adiuvante Dei gratia doctorum factionis
NEPHROLOGY: ACUTE
KIDNEY INJURY
RED text– highlighted in ppt
BLUE text – explanation
BLACK text – old trans
VIOLET LABEL – not discussed in the lec, but included in the old trans
ACUTE KIDNEY INJURY (AKI)
 Abrupt decline in GFR occurring over a period of hours to day
resulting to failure of kidney to execute nitrogenous waste
products & maintaining fluid & electrolyte
 Reversible
 When you say acute kidney injury, there is rapidly
reduction on the glomerular filtration rate only over a
period of hours to days.
 If the kidney fails abruptly, then you expect organ
damage manifestation
 The difference with chronic kidney disease is that this
is usually reversible, so there is a chance for the
kidney to go back to the usual glomerular filtration
rate
 So that was hours to days and it is reversible
CHRONIC KIDNEY DISEASE (CKD)
 Progressive & permanent decline in GFR that develops over
months or years resulting in loss
 Irreversible
 In contrast, chronic kidney disease, there is
progressive and permanent decline on the GFR that
develop over a period of more than 3 months to
several years. So this will result on permanent
damage to the kidney. There is a loss of functioning in
nephron. So, this is permanent, it is irreversible
END STAGE RENAL DISEASE (ESRD)
 The degree of CKD wherein the GFR <10ml/min that would
cause death unless renal replacement therapy is initiated
 What do you understand by end stage renal disease?
This is the terminal stage of chronic kidney disease
wherein the patient’s GFR had been to decrease to 15
ml/min. So patient cannot live without renal
replacement treatment
 There are only 2 options when you say renal
replacement treatment: chronic dialysis or renal
transplantation
UREMIA
 Constellation of signs and symptoms resulting from impaired
renal functions
 Seen in both AKI and CKD
2014-2015
DRA. ROSANNA
CORTEZ, M.D.
 When you say uremia, this can be seen both in AKI
and CKD. These are constellations of signs and
symptoms or abnormalities that may develop in
patient with renal failure
 So the full blown uremic manifestations, you will ending up
with (?) kidney disease
 These uremic manifestations maybe more prominent be seen
in patient with AKI
 So, both AKI and CKD
UREMIC EMERGENCY
 Life-threatening problems:
 Hyperkalemia
 Pulmonary edema
 Severe metabolic acidosis
 Encephalopathy
 uremic
 hypertensive
 Pericarditis
 This can be the first presentation of either AKI or CKD
 Immediate management is the same
 When you say uremic emergency, these are life
threatening problems that may be seen both in AKI and
CKD and needs immediate management
 So what are these uremic emergency? Hyperkalemia,
pulmonary edema, severe metabolic acidosis, uremic
encephalopathy. If you have these, whether it is AKI or
CKD, management is to be immediate and urgent in
regardless of the cause; you need to treat right away.
 There are situations where in you can have AKI on top of
the CKD. For example, a pt. who is diabetic or DM
nephropathy, when there is proteinuria, and the serum
creatinine is 2.6 mg/dL, then the patient develop acute
gastroenteritis, so there is an acute insult that happen that
in acutely reduce the GFR
 So when you repeated the serum creatinine, that are up to
be 6.8 mg/dL. So this condition, we use the term acute
kidney injury on top of chronic kidney disease secondary
to DM nephropathy
 All the causes of AKI that will be develop in pt. with CKD,
the diagnosis will be taken on top of CKD
NOT DISCUSSED IN THE PPT. YOU MAY READ IF YOU WANT =)
Clinical manifestations:
 Neuromuscular:
 - Paresthesia - Dose is 50-150 meq/L
- Weakness - Onset is 15-30 minutes, but delayed in CRF
- Paralysis 3. B2 Adrenergic Agonist
- Due to changes in neuromuscular conduction w/  - Increase Na+K+ATPase activity
magnitude of RMP - Albuterol 10 mg nebulization
- Does not develop until plasma K+ >8meq - Onset 30 minutes, duration 2-4 hours
 Cardiovascular: - Tachycardia is common
- Due to delayed depolarization - Dose is higher than the dose used to promote bronchial
- Cardiac toxicity enhanced by: dilatation
- hypocalcemia
- Hyponatremia Delayed Onset:
- Metabolic acidosis  Removes K+ out from the body
 Normal renal function
ECG changes – lack predictability: - NSS (125-150 m/hr)  delivery of Na+
 Peaked & narrow T wave - Loop diuretics to increase the flow rate & urinary K+
 Shortened QT interval excretion
 Widened QRS - Cation Exchange Resin
 Prolonged PR interval  Sodium Polystyrene sulfonate (Kayexalate)
 Flat P wave  Oral: 20-40g with 100mL 20% sorbitol
 Complete heart block  Onset: 2hrs repeated every 4-6hrs
 Ventricular arrhythmias  Retention Enema: 50g with 50mL 70% sorbitol plus
100-150 mL tap water and kept in the colon
Severity according to plasma K+ and ECG changes:  Absent Renal Function
 Mild - Cation Exchange Resin
- plasma K+ <6meq/L  Na polysterene Sulfonate (Kayexalate)
- ECG limited to peak T wave - Oral:
 Moderate  20-40 gm w/ 100 ml 20% sorbitol
- plasma K+ 6-8meq/L  Onset is 2 hrs; rptd every 4-6hrs
- ECG only peak T wave - Retention enema:
 Severe  50gm w/ 50ml 70% sorbitol plus 100-150 ml tap
- plasma K+>8meq/L or water & kept in the colon for 1-3 hrs
- ECG absent P wave, widened QRS or ventricular  Onset is 30 mins; rptd every 2-4 hrs
arrhythmias asystole  Each enema lower plasma K+ 0.5-1 meq/hr
 SE:?
Treatment:
 Reverse the effect of hyperK+: Absent Renal Function
1. Direct antagonism of its membrane action  Cation exchange Resin
2. Lowering the plasma K+  Dialysis:
 Driving K+ into cells - Onset immediate
 Remove K+ from body - Hemodialysis is preferred
- Removes 25-30 meq/hr on total body K+
Immediate Onset:
 Calcium gluconate Metabolic Acidosis
- 10% 10ml soln over 2-3 mins. 1. Kaussmaul Respiration – results of respiratory compensation
- Can be repeated after 5 mins - Inc RR fatigue respiratory failure
- Onset of action 1-3 minutes 2. Cardiovascular
- Antagonizes the effect of K+ resting membrane excitability - pH >7.20: 2 counteracting forces & myocardial function
towards… remains largely unchanged
- Reverse sinus rhythm a. positive inotropic effect of released epinephrine
- Immediate action reverse K+ effect b. direct inhibitory effect of acidosis on myocardial
contractility
Intermediate Onset: - pH <7.20: epinephrine effect are blocked, unmasking
 Shift K+ into the cells negative inotropic effect of acidosis
1. Insulin + Glucose  may lead to:
- Stimulates Na+K+ATPase o heart failure
- Regular insulin 4-8 u + D50-50 o hypertension
- This combination can cause hypoglycemia o cardiac arrest
- Onset 5-10 mins; lasted for 4-6 hrs 3. CNS - decrease level of consciousness: confusion, stupor, then
- Lower plasma K+ by 0.5-1.5 meq/L coma.
2. Sodium bicarbonate - seizures
- Helpful in patients with renal failure and metabolic - secondary to decrease in the intracerebral pH
acidosis 4. Potassium – hyperkalemia, due to shift of K+ out of the cells
leading to cardiac arryhtmias.

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 ++
5. Calcium – chronic metabolic acidosis enhances Ca resorption  Seizures
from bones  Changes in sensorium  coma

Treatment:
HCO3 deficit = (desired HCO3 – actual HCO3) Consequence Management
x 0.5 x weight in Kg
 ½ calculated deficit maybe replaced in 3-4 hours if severe heart 1) Protect the airway
failure is not present
2) Check fundi reflexes and coma score
 No further HCO3 therapy should be given once pH is 7.20
+ 3) Phenytoin 300 mg PO for consciuous
 K+ supplementation should be undertaken if serum K begin to
fall during correction of acidosis Hypertensive patient or Valproic Acid (sodium
Encephalopathy valproate) 10mg/kg IV for comatose
Complication of HCO3 replacement: patient
1. Sodium and volume overload 4) Gradual reduction in blood pressure
2. Hypernatremia to avoid watershed zone infarction,
3. Hypokalemia
IV labetalol or nitroprusside.
4. Post-treatment alkalosis

Pericarditis
Clinical manifestations: 1. Protect the airway
 Chest pain with respiratory accentuation 2. Options: chosen to avoid
 Friction rub disequilibrium
 Cardiac tamponade Uremic a. Consider peritoneal dialysis
- Falling BP Encephalopathy as first option
- Widened pulse pressure
b. Hemodialysis 2 hours daily;
-  JVP
- Pulsus paradoxicus blood flow at ~150ml/min
- Cold extremities c. Hemofiltration over 24 hours
d. Peritoneal dialysis
 Pericardial fluid is hemorrhagic 3. Valproic Acid 10 mg/kg IV if risk of
seizure high.
Diagnosis:
1. Chest x-ray – marked cardiomegaly Uremic Neuropathy
2. 2D Echocardiography – definitive & can estimate how much fluid  Bilateral symmetrical disturbances of both sensory and
accumulate motor function
 Sensory
Treatment:
 “stocking-gloves” distribution
 Pericardiocentesis/pericardiostomy
 Lower extremities > upper extremities
 Pericardiectomy
 Dialysis  Distal parts > proximal
 Motor
 Muscle wasting, weakness
Consequence Management
 Restless leg syndrome – ill-defined sensation or
discomfort in feet & lower legs relieved by leg movement.
 Pre-neuretic sypmtoms – indication to start dialysis

