Acute Kidney Injury Abi

ACUTE KIDNEY INJURY
DR ABIRRAMIE VIJAYARAJ
Clinical approach
• 72 MALAY MALE
• U/L T2DM
• HPT
• CKD 3A
• BPH
• PRESENTED WITH DYSURIA 2/7

• A/W SUPRAPUBIC PAIN
• HESISTANCY, VOIDING 2/7
• BASELINE UREA 4.6/CREAT127
• UPON ADMISSION UREA 7.19
/CREAT 137
• UFEME LEU 2+NITRITE NEGATIVE
PROTEIN 3+
TREATED AS AKI ON CKD 2 to

urosepsis
D2 OF ADMISSION
• NOTED RP WORSENING UREA 10.9/CREAT 239
• CLINICALLY PATIENT WAS DEHYDRATED.
• UPON EXAMINATION, DRY TONGUE,
• URINE IN CBD CONCENTRATED.
• URINE OUTPUT ABOUT 300 CC
• WAS STARTED ON IVD 2 PINT NS/24 HOURS
• Patient was also on iv cefuroxime 1.5g TDS
D3 OF ADMISSION
• UREA 8.3/CREAT 162
• GOOD URINE OUTPUT( 1L IN CBD)
• HYDRATION IMPROVED.
DEFINITION
• ACUTE KIDNEY INJURY has variably been defined
as an abrupt deterioration in parenchymal renal
function, as evidenced by changes in laboratory
values, serum creatinine (Scr), blood urea
nitrogen (BUN), and urine output which is
usually but not invariably, reversible over a
period of days or weeks.
EPIDEMIOLOGY
CLASSIFICATION OF AKI
Criteria used for AKI classification
RIFLE: Risk, Injury, Failure, Loss of Kidney
Function and End Stage Renal Disease).
AKIN: Acute Kidney Injury Network
KDIGO: Kidney Disease Improving

Global Outcome
AKI CLASSIFICATION SYSTEMS
AKI is staged for severity according to the following
criteria
The cause of AKI should be determined whenever
possible
PATHOPHYSIOLOGY OF PRE RENAL AKI & ISCHEMIC INTRINSIC AKI
Decrease in Effective circulatory volume
Activation of central baroreceptor
Angiotensin-II Norepinephrine AVP/ADH
Vasoconstriction of non
1. Preferential essential vascular beds
constriction of
efferent arterioles
Maintain renal blood flow & GFR
2. Prostaglandi
n synthesis If hypotension sufficient to overwhelm
renal autoregulatory defense
3. Auto regulation
Ischemic injury to renal parenchyma

reduction in GFR
Recovery of
GFR
Harrison's Principles of Internal Medicine 15th ed.
Clinical Prerenal AKI-
features
H/O
1) Excessive Fluid Losses from vomiting or diarrhea;
third- space losses in burn and pancreatitis.
2) Compromised cardiac function in patients with congestive
heart failure; recent myocardial infarction.
3) Liver cirrhosis and failure (hepatorenal
syndrome);
4) Drugs- cyclosporine, NSAID, or ACE inhibitor
use.
Symptoms related to hypovolemia- increased thirst ,

decrease urine Manual
output, postural Diagnosis
of Nephrology: hypotension, dizziness,
and Therapy 7th edition
Physical findings
1) Reduction in ECF volume
a. Tachycardia
b. Orthostatic hypotension
c. Dry mucus membrane
d. Absence of axillary sweat
e. A recent reduction in body weight
f. “Tenting” of upper thorax skin when pinched between the fingers
g. Jugular venous pulse not visible
2)Arterial underfilling with expanded ECF

h. Elevated jugular venous pressure,
i. Ascites,
j. Peripheral edema
k. CHF may be identified by Pulmonary crackles & S3 gallop
e .Liver failure may be identified by Jaundice, palmer erythema,
spider angiomas, decrease liver size.
Manual of Nephrology: Diagnosis and Therapy 7th edition
Intrinsic/Intrarenal
AKI: H/O -
1)Use of Nephrotoxic agents, Current
medications , Contrast agent.
2)Glomerular disease- Nephrotic / Nephritic syndrome with
hematuria, edema and hypertension .
3)Tubular disease: ATN should be suspected in any patient
presenting after a period of hypotension secondary to
cardiac arrest, hemorrhage or sepsis.
Physical finding:
• Peripheral edema
• Raised JVP
• Pulmonary rales
• Signs of uremia- Asterixis, myoclonus, pericardial rub.
POST RENAL FAILURE
Usually occur in elderly male with prostatic

obstruction.
H/O – Urinary Frequency, urgency &
Hesitancy
PHYSICAL FINDINGS –
a. Costovertebral Angle Tenderness
b. Pelvic & Rectal Masses
c. Prostatic Hypertrophy
d. Distended Bladder
Manual of Nephrology: Diagnosis and Therapy 7th edition

EVALUATION OF PATIENT WITH AKI
MANAGEME
NT
• Optimization of systemic and renal
hemodynamic through volume resuscitation and
judicious use of vasopressors .
• Elimination of nephrotoxic agents (e.g.,
ACE inhibitors, ARBs, NSAIDs,
aminoglycosides) if possible .
• Initiation of renal replacement therapy
when indicated.
DIETARY
MEASURES
• Adequate nutritional support should be
ensured.
• High protein intake should be avoided.
• Enteral/ parenteral nutrition may be required.
•Providing nutrition preferentially via the enteral

route in patients with AKI
NUTRITIONAL AND
GLYCEMIC
CONTROL
• Insulin therapy targeting plasma glucose 110–149 mg/dl
• Total energy intake of 20–30 kcal/kg/d in patients with any stage
of AKI.
• 0.8–1.0 g/kg/d of protein in non catabolic AKI patients
without need for dialysis.

