Teaching slide on AKI for all under graduate & post graduate students of medicine

1. OVERVIEW OF ACUTE
KIDNEY INJURY (AKI)
BY DR. SAQUIB NAVID SIDDIQUI
MBBS, MRCP (UK)
SpR, HCOOP & Acute Medicine
WHH

2. 1) Early identification of AKI
2) Differentiating AKI from CKD
3) Differentiating Pre- renal Vs Renal Vs Post renal causes of AKI
4) Treating electrolyte and metabolic imbalances that arise during AKI
5) Identify patients who need ITU/nephrology urgent referral for RRT
LEARNING
OBJECTIVES

3. AKI Or CKD
???

4. AKI or CKD
1) Previous CR, eGFR records
2) Presence of anaemia, hypertension favours CKD
3) Imbalance between calcium, phosphate, vitamin
D3 levels, PTH favours CKD
4) USS features suggestive of CKD related renal
parenchymal changes will help to differentiate
between AKI & CKD

5. Defination : Sudden,reversible deterioration of renal function
which
develops over hours & days associated with reduction in
urine volume.
CLASSIFICATION
1) RIFLE
2) AKIN
3) KDIGO
*** Based on Creatinine & Urine Output***

7. CAUSES
???

9. Aetiology
Pre- renal : a) Fluid loss ( vomiting, diarrhea,
hmg etc)
b) Cardiac Failure, hepatic Failure
c) Drugs :
Diuretics,NSAID,ACEI,ARB
d) Sepsis
e) Vascular Occlusion

10. AETIOLOGY
Renal Causes : (Think of anatomical structures!! –
tubules, glomerulus, interstitium, vessels)
1) Acute Tubular necrosis
2) Acute Interstitial Nephritis
3) Acute Glomerulonephritis
4) Vascular

11. Aetiology
ACUTE TUBULAR NECROSIS
A) Drugs :
Penicillin,cephalosporin,aminoglycosides,
cyclosporin,contrast agents.
B) Toxin : Hb (Haemolysis)
Myoglobin (Rhabdomyolysis)
Tumour lysis syndrome
Sepsis
C) Hypotension

12. AETIOLOGY
ACUTE INTERSTITIAL NEPHRITIS
A) Drugs :
Penicillin,Diuretics,PPI,Mesalazine,NSAID
B) Infection :Tb, leptospira, bacterial
pyeloneohritis,hunta virus
C) Auto-Immune Nephritis, transplant
rejection
D) Mushroom poisoning, myeloma light
chain

13. AETIOLOGY
GLOMERULAR CAUSES
A) RPGN ( SLE, Vasculitis,
GPS)
B) DPGN
C) IgA Nephropathy
D) FPGN

14. VASCULAR
A) Renal Vein ( Renal Vein Thrombosis)
B) Renal Artery ( Renal Artery Stenosis, Thrombotic
micro angiopathy, cholesterol embolism)
C) Vasculitis
*** Thrombotic Microangiopathy : A) Primary causes
are HUS,TTP
B) Secondary causes
are DIC, malignant HTN, systemic sclerosis, pre-
eclampsia & HELLP Syndrome

15. AETIOLOGY
POST RENAL
A) Luminal : Stone
B) Wall : Carcinoma
C) Outside the Wall : BEP, Uterine Enlargement,
Constipation
D) Urinary Bladder Causes : Stone, malignancy

18. Diagnosing Pre-renal AKI
• Is the patient hypovolemic ?
• Is there any cardiac/hepatic failure ?
• Any evidence of sepsis ?
• Any nephrotoxin drugs ?

20. 2) Signs of hypervolemia
:
• Peripheral oedema
• Ascites
• Pulmonary Oedema
• Raised JVP

24. IMPORTANT BIOMARKERS
• Cystein C
• Neutrophil gelatinase associated lipocalin
(NGAL)
• Interleukin-18
• Kidney Injury Molecules
• N-acetyl-D- glucosaminidase

26. KIM-1 (Kidney Injury Molecule – 1)
• Kim-1 is a type 1 trans - membrane
glycoprotein
• Used as a marker of severity
• Can be used as a marker to predict adverse
outcomes in hospitalized patients.

28. How to treat ??

29. The principles of management of AKI are
two-fold
• Rapid identification and correction of those
conditions contributing to or causing AKI
• Support of kidney function (where indicated and if
appropriate) with dialysis until self-supporting renal
function returns.
Remember that there is currently no widely accepted, specific pharmacological treatment for
established AKI. There is no evidence to support the routine use of diuretics or dopamine to
treat it

30. Identification and correction of
conditions causing Pre-renal AKI
1) IV fluids if hypovolemic (Ideally
crystalloids, choice of fluid selection will
depend on K+ levels. Not recommended to
give Hartmann's solution in patients with high
potassium)
2) Holding any nephrotoxic medications.
3) Anti-biotics for infection (Renal Dose)

