RENAL DISORDERS

URINARY TRACT INFECTION

Are bacterial infection of the kidneys, ureters, bladder and
urethra
Are common causes of hospital attendance worldwide
and are second most common bacterial infections.
Prevalence of UTI’S is about eight times higher in women
than in men. This is mainly because female urethra is
shorter and lies closer to the anal and vaginal orifice. At
least 1/3 of women develop UTI before the age of 24
years. The risk increases in pregnancy.
The risk in men is lower because of the length of their
urethra and the antibacterial properties of prostatic fluid
UTI’S are also common nosocomial infections (hospital
acquired) due to urinary instrumentation and
catheterization. Catheter associated urinary infections
account for about 40% of all nosocomial infection.
URINARY TRACT INFECTION: CLASSIFICATION

A) Classification based on location of UTI within the urinary

system.
1) Upper UTI
Are infections involving renal parenchyma, pelvis, and
ureters
Are less common and include:-
Pyelonephritis- inflammation of renal pelvis and renal
parenchyma
Renal abscesses
Urosepsis- UTI that has spread to the systemic
circulation and may be life threatening.
Ureteritis- inflammation of the ureters
Present with fever, chills and frank pain in addition
features of lower urinary tract infections. This is because
a patient may have simultaneous infection in both lower
and upper urinary tract.
URINARY TRACT INFECTION:
CLASSIFICATION
2) Lower UTI
Are infection involving bladder, urethra and prostate
gland
Are not usually accompanied by systemic feature such
as fever, chills and frank pain
Are the most common form of UTI
They include:-
Bacterial cystitis- inflammation of the urinary bladder
Bacterial prostitis – inflammation of the prostate
gland.
Bacterial urethritis – inflammation of the urethra
URINARY TRACT INFECTION: CLASSIFICATION
b) UTI can be classified as complicated or
uncomplicated
1.Complicated UTI’S are mainly hospital acquired
(nosocomial) or may occur in patients with co-existing
urologic abnormalities such as renal stones,
obstructions and recurrent infections; pregnancy;
immunosuppresion; and diabetes mellitus. The
individual with complicated UTI is at risk for
pyelonephritis, Urosepsis, and renal damage.
 
2. Uncomplicated UTI’S are those that occur in an
otherwise normal urinary tract and involve the lower
urinary tract. They are not usually recurrent and are
common in young girls.
URINARY TRACT INFECTION: CLASSIFICATION
c) UTI can be classified according to their natural history
(clinical course)
1. Initial/isolated infection
Refers to uncomplicated UTI in a person who has
never had an infection or has had a remote infection
separated by a period of years from the current one. 
2. Recurrent UTI
Recurrent UTI may be classified into;
Reinfection: recurrence caused by a second (new)
pathogen in a person who has experienced a previous
UTI that was successfully treated.
Relapses: Recurrence caused by the same strain of
bacteria from within the urinary tract and occurs
within 1-2 weeks of stopping antibiotic therapy.
URINARY TRACT INFECTION: CLASSIFICATION
3. Unresolved Bacteriuria
Refers to a type of relapse that occurs due to
inadequate treatment of the initial urinary tract
infection. This results in persistence bacteriuria.
This occurs as result of non-compliance to the
treatment, dug resistant infection, and inadequate
dosage.
URINARY TRACT INFECTION:
CAUSATIVE ORGANISMS
a) Gram negative bacteria namely Escherichia coli,
Enterococci, Klebsiella, Proteus, Enterobacter,
Pseudomonas, and Serratia.
NB: most common cause accounts for over 80% of
UTI’S
b) Gram positive bacteria namely Staphylococcus
c) Organisms that causes sexually transmitted infections
such as
Candida albicans
Chlamydia trachomatis
Trichomonas vaginalis
Neisseria gonorrhea
Herpes simplex
URINARY TRACT INFECTION:
RISK FACTORS

a) Factors increasing urinary stasis

1) Intrinsic obstruction secondary to other urinary tract
disorders such as ;
Urethra strictures
Tumors of urinary tract (bladder Tumors)
Renal stones
BPH (Benign Prostate Hyperplasia)
Contracture of bladder neck.
 2. Extrinsic obstruction due to condition outside the
urinary tract such as tumors, fibrosis.
3. Urinary retention including neurogenic bladder.
 URINARY TRACT INFECTION:
RISK FACTORS

b) Foreign bodies
Urinary tract calculi
Instrumentation of the urinary tract such as cystoscopy
Catheterization (Indwelling catheter, Ureteral stent,
Nephrostomy tube, intermittent catheterization) 
c) Factors compromising immune response
Decreased immune status (immunosuppresion) especially HIV
infection
Diabetes mellitus – compromises immune response and
increases the risk of neuropathy. Also the high glucose levels
provide a conducive environment for growth of microbes
Pregnancy-compromises immune response and hormonal
changes exposes the woman to UTI.
Aging due to lowered immunity
 URINARY TRACT INFECTION:
RISK FACTORS
d) Anatomical Factors
Shorter female urethra and colonization by normal vaginal.
Fistula exposing urinary tract to vaginal or lower GIT pathogens.
Obesity
Congenital abnormalities leading to obstruction or urinary stasis 
e) Other factors
Multiple sexual partners- predispose to STI and bacterial colonization
of the bladder
Poor personal hygiene especially in women
Use of spermicidal agents and diaphragms for contraception
Sexual intercourse especially in women
Hormonal changes in postmenopausal women
Synthetic underwear and irritants such as spray, sanitary pads, soaps
Female genital mutilation is associated with urinary retention, fibrosis
of urethral opening and recurrent UTI
URINARY TRACT INFECTION:
ROUTES OF INFECTION ENTRY

