Primary responsibility of the kidney is to maintain the composition and volume of the body fluids in equilibrium. Secondary function of the kidney is the production of certain humoral substances: enzyme: erythropoitin stimulating factor (ESF) or erythrogenin, which acts on a plasma globulin to form erythropoietin which in turn stimulates erythropoiesis in the bone marrow. Enzyme: renin, secreted in response to reduced blood volume, decreased blood pressure or increased secretion of catecholamines. Renin stimulates the production of the amgiotensins, which produce arteriolar constriction and elevation in blood pressure.
The structural and functional unit of the kidney is the nephron, which is composed of a complex system of tubules, arterioles, venules and capillaries (glomerular , filtrating unit) enclosed by a doublee-walled chamber called Bowman’s capsule. In glomerulus; water and solutes are filtered from the blood.
Renal disease cause impaired glomerular and tubular function thus nonprotein nitrogenous substances(creatinine, ures, ammonia) rather being excreted are retained in the blood. Urea is formed from the breakdown of amino acids by the liver. Creatinine is released during cell metabolism.
Development of the kidney begins within the first weeks of embryonic life but is not completed until a bout the end of the first year. The nephrons increase in number throughout gestation and reach their full complement by birth but still immature and less effective. Glomerular filtration and absorption are relatively low and do not reach adult values until 1-2 years.
Loop of Henle (site of the urine concentrating mechanism) is short in the newborn which reduces the ability of the newborn to reabsorb sodium and water ( urine is very diluted). Concentrating ability reaches adult levels by around 3rd month of age.
Amount of urine excreted in 24 hours depends on : fluid intake, state of kidney health, and age:
6 month-2 years 540-600 ml/24 hour
2-5 years 500-780 ml/24 hour
5-8 years 600-1200 ml/24 hour
8-14 years 1000-1500 ml/24 hour
> 14 year 1500 ml/24 hour
With renal disease: Impaired glomerular and tubular function: metabolic waste products (creatinine, urea, uric acid) rather being excreted are retained in the blood.
– Urea is formed from the breakdown of amino acids by the liver
– Creatinine: Due to breakdown of creatinine kinase (important in muscle contraction)
• Urine analysis: presence of glucose, protein, occult blood & measure pH (4.5-8) & SG (1.015- 1.025)
• Urine C & S: suprapubic aspiration/ clean catch
• Glomerular filtration rate: measured by the creatinine clearance test (100ml/min) or assessed by administration of IV radioactive substances and observe/scan flowing through the kidney
• BUN: it test glomerular function (may not increase until ~ 50% of glomeruli are destroyed (N=
5 – 20 mg/ 100ml)
• Serum creatinine: 0.7 – 1.5 mg/ 100ml
• Sonography & MRI: sizes of kidneys, ureters, differentiate between solid or cystic masses.
• X-ray: KUB
• IVP: intravenous pyelogram: a radiopaque dye is injected IV, x-ray films is then taken at frequent intervals (dye is iodine-based, child may experiences flushing of face, warmth, & salty taste in mouth)
• CT scan: size & density of kidneys, adequacy of urine flow. Sedative may be used.
• Cystoscopy: examination of the bladder & ureter opening (evaluate for VUR or stenosis)
• Voiding Cystourethrogram (VCUG): a dye is injected into the bladder to study the lower urinary tract. It shows the urethra, bladder and the presence & grade of reflux into the ureters.
• A clean-catch urine specimen for culture is required before VCUG in case of UTI
• Renal biopsy: extent of renal disease, after biopsy:
• Bloody urine
• Restrict activity for 24 hrs
• Urine samples for hematuria
• VS Q 15 min
• Observe biopsy site
• Increase intake
• Chief concern:
– Burning or cries during urination
– Blood in urine
– Frequency of urination
– Abdominal pain
– Flank pain
– Periorbital edema
– Poor appetite
– Strong urine odor
– Diaper rash
• Family history
– Renal disease
• Pregnancy history:
– Nephrotoxic drugs
• Past illnesses:
– Recurrent URTI
GU Disorders and Defects
• Urinary Tract Infection (UTI)
• Cryptorchidism (undescended testes)
• Vesicoureteral Reflux
• Hypospadias/ Epispadias
• Nephrotic Syndrome
• Acute Glomerular Nephritis
• Renal failure
1. Urinary Tract Infection
UTI is a clinical condistion that may involve the urethra, bladder (lower urinary tract), and the ureters, renal pelvis, calyces, and renal parenchyma (upper urinary tract). Because it is often impossible to localize the infection, the broad designation “UTI” is applied to the presence of significant numbers of microorganisms anywhere within the urinary tract (except the distal one third of the urethra, which is usually colonized with bacteria)
Infection of the urinary tract may be present with or without clinical symptoms. As a result, the site of infection is often difficult to pinpoint with accuracy.
