Pediatric renal disorders

Nephron tubules filter waste fluid from blood. Waste fluid (urine) is secreted into the urinary tract while
proteins, electrolytes, and blood cells are reabsorbed by the nephron tubules and returned to the bloodstream

Regulatory functions of the kidney:

 The kidneys regulate electrolytes, fluid volume, and blood pressure. Electrolytes are sodium, potassium,
calcium, phosphorus, chloride, bicarbonate,and magnesium. Electrolytes must be balanced to ensure cell
metabolism ,muscle and nerve function.The kidneys help maintain this balance by excreting or retaining
electrolytes
 Fluid volume is maintained by the kidneys excreting or retaining urine based on the volume of fluid in the
body. When the body is dehydrated, the kidneys produce a low urine output to conserve fluid, and when the
body is overhydrated,the kidneys increase urine output to reduce fluid volume in the body.
 The kidneys produce the hormone erythropoietin (EPO), which stimulates
the production of red blood cells in the bone marrow. Therefore, renal failure causes less production of EPO
and thus decreases production of red blood cells, resulting in the patient becoming anemic.

 The kidneys also produce the enzyme renin, which regulates blood pressure by stabilizing blood vessels.
Decreased blood pressure signals the kidneys that there is insufficient blood for perfusion. In response, the
kidneys increase renin production, which indirectly causes vasoconstriction and increases secretion of
aldosterone to increase blood pressure.

1
 Nephrotic Syndrome
(N. S) is a childhood renal disorder. Nephrotic syndrome occurs as a result of increased glomerular basement
membrane permeability, which allows abnormal loss of protein in the urine.

It is characterized by:

1. Hyperprotienuria.

2. Hypoproteinemia.

3. Hyperlipidemia.

4. Generalized edema.

Pathophysiology

 When antibodies encounter and bind to antigens in the circulation, they may form very
large complexes that have difficulty staying dissolved in the blood When antigen-antibody
complexes are deposited in the glomeruli, the body responds by mounting an inflammatory
response to try to remove them ,the inflammation can cause even more damage and impair
the function of the glomeruli the basic kidney part that normally filter the blood
 Increased glomerular permeability results in the passage of larger plasma proteins through
the glomerular basement membrane. This results in excess loss of protein (albumin)in the
urine (proteinuria) and decreased protein and albumin(hypoalbuminemia) in the bloodstream.

2
  Protein loss in nephrotic syndrome tends to be almost exclusively albumin.
Hypoalbuminemia results in a change in osmotic pressure, and fluid shifts from the
bloodstream into the interstitial tissue (causing edema).
 Albumin is the major protein in the blood which maintains colloid osmotic pressure and
prevents leakage of blood from vessels into tissue
 This decrease in blood volume triggers the kidneys to respond by conserving sodium and
water, leading to further edema. The shift of fluid from the plasma to the interstitial spaces
decreases the vascular fluid volume hypovolemia )which in turn stimulates the renin
angiotensin system and the secretion of antidiuretic hormon and aldosterone. tubular
reabsorbtion of sodium and water is increased in an effort to increase intravascular volume
 The liver senses the protein loss and increases production of lipoproteins. Hyperlipidemia
then develops as the excess lipids cannot be excreted in the urine.

Types of nephrotic syndrome:

1. Congenital N.S. (hereditary)inherited as an autosomal recessive disorder. The outcome for

this type of nephrotic syndrome is extremely poor.
2. . Secondary N.S. occurs secondary to other systemic diseases such as anaphylactoid purpura,
systemic lupus erythematosus, Henoch-Schonlein purpura, or diabetes.
3. Idiopathic N.S. count for 85% of cases. Occur at any age between 1 - 7 years. Peak incidence
2 - 5 years. Uncommon in infant. Idiopathic means that a disease occurs with no known
cause .The most common type of idiopathic nephritic syndrome is called :(minimal-change
nephritic syndrome( MCNS Idiopathic nephritic syndrome is more common in boys than
girls, the disease can usually be managed and prognosis is good

Clinical Manifestation:

Most of the visible signs are usually because of obvious edema.

1. A well child begins to gain weight, process insidiously over

period of days or weeks.
2. Puffiness of eyelids and face mainly in the morning.
3. Swelling of the extremities.

3
 4. Swelling of the abdomen (ascites).
5. Labial or scrotal swelling.
6. Discomfort from abdominal swelling. Pressure on abdomen
and stomach make anorexia, vomiting.