Transurethral route: the infection ascends

through the urethra
Hematogenous route: the infections from
the blood stream.
Lymphatic route: the infection from the
lymphatic system.
Direct extension: infection from the adjacent
structures especially through a fistula such
as vesicovaginal fistula etc
URINARY TRACT INFECTION:
PATHOPHYSIOLOGY
Urinary tract above the urethra is normally sterile.
Several mechanical and physiologic defense
mechanisms assist in maintaining sterility and
preventing urinary tract infection. These defense
mechanisms include:-
Uretero-vesical junction competence to prevent
backflow of urine
Peristaltic activity of the bladder that prevent stagnation
Normal voiding with complete emptying of bladder
(urine flow sweeps the bacteria in the urethra)
Anti-adherent effect produced by mucosal cell of the
bladder.
Antibacterial enzymes and antibodies such as urinary
immunoglobin.
URINARY TRACT INFECTION:
PATHOPHYSIOLOGY
Acidic PH of urine and high urea
concentration interfere with growth of
bacteria
Abundant glycoproteins that interfere with
the growth of bacteria.
Antibacterial effects of prostate fluid
Alteration in any of these defense
mechanisms increases the risk of urinary
tract infection by giving the bacteria a
chance to invade the urinary tract mainly
through the urethra for ascending infection
or through the blood stream or lymphatic
system
URINARY TRACT INFECTION:
PATHOPHYSIOLOGY
The bacteria attach to and colonize the epithelium of the
urinary tract. They avoid being washed out with voiding,
evade host defense mechanisms and initiate
inflammation. The inflammation produces localized
clinical features such as burning on urination.
In ascending infection, the infection progresses from
urethra to the bladder then to the upper urinary tract
through the urethra.
In severe infection, the bacteria gain access to the blood
circulation resulting in a life threatening sepsis (urosepsis)
.
If the infection is not cleared, complication such as renal
abscess, urosepsis, renal failure, epididymitis, arthritis,
periurethral gland infections and bacteremia may result.
 URINARY TRACT INFECTION: CLINICAL
FEATURES
a) Clinical feature of lower UTI
Dysuria- painful/difficult urination
Burning on urination
Urinary frequency – an abnormal frequent desire to
void; and often voids only small quantities. Usually> 8
times in 24 hours period.
Urinary urgency - sudden strong or intense desire to
void immediately usually accompanied by frequency.
Nocturia - waking at night to urinate for up to 2 to 3 or
more times.
Nocturia enuresis- loss of urine during sleep.
Urinary in continence - involuntary or unwanted loss or
leakage of urine
URINARY TRACT INFECTION: CLINICAL
FEATURES
Urinary retention / incomplete emptying- inability to
empty urine from the bladder
Post voiding dribbling - urine loss after completion of
voiding.
Hesitancy - difficult starting the urine stream resulting
in a delay between initiation of urination by relaxation
of the urethral sphincter and when urine stream actually
begins.
Suprapubic discomfort/pain/pressure.
Hematuria (blood in urine).
Cloudy foul smelling urine
Lower back pain
URINARY TRACT INFECTION: CLINICAL
FEATURES
b) Clinical features of upper UTI
Flank pain
Fever
Chills
General malaise
Nausea and vomiting
NB/upper UTI may or may not be accompanied by
features of lower UTI
URINARY TRACT INFECTION: DIAGNOSTIC
STUDIES

1) History and physical examination- Reveals

the clinical features.
2) Laboratory investigation
Urine for urinalysis
Urine for microscopy
Urine for culture and sensitivity
Full hemogram
High vaginal swab for microscopy culture
and sensitivity to rule out STI’S
URINARY TRACT INFECTION: DIAGNOSTIC
STUDIES

3) Imaging studies
Abdominal ultrasound
Abdominal CT scan
IV urogram to visualize urethra
IV pyelogram
Transrectal ultrasound in men

4) Cystoscopic examination
URINARY TRACT INFECTION:
MANAGEMENT
Patient are usually managed as outpatient unless in
presence of severe upper UTI or complications.
A) Medical management
Antibiotics such as Norfloxacin, Ciprofloxacin or
Lerofloxacin or Ofloxacin; or Septrin/ Cotrimoxazole
BD; or Nitrofuratoin for 7-14 days. Results of culture
and sensitivity guides in the choice of appropriate
antibiotic.
Antispasmodics to relieve bladder Irritability and pain e.
g. Buscopan
Analgesics such as paracetamol or NSAIDs to relief
pain and reduce inflammation.
Rx of underlying cause incase of urologic
URINARY TRACT INFECTION:
MANAGEMENT

Nursing management

DISCUSSION
URINARY TRACT INFECTION:
COMPLICATIONS

Renal abscesses
Arthritis
Epididymitis
Periureteral gland infection
Urosepsis / bacteremia
Renal failure
Urinary strictures
Urinary obstruction
Hydronephrosis
PYELONEPHRITIS
PYELONEPHRITIS

Pyelonephritis is bacterial infection of the renal pelvis,

renal tubules and interstitial tissue of one or both
kidneys.

