ACUTE KIDNEY INJURY

AND CHRONIC KIDNEY

DISEASE (AKI and CKD)

AA Gde Oka
Sub Bag/SMF Urologi Fk Unud/RSUP
Sanglah Denpasar
ACUTE KIDNEY INJURY
(AKI)
Dr. Hamed Shakhatreh
consultant nephrologist, Head of nephrology department, Al-basher hospital, M.O.H.
http://www.jmc.gov.jo/UploadedFiles/Documents/af61a37b-98cd-4fa4-b55e-
d3bee0177ef5.pdf
AKI Definition
 Increase in SCr by >0.3 mg/dl (>26.5 micro mol/l)
within 48 hours; or
 Increase in SCr to>1.5 times baseline, which is
known or presumed to have occurred within the
prior 7 days; or
 Urine volume <0.5 ml/kg/h for 6 hours.

Dr. Hamed Shakhatreh

consultant nephrologist, Head of nephrology department, Al-basher hospital, M.O.H.
http://www.jmc.gov.jo/UploadedFiles/Documents/af61a37b-98cd-4fa4-b55e-d3bee0177ef5.pdf
 Stage of AKI:
 Stage 1
 Increase SC 1.5-1.9 times baseline, OR ≥0.3 mg/dl (≥26.5 micromol/l) ,
OR
 Urine output <0.5 ml/kg per hour for 6 to 12 hours.
 Stage 2
 Increase SC 2.0-2.9 times baseline, OR
 Urine output <0.5 ml/kg per hour for ≥12 hours.
 Stage 3
 Increase SC 3.0 times baseline increase,
 OR Increase SC to ≥4.0 mg/dl (≥353.6 micromol/l), OR

 Urine output of <0.3 ml/kg per hour for ≥24 hours,

OR anuria for ≥12 hours OR the initiation of renal replacement therapy

OR, in patients <18 years, decrease in estimated GFR to <35 ml/min per
1.73m2
Types of Acute Kidney Injury
(AKI/ARF)
 I. Pre-renal injury
 Renal tissue is intact and normal renal histology.
 Oliguria and high serum creatinine.
 Most common cause: hypotension, hypovolaemia.
 Early diagnosis and correction: immediate diuresis and rapid
drop in serum creatinine and blood urea levels.
 If neglected:
 Fail renal compensatory mechanisms and ATN occurs.
 Hypoperfusion correction will not be followed by diuresis or drop in
serum creatinine.
 Tubular regeneration and recovery of kidney function: 2-3 weeks.
 II. Intrinsic-renal injury
 This includes
 Acute Tubular Necrosis (ATN)
 Acute Interstitial Nephritis
 Acute Glomerulonephritis
 Acute Tubular Necrosis
 Acute tubular necrosis can be induced by :
 Renal hypoperfusion (ischemia).
 Exposure to nephrotoxins (exogenous or endogenous
toxins).
 And frequently by a combination of both.
 Causes of Ischaemic ATN
 A- Blood Loss
 Haemorrhage (post partum,
surgical or gastrointestinal).
 Major trauma
 B- Fluid Loss
 Gastrointestinal (vomiting or
diarrhoea)
 Renal (aggressive diuresis or
polyuria)
 C- Third Space
 Haematoma, Illius, Peritonitis
 D- Severe vasodilatation
 septicaemia, rapid oedema
formation, liver cell failure.
 E- Renovascular disease
 Renal artery occlusion by
stenosis, embolism or
compression.
 Renal vein thrombosis or
compression.
 Causes of Toxic ATN
(A) Exogenous nephrotoxins include:
 Antibiotics: Aminoglycosides
,Amphotericin ,Cephalosporin,
Acyclovir, Sulfonamide,
Tetracyclines Bacitracin.
 Anaesthetic agents: Methoxy
fluorane
 Contrast Media: (B) Endogenous nephrotoxins
 Analgesics:Metals: as Mercury, lead, include
arsenic, bismuth, cadmium,  Pigments: Myoglobin,
antimony, Hemoglobin, Methemoglobin
 Organic solvents: Glycols  Crystals: Uric acid, Calcium,
 Poisons: snake bite, stings, bacterial Oxalate
toxins.
 III. Post –renal injury
 Obstruction of the urinary tract
 Increasing the pressure above the level of the obstruction
up to the nephron including the urinary space of the renal
glomeruli.

