This document discusses when intensive care unit patients should be referred to renal physicians. It notes key indicators for referral include single organ renal failure requiring ongoing care or abnormal kidney function that requires a renal diagnosis. The document outlines various acute and chronic kidney conditions and diseases that renal physicians evaluate and manage, including acute kidney injury, chronic kidney disease, glomerulonephritis, vasculitis, and issues in transplant patients like acute rejection. It emphasizes the importance of establishing diagnoses and developing management plans for renal patients that may involve specialized treatments.

1. 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

2. 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

3. 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)

4. 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

5. Management in ICU: what is the aim?
Time (Yrs)
PhysiologicalReserve ICU Intervention
DEATH
Estate sorting/
New lease

6. Acute Kidney Injury
• Defined in stages
• Often associated with
hypoperfusion/oilgoanuria (<500ml/d)
• Linked to a different cause
– Pre-Renal
– Renal
– Post-Renal

7. Causes
• Pre-Renal
– Hypoperfusion
• Post-Renal
– Obstruction
NB: - Think age related.

8. Intrinsic Renal Disease
• Acute Tubular Necrosis (ATN)
• TubuloInterstitial Nephritis (TIN)
• Glomerular Nephritis (GN)
• Vasculitis

9. 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 RRT
NB: - Mortality 19-37% in hospital

10. Tubular epithelial
vacuolation
Tubular epithelial
flattening
Tubular epithelial
sloughing into the
tubular lumen
ATN Histological changes
(classically)

11. 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
– Remove offending cause
• Drug vs bug
– Consider steroids (no convincing evidence)

12. Causes and treatment
• Drugs
• NSAIDS
• Penicillins, cephalosporins,
rifampicin, sulphonamies
• Diuretics
• PPI’s
• Allopurinol
• Anti-retrovirals
• TB, Sarcoidosis,
legionella, leptospirosis
• Autoimmune disease
association
• Steroid consideration
– HD needing
• Steroids
– HD independent,
observe for 10d
• No improvement – Pred
• Improvement – masterful
inactivity
• Dose Pred 1mg/kg on
reducing course for 3-
6months

13. Inflammatory cell infiltrate
- Mononuclear cells
- Eosinophils
Note: - the presence of
interstitial fibrosis
imparts a worse prognosis
Tubulointerstitial Nephritis

14. GlomeruloNephritis
• Syndrome of
– AKI
– Haematuria and proteinuria
– Salt and water retention
• General principals
– TIGHT fluid balance
– Na/water restriction
– BP control <130/80
– Loop diuretics
– ACEi/ARBs

15. IgA vs Post-Infectious
• IgA – autoimmune condition
– IgA1 deposition in the mesangium setting inflammation and fibrosis
– Onset at any point; can occur at the time of upper airways infections
“synpharyngetic haematuria”
NB: - Associated condition Henoch-Schonlein Purpura
– Tetrad – abdo pain, arthralgia, rash and AKI
– Rash buttocks, legs and arms – self limiting
– Adults – worse prognosis
• Post-infectious
– Staph, strep, syphilis
– Influenza B, Mumps, coxsackie, HBV, EBV
– Malaria, toxoplasmosis, schistosomiasis
– IC mediated 3-21 days after infection
– Self limiting, requires symptomatic treatment and of the cause

16. IgA Glomerular deposition in
Henoch-Schonlein Purpura

17. TTP vs HUS
• TTP
• ADAMTS13 cleaves vWF to mature smaller molecule
– Doesn’t in TTP causing TMA
• Classic pentad
– Fever, MAHA, thrombocytopenic purpura, renal failure and
neurological symptoms
• Management – PEX
• HUS– MAHA, thrombocytopenia and AKI
• Diarrhoea positive – shiga-like toxin
• Diarrhoea negative – Factor H deficiency (or one of a
multitude now)
• Supportive therapy inc PEX, Eculizumab (Mab C5
complement)

18. Nephrotic Syndrome
• Triad – Hypoalbuminaemia, oedema and
Proteinuria (>3g/d)
• Causes
– Diabetic nephropathy – diabetes (!), do not miss other causes
– Minimal Change – Unchanged secretory renal function
– Membranous Nephropathy – malignant concern
– FSGS – rapidly progressive and long-term damaging
– MCGN – as above
– HIVAN – black HIV +ve
– Amyloid, myeloma, light chain disease – haemotology diagnosis, renal
complications
– SLE – rheumatology diagnosis, renal complications

19. Considerations
• Protein loss
• Anticoagulation
• Causes
• Treatment
– Prednisolone
– Immune suppression

20. Vasculitis
• Fever, weight loss, myalgia
• Flitting symptoms
• Multisystem – consider in situation where
“nothing fits” and AKI
• Investigations
– Full bloods inc
• Immunoglobulins, ANCA, ANA, complement, protein
electrophoresis, coagulation
– AUSS
– CXR film
– Urine dip and quantification (protein)

22. ANCA Positive
• Biopsy – FSGS, crescents ± granulomata
• Treatment
– Prednisolone
• MP 500mg IV stat if Cr^, Cr>500 or pulm haemorrhage
• Pred 1mg/kg/day
– Cyclophosphamide
• 1-2mg/kd/day
– PEX
• Pulm haemorrhage
• Cr >500
• Anti-GBM +ve
• NB: Key difference with MP vs PEX, MP less risk and used at lower
threshold.

