May.Yvette.Allain.Cristina.Ralph.Sheryl.Bart.Heinrich.Pipoy.KC.Jam.Cecille.Denesse.Mike.Hoops.Ces.Christian.Elaine.Riza.Kristel.Ezra.Goldi.
Buf
f.Mona.AM.Maan.Adi.KC.Peng.Karla.Alphe.Aaron.Kyth.Anne.Eisa.Kring.Candy.Isay.Marco.Joshua.Fars.Rain.Jassie.Mika.Shar.Erika.Macky.Viki.Joan
.Precious.Kate.Katrina.Ams.Hannah. Memay.Pau.Rachelle.Esther.Joel.Glenn.Toni
PEDIATRICS 2
THE URINARY SYSTEM and URINARY TRACT INFECTIONS
Dr. Victor S. Doctor
Trans grUp: Goldie and Her Invisible Frends!!!
THE NORMAL KIDNEY
ANATOMY
Kidneys of Newborn Infant
relatively large and can usually be palpated through
the anterior abdominal wall
mean combined weight of both kidneys at birth:
at 6 mos = 24 grams
at 12 mos = 70 grams
at 6 y/o = 140 grams
adult weight approx. 300 grams
Nephron
structural and functional unit of the renal parenchyma
36 week of gestation, nephrogenesis stops and each
th
kidney has 850,000-1M nephrons
each nephron consists of a glomerulus and its tubules
for urine formation, acid-base balance, secretion of
certain substances
 each glomerulus is a rete of capillary tufts enclosed
in Bowman’s capsule
 capillary tufts consist of loops bound together in a
central area called Mesangium
 mesangium is composed of cytoplasmic matrix and
cells (mesangial or capillary); it is usually the FIRST
TO REACT IN THE EVENT OF GLOMERULAR INSULT
 3 Fixed cells of the Glomerulus:
•endothelial or intracapillary cell
•mesangial cell
•epithelial or extracapillary cell
Notes from Nelson:
Each kidney contains approximately 1 million
nephrons (glomeruli and associated tubules). In
humans, formation of nephrons is complete at
birth, but functional maturation with tubular
growth and elongation continues during the first
decade of life. Because new nephrons cannot be
formed after birth, progressive loss of nephrons
may lead to renal insufficiency. Decreased
nephron number at birth may be associated with
hypertension in adulthood, presumably related to
hyperfiltration and “premature” sclerosis of
overworked nephron units. This provocative
hypothesis, if proven, could identify a major risk
factor for hypertension and its associated
cardiovascular complications in the newborn
period.
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07-july-08
PHYSIOLOGY
Notes from Nelson:
Glomerular Filtration - net result of opposing forces across
the capillary wall. The force for ultrafiltration (glomerular
capillary hydrostatic pressure) is a result of systemic arterial
pressure, modified by the tone of the afferent and efferent
arterioles. The major force opposing ultrafiltration is the
glomerular capillary oncotic pressure, which is created by the
gradient between the high concentration of plasma proteins
within the capillary and the almost protein-free ultrafiltrate in
Bowman's space. Filtration may be modified by the rate of
glomerular plasma flow, the hydrostatic pressure within
Bowman's space, and the permeability of the glomerular
capillary wall.
The GFR may be estimated by measurement of the serum
creatinine level. Creatinine is derived from muscle
metabolism. Its production is relatively constant, and its
excretion is primarily through glomerular filtration, although
tubular secretion may become important in renal insufficiency.
In contrast to the concentration of blood urea nitrogen, which
is affected by state of hydration and nitrogen balance, the
serum creatinine level is primarily influenced by the level of
glomerular function. The serum creatinine is of value only in
estimating the GFR in the steady state. A patient may have a
normal creatinine level without effective renal function very
shortly after the onset of acute renal failure with anuria. In this
clinical setting, serum creatinine may be an insensitive
measure of decreased renal function because its level does not
rise above normal until the GFR falls by 30–40%.
3 Principal Kidney Functions
1. maintain constancy of internal environment by
adjusting volume, concentration and composition of
body fluids
2. elimination of metabolic wastes such as urea &
creatinine
3. elaborate the hormones rennin, erythropoietin,
prostaglandins, kallikrein-kinin
Urine Formation
1. initiated by elaboration of a large volume of protein-
free plasma ultrainfiltrate thru glomerular filtration
2. concentration and alteration of filtrate composition in
the tubules (thru tubular reabsorption of essential
substances and elimination of waste products)
Proximal Tubule
- reabsorbs 80% of filtrate volume and sodium
- all the glucose and amino acids (small portion)
and much of the filtered phosphate, minute amt
of protein that pass thru the glomeruli
- primary active process is sodium reabsorption
May.Yvette.Allain.Cristina.Ralph.Sheryl.Bart.Heinrich.Pipoy.KC.Jam.Cecille.Denesse.Mike.Hoops.Ces.Christian.Elaine.Riza.Kristel.Ezra.Goldi.Buf
f.Mona.AM.Maan.Adi.KC.Peng.Karla.Alphe.Aaron.Kyth.Anne.Eisa.Kring.Candy.Isay.Marco.Joshua.Fars.Rain.Jassie.Mika.Shar.Erika.Macky.Viki.Joan
.Precious.Kate.Katrina.Ams.Hannah. Memay.Pau.Rachelle.Esther.Joel.Glenn.Toni