CAUSES
Bacterial infection. This is the most common cause
and may be due to bacteria ascending from the lower
urinary tract or by bacteria from elsewhere in the body
through the bloodstream.
Fungi
Protozoa
viruses
PYELONEPHRITIS: TYPES
Pyelonephritis may be acute a chronic. Acute
pyelonephritis is sudden inflammation while
chronic pyelonephritis is persistent kidney
scarring and may lead to chronic renal failure.
Predisposing factors are same as for lower UTI
but the key are:-
Urinary obstructions such as stricture, BPH,
urinary stone.
vesicoureteral reflux
Urinary instrumentation such as insertion of
urinary catheter and cystoscopy.
PYELONEPHRITIS: PATHOPHYSIOLOGY
Infection gain entry to the kidneys through the urethra
from ascending infection or through the bloodstream. The
bacteria initiate inflammation response, starting in the
renal medulla and spreading to the adjacent cortex.
The inflammation is characterized by an increase in white
blood cell count around the renal tubules and edema/
swelling of the involved tissue hence enlargement of the
kidneys. The infection may progress causing abscesses in
the renal pelvis, atrophy and destruction of renal tubules
and glomeruli.
In chronic inflammation, scaring/fibrosis of the kidney
occurs and the kidney becomes contracted and non-
functional leading to chronic renal disease. Chronic
pyelonephritis is also referred to as interstitial nephritis
PYELONEPHRITIS: CLINICAL FEATURES

A) Features of acute pyelonephritis

Fairly high fever
Chills
Nausea and vomiting
Flank pain/back pain
Lethargy/ malaise
Headache
Costovertebral tenderness on the affected side.
NB/features of lower UTI may or may not be
present.
PYELONEPHRITIS: CLINICAL FEATURES

B) Clinical feature of chronic pyelonephritis.

Fatigue
Headache
Poor appetite
Polyuria
Excessive thirst
Weight loss
PYELONEPHRITIS: DIAGNOSTIC STUDIES
History and physical examination
Urine for urinalysis: shows pyuria, bacteriuria, hematuria and
WBCs casts. Urinalysis reveals azotemia, pyuria, acidosis, and
proteinuria
Blood and urine cultures
Complete blood count shows leukocytosis
Culture and sensitivity
Imaging studies
KUB
Ultrasound
CT Scan
IVP and CT scan to assess complications.
Renal function tests: Creatinine levels, and Blood urea and
nitrogen
PYELONEPHRITIS: MANAGEMENT
NB: Patient with mild infection is treated as an outpatient with
antibiotics for 14 to 21 days.
Admission is only necessary in severe infection
Admission for bed rest
IV fluids in addition to oral intake. Monitor intake and output
Ensure adequate fluid intake of 3-4 liters per day to dilute
urine, decrease burning and prevent dehydration.
Monitor vital signs 4 hourly. Also assess the general condition
of the patient. Follow-up laboratory test may be done in the
course of the management
Antibiotics to clear infection. The choice is guided by results
of culture and sensitivity.
IV antibiotics for 24-48hours then orals for 10-14 days. This
may be cotrimoxazole or nitrofurantion or quinolones or
ampiclox or third generation cephalosporin.
PYELONEPHRITIS: MANAGEMENT
Analgesics such as paracetamol/NSAIDS to relief pain
and reduce fever.
Local heat application to relief pain in the frank area with
a hot water bottle or heating pad.
Diet- balanced diet encourage oral fluid intake
Assist with ADL
Psychological care
Education:-
Personal hygiene
Adequate fluid intake (3-4 l)
Frequent voiding
Drug compliance
Regular follow up
Long term therapy to prevent recurrence with
cotrimoxazole or nitrofurantion.
PYELONEPHRITIS: COMPLICATIONS

Renal abscesses
Renal stones
Renal fibrosis/ scarring
Hypertension
Renal failure
GLOMERULONEPHRITIS
I) ACUTE GLOMERULONEPHRITIS

Glomerulonephritis is the inflammation of the

glomeruli, and may be acute or chronic.
Acute glomerulonephritis is an autoimmune
renal disorder that follows pneumococcal,
streptococcal and viral infections.
It affects both kidneys and is a leading cause of
acute renal failure.
The primary site of inflammation is the
glomeruli. However, the inflammatory process
also involves the renal tubules, renal interstitial
and renal blood vessels.
I) ACUTE GLOMERULONEPHRITIS

Occurs at any age but affects primarily early school

age children. The peak incidence is between 6-7
years of age
It is uncommon in children younger than 2 years of
age
More common in males than females.
Prognosis is good with over 95% achieving
complete recovery. However, a few cases may
progress to chronic glomerulonephritis or renal
failure.
I)ACUTE GLOMERULONEPHRITIS: CAUSES

Bacterial especially group A beta hemolytic

streptococci
Viral infections such as hepatitis B or C and
rubella.
Nephrotoxic agents such as drugs
Systemic lupus erythematosus (SLE).
Sickle cell disease
Polyarteritis nodosa.
Bacterial endocarditis
Prolonged bacteremia
ACUTE GLOMERULONEPHRITIS:
PATHOPHYSIOLOGY
Acute glomerulonephritis is an immune complex disease
that is characterized by an accumulation of antigen,
antibody and complement in the glomeruli, which result
in tissue injury.
Normally, antibodies are formed following an infection or
presence of foreign antigens in the circulation. In this
case, the antigens may be within the glomerular
basement membrane (GBM) or may be circulating non-
glomerular antigens such as viruses, bacteria, drugs etc.
The antibodies react with these antigens forming
antibody-antigen complexes. These complexes circulate
in the blood and some are trapped or deposited in the
glomerular, which activates the complement.
ACUTE GLOMERULONEPHRITIS:
PATHOPHYSIOLOGY
Activation of complement initiates an inflammatory
process.
The inflammation causes swelling, increased capillary
permeability, exudate formation and mobilization of
leukocytes.
This causes congestion of the glomerular and reduces its
ability to form filtrate.
Since the capillary lumens are occluded by edema, there is
reduced renal blood flow renal blood flow.
The reduced renal blood flow coupled with decreased
filtration rate result in excessive accumulation of water and
sodium in the body.
The end result is glomerular injury with subsequent clinical
PATHOPHYSIOLOGY
ACUTE GLOMERULONEPHRITIS: CLINICAL
FEATURES

Generalized features headache, lethargy, irritability,

nausea, anorexia and vomiting
Oliguria – reduced urine output.
Puffiness of the face especially, around the eyes
(periorbital edema). The edema is more prominent in the
morning.
Peripheral edema involving the extremities, sacral area
and the abdomen.
Hematuria –the urine is cloudy/smoky brown/dark
colored/cola colored.
Urinalysis reveals proteinuria, RBCs, WBCs, and Casts
Elevated BUN and serum creatinine levels.
ACUTE GLOMERULONEPHRITIS: CLINICAL
FEATURES

Elevated BUN and serum creatinine levels.