The peak incidence of UTI not caused by structural anomalies occurs between 2 and 6 years of age.
Except for the neonatal period, females have 10 to 30 times greater risk for developing UTI than males. It is estimated that 5% to 6% of girls will have had at least one episode of bacteriuria between the time they enter first grade and graduate from high school. The likelihood of recurrence is 50% or greater in girls.
UTI in newborns differs in some respects from infections occuring in older children. In this age group, males out-number females. The prevalence of bacteriuria in infants is 3.7% in boys and 2% in girls.
A variety of organisms can be responsible for UTI. Escherichia coli (80% of cases) and other gramnegative enteric-organisms are most commonly implicated.
Anumber of factors contribute to the development of UTI, including anatomic, physical, and chemical conditions or properties of the host’s urinary tract.
Anatomic and Physical Factors
• Shorter urethra in females (2cm in young- 4 cm in adult female, 20 cm in adult male)
• Uncircumcised males
• Incomplete bladder emptying (reflux, stenosis)
• Altered urine and bladder chemistry/ sterility:
– Adequate fluid intake promote urine sterility
– Use of cranberry juice increased urine acidity and so prevent UTI
• Extrinsic factors:
– Bladder neck obstruction: pregnancy, chronic constipation, tight clothing/ diapers
– Altered N. flora: antimicrobial agents
– Poor hygiene, use of bubble bath, hot tubs
• Any child with fever should be evaluated for UTI
• Clean – catch urine for culture & sensitivity
• With UTI, urine is positive for proteinuria due to bacterial growth
• Hematuria due to mucosal irritation
• Increase WBC
• Urine pH is more alkaline (>7)
– GI disorders
– Feeding problems
– Diaper rashes
– Strong smelling urine
• Older children, Typical symptoms:
– Pain in urination
• Cystitis (infection of bladder):
– Mild abdominal pain
• Pyelonephritis (kidneys):
– Symptoms are more acute
– High fever
– Flank or abdominal pain
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• Treatment objectives:
– Eliminate the current infection
– Identify contributing factors to reduce the risk of recurrence
– Prevent urosepsis
– Preserve renal function
• 10 days antibiotics (penicillins, sulfonamide, cephalosporins, tetracyclines)
• Mild analgesics/ antipyretics
• Increase fluid intake: flush out infection
• Clean – catch urine after 72 h to assess effectiveness
• For recurrent UTI, a
prophylactic antibiotics for
• Identify child with UTI
• Education regarding
prevention & treatment
• Instruct parents to observe
for clues that suggest UTI:
– Incontinence in a
– Strong-smelling urine
– Frequency or
2. Cryptorchidism (Crptorchism)
Cryptorchidism is failure of one or both testes to descend normally through the inguinal canal into the scrotum. Absence of testes within the srotum can be a result of (1) undescended (cryptorchid) testes,
(2) retractile testes, or (3) anorchia (absence of testes). Undescended testes can be categorized further according to location:
Abdominal: Proximal to the internal inguinal ring
Canalicular: Between the internal and external inguinal rings
Ectopic: outside the normal pathways of descent between the abdominal cavity and the scrotum The incidence of cryptorchidism is approximately 33% in preterm males; by the age of 1 year the incidence decreases to less than 1% and does not change thereafter.
Testicular development is influenced by a number of genes, but the dominant one is located on the Y chromosome. This gene stimulates the medullary sex cords of the embryonic gonad to differentiate into secretory Sertoli cells. Beginning around week 7, these cells secrete a glycoprotein that leads to development of a male genital system. Between weeks 8 and 15 a cord-like structure, the gudernaculum, extends from the developing testis (located in the lower abdomen) to the labioscrotal sweeling. The fetus grows, but the length of this gubernaculum remains relatively fixed, anchoring the testis to the developing inguinal canal (transabdominal migration) in preparation for the second phase of descent.