- followed by passive reabsorption of chloride and
water by diffusion
- volume is greatly reduced but Na and Cl- not
altered
Loop of Henle
 water is reabsorbed in the descending limb
 sodium is reabsorbed in the ascending limb
result is an environment in the interstitial tissue of
medulla that is hypertonic to plasma thus  urine
concentration takes place in the adjacent collecting
ducts
 fluid at end of loop is Hypertonic.
Distal Tubules
 fluid initially hypotonic to plasma d/t large amt of
sodium reabsorbed in the ascending limb
 more sodium reabsorbed d/t aldosterone
 potassium is secreted
 acidification takes place
 there is diluted urine d/t failure to concentrate
 glomerulus is not affected so filtration is not affected
 creatinine clearance – for kidney function test
3. Loss of Renal Function
 decreased number of nephrons
nephron hypertrophy  early aging 
hyperfiltration  nephrosclerosis  eventual
destruction (proteinuria and HPN)  renal
insufficiency  renal failure
4. Necrosis of Renal Parenchyma
 tubule and surrounding intersitium are inflamed
 destruction of the growth of functional cells (growth
factors, vit D, erythropoietin, prostaglandins,
hormones)
 tubule destroyed, glomerulus obliterates
 area replaced by non-functional scar TISSUE
 # of nephrons are reduced
 remaining nephrons are overworked

Collecting Ducts Notes from Nelson:

- final concentration mediated by vasopressin (ADH)
acting on the lining cells of the duct making them more
permeable to water The 3 basic forms of UTI are pyelonephritis, cystitis, and
asymptomatic bacteriuria.

Now we come to Doctor Doctor’s lecture.. Have fun.. Clinical pyelonephritis is characterized by any or all of the
following: abdominal or flank pain, fever, malaise, nausea,
URINARY TRACT INFECTIONS vomiting, and, occasionally, diarrhea. Newborns may show
- there is bacterial invasion and multiplication nonspecific symptoms such as poor feeding, irritability, and weight
- inflammation and host reaction
loss. Pyelonephritis is the most common serious bacterial infection
- loss of normal renal function
in infants <24 mo of age who have fever without a focus. These
- necrosis of renal tissue
symptoms are an indication that there is bacterial involvement of
1. Bacterial Invasion and Multiplication the upper urinary tract. Involvement of the renal parenchyma is
 bacteria from stools termed acute pyelonephritis, whereas if there is no parenchymal
 proximity of urethra involvement, the condition may be termed pyelitis. Acute
 adherence of e.coli that resists urine flow pyelonephritis may result in renal injury, termed pyelonephritic
 ascends from urethra to bladder (cystitis; lower UTI) scarring.
 ascends from bladder to ureters ( reflux)
 ascends from ureters to kidneys (pyelonephritis: Cystitis indicates that there is bladder involvement; symptoms
Upper UTI) include dysuria, urgency, frequency, suprapubic pain, incontinence,
 low to negative bacterial growth by culture & and malodorous urine. Cystitis does not cause fever and does not
sensitivity result in renal injury. Malodorous urine, however, is not specific
 short bladder time: newborn & infants
for a UTI.Asymptomatic bacteriuria refers to a condition that
 acidic urine
results in a positive urine culture without any manifestations of
 low dose antibiotics
infection. It is most common in girls. The incidence is 1–2% in
 wrong culture media
preschool and school-age girls and 0.03% in boys. The incidence
2. Inflammation and Host Reaction declines with increasing age. This condition is benign and does not
 Urethritis – dysuria, burning sensation cause renal injury, except in pregnant women, in whom
asymptomatic bacteriuria, if left untreated, can result in a
Cystitis – dysuria, bladder tenderness, frequent symptomatic UTI. Some girls are mistakenly identified as having
urination with fever; on ultrasound: thickened asymptomatic bacteriuria, whereas they actually are symptomatic,
bladder wall experiencing day or night incontinence or perineal discomfort.
Pyelonephritis – systemic SSx