Dysuria – pain on urination
Abdominal discomfort(dull bilateral frank pain)
High blood pressure: Systolic- 120-180mmHg and
Diastolic- 80-120mmHg
NB: The clinical features vary among patients and
at times the patient is asymptomatic and only
diagnosed following routine urinalysis.
ACUTE GLOMERULONEPHRITIS: CLINICAL
COURSE AND PROGNOSIS
The acute edematous phase of glomerulonephritis usually
persists from 4-10 days. In some cases it may persist for
2-3 weeks.
During this period the patient is sick looking, anorexic and
lethargic. This phase is followed by a period of dramatic
improvement and complete recovered within 1 to 2 years.
The first signs of improvement are increase in urine output
and decrease in body weight. There may be copious
diuresis for the first 1-2 days. The blood pressure decrease
to normal and Hematuria diminishes.
The blood urea nitrogen and proteinuria decreases but
may persist for several weeks. Most patients recover
completely in 2 years. However, precautions should be
ACUTE GLOMERULONEPHRITIS: DIAGNOSTIC
STUDIES

History and physical evaluation which gives clues on the causative

factor and reveals the clinical features
Laboratory studies
Urinalysis which shows Hematuria, proteinuria and increased specific
gravity. There are sediments of RBCs, WBCs and epithelial cells
Urine culture – negative.
Blood urea nitrogen (BUN)- elevated
Serum creatine – elevated.
Throat culture for streptococci.
Serologic test to identify presence of antibodies to several known
antigens (e.g.) antistreptolysin O, hepatitis B antigen,
Erythrocyte sedimentation rate (ESR) -elevated
Renal biopsy to confirm presence of the disease.
 ACUTE GLOMERULONEPHRITIS:
MANAGEMENT
a) Medical management is mainly supportive and focuses on
symptomatic relief, and include;
Bed rest in acute phase
Fluid restriction (usually insensible loss + volume of excreted urine)
Corticosteroids to reduce inflammation and formation of antibody
Diuretics such as lasix (20-160mg/24hrs) or Aldactone (25-200mg
/24hrs): To promote diuresis (i.e.) increase urine output hence reduce
edema
Antibiotics to clear existing infection and prevent development of new
infection
Antihypertensive to treat severe hypertension.
Dietary restriction: low sodium, low protein, low potassium diet, and
high carbohydrate
 ACUTE GLOMERULONEPHRITIS:
MANAGEMENT

b) Nursing management
Bed rest during acute phase
Observations
-vital signs especially blood pressure 4 hourly
-Assess for edema distended neck veins and tachycardia
which indicate fluid are load
-General condition
Maintain strict input and output. Observe the colour of
urine
Daily weight monitoring to assess fluid loss
-Measure weight same time each day.
 ACUTE GLOMERULONEPHRITIS:
MANAGEMENT; NURSING CARE
Fluid restriction- the calculation is done as follows (
insensible loss and urine output for the past 24 hours)
-Ice chips to minimize thirst in a fluid restricted patient
-Frequent mouth care to reduce thirst.
-Serve fluid in a small cup
Drugs
-Proper administration observing the five right
-Assess for signs of side effects
Diet
-Low sodium potassium and protein
-High caloric diet
ACUTE GLOMERULONEPHRITIS:
MANAGEMENT; NURSING CARE

Infection prevention- observe aseptic technique,

hand washing and protect the patient from
individuals with bacterial infections etc
Activity
-As patient improves, allows gradual ambulation
-Balance activity with adequate period of rest
Assist with activity of daily living
Hygiene to include bathing with mild soap and skin
care, apply jelly, assess skin integrity, and assist/
encourage with oral care.
ACUTE GLOMERULONEPHRITIS:
MANAGEMENT; NURSING CARE

Elimination
-Measure the urine output hence provide patient with
a urine or bedpan and a measuring jug involve
parents in the urine collection and measuring
-Monitor bowel movements
Psychological care
Health education and discharge: Condition,
Medications, Diet, Activity, Infection prevention,
Monitoring input/output, Signs of complications,
Follow-up care.
ACUTE GLOMERULONEPHRITIS:
COMPLICATIONS

Chronic glomerulonephritis
Acute cardiac failure
Acute renal failure
Hypertensive encephalopathy
II) CHRONIC GLOMERULONEPHRITIS
Is a syndrome that reflects end stage of
glomerular inflammatory disease.
The syndrome is characterized by proteinuria,
Hematuria, and slow development of uremia as a
result of decreasing renal function.
The clinical course may take as many as 30 years.
Commonly diagnosed coincidentally during a
routine urinalysis. Diagnosis may be confirmed
through a renal biopsy, renal ultrasound or CT scan.
Management is usually supportive and
symptomatic similar to that of chronic renal failure.
NEPHROTIC SYNDROME
NEPHROTIC SYNDROME