 When this back pressure exceeds that of the filtration

pressure in the renal glomeruli, the process of urine
formation will stop.

 Progressive accumulation of wastes and increase of serum

creatinine and blood urea.
 Clinical features of AKI:
 Usually
 History of the etiologic cause such as trauma, shock, haemolysis, drug
intake, infection, or stone disease.
 Patient may notice
 Change in urine volume and character, oliguria is common, but in 10-
50% of cases urine volume will be normal or even higher (as in toxic
ATN) this is called polyuric ATN.
 Absolute anuria is highly suggestive of obstructive ARF (post-renal) or
very severe form of ATN (cortical necrosis).
 Manifestation of salt and water retention
 Oedema, puffiness, hypertension and even heart failure.
 Manifestations of uraemia
 Acidotic breathing, dyspnea, nausea, vomiting, headache, muscle
twitches and even frank encephalopathy and coma.
 Patient may present as well with any of complications
 Complications Of AKI
 Cardiovascular
 Pulmonary Odema,
Arrhythmias, Hypertension,
Pericardial Effusion, Myocardial
Infarction, Pulmonary
Embolism
 Metabolic
 Hyponatremia, Hyperkalemia,
Acidosis Hypocalcemia,
Hyperphosphatemia
 Neurologic
 Coma, seizures
 Gastrointestinal
 Gastritis, gastroduodenal ulcers
 Haematologic
 Anaemia, hemorrhagic
diathesis
 Infections
 Pneumonia,septicemia, UTI
 Investigations of AKI:
A-Urinary indices
May be helpful in the differentiation between
 Pre-renal failure and acute tubular necrosis.
 Diuretics should not be given at least during the preceeding 48 hours for these
parameters to be valid.

B- Urinary sediment
 Centrifugation of fresh urine sample and examination of the urinary sediment
may be helpful in diagnosing different causes of ARF

C- Renal Imaging

D-Renal Biopsy
 Differentiation between
Pre-renal failure and ATN

• milliosmoles/liter (mOsm/L)
• Fractional Excretion of Sodium (FENa)
 TREATMENT OF AKI
A- Treatment of the cause
 Causing renal hypoperfusion, exposure to toxic drug or chemical or
systemic disease.

B- Prevention of AKI
 The timing of intervention to prevent ATN is important.
 Protective agents must be administered at the time of, or immediately
following potential renal insult.
 This intervention may prevent or at least blunt the severity of ATN.
 TREATMENT OF AKI
 The intervention could be through the following approaches. In
different combinations according to the clinical situation:
 Volume expansion by saline loading.

 Diuretic as mannitol and furosemide.

 Calcium channel blockers as verapamil and nifedipine.

 Vasodilating agents as dopamine in renal dose 1-2

ug/kg/min
 ATP-magnesium chloride.
 In case of contrast media, the following additional
points should be adopted, these are:

 Avoid unnecessary contrast procedures.

 Avoid multiple contrast exposure within a few days.
 Avoid contrast exposure in high risk patient.
 Use the smallest dose possible.
 Use of non-ionic contrast is to somewhat safer.
 In high risk patient with renal impairment we can manage to
wash the contrast out immediately after the technique (e.g.
coronary angiography) by haemodialysis.
 CHRONIC KIDNEY
DISEASE (CKD)
Dr. Hamed Shakhatreh
consultant nephrologist, Head of nephrology department, Al-basher hospital, M.O.H.
http://www.jmc.gov.jo/UploadedFiles/Documents/af61a37b-98cd-4fa4-b55e-
d3bee0177ef5.pdf
What is CKD?
 Presence of markers of kidney damage for three months,
 as defined by structural or functional abnormalities of the kidney
with or without decreased GFR,
 manifest by either pathological abnormalities or other markers of
kidney damage, including abnormalities in the composition of
blood or urine, or abnormalities in imaging tests.

 The presence of GFR <60 mL/min/1.73 m2 for three

months, with or without other signs of kidney damage as
described above.
Epidemiology
 19 million Americans have CKD
 Approx 435,000 have ESRD/HD

 Annual mortality rate for ESRD: 24%

 CAUSE OF CKD:
 The most common causes of CKD are DM, HT
and glomerulonephritis. Together, these cause approximately
75% of all adult cases

 Diabetes. (35%)
 High blood sugar levels caused by DM damage blood vessels in the
kidneys.
 If the blood sugar level remains high, this damage gradually reduces the
function of the kidneys.

