A presentation which taught us about “when to refer to a renal physician would be perfect, in particular intrinsic renal failure not to be missed in an ICU presentation with AKI, and diagnostic work up prior to assessment by a renal physician?” Adam Kirk Consultant Renal Physician 23 rd October 2014
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A presentation which taught us about “when to refer to a renal physician would be perfect,
in particular intrinsic renal failure not to be missed in an ICU presentation with AKI, and diagnostic work up prior to assessment by a
renal physician?”
Adam Kirk
Consultant Renal Physician
23rd October 2014
Difficult Topic
• The relationship between ICU and Renal; pathophysiologically
• What is there that renal physicians do that ICU do not?
• Key indicators– Renal input – single organ failure with on-going care needed– Weird brain
• Key interventions
• In the acute or more chronic setting
Chronic Kidney Disease
• Aims of referral to address– Establish diagnosis– Anaemia– Bone disease– Cardiovascular risk modification
• Hypertension• Hypercholesterolaemia
– Preparation for Renal Replacement Treatment• Psychologically• Modality• Physically (AVF/Tenckhoff)
80 yrs 120yrs??
eGFR
Age of patient
ESRD
Intervention
Managing CKD: what is our aim?
Death from something other than ESRD or CVD
CONTENTED
LIFE
Management in ICU: what is the aim?
Time (Yrs)
Ph
ysio
logi
cal R
eser
veICU Intervention
DEATH
Estate sorting/New lease
Acute Kidney Injury
• Defined in stages
• Often associated with hypoperfusion/oilgoanuria (<500ml/d)
• Linked to a different cause
– Pre-Renal
– Renal
– Post-Renal
Causes
• Pre-Renal
– Hypoperfusion
• Post-Renal
– Obstruction
NB: - Think age related.
Intrinsic Renal Disease
• Acute Tubular Necrosis (ATN)
• TubuloInterstitial Nephritis (TIN)
• Glomerular Nephritis (GN)
• Vasculitis
ATN• Common and predictable (in high risk scenarios)• Causes
– Oligoanuria– Rise in creatinine– Actual structural renal parenchymal damage
• Pointers– Bland urine (poss some proteinuria 1+)– Raised fractional excretion of Na and urinary concentration
• Prognosis– 60% expect full recovery– 30% suffer residual dysfunction– 5-10% go on to require RRTNB: - Mortality 19-37% in hospital
Tubular epithelial vacuolation
Tubular epithelial flattening
Tubular epithelial sloughing into the tubular lumen
ATN Histological changes(classically)
Tubulointerstitial Nephritis
• Acute usually allergic reaction causing parenchymal AKI with fever, arthralgia and rash (in F>M, 50-60’s)
• Chronology may be 3 – 21 days preceding the onset of symptoms
• Urine can have <modest haematuria and proteinuria (<1g/d), eosinophils present
• Biochem may reveal deranged U/Cr but also Ca.• Treatment