Is a renal disorder characterized by massive

proteinuria, hypoalbuminea, hyperlipidemia
and edema as a result of glomerular injury
Common in ages between 1-8 years, hence
mainly a disease of preschool child.
In adults, the disease is associated with
systemic disease such as diabetes mellitus,
systemic lupus erythematosus.
NEPHROTIC SYNDROME: CAUSES

Idiopathic- there is no known cause in approximately 80%

of the cases.
Acute/chronic glomerulonephritis
Systemic diseases (Disseminated systemic lupus
erythematosus, Amyloidosis, Diabetes mellitus)
Drug toxicity (Penicillamine, NSAIDS, Captopril, Heroin)
Allergens (Venom/ sting, Anaphylactoid purpura)
Infections: Viral Infections (HIV/AIDS, hepatitis); Bacterial
infections (streptococcal, syphilis); Protozoal infections
(malaria)
Malignancies (Hodgkin’s disease; leukemias; and solid
tumors of lungs, colon, stomach, breast)
NEPHROTIC SYNDROME: PATHOPHYSIOLOGY

The actual process that triggers glomerular damage in

nephrotic syndrome is not clearly understood. However,
following renal glomerular damage, the membrane
becomes permeable to proteins especially albumin.
The protein is lost in urine hence hyperalbuminuria. This
reduce serum albumin hence hypoalbuminemia and
consequently reduced osmotic pressure of the blood.
As a result fluid from the vascular is pulled into the
surrounding tissues and accumulates in the interstitial
abdominal cavity hence ascites and edema.
The shift of fluid from the plasma to the interstitial space
reduce the vascular fluid volume hence hypovolemia.
NEPHROTIC SYNDROME: PATHPOPHYSIOLOGY

Hypovolemia stimulates renin-angiotensin system

and the secretion of anti-diuretic hormone and
aldosterone.
This causes reabsorption of water and sodium from
the renal tubules in order to increase intravascular
volume but may cause fluid overload if not
reversed.
Hypoalbuminemia triggers synthesis of blood
proteins and lipids by the liver and this causes
hyperlipidemia.
NEPHROTIC SYNDROME: CLINICAL FEATURES

Edema of lower extremities, abdomen, scrotum and the

face. This causes;
Puffiness of the face especial around the eyes and is
worse in the morning.
Progressive weight gain over a period of days or weeks.
Skin breakdown due to edema
Blood pressure is normal or slightly decreased
Proteinuria (4-30g/day protein loss)
Oliguria decreased urine output
Anorexia and diarrhea due to intestinal congestion and
poor intestinal absorption
Dark and frothy urine but no Hematuria
NEPHROTIC SYNDROME: DIAGNOSTIC
STUDIES
History and physical examination – reveals the clinical
features.
Laboratory studies
Urinalysis – reveals proteinuria, high urine specific
gravity.
Serum protein – reveals hypoalbuminemia and
hyperlipidemia
Serum sodium- high.
Blood cell count- normal a slightly elevated due to
blood concentration.
24 hours urine specimen.
NEPHROTIC SYNDROME: MANAGEMENT

a) Medical management
Bed rest
Antibiotic prophylaxis or to treat existing infections
Plasma volume expanders such as albumin, plasma
and dextran to raise osmotic pressure.
Low sodium, low potassium, high protein, and high
caloric diet.
Corticosteroids- prednisone 2mg/kg body weight.
Diuretics- Laxis (furosemide).
Dietary supplements such as ferrous and
multivitamins
NEPHROTIC SYNDROME: MANAGEMENT
Bed rest in acute phase.
Observations. These include assessing general conditions,
changes in edema, signs of infection, vital signs 4 hourly
and report any deviation from normal.
Strict accurate input and output monitoring.
Daily weight monitoring with the same weighing machine
and at the same time of the day. The patient should be
wearing the same clothing.
Fluid restriction during massive edema. Serve fluid with
small cups. Provide ice chips and mouth care to relief
thirst.
Drugs administration as prescribe and closely monitor the
side effects.
NEPHROTIC SYNDROME: MANAGEMENT
Infection prevention interventions to include avoiding
contact with infected individual, observing medical
asepsis such as good hand washing etc.
Hygiene with special attention to skin care. Observe skin
for breakage, change position frequently, avoid dragging
while handling the patient and apply jelly.
Elimination: monitor amount and characteristics of urine.
Also monitor bowel movements.
Psychological care: Renal conditions are usually
associated with poor prognosis and high levels of anxiety.
Hence support the patient psychologically form the
diagnosis through the treatment period.
Health education on the condition to include signs of
NEPHROTIC SYNDROME:
COMPLICATIONS

Infections due to altered immune responses

Hypercoagulability with thromboembolism
especially pulmonary emboli.
Skeletal abnormalities due to altered calcium
metabolism.
OBSTRUCTIVE UROPATHIES
OBSTRUCTIVE UROPATHIES
Urinary obstruction refers to any anatomic and functional
condition that blocks or impedes the flow of urine. It may
be acquired or congenital. An obstruction produces
damaging effects on the urinary system especially to the
organs above the level of obstruction. The damaging
effects may be in form of;
Changes in the bladder dextrusor muscle, hence interfering with
functions of the bladder.
Ureteral dilatation and kinking
Vesicoureteral reflux (backflow of urine from the bladder to the
ureters)
Hydroureter: dilatation of the renal pelvis
Hydronephrosis: dilation of the renal pelvis and calyces.
Chronic pyelonephritis
OBSTRUCTIVE UROPATHIES

The severity of these effects depends on;

The location of obstruction
Duration of obstruction
Amount of pressure exerted
Presence of urinary stasis
Presence if infection
OBSTRUCTIVE UROPATHIES

