1. Acute kidney Injury(AKI)
Dr Dana Ahmed Sharif
Renal Physician
MRCP UK/ MRCP London

2. Resource materials Davidson’s Principles & Practice of Medicine
Kumar & Clark Clinical Medicine
Oxford textbook of Clinical Nephrology
Oxford handbook of Nephrology and hypertension
Renal Association website(
K/DOQI guideline (
AKI network (

3. Renal function
Kidney has many roles:

4. Renal function
Kidney has many roles:
- Excretory function

5. Renal function Kidney has many roles: - Excretory function
- Osmolality regulation

6. Renal function Kidney has many roles: - Excretory function
- Osmolality regulation
- Acid base balance

7. Renal function Kidney has many roles: - Excretory function
- Osmolality regulation
- Acid base balance
- BP regulation through
salt and water balance

8. Renal function Kidney has many roles: - Excretory function
- Osmolality regulation
- Acid base balance
- BP regulation through
Salt and water balance
- Hormone secretion ( Erythropoietin, Vit D3)

9. Definition of Acute Kidney Injury
Acute usually reversible decline in renal function*
Rapid time course( < 48 hrs)
Reduction of kidney function:
A- Rise in serum creatinine, defined by either:
1- absolute increase in serum creatinine of >0.3mg/dl( >26µmol/l)
2- % increase in serum creatinine of > 50%
B- Reduction in urine output, defined as < 0.5ml/kg/hr for more than
6 hrs
* Acute kidney injury network

10. Incidence of AKI* 500 ppm/year – UK ( up to 38,000/yr)
Incidence of AKI needing dialysis 200 ppm/year
Pre renal and acute tubular necrosis (ATN) accounts for 75% of the cases of AKI
7% of all hospital admissions( 65% of intensive care admission)
Mortality:
5-10% in uncomplicated AKI
50-70% in AKI secondary to other organ failure( intensive care)
> 50% in dialysis requiring AKI
*Xue JL, Daniels F, Star RA et al. Incidence and mortality of acute renal failure in Medicare beneficiaries, 1992 to J Am Soc Nephrol 2006; 17: 1135–1142.

11. Acute kidney injury Pre renal Intrinsic Post renal
- ↓ Effective renal blood flow:
1- Haemorrhage
2- Volume depletion
3- Low cardiac output
4- Sepsis
5- CCF
6- Cirrhosis
- Arterial stenosis/Occlusion
- Vasomotor:
1- NSAID
2- ACEI/ ARBs
Intrinsic
Post renal

12. Diagnosing pre-renal AKI
Is the patient volume depleted?

13. Diagnosing pre-renal AKI
Is the patient volume depleted?
Is cardiac function good?

14. Diagnosing pre-renal AKI
Is the patient volume depleted?
Is cardiac function good?
Is the patient septic?

15. Diagnosing pre-renal AKI
Is the patient volume depleted?
Is cardiac function good?
Is the patient septic?
History
Examination
Investigation

16. Diagnosing pre renal AKI
History
Examination :
1- Signs of Hypovolaemia:
a- Low BP( and reduced pulse pressure)
b- Postural BP drop ( a fall in systolic BP > 10mmHg)
c- Sinus tachycardia and postural increase in heart
rate ( increase in HR > 10 beat/min).
d- Low JVP even when the patient is supine
e- Cool peripheries and vasoconstriction
f- Poor urine output

17. Diagnosing pre-renal AKI
2- Sings of hypervolaemia( high extracellular fluid):
a- Increased circulating volume:
- High BP
- Elevation of the JVP
b- Increased interstitial fluid:
- Peripheral or generalized oedema
- Pulmonary oedema (tachypnoea, tachycardia, third heart sound, basal
crackles)
- Pleural effusion
- Ascites
. Lab investigation:
- Blood tests
- urine: including urinary Na( low)

18. Case 1
67 yr man – IHD
Admitted with D&V – O/E JVP not seen, BP 100/60 lying, 80/50 standing, pulse 105 bpm
Creatinine 5.8 ( mg/dl)
x2 IV access
Given IV saline
Catheterised and started on furosemide
Function worsened and transferred to renal unit

19. What was the only helpful intervention
1- Inserting a urinary catheter 2- Inserting a CVP line 3- Administering IV fluids 4- Administering diuretics

20. What was the only helpful intervention
1- Inserting a urinary catheter 2- Inserting a CVP line 3- Administering IV fluids 4- Administering diuretics

21. Treatment of pre renal failure
DO NOT put in a urinary catheter
DO NOT GIVE DIURETICS – improving urine volume does not mean an improvement in renal function
CVP line rarely needed – and certainly not substitute for clinical examination

22. Treatment of pre-renal failure
Volume replacement
Improve cardiac function in congestive
cardiac failure

23. Treatment of pre-renal failure
Volume replacement: fluid, blood, plasma expander…
A- Resuscitate:
- Hypotensive and tachycardic
B- Replacement
C- Maintenance