 bladder irritation – hypercontracted bladder wall  Normal Urinary Tract

frequent small amt of urine  vesicoureteric junction does not allow retrograde
 to diagnose bladder infxn: ultrasound will show flow of urine from the bladder to the kidney
bladder walls thickened than normal
Vesico-ureteral Reflux
 inflammation  edema  thickening of walls  phenomenon of backward-upward flow of urine
 WBC during inflammation
May.Yvette.Allain.Cristina.Ralph.Sheryl.Bart.Heinrich.Pipoy.KC.Jam.Cecille.Denesse.Mike.Hoops.Ces.Christian.Elaine.Riza.Kristel.Ezra.Goldi.Buf
f.Mona.AM.Maan.Adi.KC.Peng.Karla.Alphe.Aaron.Kyth.Anne.Eisa.Kring.Candy.Isay.Marco.Joshua.Fars.Rain.Jassie.Mika.Shar.Erika.Macky.Viki.Joan
.Precious.Kate.Katrina.Ams.Hannah. Memay.Pau.Rachelle.Esther.Joel.Glenn.Toni
 permits transport of urine from bladder to the
kidney
 may be unilateral or bilateral
 demonstrated and graded by Voiding
Cystourethrogram (VCUG)
Notes from Nelson:
Retrograde flow of urine from the bladder to the ureter and
renal pelvis is referred to as vesicoureteral reflux. The
ureter normally is attached to the bladder in an oblique
direction, perforating the bladder muscle (detrusor) laterally
and proceeding between the bladder mucosa and detrusor
muscle, creating a flap-valve mechanism that prevents
reflux. Reflux occurs when the submucosal tunnel between
the mucosa and detrusor muscle is short or absent. Reflux
usually is congenital, occurs in families, and affects
approximately 1% of children.
Reflux predisposes to renal infection (pyelonephritis) by
facilitating the transport of bacteria from the bladder to the
upper urinary tract. The inflammatory reaction caused by a
pyelonephritic infection may result in renal injury or
scarring, also termed reflux nephropathy. Extensive renal
scarring impairs renal function and may result in renin-
mediated hypertension. renal insufficiency or end-stage
renal disease, impaired somatic growth, and morbidity
during pregnancy. Reflux nephropathy once accounted for
as much as 15–20% of end-stage renal disease in children
and young adults. With greater attention to the management
of urinary tract infections (UTIs) and a better understanding
of reflux, end-stage renal disease secondary to reflux
nephropathy is uncommon. Reflux nephropathy remains
one of the most common causes of hypertension in
children. Reflux in the absence of infection or elevated
bladder pressure does not cause renal injury.
Components of Urinalysis
• color
• volume
• consistency (cloudy or not)
• sp. gravity
• RBCs, WBCs, casts, crystals
• pH (varies normally with food intake)
• blood chemistry
• creatinine
• uric acid / other metabolic products
 if with acidosis, but kidneys are normal
 urine will be acidic
 if blood is acidic, urine is alkaline
 kidneys are non-functional
 if with high Na in blood, kidneys are normal
 there will be  Na in urine
Post-Streptococcal Acute Glomerulonephritis (PSAGN)
- most common type and most common post-
infectious form
- peak age at 7 y/o
- an immune-complex meadiated dse d/t prior
infection with the nephritogenic strains of
Group A beta-hemolytic strep
(post-strep  AGN  inflamed glomerulus
(immunologic)
*yan po ung part na me example c doc ng past,
present at future..
- low volume urine w/ high sp. gravity
- RBC PREDOMINANCE (gross hematuria)
- tubules unaffected
- glomerulus is congested
- essential elements: edema, oliguria, hematuria,
hypertension
- Tx:
a. anemia from hematuria is insignificant
b. oliguria / edema – osmotic diuretics; 
water intake and  salt intake
c. for HPN – rapid-acting anti-HPN
UTI –
Notes WBC
from Nelson:
NephroticRBC
AGN – syndrome is primarily a pediatric disorder and is
15Nephrotic
times more Syndrome
common in children than adults. The incidence
– urine should not contain WBC nor RBC; no
is 2-3/100,000 children per year; and the majority of affected
hematuria; no pyuria
children will have steroid-sensitive minimal change disease.
– contains massive amount of protein
The characteristic
–
features of nephrotic syndrome are heavy
excessive protein excretion
proteinuria (>3.5 g/24 hr in adults or 40 mg/m2/hr in children),
– hypoalbuminemia
hypoalbuminemia d/t massive
(<2.5 2g/dL), edema, proteinuria
and hyperlipidemia.
( > 1 g / m / 24 hrs)
ETIOLOGY: Most children (90%) with nephrotic syndrome
del aMundo
have form of–the
2gidiopathic nephrotic syndrome. Causes of
Harisson – 3.5
idiopathic nephroticg syndrome include minimal change
disease (85%), mesangial proliferation (5%), and focal
segmental glomerulosclerosis (10%). The remaining 10% of
children with nephrotic syndrome have secondary nephrotic
syndrome related to syste-mic ( Table 527-1 ) or glomerular
diseases such as membranous nephropathy or
membranoproliferative glomerulonephritis
PATHOPHYSIOLOGY: The underlying abnormality in
nephrotic syndrome is an increase in permeability of the
glomerular capillary wall, which leads to massive proteinuria
and hypoalbuminemia. The cause of the increased
permeability is not well understood. In minimal change
disease, it is possible that T-cell dysfunction leads to alteration
of cytokines, which causes a loss of negatively charged
glycoproteins within the glomerular capillary wall. In focal
segmental glomerulosclerosis, a plasma factor, perhaps
produced by lymphocytes, may be responsible for the increase
in capillary wall permeability. Alternately, mutations in
podocyte proteins (podocin, α-actinin 4) are associated with
focal segmental glomerulosclerosis ( Table 527-3 ). Steroid-
resistant nephrotic syndrome is associated with mutations in
NPHS2 (podocin) and WT1 genes.
Although the mechanism of edema formation in nephrotic
syndrome is incompletely understood, it seems likely that, in
most instances, massive urinary protein loss leads to
hypoalbuminemia, which causes a decrease in the plasma
oncotic pressure and transudation of fluid from the
intravascular compartment to the interstitial space. The
reduction in intravascular volume decreases renal perfusion
pressure, activating the renin-angiotensin-aldosterone system,
which stimulates tubular reabsorption of sodium. The reduced
intravascular volume also stimulates the release of antidiuretic
hormone, which enhances the reabsorption of water in the
collecting duct.
May.Yvette.Allain.Cristina.Ralph.Sheryl.Bart.Heinrich.Pipoy.KC.Jam.Cecille.Denesse.Mike.Hoops.Ces.Christian.Elaine.Riza.Kristel.Ezra.Goldi.Buf
f.Mona.AM.Maan.Adi.KC.Peng.Karla.Alphe.Aaron.Kyth.Anne.Eisa.Kring.Candy.Isay.Marco.Joshua.Fars.Rain.Jassie.Mika.Shar.Erika.Macky.Viki.Joan
.Precious.Kate.Katrina.Ams.Hannah. Memay.Pau.Rachelle.Esther.Joel.Glenn.Toni