1. Needle Drainage before dialysis to Pulmonary Edema

avoid hypertension Clinical Manifestation:
Pericardial
2. Leave drain in situ during low/no  Sudden dyspnea
Tamponade
heparin dialysis  Cardiac/noncardiac
3. Switch to or start peritoneal  Bilateral rales
dialysis as soon as possible.  May have NVE (Neck Vein Engorgement)
Diagnosis:
 Chest Xray
Uremic Encephalopathy HPNsive Encephalopathy  ABG
Clinical manifestations:
 Insomnia Consequence Management
 Restlessness
 Twitching, myoclonus, asterexis
 Irritability, depression, aggression

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  As defined earlier, when we say AKI, it develop over a
1) Sit the patient up period of hours to days.
2) Oxygen by face mask/continuous  Clinically, this will be evident on just increase on BUN, or
positive airway pressure/ventilator both BUN and Serum creatinine
3) Furosemide 100-300mg IV  What is the normal ratio of BUN to Creatinine? 10:1
Pulmonary
4) Nitroglycerin 10 - 200µg/min IV  There is a situation where in normal ratio will increase, it
Edema
5) Morphine 5 mg IV if respiratory drive means the increase on the urea is higher than the increase
not depressed in the serum creatinine
6) Remove fluid by venesection,  Why it is important for you to know the ratio (BUN:Crea
hemofiltration, or peritoneal dialysis ratio} or it may just be just increase in BUN and without
concomitant increase in serum creatinine
Acute-on-Chronic Kidney Disease  Clinically, they may be present as acute oliguria
 The degree of renal failure has been aggravated by some  When we say acute oliguria, less than 400 ml of urine in 24
intercurrent event hours or in some books, less than 500 ml in 24 hours
 Additional decline in GFR from a superimposed process as:
 Volume depletion CONSEQUENCES OF AKI
 Nephrotoxic drugs
 Disease relapse  Retention of nitrogenous waste products
 Disease acceleration  Expansion of ECF volume
 Infection  Disorders on electrolytes and Acid-Base balance
 Obstruction
 Hypercalcemia  What will happen if there is acute kidney injury? You
 Accelerated hypertension know the functions of the kidney, as an excretory organ,
 Heart failure so it will retain the nitrogenous waste products and this
will be reflected on your BUN and serum creatinine.
Hemodialysis VS Peritoneal dialysis Because of oliguria, there will be increase in the
Hemodialysis intravascular compartment or the ECF volume expansion
 Intermittent hemodialysis – 3-4 hrs/day 3-4x per week manifested as edema or pulmonary congestion. Disorder
 Slow efficiency dialysis – 6-12 hrs/day 3-6x per week (SLED) on electrolytes or acid base disorders, it will be important
 Continuous renal replacement therapy (CRRT) to know that pt. who are oliguric, will have increased
- CAVH - CVVH incidence in the development of pulmonary congestion
- CAVHD - CVVHD and hyperkalemia compared to those urine output are
- CAVHDF - CVVHDF still adequate
 Tatandaan ninyo, problema lagi ang hyperkalemia and
- More rapid removal of solutes pulmonary congestion if the patient has oliguria
- Less time required  Abnormalities in acid base – metabolic acidosis
- No risk of peritonitis, intestinal perforation,
hyperglycemia

Peritoneal dialysis
- Simpler to perform
- Easier access
- No anticoagulation or blood loss
- Fewer problems with hypotension Overlapping

ACUTE KIDNEY INJURY  So there is an overlap, as I have mentioned, CKD in which

the pt. also may develop AKI or there is acute kidney
disease without concomitant reduction on the GFR. So
 Rapid decrease in GFR occurring over period of hours to meron overlap
days
 Clinically diagnosed by one of the following: RENAL CRITERIA STRUCTURAL
1) Increase in BUN CRITERIA
2) Increased in BUN and Creatinine Acute Kidney Injury Increased in serum No criteria
3) Oliguria – urine < 400 ml/day creatinine by 50%
within 7 days or

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 increased in serum CLASSIFICATION OF AKI
creatinine by 0.3
mg/dl (26.5mmol/l) 1) NONOLIGURIC
within 2 days  Urine output > 400ml/day
Oliguria
2) OLIGURIC
Chronic Kidney GFR= <60 ml/mim Kidney damage
Disease
2
per 1.73m for 3 (>3mos)  Urine output < 400ml/day
months 3) ANURIC
Acute Kidney AKI or GFR <60 Kidney damage  Urine output < 100ml/day
2
Disease ml/min per 1.73m (<3mos)  We classify AKI, whether it is non-oliguric, oliguric or
for 3 months or anuric
decreased in GFR
>35% or increased
Low urine outputreflect:
serum creatinine by
50% for <3 months  More severe initial injury
Normal Kidney GFR >60 ml/min per No damage  Implication for: volume overload
2
Disease 1.73m f or stable Electrolytes disturbances
craetinine  Prognosis
o Better prognosis with oliguric than non-oliguric
 How do you define this different AKI? Your acute kidney
disease/disorder and the normal kidney disease or the Reduction in GFR
chronic kidney disease Obstruction to urine flow
 So this is based on the serum creatinine and the duration
 So in AKI, increased in serum Creatinine by 15% within 7  Oliguria Acute renal failure
days or an increase in serum creatinine by 0.3 mg/dL
within 2 days, the pt has oliguria. In structural criteria, no  If there is oliguria or low urine output, it will tell you that
damage the renal parenchymal injury is more severe and you will
 when you say CKD, there is reduction in the GFR that is have problem on volume overload and hyperkalemia
less than 60 ml/min that develop more than 3 months or  Prognosis will also be affected because if the patient is
evidence of structural damage oliguric, then you will be have more problem, prognosis
 Pt. with polycystic kidney disease, you know what will be poorer compared to the oliguric pt with AKI
polycystic kidney disease is, may develop over years. For  40% of pt. with AKI without oliguria and example of this
example, 15 years old, there are several cysts that may will be patient with aminoglycoside nephrotoxicity. If ever
have been focal at the age of 35. So you can consider pt. they develop AKI, the urine output is still adequate
with polycystic kidney disease as CKD even if the GFR has  The outcome will increase in level of serum creatinine
been normal  If you prognosticate also the pts if the pt. starts as oliguric
 When you say acute kidney disease, the GFR had been  If you have AKI, there is sudden reduction in the GFR or
reduced by 60% that developed less than 3 months. There there is obstruction to urine flow in general causes
can be kidney damage like proteinuria, hematuria,  Pt with acute oliguria, will soon develop AKI but not all AKI
ultrasound findings, abnormalities of the kidney and will have oliguria, 40% still with urine output
urinary tract that may develop on less than 3 months
produce acute kidney disease ADQPI
 Normal kidney disease, GFR more than 60 ml/min. For
example, pt. is chronically hypertensive, pwedeng Recently, a consensus conference sponsored by the Acute Dialysis
urinalysis ay normal kaya lang GFR niya is 75 ml/min; it can Quality Improvement Initiative (ADQI) has proposed a new definition
be normal but is more than 60 ml/min, so you can of ARF that has been widely endorsed and is increasingly being used.
consider this. In keeping with the spectrum of changes seen in AKI, a diagnostic
classification scheme was developed
 ACUTE KIDNEY INJURY  Acute Dialysis Quality Improvement Initiative (ADQI) has
 (ACUTE RENAL FAILURE) proposed a new definition for acute renal failure. So this is
 ACUTE TUBULAR NECROSIS the list on the increase in serum creatinine and the urine
output that is noted because when we see pts with AKI
 You will use interchangeably AKI, acute renal failure and usually mislead, the serum creatinine elevate later if there
acute tubular necrosis is already established renal parenchymal injury. You have
 However, not all pt. with AKI or ARF have acute tubular to get the patient Early to lessen the mortality of pt with
necrosis. Be careful in using AKI rather than ATN AKI because AKI have higher mortality compared to