24. Treatment of pre-renal failure
Volume replacement: fluid, blood, plasma expander…
A- Resuscitate:
- 0.9% Normal saline
- be aware of fluid overload (high BP, RR, basal lung crackles and low
satO2)
- fluid challenge ( trial ml N saline IV in 10min, then re-assess,
repeat if necessary)
B- Replacement: depends on
a- Degree of hypovolaemia
b- Ongoing losses
c- Whether oligo-anuric
d- Cardiovascular status

25. Treatment of pre-renal failure
A rough guide ( be aware of elderly and those with poor left ventricular function):
- first litre over 2 hours, THEN REASSESS
- second litre over 4 hours, THEN REASSESS
- third litre over 6 hours, THEN REASSESS
*Remember to add insensible loss, if not sure or think you over done it, stop all fluid and reassess the patient
C- Maintenance:
Once euvolaemic, and assume no other losses, match urine out put
plus 30mls/hour (insensible loss may be higher if febrile)

26. Acute kidney injury Pre renal Intrinsic Post renal Vascular
1- Vasculitis
2- Thrombotic microangiopathy
3- Scleroderma renal crisis
4- Renal vein thrombosis
5- Cholesterol emboli
Acute GN
Glomerluo-nephritis
Acute TIN
tubulointestitial nephritis
ATN
acute tubular necrosis
Post renal

27. Acute kidney injury Pre renal Intrinsic Post renal Vascular
1- Vasculitis
2- Thrombotic microangiopathy
3- Scleroderma renal crisis
4- Renal vein thrombosis
5- Cholesterol emboli
Acute GN
(Glomerluo-nephritis)
Acute TIN
(tubulointestitial nephritis)
ATN
acute tubular necrosis
Ischaemic
Nephrotoxic
Post renal

28. Acute kidney injury Pre renal Intrinsic Post renal Vascular
1- Vasculitis
2- Thrombotic microangiopathy
3- Scleroderma renal crisis
4- Renal vein thrombosis
5- Cholesterol emboli
Acute GN
(Glomerluo-nephritis)
Acute TIN
(tubulointestitial nephritis)
ATN
acute tubular necrosis
Ischaemic
Nephrotoxic
Endogenous
1- Haemoglobinuria
2- Myoglobinuria
3- Casts and Crystals
Exogenous
1- Nephrotoxic drugs
2- Radiocontrast
Post renal

29. Diagnosing Intrinsic Renal AKI
Has pre-renal and post renal been excluded?
History
- Drug, Rash, joints, nose bleed, haemoptysis, hearing loss, claudication, IHD,
diabetes, fever or night sweat, Recent infection
Examination
- Oedema, rash, mouth ulcer, hearing loss, uveitis, AF, ischaemic toe, bruits, evidence of scleroderma, prosthetic valve or stigmata of Endocarditis
Laboratory investigations
- Urine including microscopy for dysmorphic RBC, Protein, Bence Jones protein,
protein/creatinine ratio or 24hr protein excretion
- Blood – nephritic screen – ANA, dsDNA, ANCA, antiGBM, Immunoglobulines
protein electrophoresis, Rh-factor, HBV, HCV, HIV, cryoglobulins, blood film, CK,
C3,C4, ASO-titre , ESR and CRP
. US kidneys
. Renal biopsy

30. Criteria for distinction between pre-renal and intrinsic causes of renal dysfunction
Urine specific gravity
> 1.020
< 1.010
Urine osmolality(mOsm/Kg)
> 500
< 500
Urine Na+ (mmol/l)
< 20*
> 40
Fractional excretion of Na+
< 1%
> 1%**
* Except in diuretics or dopamine
** remains low in contrast nephropathy and myoglobinuria

31. Case 2 What did they do right?
56 years old man
Cough, haemoptysis and joint pain
O/E JVP +6cm
Creatinine 7.5mg/dl( ) on admission
IV access, started on IV fluid and diuretics- SOB worsened
Transferred to renal unit after 1 week when renal function failed to improve

32. What was done correctly
Omission of urine catheter
Administered IV fluids and diuretics
Transfer to renal unit after 1 week

33. What was done correctly
Omission of urine catheter
Administered IV fluids and diuretics
Transfer to renal unit after 1 week

34. Treatment of intrinsic renal AKI
GN – autoimmune – immune suppression/ plasma exchange
Infective Bacterial Endocarditis – antibiotics
Interstitial nephritis
- Stop offending medication
- Corticosteroids

35. Treatment of intrinsic renal AKI
ATN
- In-hospital mortality 19-37%*
- Recovery could take up to 6 weeks**
- Self correcting (full 60%, some 30%, dialysis 5-10%)
- Very severe – permanent cortical necrosis
* Oxford handbook of Nephrology and Hypertension 2009
** Kumar and Clark/ Clinical Medicine July 2012

36. Acute kidney injury Pre renal Intrinsic Post renal Obstruction
1- Bladder out-let obstruction
2- Bilateral ureteral obstruction

37. Nature of Obstruction Outside
- Tumours, prostate, retroperitoneal fibrosis, cervical Ca
Within wall
- Tumours, strictures
Within lumen
- Stones, tumours