Assignment ni doc.. kinuha ko n lng ulit sa del Mundo..

 What are the alternative methods for collecting 24-
hr urine? Figure 1: ze urineri zystem

A freshly voided urine specimen collected early in the

morning is preferable for routine urinalysis. The
specimen should be examined immediately to avoid
disintegration of formed elements. Water or softdrinks to
hasten collection of a specimen should be avoided as
these results in dilute urine, red cell lysis, and
undergraded qualitative protein testing.

Methods:
1. PEREZ REFLEX - Stimulation of urination by running
tap water or stroking the spinal column upward or
downward (recommended)
2. Plastic (U- or wee_ bags and sterile vials may be used
to collect samples after proper cleansing of the genitalia
*bags should be discarded and changed if no
urine is voided w/in 3 hrs
3. Aseptic catheterization using French 8 or 10 catheter
(or French 5 C-32 feeding tube) and suprapubic bladder
tap may be done when indicated

Figure 2: zis is e nefron

mga words of wisdom ni doc..

1. if the function of ur legs is to walk and it is severed,

what will happen? answer: you cannot walk..  akalain
mo un, nabago pananaw ko sa buhay dahil dito..
2. Know what is normal…  bawal kontrahin to..

PASENSYA NA AT MAGULO UNG TRANS.. CNUBUKAN

NAMIN KUNIN ANG PANIG NI NELSON EH..
UNFORTUNATELY, MAHIRAP CYA ISINGIT SA LEC SO
NAKA BOX NALNG CYA.. SANA MAKATULONG.. LAM KO
KULANG, ALANGAN NAMAN ILAGAY KO LAHAT DB..
HEHE.. ANYWAY, KNG MAY TNUNG, PLS REFER TO THE
FIGURES BELOW.. YAN NA MISMO UNG LEC NATIN.. UH
HUH!! UH HUH!!

Figure 3: This iz e cast