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 condition that in critical setting, when they develop AKI,
the mortality becomes higher
GFR criteria Urine Output criteria
RISK Screa x 1.5 UO <0.5ml/kg/hr x6
or hrs
GFR >25%
INJURY Screa x 2 UO <0.5ml/kg/hr x12
or hrs.
GFR >50% Oliguria
FAILURE Screa > 4mg/dl UO <0.3ml/kg/hr x24
Acute rise >0.5mg/dl hrs.
Anuria x 12hrs.
LOSS Persistent ARF = Complete loss of kidney function >
4weeks
ESKD End Stage Kidney Disease
(>3 Months)
Renal dysfunction is defined in terms of a rise in creatinine or a
reduction in urine output, the more severe of the two criteria being
selected. RIFLE-F (Failure) is present even if the risk in serum
creatinine is less that the threefold above baseline, provided that
the new serum creatinine is greater than 4mg/dL and has risen by at
least 0.5 mg/dL. When the achieved designation results from ed e.g.
RIFLE-Fo. Similarly, a subscript “c” is used to denote the presence of
preexisting chronic kidney disease.
 If there is increased in serum creatinine, 1.5 and the urine
output have been reduced by 0.5 ml. So 0.5 ml x 60 kgs =
that is 30 ml/hr
 If less than 30 ml/hr that observed in 6 hours, pt. is already
at risk for the development of AKI
 If the serum creatinine is doubled up and the urine output,
let’s say 30 ml, in 60 kg, less than 30 ml then what is your
observe for 12 hrs? The patient have already injury
 If the serum creatinine have increased for more than 4
mg/dl or an acute rise >0.5mg/dl. For example, ang serum
creatinine mo initially is 1.5 mg/dl naging 4.5, acute rise.
That is already failure or the urine output had been
reduced by 0.3ml multiply by 60 kgs – more or less than 20
ml/hr that is observe for 48 hours or the patient had been
anuric. Ano yung anuric? Less than 100 ml/24 hrs when
the pt. is considered in failure
 This was in end stage kidney disease, on how you manage
the patient. If you have persistent loss of kidney function
that will necessitate dialysis, observe the pt. in 4 weeks
then the pt. have kidney loss. This necessitate dialysis
 For example, this one, if you are doing your dialysis more
than 3 months and there is no evidence of recovery or
reversal of the renal function then the patient is in end
stage kidney disease. What does it mean? Pt. with AKI in
worst scenario and in severe type, maybe a cause of end
stage kidney disease that is observe in more than 3
months so nagfifit na siya doon sa criteria for the diagnosis
The future depends on what we do in present Page 6 of 20
of chronic kidney disease, more than 3 months.
Understood na yan ha?
FEATURES SUGGESTING CKD
1) Symptoms lasting >3months
2) BUN or Creatinine documented months earlier
3) Normocytic, normochronic anemia
4) Small kidneys < 10cm on renal UTZ
5) Retention of nitrogenous waste products
6) Expansion of ECF volume
7) Disorders on electrolytes and acid – base balance
 Can we define the reduction on the renal function? It is
easy to say that there is AKI or CKD
 There are situations wherein it is very hard for you to tell
what is the course of the illness
 You may have some clue to tell you that the patient is CKD
and not in AKI. For example, they present with uremic
emergency with uremic encephalopathy, so how will you
tell whether this patient who present with uremic enceph
is due to AKI or CKD? More than 3 months or you have
documented several months in the past, BUN and crea was
already elevated. Findings: normochromic, normocytic
anemia (di ko maintindihan ang sinabi na words) to CKD
than AKI
 You will not develop anemia in pt. with AKI unless the
cause of the AKI is blood loss. On that situation it can be
very obvious that there is acute blood loss that causes this
in AKI
 Otherwise, kung wala siyang history of blood loss and
there is normochromic, normocytic anemia and the pt. is
well compensated, 64 lang ang haemoglobin but the pt. is
still talking b ecause if it will happen acutely, then what
should expect what? There will be more symptomatic of
that acute anemia
 If you will do ultrasound (UTZ) among Filipinos, if the sizes
of the kidney is less than 10 cms, making them small
kidneys. They took also the cortical thickness, you can
measure cortical thickness in the ultrasound, if it is less
than 2 cm and if it will portray contracted kidneys wherein
the cortex had thinned out, sabihin na lang natin less than
4 cms na lang. So that it indicate chronic kidney disease
because in AKI, ultrasound findings within normal, it may
be abnormal but it is not contracted as small size kidneys,
echogenicity of the kidney will be increased. So in UTZ, the
usual kidney is blackish than liver (right) and spleen.
 But in secretion wherein kidney becomes more whiter
than the liver and the spleen, this will be label as increased
echogenicity of the kidneys, that may indicate CKD
 Evidence of retention of nitrogenous waste products. Kung
ang serum creatinine mo, 10 mg/dl and pt. is still
asymptomatic/fewer symptoms then this point to CKD
compared to AKI pt. that the serum creatinine just go up
to 5 mg/dl, they are more symptomatic. Why? Because in
CKD, even if the serum crea increases, that there is time
CooKiE 
 for variable compensate kaya may symptoms. Fluid
overload manifested as neck vein engorgement, bilateral
rales, peripheral edema, hypertension; this may be
common in AKI. But these will develop as late
consequences or late stage CKD.
 Acid base disorder – metabolic acidosis and hyperkalemia
ETIOLOGY
 Pre-renal = 50%
 Intrinsic Renal = 40%
 Post – renal = 5%
 Pre renal AKI – this is the most common
 When we say pre-renal, there is strong muscle often
repair; the problem is the renal blood flow. GFR is
dependent on the amount of renal blood flow. So if you
reduced the renal blood flow, the GFR also goes down
 When you say intrinsic, the problem is the kidney and its
structure. It maybe because of acute glomerulonephritis,
acute tubular necrosis, or ischemic or nephrotoxic injury
to the kidney or it could be injury to the renal vessel that is
affected. So intrinsic. Pwede ang renal blood flow ay okay,
pwede din abnormal
 Post renal – wala ka problem sa blood flow, walang
problem sa kidney. Ang problem mo ay mechanical, there
is obstruction to the flow of urine
 So, nabanggit ko na yung post renal, nabanggit ko na yung
pre renal. Pero higit na alamin ang cause ng intrinsic.
CAUSES OF PRERENAL AKI Prerenal AKI
 Common denominator ng all pre renal causes will be
diminished renal blood flow. There is hypoperfusion to the
kidney. So it can be reduction on the intravascular volume.
Any cause of reduction in intravascular volume will reduce
the renal blood flow and can cause pre renal AKI.
 So this can be cause of bleeding (postpartum bleeding),
fluid losses from the GI tract like yung mga sinabi natin na
fluid volume depletion. The other causes can lead to
intravascular volume. Losses in the GI, in the kidney.
Central diabetes insipidus can also cause of volume
depletion or yung may burn, exude fluid from the skin, this
can cause severe fluid losses
 Or if the patient have no losses so that fluid is shifted to
the interstitial compartment, so this maybe deficient in
hypoalbuminemia
 What are the causes of hypoalbuminemia? Pt. with
malnutrition, nephritic syndrome, liver cirrhosis. Albumin
is depleted in their blood, will deteriorate oncotic
pressure. If you have low oncotic pressure, what happen
to the water inside the intravascular compartment? It will
shoot the interstitial compartment, so that the effective
intravascular volume will be depleted
 So if you don’t have losses but the fluid is pooling blood
just in evidence of vasodilatation
 You’ve seen pt. with allergy. Ano itsura ng pasyente na
may allergy? Mapula because of vasodilatation.
 Anaphylactic shock - there is pooling of blood in the
circulation that can lead to the vasodilatation. So this can
be depleted intravascular volume
 Anesthetic agents, this can also cause vasodilatation

Reduce effective Impaired Renal

extracellular volume Autoregulation
...
 .

Hypovolemia Systemic
Hemorrhage Vasodilation
Postglomerular (efferent
Fluid loss: GI, Sepsis
arteriolar) vasodilation
renal, skin, Cirrhosis
ACE inhibitors
respiratory,surgi Anaphylaxis
Angiotensin AT1 receptor
cal Anesthesia
antagonists
Hypoalbumunem Pharmacologic
ia Vasodilation
Third Spacing

Postglomerular (afferent arteriolar)