This second phase begins around weeks 25 to 30 and is characterized by shrinking of the gubernaculum under the influence of testosterone, causing the testis to migrate down the inguinal canal and into a scrotal position (transinguinal migration).
Cryptorchidism occurs when one or both testes fail to descend through the inguinal canal and into the srotum. Several processes may slow or arrest testicular descent, including endocrinologic abnormalities affecting the hypothalamic-pituitary-testicular axis, denervation of the genitofemoral nerve, traction of the gubernaculum, abnormal development of the epididymis, or premature birth.
Cryptorchid testes are often accompanied by congenital hernias and abnormal testes, and ther are at risk for subsequent torsion.
An ectopic testis emerges outside the inguinal ring into the perineum, femoral area, or lies in a transverse scrotal or prepenile location.
Anorchia is the complete absence of a testis. Anorchia is suspected whenever one or both testes cannot be palpated in the patient with cryptorchidism.
Retractile testes can be found at any level within the path of testicular descent, but they are most commonly identified in the groin. Fortunately, they are not truly cryptorchid; instead, they are introverted to an inguinal or abdominal position because of an overactive cremasteric reflex. The cremasteric reflex, observed as withdrawal of the testis above the srotum and into the inguinal canal in response to various stimuli including exposure to cool temperature, is active during infancy and peaks around age 4 to 5 years. Unlike the cryptorchid testis, the retractile testis can be gently moved into the scrotum without residual tension and does not require treatment.
Undescended testes are a congenital problem, meaning they are present at birth. The exact cause is not known, but this problem is believed to be partly inherited, as there is a slightly higher incidence of the condition among relatives of those who have it. There may be some hormonal abnormality associated with the development of undescended testes. Twisting (torsion) of the testes within the abdomen during fetal development may also injure the testes, preventing them from developing appropriately.
The following factors increase your child’s chance of having undescended testes.
– Low birth weight
– Down syndrome (fetus)
– Hormonal abnormalities (fetus)
– Toxic exposures in the mother
– Mother younger than 20 or older than 35 years of age
– A family history of undescended testes
A nonpalpable testis is typically observed by the parent or detected during routine physical examination by a nurse or physician. If one testis is not palpable, the affected hemiscrotum will appear smaller than the other, while both hemiscrota appear small with bilateral nonplapable testes. In the case of retractile testes, the parents may report intermittently observing the testis in the scrotum, frequently when the child is being bathed in warm water.
Retractile testis can be manipulated into the scrotum. By 1 year of age, cryptorchid testes will descend spontaneously in approximately 75% of cases in both full-term and preterm infants. In contrast, true undescended testes rarely descend spontaneously after 1 year of age.
A trial of hormone therapy with luteinizing releasing hormone (nasal spray) and human chorionic gonadotropin (injection) may be attempted; however, surgical treatment is the preferred management.
Surgical repair is done to:
1. prevent damage to the undescended testicle by exposure to the higher degree of body heat in the undescended location, thus maintaining future fertility
2. decrease the incidence of tumor formation, which is higher in undescended testicles
3. avoid trauma and torsion
4. prevent the cosmetic and psychologic handicap of an empty scrotum
Postoperative care: prevention of infection and instructing parents in home care of the child, including pain control. Infection is prevented by carefully cleansing the operative site of stool and urine. Observation of the wound for complications and activity restriction are discussed. Parents are concerned about the future fertility of the child, and family is counselled regarding the prognosis. In most cases the family can be reassured of normal function in adulthood.
3. Vesicoureteral Reflux
VUR refers to the retrograde flow of urine from the bladder up the ureters and possibly to the kidneys during micturation while the bladder contracts and then allowed to empty after voiding.
Residual urine remains in the bladder until next void. The cause may be a defective bladder valve or incorrect placement of ureters. Valve defect either from birth or from repeated UTIs.
