[RENAL PHYSIOLOGY 2ND HOUR] February 8, 2014

Classification scheme for Acute Kidney

Injury* (RIFLE criteria)
___

Risk

Injury

Failure

Loss
ESKD

GFR Criteria

Increased SCreat x
1.5 or GFR decrease
>25%
Increased SCreat x
or GFR decrease
>50%
Increased SCreat x 3
or GFR decrease
75% or SCrea
>4mg/dl

Urine
Output
Criteria
UO
<5ml/kg/h x
6hr
UO
<5ml/kg/h x
12hr
UO
<3ml/kg/h x
24hrs oliguria
Anuria x
12hrs

Persistent ARF complete loss of

kidney function >4 weeks
End Stage Kidney Disease
(>3months)

*Significance of RIFLE criteria: to know if the

clinical course of the patient is improving or not
based on the serum creatinine and urine output.

Urine

output will not make the doctor wait for a

couple of days before he can act on the patients
condition. For example, if by 6 hours the patient is
producing less than 5ml/kg/h, the doctor can analyze if
the kidney injury is progressing to a more severe form.
He may hydrate the patient, give diuretics, give an
anti-inflammatory drug, and give steroids depending
on his assessment. Every 6 hours the patient should be
reassessed. If management is not aggressive, this may
lead to progression to the point of dialysis.

ACUTE KIDNEY INJURY (AKI)

A. ETIOLOGY
Pre renal - before glomerulus/kidney
(Vasomotor nephropathy)
Ischemic - blood supply to kidney has been
compromised
Hypovolemia secondary to bleeding
GI electrolye losses in diarrhea
Burns or renal salt wasting stab wound, MVA
injury
Hypotension
Shock
Hypoxia
Heart Failure

Sepsis
Intestinal obstruction
Hepatorenal syndrome due to antigen antibody
reactions
Toxic drugs:
Aminoglycosides (gentamicin, amikacin,
neomycin)
Wasp stings
Bee stings
Toxins:
Plant toxins
*weight losing drugs such as Bangkok pills
contain aristolochic acid Renal failure, renal
insufficiency
Snake bites
Rhabdomyolysis
Blackwater fever in falciform malariae
Radiocontrast agents

Renal
(Intrinsic to kidney)
Glomerulonephritis
Post infectious (post streptococcal, post viral)
SystemicLupus Erythematosus
Henoch-Schonlein Purpura (HSP)
Membranoproliferative glomerulonehritis (MPGN)
ANCA GN
Anti-neutrophil cytoplasmic autoantibodes (ANCA)
assoc. w/ necrotizing & crescentic GN
Anti-Glomerular Basement Membrane disease
Vascular: renal artery stenosis affecting blood
supply to kidneys
Hemolytic-uremic syndrome (HUS)
Renal vein thrombosis
Renal artery thrombosis
Acute tubulointerstitial nephritis allergy to drugs
causing sloughing off of tubular membrane
Infectious
Epstein-Barr virus (EBV)
Leptospirosis (hepatorenal syndrome)
Drugs including herbal preparations
Acute pyelonephritis
Tumor infiltration

Post renal - after glomerulus/kidney

[RENAL PHYSIOLOGY 2ND HOUR] February 8, 2014

Structural (identify where obstruction is to see the
cause):
Posterior urethral valve
Ureteric obstruction
Neurogenic bladder

8) Prevent fluid overload (give diuretics or

doing RRT)

Modern criteria for the initiation of RRT

in the ICU

Oliguria (UO < 200ml w/in next 12 hrs)

Crystalluria acid crystals in the tubules
Tumor lysis syndrome (seen in patients receiving
chemotherapy)
Melamine
*Illegally added to food products (ex. milk) &
may cause renal & urinary problems)
*Resin used in porcelain used as milk substitute
*Renal stones, renal failure
Calculi
Blood clot

B. MANAGING AKI
Treatment or removal of the cause to address
treatment
Maintenance of physiological homeostasis while
recovery takes place
1) Nutritional support (30-35 kcal/kg/day) as
mixture of CHO and lipids, & CHON at 12g/kg (most patients have poor appetite so
IV solutions may be given)
2) Hyperkalemia must be promptly treated
(Use hyper-K regimen: nebulize the patient
Kayexylate may be given, calcium gluconateemergency management)
a) Insulin and dextrose (D5050)
*Insulin shifts K into cell
b) Sodium bicarbonate given if metabolic
acidosis is present (orally/intravenously)
c) Calcium gluconate
*Replaces Ca and help entry of K back into
the cell
d) RRT (Renal replacement therapy w/ 2
modalities: Peritoneal & Hemodialysis)
3) Metabolic acidosis (due to failure to
conserve HCO3)
4) Anemia (due to disruption of EPO production
in renal interstitial cell)
5) Renal doses of drugs
6) Stress ulcer prophylaxis
*Preserve the viability of GI mucosa so that
you can give H2 receptor antagonists &
potent pump inhibitors (PPI)
7) Prevent infection and iatrogenic causes of
infection