Cardiac Failure Vasoconstriction
Myocardial Sepsis
Dysfunction Hypercalcemia
Valvular Hepatorenal Syndrome
Dysfunction Pharma agents: NSAIDs, Cyclosporine
Cardiac (cyclosporine A), amphotericin B, epinephrine
The future depends on what we do in present
Tamponade Page 7 of 20
(adrenaline), norepinephrine (noradrenaline) CooKiE 
Pulmo HPN
  Medications like nitrates. Ang nitrates is used that
nilalagay as patch to mask vasodilatation of the coronary
arteries. Side effects of nitrates?
 Headache. Because if you vasodilate vessels in the brain it
can cause headache
 One clue that the pt. is coming from nitrate or pt. is having
to nitrate is having experience chest pain and had
sublingual nitroglycerin
 So this vasodilatation can also be seen in pt. with taking
calcium channel blocker. So these can lead to effective
means of vascular permeability in the kidney
 More vasodilatation but the cardiac output is low
 So the effective intravascular volume will be depleted, can
be seen in pts with massive myocardial infarction, this is
what you called cardiogenic shock because the cardiac
output is low because the heart cannot pump because of
the pericardial effusion so there is cardiac tamponade
 In pt. with pulmonary hypertension, any form of
cardiomyopathy so it can reduce the cardiac output. So
this maybe the cause of diminished in neffective
intravascular volume so that can lead to prerenal AKI.
 So before you understand this, there are manifestations of
the following if ever there is intravascular volume
depletion meron kang compensation
 The compensation is you stimulate the baroreceptors, and
then stimulate sympathetic nervous system. Ano ngayon
ang problem ng sympathetic nervous system? You release
the catecholamines like norepinephrine, if you stimulate
the RAAS, you have angiotensin II and you stimulate the
release of vasopressin. These try to have vasoconstriction
to preserve the intravascular volume.
 Stimulating salt and water reabsorption in the tubules to
restore the blood volume and the blood fraction
 On the other hand, angiotensin II will have an effect on the
efferent arterioles. This efferent arterioles constriction, it
will constrict the efferent arterioles in to preserve the GFR.
The efferent must be constricted and the afferent must be
dilated
 If you give your pt. an ACE inhibitor, what is the effect of
your ACE inhibitor? On the conversion of your angiotensin
I to II, so kung wala ng angiotensin II kasi pinprevent ng
ACE or kahit yung ARB hindi mageeffect sa efferent
arterioles binablock niya so there will be sudden, instead
of constriction, so dilated yung efferent arteriole. So that
will end in dramatically reduced the GFR
 So kung magbibigay ka ng antihypertensive drugs like ACE
inhibitors or ARB, you need to watch out is the sudden
reduction on the GFR because of the effect of relaxation of
the efferent arterioles
 On the other side, resistance receptors and this will trigger
vasodilatation of afferent arterioles. This vasodilatation is
also increase or converted the synthesis of prostaglandin.
Prostaglandin are dilator to your afferent arteriole
because we want afferent to be dilated
The future depends on what we do in present Page 8 of 20
 Prostaglandin E2 and prostacyclin will dilate the afferent
arterioles
 If you give your patient NSAIDS, if you give it, for the
synthesis of prostacyclin so it will restrict the afferent
vasodilatation instead magcoconstrict, mataas yung
prostacyclin, so it can cause sudden reduction on the GFR
to this impaired autoregulatory para iniistop mo yung
autoregulation
 So nitric oxide, kallikrein and kinins are vasodilators. So it
is one of the modalities of treatment in AKI is to give a
stimulant for nitric oxide synthesis because nitric oxide can
dilate the afferent arteriole
 SUMMARY LANG TO KUNG NAINTINDIHAN MO.
 Impaired renal autoregulation.
 Those that will dilate the efferent arterioles (ACE
inhibitors, ARB will cause pre renal AKI
 Afferent arterioles are constricted so this are in pt.
with given NSAID, norepinephrine, cyclosporine
 Kaya may mga pasyente na hypotensive, if you wll
give your norepinephrine, it will constrict the afferent
arterioles pwedeng makadamage o makadagdag
doon sa AKI
 Ito din yung mechanism on how the pt. will develop
hepatorenal syndrome
 When we say hepatorenal syndrome, you have liver
failure and the pt. developed AKI but there should be
exclusion pwede siya with liver failure or cirrhosis you
may have other causes of AKI. For example, pasyente
mo may liver cirrhosis, at may ascites, you remove 5
liters of your ascites this can start drop in
intravascular volume and that can be cause of AKI. In
that situation, you will not label this as hepatorenal
syndrome. So you exclude other causes because the
failing liver can be producing substances that will
selectively cause constrict of the afferent arterioles
kaya siya sianbing hepatorenal syndrome
 So in essence, ang hepatorenal syndrome, is a clinical
eye of AKI
 Sepsis can be vasodilatation, competitive because of
constriction of afferent arteriole
HYPERVISCOSITY SYNDROME
 Multiple myeloma
 Polycythemia
 Macroglobulinemia
 In a situation wherein there is hyperviscosity syndrome,
very viscous yung blood, hindi makaflow, in pt. with
multiple myeloma, polycythemia, macroglobulinemia.
This can reduce effective intravascular volume kasi kung
tutuusin, ang intravascular volume mo magdedepleted
but the effective intravascular volume is assume
CooKiE 
 reduced because of the viscous blood that cannot, that
can be cause of reduced renal blood flow
PRERENAL AKI
 Characterized by renal hypoperfusion
 Integrity of renal parenchymal tissue is
preserved
 Most common cause of AKI
 GFR is corrected rapidly on restoration of renal
perfusion (within 24-72 hours)
Secondary to diseases characterized by:
1. Hypovolemia
2. Decreased cardiac output
3. Systemic vasodilation
4. Intrarenal vasoconstriction
 So, ang common problem with pre renal AKI is renal
hypoperfusion, the integrity of renal parenchymal
tissue is preserved and it is the most common type of
AKI. If you correct this, with 24-72 hours, you reverse
the renal function
 For example, pt. no. 1: having diarrhea for 3 days,
diarrhea and vomiting, was brought to the ER, pt. is
severely volume depleted, right away hydrate the pt.
before the pt. was brought to the ER, risk for no urine
output yung pt. dehydrated
 Pt. no. 2: having diarrhea and vomiting for 5 days,
having oliguric for 2 days also at the ER. Severely
volume depleted, hinydrate mo din. Which patient
will start to cope? Patient 1. Patient no.2, nahydrate
mo sila parehas within 24 hrs start to put out urine in
pt. 1. Yung pt. 2 3 days na di umiihi. So that is
different type of your AKI.
 So ang clue mo, sasabihin ng mga resident physicians,
“Ay, nag acute tubular necrosis na yung patient #2”,
kasi if the pt. hindi umihi that will happen in the
severe type of AKI, tubular necrosis yan.
 Urinalysis maybe normal or you may have bland
urinary sediment
 You may only have change in the specific gravity or
the most that you can see will be hyaline cast, that is
in prerenal AKI
INTRINSIC/INTRARENAL AKI
 Problem within the kidney
CAUSES
Diseases of large renal vessels:
 Renal artery stenosis/thrombosis/embolism/obstruction/
atherosclerotic plaque
 Operative arterial cross – clamping
The future depends on what we do in present Page 9 of 20
 Bilateral renal vein thrombosis/occlusion
 Ang intrinsic or intrarenal AKI ang problem is within
the kidney, because of problem of the large renal
vessels; like in renal artery stenosis or thrombosis. For
example, yung pasyente mo, nag coronary
angioplasty, nadislodge yung atheromatous plaque
nung ininsert yung catheter, nagbara dun sa renal
artery in the form of thrombosis, then the pt. now
developed oliguria. So iyan ang cause.
 Renal artery thrombosis/embolism or yung pasyente
mo, pelvic surgery because of pelvic malignancy.
Iatrogenically, nagclot byung mga renal vessels so it
can be cause of oliguria after pelvic surgery.
 It can be renal vein thrombosis or occlusion, kaya
yung pasyente may nephritic syndrome, no urine
output at may flank pain, suspect renal vein
thrombosis as the cause.
Diseases of renal microvasculature:
 Vasculitis
 Thrombotic microangiopathies
 Hemolytic Uremic syndrome
 Malignant HPN
 Thrombotic thrombocytopenic purpura
 Toxemia of pregnancy
 HELLP
 Diseases of the microvasculature – so ito yung mga
vasculitic diseases.
 Henoch Schloein purpura, Wegener’s granulomatosis,
haemolytic uremic syndrome
 So, mababarahan yung vessels sa kidney.
 Pt. with malignant hypertension, toxemia or eclampsia of
pregnancy. ito yung explanation bakit nag renal AKI yung
pasyenteng may eclampsia or the worst scenario will be in
pt. who are eclamptic with hemolysis, elevated liver
enzyme and low platelet. So that is the worst. They can
develop AkI due to this mechanism.
Glomerular disease:
 AGN
 RPGN
 Of course, glomerular diseases self explanatory yan noh.
You know that in glomerular disease, for example, if the
acute glomerulonephritis, there is injury to that
glomerulus, to the basement membrane. So the surface
area for glomerular filtration is reduced. So it can reduce
the GFR. That may be seen in acute GN and in pt. with
RPGN
Diseases of Tubulointerstitium Associated with Acute Intrinsic
Renal Azotemia
Drug-induced Allergic Interstitial Nephritis
Β-Lactams NSAIDS Other Viral
Ampicillin Aspirin A-Methlydopa CMV
CooKiE 
 Amoxicillin Celecoxib Allopurinol Measles  What do you understand by ischemic? In general? Meron
Carbenicillin Fenoprofen Azathioprine Infectious
kang coronary ischemia, ano ang ibig sabihin? Dimished
Methicillin Ibuprofen Mononucleosi
Nafcillin Indomethacin Carbamazepine s ang blood flow
Oxacillin Mefenamic acid Cimetidine Rocky  So, can we say the pt. since a common denominator
Pen G Naproxen Omeprazole Mountain
Cephalexin Phenazone Clofibrate spotted fever among the causes of prerenal AKI is diminished renal
Cephalotin Phenylbutazone Clozapine Other blood flow? Does it mean that this can also cause intrinsic
Cephradine Tolmetin Famotidine Candidiasis or ischemic AKI? Although maski sa prerenal, can it cause
Cefotaxime Sulfinpyrazone Toxoplasmosis
Diuretics Phenobarbita Miscellaneous ischemic AKI? YES. So, it depends on how severe, how
Other Chlorthalidone Infectious Systemic dse. prolong the acute insult that resulted in renal
Antibiotics Furosemide Bacterial SLE
Ethambutol Bumetanide Acute Sjogren syn. hypoperfusion, you have graded respond on the kidney.
p- Thiazides pyelonephritis Tubulointerstitial Not unless the pt. 1 at si pt.2
nephritis and
Aminosalicylate Leptospirosis
uveitis syn,  The pt. 1 prerenal lang siya. Pt. 2, nahydrate mo na,
Rifampin Scarlet fever
Cancer naoverload ka na nga di pa din umiihi, pataas pa din ng
Sulfonamides Typhoid fever
Lymphoma
Trimetoprim Legionnaire’s pataas ang serum creatinine , that will lead already to
Leukemia
Ciprofloxacin Dse,
Myeloma ischemic AKI
Levofloxacin
Sarcoidosis
Norfloxacin
Vancomycin ISCHEMIC ATN

