ACUTE KIDNEY INJURY

AND CHRONIC KIDNEY

DISEASE

Dr. Hamed Shakhatreh

consultant nephrologist,
Head of nephrology department, Al-basher hospital, M.O.H.
AKI Definition
 AKI is defined as any of the following :
- increase in SCr by >0.3 mg/dl
(>26.5lmol/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.
Stage of AKI:

 Stage 1— 1.5-1.9 times baseline OR

≥0.3 mg/dl (≥26.5 micromol/l) increase in the serum
creatinine, OR urine output <0.5 ml/kg per hour for 6
to 12 hours.
 Stage 2 — 2.0-2.9 times baseline increase in the
serum creatinine OR urine output <0.5 ml/kg per
hour for ≥12 hours.
 Stage 3 — 3.0 times baseline increase in the serum
creatinine OR increase in serum creatinine to
≥4.0mg/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
 I. Pre-renal injury

In pre-renal failure, the renal tissue is intact and kidney

biopsy shows normal renal histology. Oliguria and high
serum creatinine are due to functional impairment; since
there is no sufficient blood reaching the kidney to be
cleared of these toxins.
Combination of hypotension, hypovolaemia resulting in
diminished renal perfusion is the most common cause of
acute renal failure in hospitalized patients.
When renal hypoperfusion (due to hypotension and/or
hypovolaemia) is not severe enough to cause renal
tubular damage, it will manifest as pre-renal failure in
the form of oliguria and a rise in serum creatinine and
blood urea. Since there is no structural renal damage,
early diagnosis and correction of renal hypoperfusion
results in immediate diuresis and rapid drop in serum
creatinine and blood urea levels.
If hypoperfusion is severe or neglected, renal
compensatory mechanisms will fail and acute tubular
necrosis occurs. In this new situation, correction of
hypoperfusion will not be followed by diuresis or drop
in serum creatinine. Few days or weeks (mean 2-3
weeks) are needed for tubular regeneration and
recovery of kidney function to occur.
II.Acute Intrinsic Renal injury
This includes acute tubular necrosis
(ATN), acute interstitial nephritis and
acute glomerulonephritis.
At this presentation we well discuss ATN
as the other entity will be discussed
separately in other lectures.
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 as in 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:
Analgesics:
Metals: as Mercury, lead, arsenic, bismuth, cadmium,
antimony,
organic solvents: Glycols
Poisons: snake bite, stings, bacterial toxins.
Causes of Toxic ATN

(B) Endogenous nephrotoxins

include
Pigments: Crystals:
Myoglobin Uric acid
Hemoglobin Calcium
Methemoglobin Oxalate
Post –renal injury
In post-renal failure, the obstruction of the
urinary tract results in 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 with progressive
accumulation of wastes and increase of
serum creatinine and blood urea.
Clinical features of AKI:
1- Usually, the patient gives history of the etiologic
cause such as trauma, shock, haemolysis, drug
intake, infection, or stone disease.

2- Patient may notice a 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).
3- Manifestation of salt and water retention (oedema,
puffiness, hypertension and even heart failure).

4- By time, manifestations of uraemia appear as acidotic

breathing, dyspnea, nausea, vomiting, headache, muscle
twitches and even frank encephalopathy and coma.

5- Patient may present as well with any of the following

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 bx.
TREATMENT OF AKI:
A- Treatment of the cause e.g. any condition
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.
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
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,HTN
and glomerulonephritis. Together, these cause
approximately 75% of all adult cases
 Diabetes. It causes about 35% of all chronic kidney
disease. 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. It causes another 30% of
all kidney disease. Because HTN 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
 HTN  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
 HTN
 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)
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
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+ microscopy
and phosphorous  Spot urine for
 PTH microalbumin
 HBA1c  24-urine collection
 LFTs and FLP for 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
 HTN and proteinuria are the two most
important modifiable risk factors for
progressive CKD