermittent RRT:

Acute Kidney Injury: Diagnosis, Management and Controversies

Probably the area I feel least comfortable with on the AICU so looking forward to an update – especially with regard to RRT. Brexit jokes only allowed for first hour according to the chair….

Excellent overview from basic pathophysiology to RRT. 3 excellent reviews worth mentioning that were highlighted:

Acute kidney injury and sepsis:

Pathophysiology of acute ischaemic kidney injury:

Fluid management in AKI:

Acute Kidney Injury

Is all AKI the same? (Lui Forni)

NO! AKI is a syndrome –  IMPORTANTLY does not include the cause…


  1. Specific kidney diseases e.g. glomerulonephritis
  2. Non specific e.g. ischaemia
  3. Extra renal e.g. obstruction

Beware the hidden tiger in the AKI without obvious cause

Transjugular renal biopsy by interventional radiologists potential option in coagulopathic patient

Pathogenesis of AKI (John Prowle)

Again – reinforcing AKI is a heterogenous clinical syndrome – multifactorial

ATN first described in 1941 in Blitz survivors. Crush injuries with secondary mortality from renal failure:

Key points:

  1. Baseline risks e.g hypertension
  2. Acute pathology e.g. sepsis
  3. Nephrotoxicity e.g. drugs

Like playing the fruit machines in UK – if all three come up, highly likely to develop AKI

Treatment of the above:

  1. Recognise risks
  2. Treat and mitigate pathology
  3. Avoid unnecessary nephrotoxin exposure

Conventional belief that AKI is driven by global organ ischaemia – theory that has now been challenged

Commonest association with AKI is sepsis BUT unlikely due to purely global hypoperfusion

More important = balance between kidney ischaemia and inflammation injury

Endothelial cell activation, injury and reduced microvascular flow play major role – may not be dependent on global macrovascular flow –

Noradrenaline may increase glomerular pressure without compromising renal perfusion and restore GFR

BUT if tubular injury due to inflammation – cant be manipulated by systemic haemodynamics as reduction in renal blood flow in AKI – mediated by tubular dysfunction

Take home messages:

  1. Initially in septic shock – increasing BP may increase UO.
  2. In establised AKI – nil benefit. (except potentially in HT patients – renal hypertension challenge to assess improvement in UO)

Epidemiology of AKI – Ville Pettila

Incidence of AKI in ICU around 40-60%

RRT in AKI 300-600 per million population

Top 5 causes: Hypovolaemia/diuretics/hypotension/colloids/severe sepsis

Even stage 1 AKI associated with increased mortality

Interesting question about lack of routine followup for patients with AKI? e.g. compared to acute MI

Need to engage local nephrology services early in arranging followup review

Prevention of AKI – Miet Schetz

Reinforcing above: Patients at risk of AKI

  1. Baseline risks
  2. Acute conditions
  3. Nephrotoxicity

Interplay between risk factors v insults

Radiocontrast, aminoglycosides, ACE-I

Limited evidence in witholding ACE-I  – cardiac cath:

Seem to be functional but not structural changes to kidney – ?lack of evidence of harm

Fluid overload bad for the kidney. Two excellent papers on fluid management:

Choice of fluid also important:

General message – starches = bad

6S trial NEJM  –

Myburgh 2012 NEJM –

So then, saline or buffered crystalloid solution? – choride restrictive regime associated with reduced incidence of AKI and RRT – SPLIT trial – nil difference in renal outcomes with buffered crystalloid v saline (but ?low risk pts and low volumes crystalloids)

Take home messages:

  1. Starches nephrotoxic in sepsis and ICU
  2. Hyperchloraemia may induce renal vasoconstriction
  3. Hypotension duration/severity related to AKI
  4. Earlier use of vasopressor may be advantage
  5. No adverse effect of vasopressor on renal function in patients with vasoplegic hypotension
  6. Targets should be individualised


Renal replacement therapy

Case study? Need for RRT? (Eric Hoste)

Majority of people would not start RRT in AKI stage 1 in patient with abdominal sepsis and laparostomised abdomen

By AKI – stage 3, still a third of audience wouldnt start RRT

Such a disparity. Compared to cardiac/respiratory support – potentially clearer decisions on e.g. intubation etc

When to start RRT? (Michael Darmon)

Current practices

Survey of practice in nephrologists:

Median Ur 20/ Cr 322 for initiation of RRT

Should we start earlier in patients with haematological instability?  –  Small RCT – deleterious effect of haemofiltration during early phase sepsis

Risks/Benefits of early RRT pre-classical indications?