 All causes of pre-renal azotemia

 If it is due to drugs, parang yung hypersensitivity reaction.
Kaya ang usual manifestation ng patient, for example,
nagtake ng allopurinol, 5 days nagtatake ng allopurinol,
nagkaroon ng liver, nagkaroon ngf heart lesion, skin lesion,
then the pt. become oliguric, CBC: increased eosinophils,
so you called it as ACUTE allergic interstitial nephritis
 So there are lot of drugs implicated. Hindi lang allopurinol,
even cimetidine, anticonvulsant such as phenytoin,
Phenobarbital; NSAIDS. It also cause ALLERGIC
INTERSTITIAL NEPHRITIS, even the COX inhibitor
 Antibiotics even rifampicin and quinolones can also cause
ALLERGIC interstitial nephritis
 If the cause is due to infection, you don’t call it as allergic
interstitial nephritis but you call it as ACUTE INTERSTITIAL
NEPHRITIS. Example of this, ngayong season na to,
LEPTOSPIROSIS.
 So ang reason how is it leptospirosis causes AKI is
development of acute interstitial nephritis
 Another one, pt. with pyelonephritis tubulointerstitium
infiltration with lymphoma, leukemiaeven sarcoidosis so
these can be also cause of acute interstitial nephritis.
 Marami yan, typhoid fever, leptospirosis, acute
pyelonephritis, legionnaires disease and even viral
infection can be cause of acute interstitial nephritis
ACUTE TUBULAR NECROSIS (ATN)/ACUTE KIDNEY INJURY (AKI)
 Ischemia (Ischemic ATN) – 50%
 Nephrotoxins (Nephrotoxic ATN) – 35%
 20-30% of patients do not have morphological evidences
of tubular necrosis
 Another form of intrinsic causes of AKI will be acute
tubular necrosis, which can be ischemic or nephrotoxic
 Hypoperfusion induce ischemic injury to renal cells
 Recovery takes 1-2 wks. after normalization of renal blood
flow
 Extreme form – Complete cortical Necrosis (Irreversible
renal failure)
RENAL HYPOPERFUSION
Prerenal AKI
Ischemic ATN
Bilateral complete cortical
Necrosis
 So it means the renal hypoperfusion may have graded
respond on the kidney. So in more severe scenario, worst
at lesser ang hypoperfusion and it was addressed
immediately then it can only be prerenal AKI
 But if it is severe and prolonged. It can lead to ischemic
ATN and pagka worst, it will be bilateral
complete cortical necrosis. So this is irreversible. This may
be the cause of end stage renal disease, your bilateral
cortical necrosis
 So gagamitin natin yung patient natin, dun sa #1 pt natin.
 Si pt #2, nagdialysis, but after one month of dialysis, the
patient has serum creatinine goes down to 2 mg/dL, so
you would stop the dialysis
 Si pt. # 3 however 4 months mo na dinadialysis, walang
evidence ng reduction, recovery ng renal function. So most
probably, si pt. #3 developed bilateral cortical necrosis
that is the most extreme effect of renal hypoperfusion.
 So all the causes of prerenal, if it is severe and prolonged
can lead to development of ischemic ATN
NEPHROTOXIC ATN

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 NEPHROTOXIC ACUTE TUBULAR NECROSIS of the aminoglycoside and the contrast agent that you’ve
been used may lead to nephrotoxic ATN
 Convoluted and straight portions of proximal tubules
 Kidneys are vulnerable EXOGENOUS NEPHROTOXINS
o Rich blood supply (25% of cardiac output)
o Ability to concentrate toxins to high level within
medullary interstitium and renal epithelial cells Exogenous Nephrotoxins That are Common Cause of Acute
o Important site for xenobiotic metabolism Intrinsic Azotemia with Acute Tubular Necrosis
Antibiotics Chemotherapeutic agents
Increase incidence in: Acyclovir Cisplatin
 Elderly Cidofovir Ifosfomide
 Pre-existing CKD Indinavir Anti-inflammatory and
 True/effective hyponatremia Foscarnet immunosuppressive agents
 Concomitant exposure to other toxins Pentamidine NSAIDS (including COX-
Aminoglycosides 2 inhibitors)
 The other cause of ATN will be nephrotoxic ATN. Amphotericin B Cyclosporin/tecrolimus
 So the effect will be on convoluted and the straight Organic solvents Intravenous immune
portions of the proximal tubules. Ethylene glycol globulin
 So why it is the kidney is vulnerable to nephrotoxin? Toluene Radiocontrast agents
Poisons Bacterial toxin
Because if you will have that inherent property wherein
Paraquat
they concentrate toxins in the higher level in the Snake bites
medullary interstitium. And this can concentrate toxins or
it can cause nephrotoxic ATN  What are the nephrotoxins? Ang nephrotoxins can be
 Some of the substances cannot be harmful but it is endogenous, can be exogenous in administer sa
converted to a harmful metabolite and you know that the patient or endogenous
renal blood flow to the kidney is around 25% of the cardiac  What are the exogenous nephrotoxins? Antiviral
output agents. Saan ginagamit ang acyclovir? Pt. with herpes
 So yung substance in the blood definitely will reach the zoster. Sino nagheherpes zoster? Elderly.
kidney. 25% of the cardiac output ng blood supply to the  Apg nagheherpes zoster ang individual so usually
kidney ampong elderly. Bigyan mo siya ng IV acyclovior, try to
 So hindi lahat e magkakaroon ng nephrotoxic effect. Like watch oput for serum creatinine. Be sure when you
for example, bakit yung iba pag binigyan mo ng start that, dapat meron kang baseline na renal function
aminoglycosides ok lang? Bakit yung iba pag bingyan mo assessment
ng aminoglycosides nagkakaroon sila ng AKI (Nephrpotoxic  Other include aminoglycoside: Amphotericin B
AKI)?  some of the chemotherapeutic agents like Cisplatin
 Nephrotoxic ATN is common in individual wherein the  anong klaseng NSAIDS? For healthy individual, sila din
renal function is already impaired yung nagrerequire ng NSAID di ba? Bago niyop bigyan
 Sino ang mga impaired ang renal function? Kahit anong ng NSAID, isipin niyo muna ng mabuti. Kasi in
sakit pag dumating ka ng 60 years old, ang renal function medicine, ang dictum is “to do no harm” to the pt. may
mo hindi lang bababa definitely. Lalo na y an kung may medication ka nga, bingyan mo nga ng NSAID not
other comorbidities like hypertension, diabetes, NSAID because of the arthritis, e yung pasytente mo nag AKI,
because of the arthritis. nagdialysis pa. Sino may kasalanan? Doctor
 So elderly, pre-existing chronic kidney disease,  Do no harm – lagi mo iisipin whether this pt. will
hypovolemia, concomitant exposure to other toxins. So benefit more than the adverse effect, if medicine will
these are the population group that we have that increase be good to the pt.
incidence  Immunoglobulins – sino binibigyan ng
 In addition to these, pt, with congestive heart failure , ang immunglobulins? Pt. with Guillain Barre, pt with
cardiac output is less exposure to hepatitis
 Diabetic patient. Why diabetic patient? Uncontrolled  Contrast agent – any radiologic procedure that will be
diabetes, what happen? You have polyuria, and the use of contrast agent (CT scan with contrast, coronary
glucose acts as an osmotic diuretic, that individual prone angiogram, cerebral angiogram) so these can be use of
to develop a CKD contrast agents
 For example ang pasyente mo, in acute pyelonephritis  Even if you will using isosmotic or non iodinated
inistart mo ng aminoglycosides nagdoubt ka baka meron contrast agents , hindi pa din yung increment yung AKI
obstruction. Nagrequest ka ng IVP (intravenous
 May mga advents na that was on the management of
pyelography), this double jeopardy to the kidney because
pt. who will about to undergo contrast enhanced

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 procedure that you need to categorize whether the pt
is low risk, moderate risk or high risk. Because if it is
high risk, you need to dialyse the pt. to take rid of the
contrast agent
Some Sources of Endogenous Nephrotoxins That Cause Acute
Intrinsic Renal Azotemia with Tubular Necrosis
Nephrotoxins that provoke Acute Tubular Necrosis
Effects
Hemodynamic
Direct Tubular
Epithelial Toxicity
ENDOGENOUS NEPHROTOXINS
 Myoglobinuria (rhabdomyolysis)
 Hemoglobinuria (hemolysis)
 Hyperuricosuria (increased uric acid production)
 Ano yung mga endogenous nephrotoxins? Ang
endogenous nephrotoxins that are produced in the
body.
 Nephrotoxins may be due to myoglobin. Myoglobin is
released if there is rhabdomyolysis. Kelan
nagkakarhabdomyolysis? After muscle injury. After
The future depends on what we do in present Page 12 of 20
hazing, kaya nagrerenal failure yan is because of the
release of myoglobin. Myoglobin is toxic to the kidney.
 Yung pasyenteng binigyan ng INH (isoniazid) or
intentionally nagtake ng INH, may suicidal tendency
ang patient, nagtake ng INH. INH is not toxic to the
kidney. But how the pt. will develop AKI? What is the
effect of your INH? INH causes seizure. Seizure causes
rhabdomyolysis, it will release myoglobin so you will
see urine is reddish in color.
 Hemolysis – example of this will be in pt. with malaria.
Malaria – you have erythrocytic phase, it can lyse red
cells. When the red cells are lysed, you release
haemoglobin. Haemoglobin is also nephrotoxic to
kidney
 Intravascular hemolysis or any form of hemolysis can
also cause nephrotoxic ATN
 You also decrease uric acid or there is increase
production of uric acid. Ang common cause nito is if
you have patient with malignancy that will subject to
the radiation treatment or chemotherapy this will halt
the tumor cells kaya sinabing tumor lysis syndrome,
because that tumor cells can rise if it will increase uric
acid. Yung tubules hindi niya manhandle yung
increased uric acid so it is also toxic to the kidney and it
can also obstruct the tubules. So yun ang mechanism
kaya may tinatawag na acute uric acid nephropathy or
tumor lysis syndrome after chemotherapy or radiation
treatment
Nephrotoxins
NSAIDS, ACE-inhibitors, Angiotensin 1
receptor antagonists, (cyclosporine A),
tacrolimus (FK506), radiocontrast,
hemoglobin
Antimicrobial drugs:aminoglycosides,
vancomycin, foscarnet, amphotericin B,
pentamidine Chemotherapeutic agents:
cisplatin, ifosfamide, plicamycin
(mithramycin), 5-fluorouracil, tioguanine (6-
thioguanine), cytarabine (cytosine
arabinoside), Miscellaneous drugs: lithium,
acetaminophen (paracetamol) Recreational
drugs
Radiocontrast
Light chains
Pigments: myoglobin, hemoglobin
Other toxins: organic solvents (carbon
tetrachloride, chloroform), herbicides
(paraquat), plant poisons (mushrooms),
animal poisons (insect/snake venoms)
Urate
Oxalate (ethylene glycol poisoning)
Drugs: acyclovir (acyclovir), methotrexate,
sulfonamides, triamterine, methoxyflurane,
indinavir
CooKiE 
 -bladder neck
-urethra
-bilateral ureteric obstruction
Cystalluria -unilateral ureteric obstruction in a pt with one functioning
kidney or with significant preexisting CKD

