Renal System

Samah Suleiman20/4/2006

Urinary tract infections

is the inflammatory process resulting from bacterial invasion into urinary sterile urinary tract

Epithelial cells that line the urinary tract respond quickly to bacterial invasion, producing pathogen-destroying leukocytes

Diagnosis of UTI is confirmed by pyuria-white blood cells, and bacteriuria-bacteria in the urine

Prevalence: Childhood bacterial UTI is the second after upper respiratory tract infections

UTI affect 3-5% of all girls and 1% of boys by the age 11years

Escherichia coli which found in the GI tract is the responsible bacteria for 80% of pediatric UTI

Risk factors

Anatomic factors such as short and strait female urethra, situated close to rectum

Female infants are specially vulnerable as a result from fecal soiling

Congenital anomalies In male: UTI is associated with

prostate problems

UTI is also documented with bowel dysfunction: this believed to be due to pressure of the distended rectal segment and colonic seeding bacteria via the heamatogenic route

Host factors include reduced immune response, bacterial adherence

male found to have greater immune system immaturity and decreased resistance to pyelonephritis and septicemia

uncircumcised male infants has elevated colonization, more risk for UTI for the first 6 months of age

breast feeding offer protective benefits against UTI

Pathophysiology

The kidneys are essentially regulatory organs which maintain the volume and composition of body fluid by filtration of the blood and selective reabsorption or secretion of filtered solutes.

the kidneys are retroperitoneal organs (ie located behind the peritoneum) situated on the posterior wall of the abdomen on each side of the vertebral column, at about the level of the twelfth rib. The left kidney is lightly higher in the abdomen than the right, due to the presence of the liver pushing the right kidney down.

The kidneys take their blood supply directly from the aorta via the renal arteries; blood is returned to the inferior vena cava via the renal veins. Urine (the filtered product containing waste materials and water) excreted from the kidneys passes down the fibro muscular ureters and collects in the bladder

The bladder muscle (the detrusor muscle) is capable of distending to accept urine without increasing the pressure inside; this means that large volumes can be collected (700-1000ml) without high-pressure damage to the renal system occuring.

When urine is passed, the urethral sphincter at the base of the bladder relaxes, the detrusor contracts, and urine is voided via the urethra.

urinary tract is a sterile system, the slightly acidic urine creates hostile environment for most alkaline microorganisms

first line of defense is expulsion via bladder flushing or voiding-increase frequent voiding

immune response start and leukocytes flood the area

affected tissue become inflamed and edematous

bacteria release toxin that is alkaline in nature

nerve endings responds with painful bladder spasm to flush out the pathogen

mucosal infiltration produce hemorrhagic areas

ureterovesicle junction (UVJ) may be become incompetent

transient reflux permits the infection to ascend into the kidneys- pyelonephritis result and may cause irreversible renal involvement (renal parenchymal scarring with loss of glomeruli)

infants acquire pyelonephritis have mote extensive renal damage than children older than 4 years old- have 30% UTI recurrence after the first infection

risk of future hypertension or renal compromise in adulthood

gram-negative septic shock may result from the pyelonephritis due to bacterial endotoxins-life threatening condition

child may experience seizures, hypertension, fever and loss of consciousness

Assessments

Lower tract infections usually presented by increase urinary frequency, urgency, dysuria, hematuria, starngeuria (stopping and starting the urinary stream)

Urine may appear cloudy, blood-tinged Incontinence, mild fever, and

suprapupic pain are common

High fever->39C, flank pain, vomiting, lethargy, and genaralised malaise point to pyelonephritis

Vomiting, diarrhea, irritable cry, poor feeding, slow weight gain or weight loss, diaper rash should raise suspicion of UTI

Diagnostic tests

Collecting urine sample: Midstream urine sample: depends on

the child ability to void Adhesive urine-collection bag: from

non-toilet trained child High incidence of contamination

Recover urine from diaper via aspiration technique: do not recover urine from diapers containing gelling materials for specific gravidity, pH, or protein

Catheterization: inserting polyurethane catheter into the bladder by sterile technique

Suprapupic aspiration: with a syringe withdraw urine directly from the bladder

Blood and protein in the urine confirm UTI

Leukocyte esterase is an enzyme released during WBC destruction

Leukocyte esterase and nitrate testing are often negative because of frequent voiding and lower levels of esterase in the child’s blood

Interventions

Symptomatic relief Arrest the spread of infections Eliminate systemic infiltration of

bacteria Combined antibiotic therapy, increased

fluid intake, and frequent voiding

Urinary evaluation and monitoring for recurrence

Antibiotic therapy for lower UTI include combined sulfamethoxazole, nitrofurantoin, penicillins, and cephalosporins orally for 7-10 days

These may altered after culture results

Repeated urine specimen should be collected 48-72hours after initiation of medication

Increased fluid intake: up to 1000 cc for the older child to dilute and washed out endotoxins and tissue debris

Bladder irritants such as chocolate and caffeine rich should be avoided

Give mild analgesic such as acetaminophen

IV therapy: nursing care directed toward V/S, level of discomfort, intake and output monitoring

Child and family teaching include aspects of disease progression and management, handling of medication

Discuss the risk factors for reinfection and recommended prevention technique

Females whose first UTI before age 5 years and all males should have renal ultrasound, voiding cystourethrogram (VCUG), and intravenous pyelogram (IVP)

Glomerulonephritis

The glomeruli are the structures of the kidneys that supply blood flow to the small units (nephrons) in the kidneys that filter urine.