UO >0.5cc/kg w/in the next 6 hrs based on RIFLE

criteria
*Consider dialysis, unresponsive to fluid therapy
BUN > 80mg/dl
Normal: 20mg/dl
4x elevated BUN: consider diuretic therapy
Serum creatinine > 3mg/dL (initiate dialysis)
Normal: 1 mg/dl
75% increase: consider renal replacement
Serum K > 6.5mmol/L or rapidly rising
Arrhythmias experienced - you give bicarbonate,
Insulin, glucose, etc and yet it cannot be
corrected
Pulmonary edema unresponsive to diuretics
Uncompensated metabolic acidosis (pH<7.1)
HCO3 8 or 9
Temperature > 40 C
-Disruption of central regulator of temperature
Uremic complications (encephalopathy,
myopathy, neuropathy/pericarditis)

Overdose w/ a dialyzable toxin

Nephrotic syndrome: (3 cornerstones for
nephrosis:)
1. Proteinuria
*Urine spillage: > 2 g/day of CHON in children
> 3 g/day in adult
2. Generalized edema (ascites, periorbital
edema, bipedal edema, scrotal edema)
3. Hypoalbuminemia

Corticosteroids such as Prednisone are given

(e.g dose: 2mg/kg/day to a pediatric patient)
Some adverse effects of steroid therapy include
cushingoid appearance (bufallo hump), Hirsutism,
HTN, behavioral changes, steroid psychosis
Nephrotic
syndrome may be
precipitated by a
viral infection
(patients would
usually manifest with
cough and colds)
should be treated
first.

[RENAL PHYSIOLOGY 2ND HOUR] February 8, 2014

Obstructive Uropathy
-Renal cortex remains intact while renal medulla
has expanded and the presence of a pelvic
constriction of a ureter.
-Post renal obstruction that can eventually lead to
renal failure.
Intravenous pyelogram will show the
obstruction in the renal pelvis, dye cannot
be seen draining down into the urinary
bladder. Constriction is released via surgery
or a stent may be inserted prior to surgery
so that the urine drains out of the renal
pelvis relieving the patient from
obstruction.

Vesicoureteral Reflux (VUR)

-

Procedure that can show defect is known as

Vesico cystourethrogram (VCUG) a catheter is
inserted into the patient and dye is infused, the
dye goes to the urinary bladder, allow the patient
to void and it goes up towards the ureters.

Other post renal causes:

Duplication Anomalies
-Double ureters in one kidney
Weigert-Meyer rule
Upper pole of the kidney is drained by the
ectopic ureter w/c inserts inferomedially at
the urinary bladder (below the normal ureter)
Lower pole of the kidney is drained by normal
ureter
Upper pole hydroureteronephrosis
Ureterocele or ectopic ureter
Lower moiety reflux

Congenital CNS disorders

Voiding disturbances such as in a patient with

Kidney of newborns usually affected

Abnormal flow of urine from bladder to upper
urinary tract
A form of postrenal cause of AKI
Problem: abnormal anatomic insertion of ureter
to urinary bladder; thus, urine goes back to the
ureter
VUR grades:
Grade 1: urine reflux only into ureter w/o
any distension
Grade 2: urine reflux into ureter & renal
pelvis, still w/o any dilation
Grade 3: moderate dilation of ureter & renal
pelvis
Grade 4: dilation of renal pelvis & calyces w/
moderate ureteral tortousity
Grade 5: gross dilation of renal pelvis &
calyces & blunting of fornices
*Grades 1-3 are prone to UTI, treated with
antibiotic and urinary prophylaxis
*Grades 4 & 5 are operable: correct the insertion
of the ureter to the urinary bladder. Some degree
of renal failure may occur unless corrected by
surgery. Renal scarring will be present affecting
renal function, decreased number of nephrons

neurogenic bladder where in catheter is inserted

intermittently to drain the urine or else urine
refluxes to the kidney that leads renal function
compromise.
Dysplasias may cause pseudo obstructive
nephropathies
Myelodysplasia
Vertebral column anomalies that affect
primarily the lumbar and sacral segment of
the spinal cord
Urogenic bladder: no control of voiding
patterns

II. CHRONIC RENAL FAILURE

Results from irreversible loss of large
numbers of functioning nephrons
In AKI, there is still hope of reversibility
Serious clinical symptoms often do not occur
until the number of functional nephrons falls to
at least 70% below normal
There are patients who are asymptomatic until
only 30% of their renal function remains
Patients may have a history of
Glumerulonephritis, obstructive nephropathies,
Anemia (subtle signs)
Treatment is more of supportive, preserving the
function of the remaining nephrons
Dialysis is indicated

Causes
1.
Metabolic disorders
Diabetes mellitus most common cause

[RENAL PHYSIOLOGY 2ND HOUR] February 8, 2014

2.