•1.0–1.5 g/kg/d in patients with AKI on RRT and up to a
maximum of 1.7 g/kg/d in patients on CRRT and in hyper
catabolic patients.
FLUI
DS
• KDIGO suggest using isotonic crystalloids in absence of
hemorrhagic shock rather than colloids (albumin or
starches) .
• Colloids may be chosen in some patients to avoid
excessive fluid administration in patients requiring large
volume resuscitation, or in specific patient subsets.
• Colloids- Albumin is renoprotective and Hyperoncotic

starch shows nephrotoxicity.
POST- RENAL
AKI
• Prompt relief of urinary tract obstruction by
catheterization in urethral obstruction, correction of
ureteric obstruction by ureteric stent or percutaneous
nephrostomy.
• Relief of obstruction is usually followed by an
appropriate diuresis and may require continued
administration of intravenous fluids and electrolytes for a
period of time.
AKI - CONTRAST INDUCED
 Non-pharmacology for prevention

 Hydration to prevent contrast induced nephrotoxicity
 KDIGO guideline recommend using normal saline or
sodium bicarbonate infusion
Normal saline regimen: 1ml/kg/h for 12hours before and after
procedure.
Sodium bicarbonate regimen: 3ml/kg/hours for one hour before
procedure and 1ml/kg/hours for 6 hours postcontrast.
PHARMACOLOGICAL THERAPY
 For prevention of CIN
 Ascorbic acid:3g orally pre and 2mg orally for two doses
postprocedure and N-acetylcysteine(600-1200mg orally
every 12 hours for 2-3 days, the first two doses
precontrast
 Current KDIGO guideline suggest moderate control of
blood glucose to level of 110-149 mg/dl with insulin
prevent ICU-Acquired AKI
Dialysis therapy
The indications to start
dialysis
CLINICAL
• Anuria (< 100 mL/day)
• Uremic neuropathy, BIOCHEMICAL
• Uremic pericarditis
• Uremic bleeding • severe Metabolic
• uremic sx Acidosis
• malnutrition • Hyperkalemia
• Volume overload • uremia
• HPT resistant to drug
therapy
MODES OF
DIALYSIS
• Hemodynamically stable- HD
• Hemodynamically unstable
1. CRRT
2. PD
3. SLED (Slow Low-efficiency dialysis).

Risk factors of
AKI
• Elderly
• Pre-existing renal disease
• Surgery, trauma, sepsis or myoglobinuria
• Diabetes Mellitus
• Volume depletion states
• LV dysfunction
• Nephrotoxic drugs
RECOVERY OF RENAL
FUNCTION
• Quantifying the recovery of renal function is extremely
challenging.
• COMPLETE RECOVERY : defined as return to pre-

AKI renal function ,assessed as the GFR +/- 10% of
baseline.
• NON RECOVERY: defined as persistent requirement of

RRT.
• PARTIAL RECOVERY : defined as

persistent impairement in GFR but no
requirement of RRT.
PROGNOSIS
• Pre-renal and Post- renal better prognosis.
• Kidneys may recover even after dialysis
requiring AKI.
• 10% of cases requiring dialysis develop CKD.
• Individuals may die early even after kidney
function recovers completely.
THANK YOU..

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ACUTE KIDNEY INJURY

• PRESENTED WITH DYSURIA 2/7

TREATED AS AKI ON CKD 2 to

AKIN: Acute Kidney Injury Network

KDIGO: Kidney Disease Improving

Decrease in Effective circulatory volume

Activation of central baroreceptor

Angiotensin-II Norepinephrine AVP/ADH

Ischemic injury to renal parenchyma

Symptoms related to hypovolemia- increased thirst ,

2)Arterial underfilling with expanded ECF

Usually occur in elderly male with prostatic

Manual of Nephrology: Diagnosis and Therapy 7th edition

• Enteral/ parenteral nutrition may be required.

•Providing nutrition preferentially via the enteral

• Total energy intake of 20–30 kcal/kg/d in patients with any stage

• 0.8–1.0 g/kg/d of protein in non catabolic AKI patients

without need for dialysis.

• Colloids- Albumin is renoprotective and Hyperoncotic

appropriate diuresis and may require continued

administration of intravenous fluids and electrolytes for a

 Non-pharmacology for prevention

3. SLED (Slow Low-efficiency dialysis).

• COMPLETE RECOVERY : defined as return to pre-

• NON RECOVERY: defined as persistent requirement of

• PARTIAL RECOVERY : defined as

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