23. Immunofluorescence demonstrating ANCA
pattern of labelling
P-ANCA Pattern
(MPO)
C-ANCA Pattern
(PR3)

24. Anti-GBM disease
• Pathogenic IgG binds α3 region of collagen IV
(BM in glomeruli and alveoli)
• Usually more devastating
• Single hit disease – so make diagnosis and
treat ASAP
• Biopsy – FSNGN, ruptured Bowman’s capsule
• Treatment
– RRT
– Steroids (MP 1g x3, then Pred)
– PEX

25. Additional ones not to be missed
• Myeloma/Light chain abnormalities
– Require biopsy of some sort
• Lymphoma
– De novo OR Post-Transplant Lymphoproliferative
Disorder (PTLD)

26. Key investigations
• Immunoglobulins
• Hepatitis Serology (B/C)
• Complement
• Protein Electrophoresis
• ± Bence Jones
• Up to you. PE Strip should cover all eventualities of
secretory of non-secretory myeloma

27. Transplant
• Considerations when dealing with sick pt
– At time of transplant, ESRD
• This implies all renal complications are fair game
– Background viral activity becomes more central
• CMV/EBV/BK/HIV/Hepatitis
– Transplant career important
• Immune suppression levels
• Rejection episodes
– Time since and transplant and level of success

28. Acute Rejection
• Classic triad
• Fever, Oliguria, graft tenderness
NB: - less available now with better immune suppressants
• Prompt assessment/treatment ESSENTIAL
• Implications on long-term graft function/outcome
NB: - Successful treatment of AR within T+60d has little
affect on graft outcome.

29. Risk Factors
• High Risk
• African American
• Sensitization
– Prev Tx
– Pregnancy
– Blood Transfusion
• Delayed Graft Function
– Deceased donor source
– Increased donor age
– Prolonged ischaemic time
– Donor brain death
– Donor acute rejection
• HLA mismatch
• Positive PreTx Bcell Crossmatch
• ABOi/HLAi
• Co-existing infection
• Adolescent recipient
• Previous rejection episode
• Low Risk
• Zero mismatch
• Elderly recipient of young healthy
donor
• Pre-emptive transplant
• Living donor source
• First Transplant

30. Assessment/Treatment
• Assessment
– Urine dip
– Obs
– Biochemistry with
trough IS levels
– AUSS
– Kidney biopsy
• Treatment
– Pulsed steroids
– Consider increasing the
IS
– Continual review to
ensure improvement
– Re-review with view to
additional AR treatments
eg ATG

31. Differential diagnosis of Allograft
dysfunction
• Week 1
– ATN
– Rejection
– Obstruction/leak
– Clot art/vein
• <12 weeks post-Tx
– AR
– CNI toxicity
– Volume depletion
– Obstruction
– Infection (inc virus)
– Interstitial disease
– Recurrent primary disease
• >12 weeks post-Tx
– AR
– Volume contraction
– CNI Toxicity
– Obstruction
– Infection
– Chronic allograft
nephropathy
– Recurrent primary disease
– RAS
– PTLD

32. Post-Transplant Infections
• 1-6 months
• Opportunistic/non-
conventional
– CMV/HHV-6/HHV-
7/EBV/VZV/influenza/RS
V/adenovirus
• Aspergillus,
cryptococcus,
nocardia, listeria
• Legionella, TB, PCP
• HBV, HCV, HIV
• <1 month
• Post –op bacterial
– UTI/ Resp/ Vascular
related/ wound
• Nosocomial
– Inc legionella
• HSV
• Candida
• Untreated undeclared
disease (donor origin)
• >6 Months
• Late opportunistic
• Cryptococcus,
CMV retinitis or
collitis, VZV,
parvovirus B19,
Polyoma (BK),
HBV HCV
• Malignancy
• EBV, Papilloma,
HSV, HHV-8
• CAP/other infections

33. Summary
• Bloody difficult from ICU
• When to refer
– When there is a renal diagnosis requiring renal
intervention/advice
– When there may be and further
brains/interference may benefit the patient
prognosis
– Known renal patient esp Transplant

34. To consider on referring
• PMH is essential to understanding how the
patient got where they are
• PMH essential to understanding possible
response to considered therapies
• Masterful, highly qualified, skilful inactivity is
not always a bad thing

35. Thank you
Any questions