The international classification system describes the degree of reflux from the bladder into upper genitourinary tract structurs as follow:
• Grade I: urine refluxes part-way up the ureter
• Grade II: urine refluxes all the way up the ureter
• Grade III: urine refluxes all the way up the ureter with dilatation of the ureter and calyces (part of the kidney where urine collects)
• Grade IV: urine refluxes all the way up the ureter with marked dilatation of the ureter and calyces
• Grade V: massive reflux of urine up the ureter with marked tortuosity and dilatation of the ureter and calyces
• Primary reflux: congenital anomaly affects the ureterovesical junction
• Abnormal tunneling of the intramural ureteral segment
• Defects in the configuration of the ureter orifice
• Familial pattern
• Secondary reflux: occurs as a result of an acquired condition, UTI, neuropathic bladder dysfunction
• Renal/Bladder Ultrasound
• Voiding Cystourethrogram (VCUG)
• Spontaneous resolution over time 20-30%
• 80% probability of remission may occur in grades I and II reflux when managed medically
• Continuous low-dose antibacterial therapy
• Frequent urine cultures
• Surgical correction for grades IV & V
• Grade III is managed conservatively unless there are complications
Indication for surgery
• Significant anatomic abnormalities
• Recurrent UTIs
• High grades of VUR
• Non-compliance with medical therapy
• Intolerance to antibiotics
• VUR after puberty in females
• High risk for injury related to possibility of kidney damage from chronic infection
• Anxiety related to unfamiliar procedures
• Altered family processes related to illness of a child
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• Administration of antibiotics
– Perineal hygiene
– Complete bladder emptying
– Frequent voiding
• Conservative management – prophylactic antibiotics, routine urine cultures
Hypospadias refers to a condition in which the urethral opening is located below the glans penis or anywhere along the ventral surface (underside) of the penile shaft. In very mild cases the meatus is just below the tip of the penis. In the most severe malformations the meatus is located on the perineum between the halves of the scrotum. Chordee, or ventral curvature of the penis, results from the replacement of normal skin with a fibrous band of tissue and usually accompanies more severe forms of hypospadias.
• Circumcision delayed: save the foreskin for repair
• Surgical correction by 1 year old
– To enable voiding in standing position
– Improve physical appearance
– Sexual adequacy
• Assess for birth defects
• Maintain body image
• Preparation for operation
• Care for indwelling catheter
• Avoid tub bath, rough activities
• Antibacterial ointment
• Increase fluid intake
5. Acute Glomerulonephritis (AGN)
• Inflammation of the glomeruli occurs as an immune complex disease after infection with nephritogenic streptococcus (APSGN)
• Common in early school age, uncommon in children < 2years
• Strep. Infection followed by a release of a membranelike material from the organism into circulation
• Antibodies are formed, an immune complex reaction is then occurs after a period of time which become trapped in the glomerular capillary loop
• A reduction in glomerular filtration rate of plasma occurs leading to accumulation of water and retention of sodium
• Increased plasma and interstitial fluid volume cause circulatory congestion and edema
Post-streptococcal glomerulonephritis is form of glomerulonephritis. It is the result of an infection, not of the kidneys, but of a completely different area, such as the skin or throat, with a specific type of Group A hemolytic streptococcus bacterium. As a consequence of immune complexes (formed from streptococcal antigen, antibodies, and a substance called complement) becoming trapped in the glomeruli of the kidneys, the glomeruli become inflamed. This results in inefficient filtering and excreting function by the kidneys. Protein and blood may be present in the urine, and excess fluid commonly accumulates in the body. Hypertension is usually present. The disorder may develop 1-2 weeks after an untreated throat infection, or 3-4 weeks after a skin infection.
It may occur in people of any age, but most often occurs in children 6-10 years old. Risk factors include having a recent history of sore throat, strep throat, streptococcal skin infections (such as impetigo), and other streptococcal infections.
Macroscopic hematuria (50%)
Tea or cola colored
Oliguria/ anuria common
Periorbital, rarely severe
HTN (60-70%): headache, drowsiness, vomiting,
vision changes, convulsions (encephalopathy)
Abdomen, flank and CVA tenderness common
Additional symptoms that may be associated with this disease:
Urine analysis: ↑ WBC, epithelial cells, RBC, SG
Serum: ↑ BUN, creatinine, ESR, Hgb
Serum ASO may be elevated.
Genitourinary Disorders/ Khulood Shattnawi
There is no specific treatment for post-streptococcal glomerulonephritis. Usually resolves spontaneously. Course of disease is 1-2 weeks. Treatment is focused on relief of symptoms.
Antibiotics, such as penicillin, should be used to destroy any streptococcal bacteria that remain in the body. Antihypertensive medications and diuretic medications may be needed to control swelling and high blood pressure. Corticosteroids and other anti-inflammatory medications are generally not effective.