7. Breathlessness, ascites make pressure on diaphragm so decrease lung expansion.

8. Waste muscle.
9. Pale face.
10. Skin easy break down.
11. Diminish urine, dark in color, tea color.
12. Hepatomegaly.
13. Susceptibility to infection, because of low immunity.

Diagnosis:

1. Physical finding.
2. Urine analysis ==> proteinuria.
3. Blood test ==> hypoalbuminemia.
4. Cholesterol elevated above 220 mg/dl.
5. Elevated sedimentation rate indicating inflammation of the glomeruli membrane .
6. Renal biopsy: a procedure where a small sample of tissue is taken from the kidney
through a needle .The tissue is sent for special testing to determine the specific disease
and provide information about the glomerular status

Medical Treatment:

 Intravenous albumin may be used in the severely edematous child.

 Diuretics are also required in the edematous phase. Long-term therapy is usually required to induce
remission. The nephrologist will determine the length of therapy based on the child’s response.
 Immune suppressive therapy such as cyclophosphamide, cyclosporine A, may be necessary.
 Use of corticosteroids therapy. Decrease excretion of protein, Anti - inflammatory drug acts on the
decreasment of permeability of the basal membrane of the glumeruli to protien molecules ==> decrease
excretion of protein through urine.

Nursing Consideration

Promoting Diuresis:

 Administer diuretics if ordered, usually furosemide (Lasix). Children may develop hypokalemia because of
potassium loss as an adverse effect of furosemide. Those children may require potassium supplementation
or a diet higher in potassium containing foods.

4
 Bed rest during the edema phase of the disease encourages turning regularly to prevent tissue breakdown.
Edematous skin easily breakdown. Support edematus areas such as scrotum, abdomen, and legs.
 Monitor urine output and the amount of protein in the urine (by dipstick).
 Weigh the child daily on the same scale either naked or wearing the same amount of clothing.
 Assess for resolution of edema, Measure abdominal girth at umbilicus.
 Measure pulse rate and blood pressure every 4 hours to detect hypovolemia resulting from excessive fluid
shifts.
 Enforce oral fluid restrictions if ordered.
 In cases of severe hypoalbuminemia, intravenous albumin may be administered. Increases in the serum
albumin level cause fluid to shift from the subcutaneous spaces back into the bloodstream.
 A diuretic such as furosemide administered immediately after the albumin infusion allows for optimal
diuresis and prevents fluid overload.

Measures to prevent infection:

 Protect the child from contact with infected roomates visitors, and other personnel.
 Monitor the child’s temperature, and vital signs to detect early infection. Viral illness may trigger a relapse
in children with nephrotic syndrome who have achieved remission.
 Administer pneumococcal vaccine as prescribed.
 Administer prophylactic antibiotics, if prescribed.
 Live vaccines should be delayed until at least 2 weeks after corticosteroid or other immunosuppressive
medication therapy ceases.
 Teach parents that if the child is unimmunized and is exposed to chickenpox, the pediatrician or
nephrologist should be notified immediately, so that the child may receive varicella zoster
immunoglobulin.(vaccine for chickenpox)

Provide good nutrition:

 Restrict sodium during edema and steriod therapy.

 Give supplementary vitamins and iron as ordered.
 Fluid restriction is reserved for children with massive edema.
 Encourage protein-rich snacks.

Family support and education:

 Instruction for albumin in urine test.

 Administration of medication, teach about steroid side effects (cushingoid appearance) moon face, extra fat
at the base of neck, increase in body hair)
 Give emotional support because Nephrotic syndrome is often a chronic condition, and children who are
responsive to steroid treatment may enter remission only to experience relapse. This cycle of relapse and
remission takes an emotional effect on the child and family. Frequent hospitalizations require the child to
miss school and the parents to miss work; this creates further stress for the family.

Complications:

Venous thrombosis :due to leak of anti -thrombin3 which helps prevent thrombosis .This often occurs in
the renal veins .Treatment is with oral anticoagulants not heparin as heparin acts via anti-thrombin 3 which
is lost in the proteinuria so it will be ineffective.
5
 Infection :due to leakage of immunoglobulins ,encapsulated bacteria such as Haemophilus influenzae and
Streptococcus pneumonia can cause infection .
Pulmonary edema :again due to fluid leak, sometimes it leaks into lungs causing hypoxia and dyspnea .
Growth retardation :does not occur in MCNS.It occurs in cases of relapses or resistance to therapy .
Causes of growth retardation are protein deficiency(loss of protein in urine), anorexia(reduced protein
intake,steroid therapycatabolism .
Acute renal failure is due to hypovolemia. Despite the excess of fluid in the tissues, there is less fluid in the
vasculature. Decreased blood flow to the kidneys causes them to shutdown .Thus it is a tricky task to get rid
of excess fluid in the body while maintaining ciculalatory euvolemia.