Risks of early RRT?

  1. Unrequired RRT in pt with spontaneous recovery
  2. Risk of catheter insertion and extracorporeal circuit
  3. Depletion of drugs, nutrients, electrolytes
  4. Resource consumption

Benefits of early RRT?

  1. Prevention of electrolye disturbance
  2. Homeostasis – better fluid balance

Should we start premptive RRT then? Before classical indications? – suggestion of beneficial effect on survival but heterogeneous studies ++

AKIKI study – RCT in NEJM 2016:

  • KDIGO stage 3
  • Within 6h or discouraged until usual criteria or >12h
  • No difference in mortality. Decrease in RRT requirement by 50%

ELAIN study may provide more data –


  • Definition of delayed RRT differs across studies
  • Most of studies are at high risk of bias
  • Factors leading to RRT initiation are not taken into account
  • A single study was randomised
  • Patients with severe AKI who did not require RRT are usually excluded from observational studies

Take home messages:

  1. Optimal timing remains unknown
  2. Most interventionalists would start RRT within 24 hours in KDIGO stage 3 patients (without waiting for conventional indications)
  3. Data resulting from RCTs remains conflicting and hard to interpret 
  4. Late strategy may help avoiding RRT in up to 50% patients
  5. What is the role of uraemia (beyond fluid overload) in systemic organ failure

What modality to choose? (Heleen Oudemans-van Straaten)

Key points from the talk:

  1. Timeframe (intermittent/continuous)
  2. Mechanism (HD/HF)
  3. Type of buffer (lactate v bicarbonate)
  4. Type of A/C (heparin v citrate v nothing)

Boils down to short term benefits, long term benefits and local expertise/facilites

Intermittent HD could provoke hypotension in unstable patient

Dialysis disequilibrium syndrome. Early from cirulation, late from brain —> cerebral oedema. Due to reversed osmotic shift

Cochrane review in 2007 – no difference in mortality/renal recovery and haemodynamic stability

BUT: Higher MAP and lower need for vasopressor dose escalation

KDIGO recommendation: Use IHD and CHD as complementary techniques in ICU patients

HD v HF v HDF – need to choose dependent on patient and timing

Take home messages:

  1. Initial RRT modality? Consider
    • Haem instability
    • Fluid overload
    • ICP
    • Renal recovery
    • IHD in patients with stable clinical picture and improving
  2. No robust clinical difference between HD and HF
  3. Cautious with lactate buffering in shock/liver dysfunction

Citrate v Heparin coming later!


Which membrane for RRT? (Thomas Rimmele)

Which polymer?

Molecule removal = function of size and plasma concentration.

But uraemic toxins and essential proteins – comparable mol weights

Plasma concentration – like looking for needle in a haystack? Might want to be more specific in which molecules to focus on


Vasopressin may show benefit in less severe shock in VASS trial

  • ? Weans noradrenaline early
  • ? Dose to low
  • ? Harmful interaction

May reflect beneficial effects on renal function

VASS also suggested that vasopressin + steroids better than noradrenaline + steroids

Questions therefore

  • Should we use earlier?
  • Should we use higher doses?
  • Should we use it with steroids

Factorial 2X2 double blinded RCT < 6/24

  • Vasopressin 0.0-0.06 u/min OR noradrenaline 0-12mch/min
  • When maxed out added either Hydrocort 50mg q6h or placebo

After this, open label catecholamines could be added but would be weaned first

Included adult septic patients, first episode of shock

Exclusions other reasons for steroids, CKD needing RRT

Primary outcome renal failure free days as defined by Stage 3 AKIN

414 randomised, even split

Matched groups

  • Men > women
  • APACHE mean 22
  • 80-90% received noradrenaline pre-randomisation
  • Usually included within 3/24
  • Typical creatinine around 120-130

No difference in haemodynamics between the two groups but noradrenaline group needed more noradrenaline to do so

Fluid requirements and lactate concentrations much this same

Median creatinine level lower in vasopressin patients than noradrenaline

  • No difference in distribution of renal failure
  • No difference in survivors who ever developed renal failure
  • No difference in non-survivors or survivors who did develop renal failure

No difference in mortality. No benefit to adding steroids.

Number of patients who required RRT was significantly lower (ARR 10%) than those who didn’t but once you needed dialysis, duration of that was the same

Conclusion: Early vasopressin maintained BP and reduced noradrenaline requirements as well as reducing the need for RRT but did not reduce the number of renal failure free days