Dietary salt restriction may be necessary to control swelling and high blood pressure.
Acute renal failure
Chronic renal failure
End-stage renal disease
Congestive heart failure or pulmonary edema
Nsg Dx: Glomerulonephritis
• Fluid volume excess r/t decreased U.O.
• Risk for activity intolerance r/t fatigue
• Risk for impaired skin integrity r/t edema and decreased activity
• Altered nutrition: less than body requirements r/t fluid and diet restrictions
• Anxiety r/t hospitalization, knowledge deficit of disease
• General measures:
– No added salt diet
– Fluid restriction
– Q4h BP
– Daily weights
– I & O
– No bed rest but restrict competitive activity
• > 90% recover from their illness
– The assoc HTN etc can be fatal
• is bad when…
– When the course is prolonged
6. Nephrotic Syndrome
The exact cause of nephrotic syndrome is not known but Moore et al (1994/1995) describe it as “a clinical condition where there is heavy proteinuria leading to a low serum albumin and the development of oedema” . The symptoms of nephrotic syndrome are high levels of protein in the urine, low levels of protein in the blood and swelling resulting from the build-up of salt and water Nephrotic syndrome itself is not a disease, but it can be the first sign of a disease that damages the glomeruli in the kidney. The main protein lost through the kidneys is albumin which leads to hypoalbuminaemia. Serum albumin levels drop markedly, which reduces the osmotic pull of the fluid into circulation. Fluid instead leaks out into the surrounding tissues, causing oedema.
Normal Physiology of the Nephron
The basic functioning unit of the kidney is the nephron, of which there are between 1-1.5 million in each kidney. The nephron is a blind ended tube. The blind end forms the Bowman’s capsule which encapsulates the Glomerulus. The other parts of the nephron include the proximal tubule, loop of Henle, distal tubule and collecting duct. The glomerulus is made up of a bundle of capillaries fromwhich the filtrate drains into the blind end of the nephron called the Bowman’s capsule. The function of the glomerulus is to produce an ultrafiltrate of plasma which enters the nephrons. Each glomerulus is supplied with blood from an afferent arteriole, which divides to form the tuft of glomerular capillaries. These capillaries rejoin to form the efferent arteriole. In moving from the capillary into the Bowman’s capsule, the filtrate must traverse three layers, which are:
– The endothelial cells lining of the glomerular capillaries
– The glomerular basement membrane which is non cellular, and composed of connective tissue
– The visceral epithelial cells of the Bowman’s capsule.
These three layers make up the glomerular filter, each of which has a specific function in filtering the filtrate.
• Firstly, the capillary endothelium acts as a screen to prevent blood cells and platelets coming into contact with the main filter which is the base membrane.
• Secondly, the base membrane allows the passage of molecules depending on their molecular size, shape and charge, and is the main filtration barrier.
• The final layer is the visceral epithelial layer of the Bowman’s capsule which is up made of podocyte cells in between which are slit pores, across which are spread thin diaphragms consisting of proteins. The purpose of this layer is to maintain the base membrane by preventing the larger molecules, that have passed through the base membrane, from entering the proximal tubule.
If the glomerular filter is functioning properly then an almost protein free ultrafiltrate passes into the Bowman’s capsule from the glomerular capillaries. Molecular charge, in addition to size, influences the filtration of macromolecules across the glomerular capillary wall. Charge selectivity derives from the electrostatic interactions between the fixed negatively charged components of the capillary wall and the macromolecule. As a result the filtration of positively charged molecules is enhanced, whereas the capillary wall acts as a barrier to the circulating negatively charged molecules. The filtration of albumin, a negatively charged molecule, is therefore restricted from passing through the glomerular capillary despite being small enough to do so.
3 Forms of NS
• Primary – Minimal Change Nephrotic Syndrome (MCNS)
– 80% of all cases
– Good prognosis
• Secondary to another disorder
• Congenital: autosomal recessive gene
Physiological changes due to Nephrotic Syndrome.
Nephrotic syndrome occurs as a result of damage to the Glomerular Capillary Wall (GCW) which allows proteinuria to occur (Field et al 2001). In minimal change nephrotic syndrome, there is a disturbance in the functioning of the glomerular basement membrane, which makes it increasingly permeable to plasma proteins and allows them to pass freely into the urine.