MORPHOLOGY OF AKI

CAUSES OF ACUTE POST RENAL AKI

4 cellular fates:
Ureteric Obstruction  Cellular death by necrosis
 Intraluminal: Stones blood clot, sloughed renal papillae,  Cellular death by apoptosis
uric acid or sulfonamide crystals, fungus balls  Cellular replication and division
 Intramural: postoperative edema after ureteric surgery,  Cells may appear indifferent to stress
BK virus-induced ureteric fibrosis in renal allograft
 Extraureteric: Iatrogenic (ligation during pelvic surgery)  So what happen if there is AKI? It can have death of the
 Periureteric: Hemorrhage, tumor, or fibrosis cells, necrosis, or apoptosis, or may attributed to
replication and division or it cells may appear indifferent
 The last category will be the POST RENAL AKI to stress. Ito yung hindi natin nakikita kasi. Ito pag
 So it could be obstruction of the ureter, it is almost in nagbiopsy ka, makikita mo yan
both kidneys are functioning, it should be bilateral
obstruction dun sa ureter. Kalian nagkakaroon ng
bilateral? It can be post iatrogenic ligation in pelvic Sublethal Changes
surgery. Hindi lang blood vessel, pwedeng ureter ang
naligate noh Disruption of cell Flattening of epithelium
 It can be intraluminal – naistroke, bloodclot, sloughed cytoskeleton Loss of brush border
papillae Loss of focal cell contact
 Intramural – postoperative edema after urethral surgery
 Unilateral – pero yun lang ang functioning kidney. the
other kidney is not functioning, pwedeng hypoplastic, a Membrane proteins
genetic or sira na, tapos yung nagfufunction redistribution Disengagement of cells
nagkakabara yung ureter so it can lead to post renal AKI from substratum
(integrins, Na-K-
ATPase)
Bladder Neck Obstruction
 Intraluminal: Stones, blood clots, sloughed papillae
Intratubular obstruction
 Intramural: bladder CA, bladder infection w/mural edema,
Loss of cellular polarity
neurogenic, drugs (eg tricyclic antidepressants, ganglion
blockers)
 Extramural: Prostatic hypertrophy, prostatic carcinoma Redistribution of adhesion
Cellular Dysfunction molecules
 Next is the BLADDER NECK OBSTRUCTION, more
common.
 Bladder neck obstruction, in elderly, maybe because of
 What happen? Pt. may have sublethal changes wherein
enlarged prostate. Whether this is between age or
there is disruption of the cell cytoskeleton and this can
benign prostatic hypertrophy or prostatic Ca or it can be
cause loss of brush border and loss of focal cell contact to
also urethral obstruction from a stone or stricture or a
the individual renal cells. So disengagement of cells and
mass that cal lead to post renal AKI
this can lead to membrane protein redistribution. And
 So pag mechanical lang ito, madali lang itpo madetect.
remember integrins, we called integrins andyan ngayon
Why? Because if it is bladder neck obstruction, you will
ang research wherein they come to prevent sublethal
have distended urinary bladder. If it is
changes is to address this integrins because if not, there
ureteralobstruction, you will be guided by ultrasound,
will be loss of cellular polarity and this will lead to cellular
you have hydronephrosis. Kung bladder neck
dysfunction and also redistribution of adhesion molecules
obstruction, it may be bilateral hydronephrosis
that can cause intratubular obstruction causing AKI
Urethral Obstruction
 Phimosis, congenital valves, stricture, tumor CLINICAL FEATURES
 AKI from obstruction develops:
 Oliguria
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  S/S fluid overload/volume depletion
 S/S of underlying causes of ARF
 S/S electrolytes imbalance, acid – base disorders
 Changes in sensorium
 So what will be the manifestation of pt. with AKI?
Common: acute oliguria, signs and symptoms of fluid
overload (pulmonary congestion, increased blood
pressure, edema) or baka naman ang pasyente oliguric
kasi there is volume depletion. You must know by now
how to assess fluid overload and fluid depletion, and
depending on the cause of acute kidney injury. So kung
ang pasyente mo, may alopecia, joint pains, amy fever and
there is malar attacks, babae, pt. with evidence of pleural
effusion, pericardial effusion, pt is oliguric, with edema,
ano ang cause ng AKI? LUPUS NEPHRITIS
 Or ang pasyente mo, nagfefever for 5 days, muscke and
joint pain, icteresia, and severe muscle tenderness with
conjunctival suffusion. Just recently lang, meron diyan,
tumawid lanbg, pumunta sa Jollibee, e baha dun sa
Jollibee, so this will maybe cause of leptospirosis kaya siya
oliguric. So it depends.
 Due to interstitial nephritis, --------- di ko maintindihan
sorry :( then correlate with CBC result, baka mataas ang
eosinophils and then the cause of AKI will be allergic
interstitial nephritis
 Common in pt. with AKI, yung changes ng sensorium. In
fact, this maybe the initial manifestation of pt with AKI. It
is usually be noted on the late stage of CKD. But in the AKI,
it maybe the initial manifestation of AKI. It can be
drowsiness, can be seizures, aggression, lethargy or any
form of changes in sensorium
CLINICAL EVALUATION OF AKI
History: Fluid losses and fluid intake
Urine volume
Infection: Viral, bacteria, fungal
Drug/s intake
Radiologic procedures, Surgery
Symptoms of underlying disease
Diseases or clinical situation that leads
to development of endogenous toxins
Renal calculi
Cardiac disease
 Kasi in any pt., if you will get the history, you are not
only indicating the describing the symptoms of the pt.,
more or less you will inquire what causes the
symptoms. So if we are aking the data, ask what the
cause of the AKI to the pt is.
 So on the causes that we’ve mentioned, you need to
indicate or ask the pt. fluid losses or fluid intake, urine
volume. Paano mo macclassify if oliguric or non
oliguric kung hindi mo alam how much urine pt. is
The future depends on what we do in present Page 14 of 20
voiding. Whether the pt. have infection (viral)
pwedeng mag AKI, bacterial or fungal.
 Drug intake – kahit na hindi illicit yung drug intake, you
need to inquire.
 Radiologic procedure
 Pt have surgery – intraoperative, the pt. may develop
hypotension. Siyempre hypotension, for sure may
oliguria.
 Then evaluate, what is the cause of hypotension
intraop? It maybe cardiac, maybe effect of anesthetic
agent that is used to the surgery. So depends, it will
lead to investigate
 Symptoms of underlying disease
 diseases or clinical situations that lead to development
of endogenous toxins – oliguria; cobalt treatment for a
lymphoma or the pt. have a session of the
chemotherapy
 Cardiac disease – so yung pasyente naadmit because of
severe chest pain then ------ of acute coronary
syndrome/ acute myocardial infarction. Siyempre,
yung pt. will be oliguric. That was cardiorenal
syndrome
 Meron din cardiorenal syndrome, siguro mga 2 years
from now, meron ng neurorenal syndrome. Meron na
tayong pulmorenal syndrome, hepatorenal syndrome
and now cardiorenal syndrome.
 There are several types of this cardiorenal syndrome,
but more important for you to know is there is cardiac
disease, acute caqrdiac dysfunction that affect the
kidney causing acute kidney injury. This is the TYPE 1 of
your cardiorenal syndrome
 So yung mga nagaacute MI, massive MI, tapos nag
acute kidney injury, the cause of AKI is cardiorenal
symptoms.
Physical Examination:
 State of hydration – BP, HR, JVP, mucous membrane, skin
turgor
 Signs of chronic liver disease
 Skin Lesions
 Edema
 Abdominal findings – (+) KP, distended
 Rectal exam – enlarged prostate
 Muscle tenderness/weakness
 Physical examination, siguro alam niyo na on how to
assess the stage of hydration, stages of chronic liver
diseases baka yung pasyente mo may hepatorenal
syndrome, skin lesions or edema. Kailangn ng rectal exam
baka yung prostate nagcause ng anuric yung pt. kasi
distended yung urinary bladder, muscle tenderness or
weakness should also be noted in the examination
CLINICAL EVALUATION OF VOLUME STATUS
CooKiE 
 Volume depletion: Urine sodium <10 >40
Hx – thirst, oliguria/anuria (mmol/L)
Excessive fluid losses Fractional sodium <1 >2
Fluid balance I & O, daily weights excretion
PE – dry mucosa, poor skin turgor Renal Failure index <1 >1
Absent axillary sweat
Reduced JVP  So, I mentioned earlier that you may know whether you
Postural tachycardia/hypotension are dealing with prerenal or intrinsic or ATN whether it is
Supine tachycardia/hypotension
ischemic or nephrotoxic. But there are laboratory
Current status of new urinary biomarkers for discriminating between examinations that will differentiate the two. Madali lang
different forms of AKI. clinically pero ngayon ang practice ngayon meron ng
Biomarker CPB Contrast Sepsis or Kidney ebvidence. So these are the tests, your urinary diagnostic
name nephropathy ICU setting tx indices.
NGAL 2h post- 1-2 days pre- 2 days pre- 12-24
CPB AKI AKI hpost-tx  So lagi tatandaan, if the intravascular volume is depleted,
IL-18 6h post- Not increased 2 days pre- 12-24 may compensation pa. The compensation is to increase
CPB AKI hpost-tx
sodium and water reabsorption sa tubules.
KIM-1 12h Not tested Not tested Not
post- tested
CPB  Kung prerenal AKI lang yan, operational pa din yung
L-FABP 4h post- 1-2 days pre- Not tested Not compensation. But in the tubules, if there is already ATN,
CPB AKI tested even if there is signal to compensate, hindi siya
*The times indicated (in hours) are the earliest time points at which makaabsorb ng sodium and water. So ano mangyayari
the biomarker is increased significantly from baseline values. nagyon sa urinary sodium? Hindi makaabsorb sa acute
AKI:acute kidney injury, CPB:cardiopulmonary bypass, KIM-1 kidney
tubular, kaya mataas more than 40. So prerenal, naabsorb
injury molecule-1;l-FABP; liver-type fatty acid____; NGAL:
Neutrophil gelatinase-associated lipocalin; tx:transplant pa kaya less than 10. Since the fluid or the water is
absorbed in prerenal, ang urine osmololaity mo, mataas.
 There are newer markers of acute kidney injury
because serum creatinine is several days even several  Ang water hindi na naabsorb sa ATN kaya lesser
hours before it will elevate. While it’s too late it would
just rely on the serum creatinine. For example, yung  Yung BUN, Creatinine e bakit tumataas yung BUN? Yung
pasyenteng may cardiorenal syndrome, pwedeng in absorption ng urea goes down with absorption of water
just start of 12 hours lang serum creatinine. And if you
will be doing other markers of AKI, e elevated na. So  Pag increased ang absorption ng water sa prerenal, mas
we have to get the pt. early so we can do something matass ang BUN or pwedeng BUN ang tataas without
to prevent further progression of AKI concomitant increase ng creatinine. Kaya ang BUN crea
 This is in the form of NGAL – neutrophil gelatinase- ratio mo sa prerenal is more than 10:1. So pwedeng 40:1.
associated lipocalin, so this is available. IL-18 and KIM-
1 are also biomarkers wherein the onset of each  Pero dito, hindi naman naabsorb yung water, so ang ratio
elevation is early than the elevation of BUN or mo will be less than 10:1
creatinine
 So kung ang pasyente mo, status post bypass surgery,  Yung fractional excretion of sodium at saka renal failure
to detect after surgery, 2 -3 hours pwedeng mag MI index will be less than 1 in prerenal and more than 1 in pt.
kasi if it is elevated, nagkidney injury na yung pasyente. with ATN
So you can do something to improve the intravascular
Urine Sediment in the Differential Diagnosis of Acute Kidney Injury
volume, prevent further deterioration of renal function
Normal or Few RBC or WBC White Blood Cell Casts
 Prerenal Azotemia  Acute intestinal
Urine Chemistry in Acute Kidney Injury
 Arterial thrombosis or nephritis or exudative
embolism glomerulonephritis
Urine Chemistry Pre-renal Acute Tubular
 PreglomerularVasculitis  Sever Pyelonephritis
Necrosis
 HUS or TTP  Marked leukemic or
Urine osmolality, >500 <300
Uosm (mosm/kg)  Scleroderma crisis lymphomatous
Urine to plasma >1.5 <1.1  Postrenal Azotemia infiltration
Eosinophils (>5%)
osmolality
Granular casts  Allergic interstitial
Urine to plasma >8 <3
urea  Acute tubule necrosis nephritis(antibiotics
(muddy brown) NSAIDs)
Specific gravity >1.018 <1.015