38. Diagnosing post renal AKI
History
- pain, anuria, haematuria, prostatism
Examination
- palpable bladder, central abdo mass, PR, PV
Observation
Laboratory investigations
- Urine
- Blood
- Imaging – US, CT

40. Treatment of Post renal AKI
Obtain drainage of Urine
- Bladder catheter – per urethra, suprapubic
- Retrograde drainage
- Antegrade drainage

41. Case 3 82 years old man Not passed urine for 20 hrs
O/E: large bladder and prostate on PR
Creatinine: 8.3 mg/dl
USS- dilated bladder
Urine catheter inserted, start to pass lots of urine
Following day creatinine – 4.2 but then over subsequent days rises to 5.1 then 5.8 then 6.4. still passing lots of urine

42. What is the right intervention
A- Restrict fluid to reduce urine output B- Give IV normal saline C- Remove catheter D- Investigate for other causes of renal failure

43. What is the right intervention
A- Restrict fluid to reduce urine output B- Give IV normal saline C- Remove catheter D- Investigate for other causes of renal failure

44. Post recovery diuresis
Occurs post resolution of AKI
- Post relief of obstruction
- Post ATN
Important to check fluid status
- Clinical exam
- BP and pulse
- Daily weight
- Input and output chart
Treatment – IV fluids
replace electrolyte

45. Complication of AKI 64 years old man admitted with: Potassium 7.4
Urea: 90
Creatinine: 8.5

46. What is the first line treatment
A- Insulin and dextrose B- IV calcium gluconate C- Ca+2 resonium D- Low potassium diet E- Dialysis

47. What is the first line treatment
A- Insulin and dextrose B- IV calcium gluconate C- Ca+2 resonium D- Low potassium diet E- Dialysis

48. Other Complications of AKI
Pulmonary oedema
Acidosis
Uraemia
Other electrolyte disturbance such as hyerphosphataemia and hypocalcaemia

49. Who is a risk?
Many cases of AKI should never occur in the first place 1- Elderly 2- Pre-existing renal disease 3- Surgery, trauma, sepsis or myoglobinuria 4- Diabetes 5- Volume depletion( Nil By Mouth, bowel obstruction, burn) 6- LV dysfunction 7- Nephrotoxic drugs 8- Cirrhosis (reduce arterial volume)

50. Common nephrotoxins NSAID
Diuretics, ACEI, ARB2 especially in volume depleted patient
Antibiotics, Aminoglycosides, Vancomycin
Amphotericin B
Immunosuppressant (ciclosporin, tacroliums) and chemotherapy (Cisplatin)
IV contrast

51. Reducing risk perioperatively
Three principles:
1- Avoid dehydration
2- Avoid nephrotoxins
3- Review clinical status and renal function those
at risk
Optimize volume status
1- No patient should go to theatre dehydrated
2- Review daily weight, input and output chart
3- Calculate losses especially those NBM ( use
0.9% N saline and NOT 5% Dextrose)

52. Reducing risk perioperatively
Optimize blood sugar control in DM ( use sliding scale
Catheterize those with prostate disease
Avoid surgery if possible immediately after a contrast procedure
Stop nephrotoxic drugs 24-48hrs preoperatively
Review the patient EARLY postoperatively

53. Have you.. Have seen the result of K and acted appropriately?
Assessed the patient’s volume status and treated pulmonary oedema or corrected hypovolaemia?
Taken full history and examined patient head to toe?
Excluded palpable bladder?
Seen the patient’s regular drugs? And stopped nephro-toxins?
Arranged urgent ultrasound(within 24hr)*
Performed urine test and send for microscopy and MSU
Checked acid-base status and intervened appropriately?
Checked for any previous tests of renal function?
Checked Hb, Calcium and Phosphate?
Send blood for full nephritic and myeloma screen if you are suspecting intrinsic renal failure?
* NCEPOD recommendation/ National Confidential Enquiry in to patient outcome and death.

54. ( Glomerluo-nephritis)
Acute kidney injury
Pre renal
- ↓ Effective circulatory volume:
1- Haemorrhage
2- Volume depletion
3- Low cardiac output
4- Sepsis
5- CCF
6- Cirrhosis
- Arterial stenosis/Occlusion
- Vasomotor:
1- NSAID
2- ACEI/ ARBs
Intrinsic
Vascular:
1- vasculitis
2- Thrombotic microangiopathies
3- hypertensive emergencies
Acute GN
( Glomerluo-nephritis)
Acute TIN
(tubulo-intestitial nephritis)
ATN
(acute tubular necrosis)
Ischaemic
Nephrotoxic
Endogenous
1- Haemoglobinuria
2- Myoglobinuria
3- Myoglobin casts
4- Intratubular crystals
Exogenous
1- Nephrotoxic drugs
2- Radiocontrast
Post renal
Obstruction
1- Bladder out-let obstruction
2- Bilateral ureteral obstruction

55. Summary 3 categories of AKI
Simple clinical assessment will define which
Be aware of life threatening complications and emergency treatment
Recognise those at risk