Broyer et al (1988). This process is still not fully understood, although it is thought that both the size selective and charge selective barriers on the glomerular filtration surface fail. One theory is that the podocytes fuse together which may be the reason why albumin is able to pass through the membrane.
Another theory is that when there is a loss of the fixed negative of the glomerular capillary wall, enhanced filtration of negatively charged molecules will occur. With the loss of charge discrimination in glomerulonephritis, the capillary wall becomes size selective only. This allows the passage of albumin into the ultrafiltrate to take place as the albumin molecule is small enough to pass through the membrane (Lote 2001). As a result of increased proteins in the ultrafiltrate, there will be a change in the concentration gradient within the proximal tubule. Under normal circumstances, the balance between hydrostatic and osmotic pressure gradients across the capillaries walls prevents the formation of oedema. This is known as Starling’s forces. When there is a reduction in plasma osmotic pressure, there is an increase in capillary wall permeability or venous hydrostatic pressure which affects the Starlings forces and leads to an increase in oedema formation.
Minimal Change NS
The most common form of the nephrotic syndrome in children is called minimal change disease.
Doctors do not know what causes it. The condition is called minimal change disease because children with this form of the nephrotic syndrome have normal or nearly normal biopsies. With minimal change disease, the child will probably treated by prednisone, which belongs to a class of drugs called corticosteroids. Prednisone stops the movement of protein from the blood into the urine. Diuretics may also been used which reduces the swelling by helping the child urinate.
When protein is no longer present in the urine, we have to begin to reduce the dosage of prednisone.
This process takes several weeks. Some children never get sick again, but most do develop swelling and protein in the urine again, usually following a viral illness. However, as long as the child continues to respond to prednisone and the urine becomes protein free, he or she has an excellent long-term outlook without kidney damage.
Children who relapse frequently, or who seem to be dependent on prednisone or have side effects from it, may be given a second type of drug called a cytotoxic agent. The agents most frequently used are cyclophosphamide and chlorambucil. After reducing protein in the urine with prednisone, the doctor may prescribe the cytotoxic agent for a while. Treatment with cyclophosphamide and chlorambucil usually lasts for 8 to 12 weeks. Alternatively, cyclosporine, a drug also used in transplant patients, may be given. Treatment with cyclosporine frequently continues over an extended period.
• Progressive weight gain
• Puffiness of face, periorbital at morning which subsides during the day when swelling of abdomen, scrotum & lower extremities is more prominent
• Respiratory difficulty (pleural effusion)
• Skin pallor, breakdown
• Edema of intestinal mucosa cause diarrhea, loss of appetite, poor intestinal absorption
• Decrease urine volume/ dark, frothy
• Irritable, easily fatigued
• Marked proteinuria +1 – +4
• Minimal hematuria
• Increase serum cholesterol: > 450-1500mg/dl
• Reduce serum albumin < 2 g/dl
• Increase SG
• Elevated ESR
Genitourinary Disorders/ Khulood Shattnawi
– Reduce urinary protein excretion
– Maintain a protein-free urine
– Reduce tissue fluid retention/ control of edema
– Prevent infection
– Minimize complications
• General measures:
– Bed rest during edema
– Antibiotics with infections
– Diet: restricted salt during massive edema, high protein diet
– Corticosteroids: prednisone (↑ chance for infection)
– Immunosuppressants (do not administer immunization)
– Albumin (plasma expander) and lasix
• Risk for fluid volume deficit (intravascular) r/t proteinuria, edema, and effects of diuretics
• Risk for impaired skin integrity r/t edema and decreased circulation
• Risk for infections r/t urinary loss of gammaglobulins
• Anxiety (parental) r/t caring for child with chronic disease and hospitalization
Nursing diagnosis: Fluid volume excess related to fluid accumulation in tissues
Goal: Will exhibit no or minimal evidence of fluid accumulation
– Assess I & O
– Assess changes in edema
• Measure abd girth
• Measure edema around eyes / & dependent areas
• Weigh daily note degree of pitting
• Test urine for specific gravity and albumin (hyperalbuminuria )
• Administer corticosteroids (to reduce excretions of urinary protein)
• Administer diuretics (relieve edema)
• Limit fluids as indicated
7. Renal Failure
Renal failure is the inability of the kidneys to rxcrete waste material, concentrate urine, and conserve electrolytes. The disorder can be acute or chronic and affects most of the systems in the body. Two terms that are often usde in relation to renal failure need some clarification: azotemia is the accumulation of nitrogenous waste within the blood, whereas uremia is a more advanced condition in which retention of nitrogenous products produces toxic symptoms. Azotemia is not life-threatening, whereas uremia is a serious condition that often involves other body systems.