Location and causes of the obstruction

Ureters: Ureteral obstruction may be caused
by renal stones, tumors, clot, inflammation
and pregnancy
Bladder: obstruction at the level of the
bladder may be caused by calculi, tumors
and neurogenic bladder.
Urethra: urethra obstruction may occur due
to tumors, prostate gland hyperplasia,
prostate cancer
OBSTRUCTIVE UROPATHIES

Clinical features
The features depend on the damaging
effect of the obstruction and may include;
Altered urine output such as oliguria and
anuria
Features of urinary tract infection (refer)
Features of urinary retention (suprapubic
pain, burning pain, flank pain)
Altered renal function (elevated BUN and
OBSTRUCTIVE UROPATHIES

Management
Identification and treatment of the
underlying cause and may involve;
Insertion of a urethral or Ureteral tube
Diversion of urine above the level of
blockage
Surgical intervention
1) URINARY TRACT CALCULI
(NEPHROLITHIASIS)

This refers to formation of stones in the urinary

system.
It’s associated with UTI and is more common in
men than women.
The majority of patients are between 20 and 55
years of age.
The incidence of stone formation is more common
in whites than in blacks. Recurrence of stones can
occur in up to 50% of patients.
I) URINARY TRACT CALCULI:
PREDISPOSING FACTORS

Metabolic abnormalities that result in increased

urine levels of calcium, oxaluric acid, uric acid, or
citric acid.
Obstruction with urinary stasis and bacterial urinary
tract infection
Long term indwelling catheter and other external
urinary diversion
Neurogenic bladder or urinary retention
Warm climates that cause increase fluid loss, low
urine volume, and increased solute concentration in
the urine
I) URINARY TRACT CALCULI:
PREDISPOSING FACTORS

Dietary factors: high intake of proteins that

increases uric acid excretion; large intake of
calcium and oxalate; low fluid intake that increases
urinary concentration and excessive amount of tea
or fruit juices that elevate urinary oxalate level.
Genetic factors: family history of stone formation,
cystinuria, gout, or renal acidosis.
Lifestyle factors: immobility and sedentary
occupation.
I) URINARY TRACT CALCULI:
PATHOPHYSIOLOGY

The actual process of renal stone formation is not clear,

and so many theories have been advanced in an attempt
to explain the pathophysiology. These include;
Crystals in supersaturated urine may precipitate and
form a stone.
Mucoprotein formed in the kidneys may form stones.
Urinary pH, solute load, and inhibitors in the urine affect
formation of stones. The higher the pH, the higher the
risk for calcium and phosphate stones. The lower the pH
the, the higher the risk for uric acid and cystine stones.
I) URINARY TRACT CALCULI: TYPES OF
RENAL STONES

There are five major categories of renal stones;

Calcium phosphate.
Calcium oxalate.
Uric acid.
Cystine.
Struvite (magnesium ammonium phosphate).
I) URINARY TRACT CALCULI: CLINICAL
FEATURES

The features are due to urinary obstruction and include;

Severe abdominal or lateral flank pain, which may cause
shock
Hematuria
Renal colic: Due to increased peristalsis in the ureters in
response to the passage of small stones along the
ureters.
Nausea and vomiting
Fever and chills in case of urinary infection
I) URINARY TRACT CALCULI: DIAGNOSTIC
STUDIES

Health history focusing on previous stone formation,

medications, dietary supplements and family history of
urinary calculi.
Physical examination which confirms clinical features
Laboratory studies:
Urinalysis: assess urine pH and presence of infections
24 hour urinary measurement of calcium, phosphorous,
magnesium, sodium, oxalate, citrate, sulfate, potassium,
uric acid, and total volume.
Blood for Serum calcium, phosphorous, sodium,
potassium, bicarbonate, uric acid, BUN, and creatinine
levels.
I) URINARY TRACT CALCULI: DIAGNOSTIC
STUDIES

Renal Ultrasound: identifies radiopaque stones in

the renal pelvis, calyx, or proximal ureters.
Radiological studies:
IVP: reveals the site of obstruction and confirm
presence of stones
Retrograde pyelogram: reveals the site of
obstruction
CT scan: used to differentiate the stone from a
tumor.
Cystoscopy
 I) URINARY TRACT CALCULI: MANAGEMENT

Medical management
Management of the underlying cause in order to prevent
further development of stones. This involves detailed
assessment of the predisposing factors.
Opiods to relief renal colic pain
Antibiotics and acetohydroxamic acid to treat infections in
case of Struvite stones.
Drugs to minimize urinary stone formation.
Insertion of Ureteral stent to prevent obstruction of the
ureters by the large stones
Adequate hydration to achieve dilution of the urine; at least
3 litres per day to produce urine output of 2 litres per day.
I) URINARY TRACT CALCULI: MEDICAL
MANAGEMENT
Low sodium diet. This is because high sodium intake increases
calcium excretion in the urine.
Dietary interventions especially reduction in the intake of foods with
high purine, calcium and oxalate. These include organ meat, milk and
milk products, beans, fish, dried fruits, nuts, chocolate and cocoa, and
vegetables such as spinach, cabbage, parley, celery, asparagus and
beets
Surgical removal of the urinary stones and the indications are;
Stones too large for spontaneous passage
Stones associated with infection
Stones causing renal impairment
Stones causing persistent pain, nausea, or ileus.
Stones that cannot be treated medically
I) URINARY TRACT CALCULI: SURGICAL
PROCEDURES
Surgical removal may be achieved through endourologic,
lithotripsy or open surgical stone removal.
Endourologic procedures: involves use of endoscopes to
remove small stones. This may be Cystoscope to remove
stones in the bladder and ureteroscopes to remove stones
in the ureters. Complications of endoscopic procedures
include hemorrhage, retained stone fragments, and
infection.
Lithotripsy: involves use of a device called Lithotrite (stone
crusher) to break large stones. The small stones are then
removed using bladder irrigation or are removed by use of
endoscopes. Complications of lithotripsy include
hematuria and secondary obstruction by the fine stone
I) URINARY TRACT CALCULI: SURGICAL
PROCEDURES