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  Glomerulonephritis or  Athereombolic then you inject the dye dumadaan sa blood. It is replaced
vasculitis Disease now with CT scan or CT stonogram
 Interstitial nephritis Crystalluria  If you suspect better, then you may have to do CT
 Acute angiogram or Doppler study
Red Blood Cell Casts uratenephrophaty
 Glomerulonephritis or  Calcium Oxalate
 Renal Biopsy
vasculitis  Acyclovir
>If the cause of intrinsic renal failure is unclear
 Malignant Hypertension  Indinavir
>if the cause of glomerular disease is not known
 Rarely interstitial nephritis  Sulfonamides >in allergic interstial nephritis
 Radiocontrast Agents >pts on supportive renal replacement for a
period of 3 months w/o evidence of recovery
 Depending on what is the cause, urinalysis may give you
the cause of AKI. Kung ang pasyente mo, may ATN  Renal biopsy? You will do renal biopsy if you suspect
whether it is ischemic or nephrotoxic so you have intrinsic and it is not obvious what is the cause of
MUDDY BROWN GRANULAR CAST. Prerenal pwedeng intrinsic AKI or if it is glomerular, and the cause of
normal, ang findings is said to be hyaline casts. glomerular disease is not known. Of course, in pt.
 Pag ang cause mo is interstitial or glomerular, pwedeng with allergic interstitial nephritis, and to confirm
pus cells, red cells in the urine and the different casts whether the pt. have complete cortical necrosis
 Eosinophils may be seen in pt with allergic interstitial  Kung ang pasyente mo 4 months na nagdidialysis, no
nephritis and atheroembolism of renal vessels evidence of recovery, to confirm if the pt. already
 Crystals, depende. Uric acid crystals, urate, or calcium have end stage kidney disease, do renal biopsy.
oxalate Kailangan iconfirm yan, mahirap tanggapin on the
 RBC Cats seen in pt. with acute glomerulonephritis or part of the pt. na both kidneys are not functioning
RPGN or vasculitic diseases and Leydig interstitial and have dialysis for life
nephritis
COMPLICATIONS
BUN and SERUM Creatinine
Rapid elevation (within 24- 48 hrs)
 Renal ischemia  Volume overload
 Radiocontrast  Electrolyte disorders
 Atheroembolism  Metabolic acidosis
 Elevation later (10-14 days) – toxins  Hyperphosphatemia/ hypocalcemia
 Increase in SK+, Uric acid, PO4  Anemia, bleeding time
 Decrease in SCa+2  Uremic syndrome
 Metabolic Acidosis -increase AnionGap:  Infection- common and accounts for 75%of deaths
>ethylene glycol  Cardiac abnormalities: arrhythmia, AMI, pulmonary
>methanol toxicity embolism
 GI bleeding – 10 -30% due to stress ulceration on
 BUN and serum creatinine will be elevated and there may gastric or small intestinal mucosa
be also increase in potassium and metabolic acidosis
wherein there is increased in anion gap especially if the  Complications: common e di depende kung ano yung
cause is methanol or ethylene glycol toxicity cause and the same pwede yung fluid overload, electrolyte
(hyperkalemia, metabolic acidosis) Hyperkalemia can
 Laboratory evaluation: cause arrhtymia, metabolic acidosis can also cause seizure,
1. UTZ cardiac depressant also, infection is the most common
2. X-ray - KUB cause of mortality – 75% so posibilidad na mamatay sa
-IVP, retrogade pyelography renal failure kung magdidialysis pa.
3. Ct scan – stonogram/ unenhanced helical
 GI abnormalities
Ct, CT angio
4. MRI/MRA  Can develop arrhythmia or even distress causing acute
5. Doppler UTZ coronary syndrome

 What laboratory will you request depends on what you COURSE OF ATN
think is the cause. Ultrasound –possible findings. Do you
1. Initiation Phase
need to IVP? And then if may have some benefits
2. Extension Phase
because you don’t infuse the contrast agent
3. Maintenance Phase / Oliguric/ Renal Failure
intravenously, but it is retrograde. May cystoscope and 4. Recovery Phase
Slower recovery &
Severe Oiguria
greater chances of
The future depends on what we do in present
CooKiE 
permanent renal
Page 16 of 20
impairment.
 Prolonged maintenance phase TREATMENT