Acute Renal Failure
ARF is an abrupt decline in glomerular and tubular function, resulting in the failure of the kidneys to excrete nitrogenous waste products and to maintain fluid and electrolyte homeostasis.
• Severe reduction in the glomerular filtration rate, an elevated blood urea nitrogen level, and decreased tubular reabsorption of sodium from the proximal tubule.
Manifestations APGN MCNS
Strep. antibody titers Elevated Normal
Blood pressure Elevated Normal or decreased
Edema Primarily periorbital and
Circulatory congestion Common Absent
Proteinuria Mild to moderate Massive
Hematuria Gross or microscopic Microscopic or none
Serum protein levels Minimal reduction Markedly decreased
Serum lipid levels Normal Elevated
Peak age at onset 5 – 7 2 – 3
• Increase concentration of sodium in the distal tubule which causes stimulation of the renin mechanism.
• The local action of angiotensin causes vasoconstriction of afferent arteriole which further reduces glomerular filtration and prevents urinary losses of sodium. There is a significant reduction in renal blood flow
ARF common clinical features
• circulatory congestion/ hypervolemia
• electrolytes abnormalities:
– K+ (Signs of hyperkalemia: ECG abnormalities, arrhythmia bradycardia, serum potassium level > 7mEq/L)
– Na+ (seizures)
• metabolic acidosis (tachypnea)
• oliguria: output < 1ml/kg/hr
• Anuria: no urinary output in 24 hours
• Nausea, Vomiting
Causes are classified into:
• Prerenal (hypoperfusion)
• Renal (intrinsic)
• Postrenal (obstructive)
Prerenal/ most common
• decreased perfusion without cellular injury
• renal tubular and glomerular functions are intact
• reversible if underlying cause is corrected
• common etiologies:
– hemodynamic factors that can compromise renal perfusion (CHF, shock)
• obstruction of urinary tract
• important to rule out quickly:
– potential for recovery of renal function is often inversely related to the duration of the obstruction
Intrinsic Renal Causes
• Classified according primary site of injury:
• recognize patients at risk (postoperative states, cardiac surgery, septic shock)
• prevent progression from prerenal to renal
• preserve renal perfusion
– isovolemia, cardiac output, normal blood pressure
– avoid nephrotoxins (aminoglycosides, NSAIDS)
• treat the underlying disease
• Management of the complications
• Provision of supportive therapy
• strictly monitor intake and output (weight, urine output, insensible losses, IVF)
• monitor serum electrolytes
• adjust medication dosages according to GFR
• provide adequate caloric intake
• limit protein intake to control increases in BUN
• minimize potassium and phosphorus intake
• limit fluid intake
If adequate caloric intake can not be achieved due to fluid limitations, some form of dialysis should be considered
• Vital signs
• Strict I & O, daily weights
• Fluid restriction
• Monitor electrolytes
• Minimize risk of infection
• Provide comfort and stability
Chronic Renal Failure
The kidneys are able to maintain the chemical composition of fluids within normal limits until more than 50% of functional renal capacity is destroyed by disease or injury. Chronic renal failure or insufficiency begins when the diseased kidneys can no longer maintain the normal chemical structure of body fluids under normal conditions. Progressive deterioration over months or years produces a variety of clinical and biochemical disturbances that eventually culminate in the clinical syndrome known as uremia.
The final stage of chronic renal failure, end-stage renal disease (ESRD), is irreversible. Treatment with dialysis or transplantation is required when the glomerular filtration rate decreases below 10% to 15% of normal.
– Retention of waste products
– Water and sodium retention
– Metabolic acidosis
– Calcium & phosphorus disturbances
– Growth disturbance
• Calcium and Vitamin D
Treatment of CRF
• Peritoneal Dialysis
• LRD – living related donor
• CAD – cadaver donor
• Watch for
– Swelling and tenderness over graft area
– Decreased urine output
– Elevated blood pressure