It's a syndrome not a diagnosis like nephrotic, nephritis and so on.

It's defined as sudden loss of renal function because of a certain cause

(which needs investigations to determine) over several hours or days.
Rapidly progressive glomerulonephritis (RPGN) is a type of nephritis which
causes secondary ARF over several hours to days.
ARF always is associated with oliguria which is defined as:
In adults: urine output less than 400 cc/day.
In infants: urine output less than 1ml/kg/hour.
In older children: urine output less than 0.5 ml/kg/hour.
The causes of ARF could be: pre renal, renal, post renal.

o Pre renal causes:

The most important cause is hypovolemia due to hemorrhage or
dehydration or whatever.
It could be a vascular problem (decreased renal blood flow) in case of
renal artery stenosis.
Abnormal hemodynamics due to localized causes like (NSAIDs which
cause afferent and efferent arteriolar constriction) or could be generalized
vascular causes in case of sepsis.

o Renal causes:
Could be glomerular (glomerulonephritis) or tubular (acute tubular
necrosis) or interstitial nephritis.

o Post renal:
Tubular obstruction (stones or crystals) or could be uretral stones or
urethral obstruction (posterior urethral valve obstruction).

 How to approach a patient with ARF?

You have to take a good history asking about fever, diarrhea, vomiting,
flank pain, urine out put, color, weight loss, previous surgeries complicated by
hypovolemia, nephrotoxic drugs, sepsis, chemotherapy and so on then you
have to go back to the records to investigate the previous lab data and
compare it with the recent ones. For example, if you find the creatinine of a
patient = 70 and the normal was 50-100 so you will say this is normal but if you
go back to the previous reading of your patient and his creatinine was 20 or 30
then his current creatinine is abnormal because there is much increase.
In examination:
The most important step is to asses the volume status (dehydrated or not)
and correct the dehydration rapidly.
Then you should evaluate the bladder (full or not), if you can't evaluate the
status of bladder then move to step two (put a foley's catheter).
Then do urine analysis:
If you see muddy granular casts (tubular epithelial cells) = acute tubular
necrosis. Urethral or vaginal epithelial cells (in small amounts) could be
normally seen in urine but tubular cells are always pathological.
Check for RBCs or dysmorphic RBCs which mean glomerular injury, RBC
casts (accumulation of stacked RBCs in the tubules) which mean nephritis.
Presence of WBCs or WBC casts means that there's infection
(pyelonephritis).
> Eosinophiles = interstitial nephritis.
Presence of crystals (oxalate, cystine, tyrosine ) means the presence of
stones but oxaluria could lead to renal failure without any obvious changes in
urine.
Fat crystals in sever nephrotic syndrome.
If you didn't find any thing in urine analysis then move to step 2 which
includes: urine indices, imaging (ultrasound, GFR scan, MAG3 and MCUG),
additional volume status (in case you can't determine if he has low volume or

not then we put a central line), renal vascular status by ultrasound or

angiography and other blood tests (C3 and C4 etc).
In urine indices, we depend mainly on fractional excretion of Na.
e.g. if a patient has hypovolemia he will hold on to the water and Na so
we'll find low Na in urine and the urine will be very concentrated.
Note: urine indices aren't used to predict or evaluate chronic renal failure
because there's no tubular concentration in CRF.
Always remember, urine indices are only used in ARF.
We can use the spot Na measurement but mainly we use fractional
excretion of Na =
(urine Na /plasma Na) / (urine creatinine/plasma creatinine)
Another important thing to remember: if the urea was very high compared
to creatinine then this is mostly pre renal.
Renal imaging:
o We can use the ultrasound to detect hydronephrosis or stones or as
Doppler ultrasound to show renal blood flow or renal vein thrombosis.

This is the hydronephrosis (dark black areas) with dilated calyces

o GFR scan which is a type of DTPA scan measuring the uptake of radioactive
substances by the kidneys. So it's a dynamic test to measure GFR.

After imaging, we can use volume challenge or certain drugs (dopamine) to

rise B.P or we can check the bladder or put foley's catheter to be sure there's
no obstruction.
If we don't find anything after doing all previous investigations then we
should start thinking of renal biopsy.
Sometimes we consider empirical therapy as in RPGN, we don't wait till the
results but we give steroids and cyclophosphamide immediately.