31. Treating the Renal causes of AKI
1)AIN : A) Hold any offending drugs B) Steroids if
required
2)Glomerular cause : Treat as per the cause
of glomerulonephritis
3) ATN : A) Treat with anti-biotics if infection
B) Hold any nephrotoxic drugs if ATN due
to nephrotoxic drugs
C) Treat as per required if ATN due to
rhabdomyolysis/haemolysis/tumour lysis
syndrome

33. TREATING ELECTROLYTE &
METABOLIC DISTURBANCES
ARISING FROM AKI
Treating Hyperkalemia due to AKI : as per trust guidelines.
1) Potassium 5.5 to 6 : oral calcium resonium 15g QDS with lactulose
2) Potassium 6.1 to 6.5 without ecg changes : Nebulization with Salbutamol (
2 nebs of 5mg back to back) & 50% dextrose 50ml with 10unit actrapid over
15-30mins.
3) Potassium more than 6.5 or potassium 6.1 to 6.5 with ecg changes : A) IV
10% calcium chloride 10ml or 10% calcium gluconate 30ml over 10mins.

34. TREATING ELECTROLYTE &
METABOLIC DISTURBANCES ARISING
FROM AKITreating metabolic acidosis :
IV Sodium Bi
carbonate 1.26% can be given 250 to 500ml
over 2 to 4 hours if pH below 7.1 with hco3
below 20

36. Support of kidney function with
renal replacement therapy
The absolute indications for dialysis treatment
are:
• Pulmonary oedema refractory to medical management
• Hyperkalaemia refractory to medical management
• Severe metabolic acidosis
• Uraemia causing complications (generally above 35 -40
mmol/l), e.g. encephalopathy, pericarditis.

37. Introduction to RRT
The most common types of renal replacement
therapy (RRT) are:
• Haemodialysis (HD) or haemodiafiltration
(intermittent)
• Haemofiltration (HF) (often continuous)
• Peritoneal dialysis (PD)
• Transplantation.

38. Outcome of AKI
Historically, it was thought that if patients recovered
from an episode of AKI, they were unlikely to suffer
any long-term sequelae. There is, however,
increasing evidence to suggest that this is not the
case and that abnormal physiological processes
established during the episode of AKI can result in
residual renal injury that may predispose the
individual to chronic kidney disease and loss of renal
function over time. This may be of particular
significance in persons who undergo repeated, even
if apparently mild, episodes of AKI.

39. Re-assessing our learning
objectives
1) Can we now identify onset of AKI?
2) Can we differentiate between AKI & CKD ?
3) Can we differentiate between pre-renal,renal and
post-renal causes of AKI?
4) Can we treat the metabolic & electrolyte
disturbances that arise during AKI?
5) Can we identify the patients who need urgent
referral for RRT?

40. Lets put our learning into test

41. 79 years old male comes with h/o fever,
cough with greenish sputum and
palpitations on the background of
T2DM,HTN,AF,BEP; not known to have any
previous renal disease. Also says not eating
& drinking adequately over past few days

42. O/E : His NEWS is 09. He looks dry,
dehydrated, temp 39.6 degrees, his HR is
132, irregular with his ecg revealing fast AF,
BP 92/60, RR 23, Spo2 maintain at 91% on
RA, ABG is not acidotic, not retaining. Chest
reveals right basal crackles without wheeze,
abdomen is soft, non tender, no
urinary bladder palpable, PR reveals an
enlarged prostate.

43. Bloods reveal : FBC : Hb 137, MCV 89,
WBC 17.9 with NEUH 14.2, PLT 445, CRP
217, CR 210 ( baseline 92) , eGFR 27
(baseline 78), U 10.2, NA 131, K 5.1 ,
Gas is not acidotic, Lactate of 3.7, CXR
reveals right basal consolidation. ECG
shows Fast AF

44. Thoughts
???

45. Impressions : A) AKI sec to : 1) Pre-renal
(dehydration as not eating & drinking adequately) +
sepsis (source : chest)
2) Renal : ATN due to
sepsis
B) Chest sepsis (Right CAP) QSOFA score 2
C) Fast AF sec to chest sepsis

46. HOW TO TREAT ??

47. 1) For chest sepsis : Do the sepsis 6
2) For Fast AF : Primary target is infection control; as it is the driving force for
fast AF. For rate control choice will be beta blocker (cardio-selective) as it is
the 1st line choice of medication in Fast AF, digoxin isn't suitable option as
patient has renal failure; therefore likely to cause digoxin toxicity.
3) For AKI :
A) IV fluids to correct dehydration. Patient will need 500ml bolus stat (as
hypotensive) and further fluid as per assessment. Dehydration correction
will help to resolve the pre renal aspect of AKI.
B) Anti-biotics for infection ( Would require renal dose adjustment as eGFR
is below 30)
C) All his regular medications needs to be checked for any renal dose
adjustments or withholding of drugs
D) Monitor urine output, U & E, FBC,CRP And VBG.
E) No need for RRT at present.

49. ANY QUESTIONS
???