Open surgical procedures: the type of open surgery

done depends on the location of the stone as follows;
Nephrolithotomy involves removal of stones from the
kidneys.
Pyelolithotomy is removal of stones from the renal
pelvis.
Ureterolithotomy involves removal of stones form the
ureters.
Cystotomy to remove stones from the bladder.
Hemorrhage is the most common complication of open
surgical procedures.
 I) URINARY TRACT CALCULI:
b) Nursing management
Adequate fluid intake
Observations
Drug administration: antibiotics and analgesics
Dietary intervention
Elimination: all the urine should be emptied into another
container and strain to retrieve any stone passed
spontaneously.
Encourage ambulation to facilitate movement of the
stones from upper to lower urinary tract.
Psychological support
2) URINARY STRICTURES

Urinary stricture is a narrowing of the lumen of the

ureters or urethra. It may be congenital or acquired.
Strictures may occur in the bladder neck, urethra, or
ureters.

CAUSES
a) Causes of urethral strictures
Trauma form accidents
Gonorrheal infections
Urethral instrumentation
II) URINARY STRICTURES

b) Causes of bladder neck strictures

Congenital
Chronic prostitis in men
Chronic cystitis in women
 
c) Causes of Ureteral strictures
Severe/chronic Ureteritis
Radiation therapy
Retroperitoneal abscess secondary to inflammatory
bowel disease and perforation
II) URINARY STRICTURES: MANAGEMENT

Urinary catheter for temporary or permanent

relief of Ureteral or urethral strictures.
Endoscopic dilatation
Surgical correction of the stricture.
3) BENIGN PROSTATE HYPERPLASIA

BPH is a benign enlargement of the prostate

gland characterized by hyperplasia (increase in
the number of epithelial cells) of the glandular
tissue.
It occurs in about 50% of men over 50 years of
age and 75% of the men over 70 years of age.
It commonly develops in the inner part of the
prostate gland.
It does not predispose to development of cancer
of the prostate.
Prostate gland
It is a Walnut-shaped rudimentary gland that lies
posterior to the urinary bladder
It surrounds the urethra
It is the genital organ most commonly affected by
benign and malignant neoplasms
The prostate from age 0 to puberty weighs 0gms.
Its growth is stimulated by testosterone
Age 15- 10gms
Age 20 – 20gms
FUNCTIONS OF THE PROSTATE GLAND
1. Ejaculation process.
The prostate plays a very important role in the
ejaculation process.
At every ejaculation session 2mls of semen is
emitted
During orgasm, prostate muscles contract and
propel ejaculate out of the penis
The following are three stages in
ejaculation;
1st part comes from the prostate which
is alkaline
2nd portion comes from the seminal
vesicles which contains fructose
3rd part comes from the testis, which
contains the gonad
Control of urine
The internal sphincter which is involuntary and the
external sphincter is voluntary
External sphincter gets support from the prostate
gland
Residual volume of urine in male about 20 mls
In female residual urine is 0
 III) BENIGN PROSTATE HYPERPLASIA:
CLINICAL FEATURES
The onset of the symptoms is gradual and the symptoms
are only noticed by the patient once the prostate
enlargement starts causing obstructive symptoms.
a) Obstructive symptoms:
Weak stream of urine
Hesitancy in initiating voiding
Dribbling at the end of urination
A feeling of incomplete emptying because of urinary
retention
Straining to pass urine
Prolonged micturition
b) Irritative symptoms:
Nocturia 3-4-5 times
Urgency of passing urine
Dysuria- residual urine which could be infected
Haematuria – bleeding of the large veins
Acute urinary retention- very large prostate

Indications for prostatectomy

Severe symptoms
Cancer prostate
III) BENIGN PROSTATE HYPERPLASIA:
DIAGNOSIS

Health history and physical examination- reveals the

clinical features
Digital Rectal examination (DRE):palpation to assess the
enlargement of the prostate gland
Urinalysis to assess presence of infection and specific
gravity
Blood urea nitrogen (BUN) and serum creatinine to
assess renal involvement.
Cystourethroscopy to evaluate bladder neck obstruction.
Post voiding catheterization to determine the extent of
the obstruction
Normal BPH

Normal bladder, normal Bladder hypertrophy, urine

prostate gland obstruction
III) BPH MANAGEMENT

1. SURGERY
Open prostatectomy
TURP- Trans Urethral Prostatectomy
TURP
A three way catheter is used
i- to push in fluid to wash out clots
ii- to drain out the waste
iii- for ballooning
POSTOPERATIVE MANAGEMENT

Close monitoring of vital signs especially BP

Irrigation washout must flow continuously
Observe for haemorrage in the washed out fluid
Antibiotics, analgesics
Irrigation may be stopped day 2-4 post op
depending on patient
COMPLICATIONS POSTOPERATIVELY

Immediate
Hemorrhage
Blocking of catheters
Injury to the associate structures e.g. rectum, gut
Fluid overload in TURP
Late complications
Incontinence of urine
Impotence due to nerve injury
Erectile dysfunction
Retro grade ejaculation
URINARY TRACT CANCERS
A) KIDNEY CANCER