Longterm outcome of nephritic syndrome

Relapses do occur throughout childhood .However ,once a child reaches puberty ,The disease usually stays
in remission)complete or partial absence of symptoms .It is uncommon for symptoms to return during
adulthood, however ,it is possible .

Glomerulonephritis
Glomerulonephritis is an inflammation of the glomerulus. There are two types of glomerulonephritis:

_ Acute: This might occur up to 6 weeks following a respiratory tract streptococcal bacterial infection or from
a skin infection as a result of antigen/antibody groups trapped in the tubules causing edema that decreases
filtering and thus causes urine to be retained.

_ Chronic: An abnormal immune system, bacterial or viral infection, disease or toxin causes progressive
dysfunction of the glomerulus over the years.

AGN is a result of immune complexes antigen/antibody reaction secondary to toxins of the streptococcus on
the glomerular membrane in the glomerular capsule of the nephrone.

What happens ?

The immune complex causes an inflammatory process of the glomerulus = edema and infiltration of
leukocytes = occlude the capillary lumen = decreased plasma filtration = increased accumulation of water
and sodium = increased plasma and interstitial fluid volume = increased circulatory congestion and edema .

All these changes can cause the following :

 Decreased glomerular filtration .

 Increased glomerular capillaries permeability inflammatory reaction.
 Increase vascular spasm .
 Increased blood pressure (increased blood volume

Signs and Symptoms

_ Acute:
• Lower than normal urine output (oliguria).
• Fever.
• Edema of the face and extremities.

6
• Hypertension
• Lethargy.
_ Chronic:
• Lower than normal urine output (oliguria).
• Hypertension.
• Does not respond to treatment for acute glomerulonephritis.

Test Results
Acute:
• Urine analysis: Blood in the urine (hematuria), cola-color urine, high specific gravity, and protein in the
urine (proteinuria).
• Serum: Elevated creatinine and blood urea nitrogen (BUN)
• Antistreptolysin-O test: Positive for streptococcal bacteria
• Throat culture: Positive for streptococcal bacteria
• Renal ultrasound: Shows enlarged kidneys
• Renal biopsy: Positive for glomerulonephritis
Chronic:
• Urine analysis: Blood in the urine (hematuria), cola-color urine, high specific gravity, and protein in the
urine (proteinuria)
• Serum: Elevated potassium (hyperkalemia), creatinine, and BUN
• Computed tomography (CT) scan: Shows decreased size of kidneys
• Ultrasound: Shows decreased size of kidneys
• Renal biopsy: Shows glomeruli scarring and tests positive for glomerulonephritis
• Electrocardiogram (ECG): Abnormal; possibly indicating hyperkalemia
1

Treatment

Acute:
• Administer antibiotics for 10 days.
• Administer diuretics to reduce edema.
• Administer corticosteroids to reduce the inflammatory response.
• Administer antihypertensive medication to reduce blood pressure.
• Low-sodium, low-protein diet to prevent fluid retention.
• Fluid restriction.
• Dialysis if the patient experiences renal failure.
Chronic:
• Administer corticosteroids to reduce the inflammatory response..
• For hyperkalemia:
For emergency reduction of potassium, administer insulin, hypertonic glucose, and calcium gluconate.
To remove potassium, administer sodium polystyrene sulfonate(Kayexalate).

Nursing Intervention
-Strict intake and output.
-Daily weights.
Acute:
• Provide a quiet environment.
• Monitor vital signs and report changes to the health-care provider.
• Explain to the family the importance of a low-salt, low-protein, and fluid restricted diet, and teach the
family not to stop administering antibiotics when the child’s condition improves.

7
 Chronic:
• Monitor for signs of hyperkalemia (muscle weakness, paresthesia,anorexia, and malaise).
• Explain to the family the importance of a low-salt, low-protein, low potassium, and fluid-restricted diet and
the importance of ongoing monitoring of the child by their health-care provider.
♣Nursing alert: Monitor for renal failure where urine output <1 mL/kg per hour in infants and <0.5 mL/kg
per hour in children, and creatinine, BUN, and urine creatinine clearance are elevated.

8
9