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Pronephros
Mesonephros
Metanephros
Ureteric bud
Metanephrogenic blastema
Urine formation and excretion begin by the third month of gestation
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Blood flow to the kidney in a newborn is primarily to the medullary nephrons
Because of short loops of Henle in the medullary nephrons, an infant produces more dilute urine
Infants are in a high anabolic state, so their urea excretion is low
Urea is required to establish the concentration gradient in the medulla
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Infants: narrow chemical safety margin
High hydrogen ion concentration
Low osmotic pressure
Limited ability to regulate internal environment
Immaturity and smaller tubule surface area diminish the water reabsorption response to antidiuretic hormone (ADH)
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Immature tubular transport capacity
The ability to excrete a potassium load, reabsorb bicarbonate, or buffer hydrogen with ammonia does not become efficient until approximately 2 years of age
Diarrhea, infection, fasting, and poor feeding can rapidly lead to severe acidosis and fluid imbalance
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After birth the proportion of total body water to body weight does not change markedly but location of water does
Extracellular fluid volume (ECF) of the newborn infant is nearly double that of the adult
Decrease in ECF occurs during periods of rapid growth —infancy and adolescence
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Adults take in and excrete approximately 2000 ml of water daily (5% of total body fluid and 14% of ECF)
Infants exchange 600 to 700 ml (290% of the total or nearly 50% of the extracellular volume)
Makes control of dehydration and overhydration more difficult
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Congenital abnormalities of the kidney and urinary tract occur in about 1 out of 500 newborns
Abnormalities
Minor
Nonpathologic
Easily correctable anomalies
Anomalies that are incompatible with life
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Ectopic kidneys
Horseshoe kidneys (1 per 600 births)
Hypospadias (1 in 300 infant boys)
Chordee
Epispadias (1 in 40,000 to 118,000 births M>F)
Exstrophy of the bladder
Ideally the bladder and pubic defect should be closed before the infant is 48 hours old
Surgical reconstruction is performed usually within the first year
Staged procedures include bladder augmentation, bladder neck closure, or reconstruction of both bladder neck closures and reconstruction
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Ureteropelvic junction obstruction
Blockage of the tapered point where the renal pelvis transitions into the ureter; variety of causes
Bladder outlet obstruction
Urethral valves, urethral polyps, urethral atresia
Hypoplastic or dysplastic kidneys
Unilateral or bilateral; occurrence may be incidental or familial
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Renal agenesis
Absence of one or both kidneys
Polycystic kidney disease
Autosomal dominant (1 in 1000 live births)
Cyst formation and obstruction accompanied by destruction of renal parenchyma, interstitial fibrosis, and loss of functional nephrons
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Poststreptococcal glomerulonephritis (PSGN)
PSGN occurs after a throat or skin infection with certain strains of group A α-hemolytic streptococci
A sudden onset of hematuria, edema, hypertension, and renal insufficiency
Antigen-antibody complexes and complement are deposited in the glomerulus
The immune complexes initiate inflammation and glomerular injury
One of the most common postinfectious renal diseases in children ages 5 to 15 years
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Immunoglobulin A (IgA) nephropathy
Characterized by deposition of mostly IgA but some IgM antibodies and complement in the mesangium of the glomerular capillaries
Henoch-Sch önlein purpura nephritis
Also referred to as anaphylactoid purpura
IgA nephropathy that causes inflammation and damage to the glomerular blood vessels
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Most common cause of acute renal failure in children
HUS associated with bacterial and viral agents
Escherichia coli O157:H7
The bacterial toxin from E. coli damages red cells and endothelial cells
The endothelial lining of the glomerulus becomes swollen and occluded with fibrin clots
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Causes a decreased glomerular filtration rate with hematuria and proteinuria
Swollen vessels damage red cells as they pass
The damaged red cells are removed from the circulation by the spleen, causing acute hemolytic anemia
The microcirculation develops numerous thrombi
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A group of symptoms characterized by proteinuria, hypoproteinemia, hyperlipidemia, and edema
Minimal change nephropathy (MCN)
Focal segmental glomerulosclerosis (FSGS)
Mesangial proliferation
Can develop as part of many renal diseases
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Common in 7- to 13-year-old girls
E. coli, the most common pathogen, ascends the urethra in cystitis or the ureter in pyelonephritis
Cystitis
Acute pyelonephritis
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Retrograde flow of urine from the bladder into the ureters
Reflux encourages infected urine from the bladder to be swept up into the kidneys
Leads to frequent pyelonephritis
Caused by a congenital abnormality or ectopic insertion of the ureter into the bladder
Diagnosed by a voiding cystourethrogram
(VCUG) and an intravenous pyelogram (IVP)
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An embryonal tumor of the kidney
Arises from the proliferation of abnormal renal stem cells (metanephric blastema)
Three cellular components
Stromal, epithelial, and blastemic
Inherited and sporadic forms
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Involuntary passage of urine by child who is beyond the age when voluntary bladder control should have been acquired
4 to 5 years old
Primary enuresis
The child has never been continent
Secondary enuresis
Diurnal, nocturnal, or both
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Theories
Organic causes
Maturational lag
Genetic factors
Sleep patterns
Psychosocial theories
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