In glomerulonephritis, the glomeruli become inflamed and impair the kidney's ability to filter urine.

Causes systemic immune disease such as

systemic lupus erythematosus (SLE, or lupus)

Henoch-Schönlein purpura - A disease usually seen in children that is associated with purpura (small or large purple lesions on the skin and internally on the organs) and involves multiple organ systems.

Anti-Glomerular Basement Membrane Disease (Goodpasture's

syndrome)

Is a clinical group of glomerulonephritis and pulmonary hemorrhage, mediated by an anti-glomerular basement membrane antibody which also reacts with the basement membrane of pulmonary capillaries.

Antibody response is directed toward a normal antigen present in the GBM

Goodpasture's syndrome and anti-GBM disease are classic examples of autoimmune disorders. 

Clinical Course

Goodpasture's syndrome may occur at any time, but peaks in the spring and summer months are common.

It frequently begins with a flu-like illness with evidence of pulmonary compromise. Progressive dyspnea, hemoptysis and occasionally ventilatory failure occur.

Urinalysis reveals hematuria with red blood cell casts and variable proteinuria. 

Patients with Goodpasture's syndrome require immediate institution of plasma exchange and immunosuppressive therapy. 

Patients with an initial serum creatinine less than 7 mg/dl have a greater responding favorably to therapy. 

Post-Infectious Glomerulonephritis

It is the most common form of glomerulonephritis in children

A common cause is from a streptococcal infection, such as upper respiratory infection. Usually from group A beta-hemolytic streptococci. 

usually occurs more than one week after an infection and referred to as acute post-streptococcal glomerulonephritis, APSGN

The post-streptococcal glomerulonephritis is primarily a disease of children, 6 to 7 years of age

The onset is usually abrupt, with a latent period of 7 to 21 days between infection and the development of nephritis

Common initial clinical manifestations of post-

streptococcal glomerulonephritis

Hematuria Edema Hypertension Oliguria In most patients hematuria disappears

by 6 months but proteinuria may persist for two years in a third of patients

The prognosis for complete recovery is excellent in children even accompanied by initial impairment in renal function, persistent proteinuria and the nephrotic syndrome

Children prostacycline and prostaglandin E promote the maintenance of glomerular filtration

It is evidenced that they reduced by the reduction of their output in the stage of chronic renal failure.

The growth of renin and antidiuretic hormone synthesis in children suffering from nephrotic glomerulonephritis is not accompanied by the increase of the output of prostaglandin E, their renal antagonist,

This lead to the development of the edematous syndrome

Generally, Symptoms may include

Dark brown-colored urine (from blood and protein)

Sore throat Diminished urine

output Fatigue

Lethargy Increased

breathing effort Headache High blood

pressure Joint pain

Seizures (may occur as a result of high blood pressure)

Pale skin color Fluid

accumulation in the tissues (edema)

Diagnosis

Thorough physical examination

Complete medical history

Throat culture Urine tests

Blood tests Electrocardiogra

m (ECG) - to detects heart muscle damage.

Renal ultrasound - to determine the size and shape of the kidney, and to detect a mass, kidney stone, cyst, or other obstruction or abnormalities.

Chest x-ray - to produce images of internal tissues, and organs onto film.

Renal biopsy - kidney tissue is sent for special testing to determine the specific disease.

Treatment

Specific treatment will be determined based on:

Child's age, overall health, and medical history

The extent of the disease Child's tolerance for specific

medications, procedures, or therapies

Expectations for the course of the disease

Family preference If glomerulonephritis is caused by a

streptococcal infection, then treatment will be focused on curing the infection and treating the symptoms associated with the infection.

Other different reason cannot be cured, so treatments focus on slowing the progression of the disease and preventing complications.

Treatment

Fluid restriction Decreased protein diet Decreased salt and potassium diet Medication, such as diuretics, blood

pressure medications, phosphate binders - medications to decrease the amount of the mineral phosphorus in the blood. immunosuppressive agents

Dialysis: used for short-term or long-term therapy to remove wastes and additional fluid from the blood after the kidneys have stopped functioning.

If glomerulonephritis does not resolve, long-term kidney failure may need to be addressed.

Acute renal failure

Develop rapidly over days or weeks and classified according to the site of injury to the kidney:

Prerenal: result from impared blood flow to or oxygenation of the kidneys

Usuallu cured with early supportive treatment

Renal or parenchymal: injury or malformation of the kidney tissue-Need dialysis

Postrenal: obstruction of the urinary flow at some level between the kidney and the urinary meatus –require surgical removal of the obstruction