Prevention
Initiation Phase  Cardiac function
 Patients are exposed to ischemic or toxic insults and  Intravascular volume
parenchymal renal injury is evolving but not established  Nephrotoxic drugs administration should be adjusted
 ATN is preventable at this time  Diuretics, NSAID’s, ACE inhibitors, ARB, vasodilator
 Acute urate nephropathy:
Extension Phase Allopurinol
 Continued ischemic injury and inflammation Forced alkaline diuresis
 Endothelial damage results in vascular congestion Rasburicase
 Contrast Nephropathy:
Maintenance Phase Hydration
 Parenchymal injury is established, decreased GFR Loop diuretics, Mannitol
stabilized at 5-10ml/min Dopamine
 Urine output lowest Fenoldopam
 Lasts 1-2 weeks (maybe longer) N-acetylcysteine
 Uremic complications arise during this phase Theophylline
 GFR remains low despite correction of systemic Sodium bicarbonate
hemodynamics Low or isoosmolar contrast media
 Mechanism :
 Persistent intrarenal vasoconstriction Therapeutic targets of treatment
 Medularry ischemia trigger by release of 1) Offsetting vasoconstriction
vasoactive mediators  Ca channel blockage
 Tubuloglomerular feedback by injured epithelial  Atrial natriuretic factor
cells  Endothelin blockade
 Adenosine-receptor blockade
Intrarenal Vasoconstrictions and Medullary Ischemia  Nitric oxide regulation, PG analogues
 Decreased nitric oxide
 Increased endothelin 2) Limiting inflammation
 Alpha melanocyte stimulating hormone
Recovery Phase  Anti-adhesion strategies: anti-ICAM
 Patiens recover reanl function through repair and Anti-integrins
regeneration of renal tissues 3) Altering cell outcome-Growth Factors
 Onset heralded by: = gradual in urine
output  Depending on what is the cause
= Serum creatinine  You know the pt with AKI is hypercatabolic. When you say
hypercatabolic, mabilis ang production ng nitrogenous
Post ATN diuresis: (3-5L urine/ day)
1. Approximate excretion salt and water accumulated waste products
2. Osmotic diuresis induced by filtered urea &other retained  So if you will do dialysis on this pt., hemodialysis or
solutes peritoneal dialysis
3. Overzealous use of diuretics  So prevention that may observe if you suspect, sinabi natin
4. Recovery of tubule reabsorptive process lags behind GFR mga risk factors that will cause nephropathy, so it will
prevent and if you use nephrotoxic drugs and drugs that
 I just want to point out that during recovery phase, the
will alter the autoregulatory mechanism like NSAIDS, ACE
urine output may be excessively. First clue that your pt.
and ARB and other antihypertensive agents that will cause
is improving is pt. started to put out urine if they are
vasodilatation like calcium channel blocker even nitrate
oliguric. Or if not oliguric, yung creatinine mo
can also cause.
bumababa na.
 In pt. to prevent acute uric acid nephropathy or in those pt
 But there is diuretic phase wherein the urine output is
will undergo chemotherapy or radiation treatment, you
excessive. This maybe because nagyon lang umeepekto
can give allopurinol. But take note, it can cause allergic
yung bingay na diuretic o nailalabas ng pasyente yung
interstitial nephritis. So i don’t give much that drug
excess urea and water, attract urea, attract water and
 But you can increase dieresis by giving sodium bicarbonate
comes the urine. Recovery of the tubule and absorptive
 To prevent contrast nephropathy, all of these had been
process, kahit na may signal na sa organ of
tried but the known effective is hydration and
reabsorption, pero hindi pa siya nagrereabsorb, kasi di
acetylcysteine. The rest may have some benefits but that
ba nag ATN siya so it takes time para makarecover siya.
is not conclusive. I recoomended fluid hydration and
Yan ang cause kaya maraming ihi.
acetylcysteine that can be given a day before, on the day
and one day after the procedure.

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  Center of research now wherein you medicate nitric oxide Hemodialysis
para magvasodilate, can give vasopressin analog and  Intermittent hemodialysis – 3-4hrs./day 3-4 x per week
endothelin blockade. Endothelin is a potent  Slow efficiency dialysis – 6-12hrs./day 3-6 x per week
 Continuous renal replacement therapy
vasoconstrictor so you don’t want endothelin.
(CRRT) - CAVH - CVVH
 You can give atrial natriuretic factor - CAVHD - CVVHD
 Limiting inflammation, you can give anti-ICAM and Anti- - CAVHDF - CVVHDF
integrins, these will disintegrate the cells that will lead to  Dialysis: peritoneal or hemodialysis is indicated in
cellular dysfunction regardless of the increase in serum creatinine. Kapag ang
 Alter the cell outcome – probably in the future meron ng pasyente may changes ng sensorium, and the cause is due
mga conclusive na that will prevent the development of to uremia, you need to dialyse the pt.
AKI to lessen the mortality  Since they are more hypercatabolic, it is advisable to do
hemodialysis than peritoneal dialysis.
TREATMENT  Question: pag ang pt. na hypotensive, ipapahemodialysis
mo ba?
1) Correction of underlying disorder
 Indications for dialysis:, Uremic encephalopathy,
2) Diuretics
Intractable fluid overload, Nonresponsive hyperkalemia,
Mannitol
Refractory metabolic acidosis
Furosemide
 We have several indications for hemodialysis, kahit na
Bumethanide
nagbbleed ang pasyente, kahit na hypotensive ang
3) Renal dose dopamine
pasyente, you can continue renal replacement treatment.
4) Fenoldopam
So it is very slow that you remove the excess fluid and the
5) Natriuretic peptides
excess uremic toxin not compromising the cardiovascular
6) Fluid therapy
status so you can go hemodialysis even the pt. Is
hypotensive. Pag hybrid yung stent, 6-12 hrs pag
 Pag ang pasyente ay oliguric, you convert the pt to non
hypotensive you will not do this because in 3-4 hrs time,
oliguric. Before you convert that to non oliguric, be sure the you want to remove the --- hindi mo mareremove muna 3-
pt is not volume depleted, kahit na bigyan mo ng diuretic and 4 hrs if the pt. is hypotensive
if the pt is volume depleted, hindi iihi.
 You can use furosemide, Mannitol, Bumethanide ang
drawback with mannitol, you are infusinh hypertonic Non-dialytic Management of Acute tubular necrosis:
solution, it can attract water lalo na kung pulmonary
Complication Treatment
congestion ang pasyente kaya we avoid mannitol. We give
Intravascular Restrict salt (1-2g/day) and water (usually
100 ml fastdrip. So we prefer furosemide and bumethanide Volume Overload <1L/day) Diuretics (usually loop diuretics+
in higher dose, ceiling dose thiazides)
 Renal dose of dopamine is not routinely done because it can Hyponatremia Restrict enteral water intake (<1L/day)
cause arrhythmia. Dopamine is vasoconstrictor to the renal Avoid hypotonic intravenous solutions
vessel however in lower dosage, yung tinatawag na renal (including dextrose solution)
dose of dopamine, (1-5 microgram/kg/min) pag yan ang dose Hyperkalemia -Restrict dietary potassium intake usually
<40 mmol/day)
ng dopamine sinasabi nila vasodilator to the kidney.
-Eliminate poatassium supplements &
However, kapag unstable ang cardiovascular status ng pt. sparing diuretics
wag mo bigyan nyan baka magarrhythmia, mamamatay lang -Potassium – binding ion – exchange resins
yan. The effect on afferent arteriole, it vasodilates. It is a e.g. sodium polystyrene sulfonate (calcium
calcium channel blocker resonium)
 Natriuretic peptide had been tried Glucose (50 ml of 50% dextrose) and insulin
(10 units regular)
-Sodium bicarbonate (usually 50-100 mmol)
7) Dialysis β2 agonist (e.g. Albuterol 10-20 mg inhaled
 Peritoneal or 0.5 – 1 mg IV)
 Hemodialysis -Calcium gluconate (10ml 10% solution over
2-5minutes)
Indications of Dialysis:
 Uremic encephalopathy
 Intractable fluid overload NOT DISCUSSED
 Nonresponsive hyperkalemia
 Refractory metabolic acidosis Uremia
 BUN > 100mg/dl  Clinical and laboratory syndrome reflecting dysfunction of
all organ systems as aresult of profound loss of renal
HEMODIALYSIS VS PERITONEAL DIALYSIS function

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 REDUCTION in RENAL MASS
Azotemia Vasoactive molecules
 Retention of nitrogenous waste products, evident by Cytokines
increase BUN and serum creatinine. Px may be GF
asymptomatic
Intrarenal activity
Chronic Renal Failure of RAAS
 Characterized by permanent decreased GFR associated
with loss of functional nephron population
glomerular capillary pressure
Guidelines in the care of CKD
 What is the definition of Chronic Kidney Disease? GFR (Hyperfiltration)
CKD is defined as either: (Remaining Functioning Nephron)
1) Kidney damage for at least 3 months
 Defined by structural or functional
abnormalities of the kidney HYPERTROPHY
 With or without GFR
 Manifest by:
pathologicabnormalities
markers of kidney damage GLOMERULOSCLEROSIS
- Abnormalities in blood
- Abnormalities in urine
- Imaging tests ETIOLOGY
2) GFR < 60mL/min/1.73m2 for at least 3 months, with
or without kidney damage Diabetes mellitus 40.3%
Hypertension 27.1%
 What are the different stages of CKD? Glomerulonephritis 12.9%
Stages of CKD: Interstitial disease 4.2%
Cystic/hereditary/congenital 3.4%
Stage1 Evidence of CKD Neoplasm/tumor 1.7%
GFR>90mL/min/1.73m2
Stage 2 GFR 60-89mL/min/1.73m2
Stage 3 GFR 30-59mL/min/1.73m2
Stage 4 GFR 15-29mL/min/1.73m2
Stage 5 GFR <15 mL/min/1.73m2 or on
dialysis

Stages of Chronic Kidney Disease

Stage of complete compensation
GFR 50-70 ml/min.
Serum creatinine may still be normal
Asymptomatic
Loss of renal reserve
Stage of compensated retention
GFR 20-40 ml/min
Increased serum creatinine (120-700umol/L)
Maybe asymptomatic
Anorexia
Nocturia
Anemia
Loss of energy
Increased phosphate
Decreased calcium
GI symptoms
Stage of decompensated retention (overt renal failure)
GFR 10-20 ml/min.
Uremic symptoms intensified
Serum creatinine> 700umol/L
Can still be managed conservatively
Terminal stage (ESRD)
GFR 5-10 ml/min.
Survival needs renal replacement therapy

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The future depends on what we do in present Page 20 of 20 CooKiE 