 Hypertension (30%)
 Because HT often rises with chronic kidney disease, high blood pressure
may further damage kidney function even when another medical
condition initially caused the disease.
 Other etiologies
 Renovascular disease
 Nephrotic syndrome
 Hypercalcemia
 Multiple myeloma
 Chronic UTI
Signs & Symptoms
 General  GI
 Fatigue & malaise  Anorexia
 Edema  Nausea/vomiting
 Ophthalmologic  Skin
 AV nicking  Pruritis
 Cardiac  Pallor
 HT  Neurological
 Heart failure  MS changes
 Pericarditis  Seizures
 CAD
GFR Calculations
 Cockcroft-Gault
 Men: CrCl (mL/min) = (140 - age) x wt (kg)
SCr x 0.81

 Women: multiply by 0.85

 MDRD: USUALLY WE USE COMPUTARISED

FORMULA TO CALCULAT IT :
 GFR (mL/min per 1.73 m2) = 186 x (SCr x 0.0113)-
1.154 x (age)-0.203 x (0.742 if female) x (1.12 if
African-American)
Stages of CKD
 Stage 1*: GFR >= 90 mL/min/1.73 m2
 Normal or elevated GFR

 Stage 2*: GFR 60-89 (mild)

 Stage 3: GFR 30-59 (moderate)

 Stage 4: GFR 15-29 (severe; pre-HD)

 Stage 5: GFR < 15 (kidney failure)

Management
 Identify and treat factors associated with
progression of CKD
 HT
 Proteinuria
 Glucose control
 Hypertension
 Target BP
 <130/80 mm Hg
 <125/75 mm Hg
 pts with proteinuria (> 1 g/d)

 Consider several anti-HTN medications with

different mechanisms of activity
 ACEs/ARBs
 Diuretics
 CCBs
 HCTZ (less effective when GFR < 20)
ACEs ARBs Diuretics CCBs HCTZ
Proteinuria
 Single best predictor of disease progression

 Normal albumin excretion

 <30 mg/24 hours
 Microalbuminuria
 20-200 g/min or 30-300 mg/24 hours
 Macroalbuminuria
 >300 mg/24 hours
 Nephrotic range proteinuria
 >3 g/24 hours
Metabolic changes with CKD
 Hemoglobin/hematocrit 
 Bicarbonate 
 Calcium
 Phosphate 
 PTH 
 Triglycerides 
Metabolic changes…
 Monitor and treat biochemical
abnormalities
 Anemia
 Metabolic acidosis
 Mineral metabolism
 Dyslipidemia
 Nutrition
Anemia
 Common in CKD
 HD pts have increased rates of:
 Hospital admission
 CAD/LVH
 Reduced quality of life
 Managing anemia Can improve energy
levels, sleep, cognitive function, and quality
of life in HD pts
 Metabolic acidosis
 Muscle catabolism

 Metabolic bone disease

 Sodium bicarbonate
 Maintain serum bicarbonate > 22 meq/L
 0.5-1.0 meq/kg per day
 Watch for sodium loading
 Volume expansion
 HTN

*HTN (hypertension)
Mineral metabolism
 Calcium and phosphate metabolism
abnormalities associated with:
 Renal osteodystrophy
 Calciphylaxis and vascular calcification

 14 of 16 ESRD/HD pts (20-30 yrs) had

calcification on CT scan
 3 of 60 in the control group
Dyslipidemia
 Abnormalities in the lipid profile
 Triglycerides
 Total cholesterol
 NCEP recommends reducing lipid levels in
high-risk populations
 Targets for lipid-lowering therapy
considered the same as those for the
secondary prevention of CV disease
Nutrition
 Think about uremia
 Catabolic state
 Anorexia
 Decreased protein intake
CV disease
 70% of HD patients have concomitant CV
disease

 Heart disease leading cause of death in HD

patients

 LVH can be a risk factor

Evaluation for CKD
 Blood  Urine
 CBC with diff  Urinalysis with
 SMA-7 with Ca2+ and microscopy
phosphorous  Spot urine for
 PTH microalbumin
 HBA1c  24-urine collection for
 LFTs and FLP protein and creatinine
 Uric acid and Fe2+
studies  Ultrasound
 Key points
 The serum creatinine level is not enough!
 Target BP for CKD
 <130/80 mm Hg
 <125/75 mm Hg in proteinuria
 HT and proteinuria are the two most
important modifiable risk factors for
progressive CKD