Treatment of ARF:
It's mainly supportive but we can give immunosuppressants. If it's pre renal
failure we should give fluid to increase the volume or we could use
iontropes (digoxin), if the patient doesn't improve on fluid and the volume
is good then I have to stop fluid to prevent the overload.
If the patient takes antibiotics or other drugs then we should reduce the
dose and adjust it accordingly.
Hemodynamic support and respiratory support if there's pulmonary edema
or overload.
Fluid management is important; could be fluid giving or restriction.
To be on the safe side always give urine output + insensible loss.
ARF starts with oliguria then when start recovering he develops polyuria so
if we don't give the maintenance he will develop ARF again and again.
For electrolytes, the most important one to monitor is K because it's the
only electrolyte that can kill the patient so we have to give him K free diet
and adjust according to his K level. If you want to give K you shouldn't give
it continuously.
Acid base level should be monitored and the acidosis should be corrected
because it will not be corrected by itself (the kidneys are the major site for
acidity control).
Ca is decreased in sever cases so you should provide it.
Phosphorus is increased in ARF but it's not significant whatever the level.

 When do we do dialysis??
o if the failure is rapidly progressive and there's no steadiness in creatinine
levels.
o Major electrolyte abnormalities (especially hyperkalemia) unresponsive to
medical therapy; so we restrict the K, give K oxalate, protect the heart and
correct the acidosis then if all these aren't working we have to do dialysis.
o Fluid overload (hypervolemia) not responding to diuretics or fluid
restriction and you need to give fluids to the patient then we should start
him on dialysis.
o Uremic Pericarditis (can't be treated without dialysis).
o Uremic encephalopathy.

It's not called chronic renal failure any more because the definition has
spread to include chronic kidney problems with normal function (normal
creatinine level) like kidney scars or persistent hematuria or proteinuria or IgA
nephropathy with normal kidney function. So now it's called chronic kidney
disease.
It's defined as a state of irreversible kidney damage and/or reduction of
kidney function, which can lead to future decreases in kidney function, e.g. a
patient with kidney scar and normal function he may develop renal failure in
the future.

Stages of chronic kidney disease:

There're 5 stages but you should know that it's not mandatory to go into
that sequence so you can diagnose a patient in stage 4 or 5 without going
through stage 1 or 2 or 3.

Stage
1
2
3
4
5

Description
Kidney damage with normal or GFR
Kidney damage with mild GFR
Moderate GFR
Severe GFR
Kidney failure

GFR (mL/min/1.73 m2)

90
60-89
30-59
15-29
<15 (or dialysis)

You should know that some patients stay in a certain stage and don't
develop renal failure, e.g. 50% of IgA nephropathy patients don't develop renal
failure, they only have hematuria.
- GFR:
GFR is the sum of functioning glomeruli so a reduction in GFR implies a
decrease in the number of functioning glomeruli.
We can calculate the GFR by either imaging studies or by Schwartz formula
which depends on the age, gender and body size (height) so:
GFR = k * (height or length / serum creatinine)
K depends on the age and gender.
Newborns have small GFR due to there immature kidney.
GFR of male > GFR of female but you should know that GFR > 90 is normal
in both sexes.
Normal GFR in children and young adults
Age (gender)c

Schwartz equation

Mean GFR SD
mL/min/1.73m2

1 week (males and females)

2-8 weeks (males and females)
>8 weeks (males and females)
2-12 years (males and females)
13-21 years (males)
13-21 years (females)

GFR=0.33*(Length/SCr) in Preterm
GFR=0.45*(Length/SCr) in Term
GFR=0.45*(Length/SCr)
GFR=0.45*(Length/SCr)
GFR=0.55*(Length/SCr)
GFR=0.70*(Length/SCr)
GFR=0.55*(Length/SCr)

40.6 14.8
65.8 24.8
95.7 21.7
133.0 27.0
140.0 30.0
126.0 22.0

Distribution of the etiology of chronic kidney disease

(CKD) in children based upon age:

The younger the patient, the more likely the cause to be congenital or
structural (VUR, neurogenic bladder, polycystic kidney, obstruction ..etc) or
HUS.
As he/she grows up, glomerular diseases are more likely.
So the etiology of chronic kidney disease:
o Congenital renal anomalies were present in 57 percent of cases.
o Glomerular disease was present in 17 percent of patients.
o Other causes accounted for approximately 25 percent of cases (around
20% of these causes are idiopathic).