3.

4.

5.

6.

7.

(*usual focus of researches, some new drugs

made cause hepatotoxicity)
Amyloidosis deposition of amyloids in the
kidneys
Renal vascular disorders
Atherosclerosis - cholesterol plaque deposition
Nephroclerosis - hypertension
Immunologic disorders
Glomerulonephritis
Polyarteritis nodosa
Lupus Erythromatosus increasing in number
Infections
Pyelonephritis
Tuberculosis
Primary tubular disorders
Nephrotoxins (analgesics & heavy metals)
Urinary tract obstruction
Renal calculi
Hypertophy of the prostate
Urethral constriction
Congenital disorders
Polycystic disease
Congenital absence of kidney tissue (renal
hypoplasia)

person must be placed on dialysis (temporary

treatment) a bridge to the treatment of
transplantation(true treatment) w/ a functional
kidney to survive
Renal Replacement Therapy (2 modalities)
Peritoneal Dialysis
Uses a fluid system that is compatible w/
peritoneal fluid
Peritoneum acts as the glomerulus w/c
serves as a semi permeable membrane
Peritoneal catheter inserted in posterior cul
de sac
Exchange of solutes in peritoneum, drain
fluid after 4-6 hrs
Done every day; usually 4x a day

History taking is very important (such as

NSAIDs taken, recurrent UTI)
5 Stages of Chronic Kidney Disease (CKD)
-IRREVERIBLE renal damage staging

Stage

Creatinine
clearance

Conditions
/associated

90 or more
ml/min/1.73 m2

with risks of
developing CKD
(lupus, nephrotic
syndrome)

II

60-89 ml/min/1.73
m2 (mild)
30-59 ml/min/1.73
m2 (moderate)
15-29 ml/min/1.73
m2 (severe) S/S of

III
IV

S/s present:
encephalopathy,
uremia, HTN,
hypercalemia,

<15 ml/min/1.73 m2
(end stage)
Dialysis is indicated usually in stages IV and V
End Stage Renal Disease
Progressive deterioration of renal function and
further loss of nephrons to a point at w/c the

emodialysis
Dialyzer serves as glomerulus

[RENAL PHYSIOLOGY 2ND HOUR] February 8, 2014

Optimum prescription for dialysis should be

done 3x/week but in the Philippines,

patients usually have it 2x/ week. (45 times
allotted by Philhealth)
Kidney transplant
-Insertion is in the iliac (sa may singit)
-

Native kidney is not removed or remains due to

higher infection risks, the new kidney is attached
Wrap ups
Clearance: In a steady state condition, the
serum level if an endogeneous marker s
correlated w/ the reciprocal of the level of GFR,
making it possible to estimate GFR w/o urine
collection
AKI in the Elderly
GFR declines w/ aging (> 65 years)
Age related decline in GFR is part of normal
aging
Decreased GFR in the elderly is an independent
predictor of adverse outcomes such as death
and cardiovascular disease
Decreased GFR in elderly requires adjustment in
drug dosages as in CKD

40 years old up will have a decline in glomeruli

every year
Upon reaching 70-80 years of age, 40%
functioning nephrons remain
Age related diseases occur, adjustment of drugs
because of decreased
Increased incidence of Adult Respiratory
Distress Syndromes, Spesis, Trauma
Mortality rate increases
Independent Risk Factors for AKI in the Elderly
Hypovolemia
Hypotension
Hypoxia
Sepsis
Be wary of renal function alongside with
associated co-morbidities (such as diarrhea and
diabetes) making them vulnerable to Kidney
injury.
Modification of Diet in Renal Disease
(MDRD)
Modification of diet in renal disease equation
This equation uses the serum creatinine value
in combination w/ age, sex, and race to
estimate GFR, and therefore avoids several of
the limitations to the use of serum creatinine
value alone
NOTETAKERS:
BANIZAL, Sigrid/CHOMAPOY,
Becky/CLAUDIO, Dennis