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

0.3mg/dl(26.5micromol/l)increase in the serum
creatinine, OR urine output <0.5ml/kgper hour for 6
to 12 hours.
Stage 2 2.0-2.9 times baseline increase in the serum
creatinine OR urine output <0.5ml/kgper hour for 12
hours.
Stage 3 3.0 times baseline increase in the serum
creatinine OR increase in serum creatinine to
4.0mg/dl(353.6micromol/l)OR urine output of
<0.3ml/kgper 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 <35ml/minper 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

Severe vasodilatation as in septicaemia, rapid

oedema formation, liver cell failure.
E- Renovascular disease
D-

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 1050% 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

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 areDM,HTN

andglomerulonephritis.Together, these cause
approximately 75% of all adult cases
Diabetes. It causes about 35% of all chronic kidney
disease. Highblood sugar levels caused
byDMdamage 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
allkidneydisease. BecauseHTNoften 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

Fatigue & malaise

Edema

Ophthalmologic

AV nicking

HTN
Heart failure
Pericarditis
CAD

Anorexia
Nausea/vomiting

Skin

Cardiac

GI

Pruritis
Pallor

Neurological

MS changes
Seizures

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

Microalbuminuria

20-200 g/min or 30-300 mg/24 hours

Macroalbuminuria

<30 mg/24 hours

>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

CBC with diff

SMA-7 with Ca2+
and phosphorous
PTH
HBA1c
LFTs and FLP
Uric acid and
Fe2+ studies

Urine

Urinalysis with
microscopy
Spot urine for
microalbumin
24-urine collection
for protein and
creatinine

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