CLINICAL PRESENTATION:
o Early stages of CKD (asymptomatic).
o Direct kidney injury or disease (ARF on top of CRF).
o Incidental findings of an elevation in the serum creatinine concentration
and/or abnormalities on urinalysis.
o Detection of congenital or structural anomalies by imaging studies.

o Poor growth.
o Symptoms and/or signs of severe renal impairment (acidosis).
o Systemic symptoms and findings due to a concurrent systemic disease (skin
rash in case of SLE or seizures etc).

COMPLICATIONS OF CKD:

Disorders of fluid and electrolytes

Renal Osteodystrophy
Anemia due to lack of erythropoietin.
Hypertension
Dyslipidemia
Endocrine abnormalities
Growth impairment
Decreased clearance of renally excreted substances from the body (uremia).

The doctor didn't explain anything about the complications so for more
information go to the slides.
The follow up of the patient depends on the stage of the disease; a patient
in the early stages you should see him every 3 6 months but a patient in the
end stages you have to see him every week or maybe every day.
Every visit we should check the GFR, diet, growth parameters, PTH,
haematology, CVS and so on.

Management:
General principals:
o Treat reversible renal dysfunction ( a patient with CRF has UTI then you
have to treat the UTI aggressively).
o Prevent or slow the progression of renal disease.
o Treat the complications of CKD.
o Identify and adequately prepare the child/family in whom renal
replacement therapy will be required.

Reversible renal dysfunction:

o Decreased renal perfusion; e.g. renal artery stenosis.
o Don't give any Nephrotoxic drugs.
Management of complications:
o Sodium & water retention:
Water retention develops in the later stages (stage 4 or 5), you have to
restrict dietary Na intake and use the diuretics but you should supply the
patient with his needs of Na and fluid. If this doesn't work you should start
dialysis.
Patients with chronic kidney disease due to congenital anomalies have
polyuria not oliguria so they need more fluid and Na.
o hyperkalemia:
The most important thing is to control the diet. The problem is that
foods which children like is rich in K (potato, tomato, banana ..etc) so it's
difficult to prevent the child from eating such foods.
We give K oxalate to bind with K in the gut.
o Metabolic acidosis:
We give NaHCO3 (the only treatment).
o Renal osteodystrophy:
Decreased Vit D leads to hypocalcemia which leads to bone resorption
(Ca resorped from the bone along with Ph) so this will lead increased Ph
which stimulates PTH production (to get rid of the Ph through the kidneys)
but the kidneys are failed so increased Ph more and more causing more PTH
and more bone resorption. It's like a cycle and we have to break this cycle
by giving Ph binders.
Don't give Vit D because it'll worsen the condition more by increasing Ph
absorbtion from the gut so you break the cycle then give Vit D.
o Hypertension:
Because of fluid overload and activation of rennin-angiotensin system
(due to decreased GFR) so we give diuretics, salt restriction and ACE
inhibitors + ARBs.

o Anemia:
Could be due to iron or folate or B12 deficiency Or due to decreased
production of erythropoietin or frequent blood loss during dialysis. So we
give iron and folate to be sure then we give erythropoietin.
Hgb levels should be between 10 12 not above that because they are
prone to dyslipidemia and atherosclerosis, not below 10 because it will
affect cognitive functions.
o nutrition:
They have very limited choices regarding their nutrition so they have to
avoid K rich foods and Ph rich foods like canned food, juices etc.
o growth:
They have growth retardation due to many factors (anemia,
osteodystrophy, recurrent illnesses and admitions, growth hormone
resistance etc).
o dyslipidemia.
o uremic bleeding.
o uremic Pericarditis.
The Dr. didn't talk about the treatment of the last three complications.
Renal replacement therapy:
It depends on the family, patient, severity of the condition and availability
of the service.
Three types of renal replacement therapy:
o Renal transplant.
o Hemodialysis.
o Peritoneal dialysis.
We do living transplant means that one of the parents should donate so if
the parents are healthy and there's a match then we prefer the transplantation.
But if the parents are old and have health problems (DM, HTN) or the family
has a kidney problems (polycystic kidney disease or familial condition) then we
don't do the transplant from the family.

We don't do the transplant for patients less than 10 years of age.

To distinguish between ARF and CRF look for anemia, very high PTH and
small kidney size. These are only present in CRF.

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