Chapter 37 Alterations of Renal and Urinary Tract Function in Children

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Chapter 37

Alterations of Renal and Urinary

Tract Function in Children

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Development of the

Urinary Renal System

Pronephros

Mesonephros

Metanephros

 Ureteric bud

 Metanephrogenic blastema

Urine formation and excretion begin by the third month of gestation

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Fluid and Electrolyte Balance

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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Fluid and Electrolyte Balance

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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Fluid and Electrolyte Balance

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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Location of Body Water

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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Exchange of Body Water

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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Structural Abnormalities

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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Structural Abnormalities

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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Structural Abnormalities

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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Structural Abnormalities

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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Glomerulonephritis

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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Glomerulonephritis

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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Hemolytic-Uremic Syndrome

(HUS)

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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Hemolytic-Uremic Syndrome

(HUS)

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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Nephrotic Syndrome

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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Urinary Tract Infections (UTIs)

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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Vesicoureteral Reflux (VUR)

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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Vesicoureteral Reflux (VUR)

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Vesicoureteral Reflux (VUR)

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Wilms Tumor

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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Enuresis

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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Enuresis

Theories

 Organic causes

 Maturational lag

 Genetic factors

 Sleep patterns

 Psychosocial theories

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