Kidney cancers arise from the cortex or pelvis (and

calyces) and may be benign or malignant.
However malignant tumors are more frequent and
renal cell carcinoma (adenocarcinoma) is the most
common type.
Adenocarcinoma occurs twice as often in men as
in women.
Usually discovered in persons 50 to 70 years of age.
A) KIDNEY CANCER: PREDISPOSING
FACTORS

No known cause. The predisposing factors are;

Cigarette smoking
Genetic /familial factor. There is increased
incidence has also been seen in the first degree
relatives.
Obesity
Hypertension
Exposure to asbestos, gasoline, and Cadmium
Cystic kidney disease associated with end-stage
renal disease.
A) KIDNEY CANCER: CLINICAL FEATURES
Clinical features appear in the late stages. Kidney
tumors cause symptoms by compressing,
stretching or invading structures near or within the
kidney. The features include:-
Hematuria
Flank pain
Palpable mass in the frank or abdomen
Hypertension
Anemia
Weight loss
Fever
A) KIDNEY CANCER: DIAGNOSTIC
STUDIES

Health history
Physical examination
Laboratory tests: urinalysis, blood tests such as
BUN and creatinine.
Renal ultrasound
IVP with nephrotomography
CT scan and MRI
Radionuclide isotope scanning is use to detect
metastases
A) KIDNEY CANCER: STAGING

Stage 1: Cancer limited to renal capsule

Stage 2: Cancer spread to perirenal fat but confined
within the fascia. It includes metastases
to adrenal gland
Stage 3: Regional lymph node involvement. It also
involves renal vein and vena cava
Formation of tumor thrombus may be present in the
renal vein or vena cava
Stage 4: Presence of distant metastases especially
liver, lungs and bones.
A) KIDNEY CANCER: MANAGEMENT

A) Medical/surgical management
1. Radical nephrectomy for stages I, II and some
cases of stage III. This surgical procedure involves
removal of the kidney, adrenal gland, surrounding
fascia, part of the ureters, and draining lymph
nodes. Indications of nephrectomy are;
Renal tumor
Polycystic kidneys that are bleeding or severely
infected
Massive traumatic injury
Elective removal of kidney from a donor
A) KIDNEY CANCER: MANAGEMENT

2. Radiation therapy: For palliative management of

advanced disease (stage IV).
3. Chemotherapy is used to treat metastatic disease
(Stage IV)
4. Biologic therapy (interferons and interleukins) are
used in the treatment of metastatic disease
5. Supportive care to relief the symptoms of various
treatments
A) KIDNEY CANCER: MANAGEMENT

B) Nursing care
1. Nursing preoperative care
Admit
Observations (vital sign and general condition)
Fluid therapy: observe any fluid restriction and
maintain strict input and output.
Baseline investigations such as;
Serum electrolytes
BUN
Urinalysis
A) KIDNEY CANCER: PREOPERATIVE NURSING
CARE
Nutrition diet: ensure a high vitamin, caloric diet. Restrict sodium,
potassium and protein. Ensure adequate
Fasting- ensure the patient fast for about 6 to 8 hours before the
operation to prevent intraoperative complications.
Patient education and obtaining an informed consent. This is a
collaborative intervention that involves the surgeon, anesthetist and
the nurse. The information given include:-
The type of surgical procedure and its indication.
Flank incision will be made on the affected side.
Patient will be placed in hyper extended side lying position. This may
cause muscle aches after surgical
Psychological care to allay fear and anxiety
Immediate preoperative care using the checklist as per the hospital
procedures.
A) KIDNEY CANCER: MANAGEMENT
2. Post operative nursing care
Patient reception
Receive the patient from theatre.
Ensure the patient is conscious and that all the vital
signs are within the normal range.
Position the patient on the lateral position away from
the incision site.
Respiration
Monitor breathing pattern (rate & rhythm)
Ensure adequate ventilation
Adequate medication to relief pain and allow patient to
 A) KIDNEY CANCER: MANAGEMENT

Observations:
Monitor vital signs ½ hourly and reduce the frequent as the patient
improves to four hourly.
Monitor signs of hemorrhage such as hypotension, restlessness,
lethargy etc.
Monitor signs of infection generally and at the incision site
Report promptly to the doctor in case of anything unusual
Daily weighing of PT to rule out edema using same scale and wearing
similar clothing.
Fluid therapy:
Ensure the patient receives the intravenous fluids as prescribed.
Maintain asepsis in the care of the venipuncture site
Maintain nil per oral until the bowel sounds are present
 A) KIDNEY CANCER: MANAGEMENT
Pain management:
Administer prescribed analgesics
Instruct patient to use relaxation techniques
Report in case of severe pain
Drainage and indwelling catheter care:
The patient comes for theater with a closed drainage
system to drain the operation and reduce tension at the
incision site.
Observe asepsis in the care of the drainage system and
record the drainage in 24 hour. It’s usually removed in 24 to
72 hours depending on the amount of drainage.
Observe aseptic technique in the care of the indwelling
catheter to prevent introducing the infection. The catheter
 A) KIDNEY CANCER: MANAGEMENT

Nutrition:
The patient is on nil per oral until the bowel sounds are
present. Then the patient is started on a fluid diet and
gradually progresses to normal diet.
High fiber diet to avoid constipation
Encourage adequate oral fluid intake and discontinue IV
fluids
Drug administration
Administer prescribed antibiotics and analgesics.
Usually the patient is on injectables for 24-48 hours due
to nil per oral and is put on oral treatment once the bowel
sounds are present.
A) KIDNEY CANCER: MANAGEMENT

Ambulation and exercises

Early & frequent ambulation assists in maintaining
adequate respiration function. This also promotes
urinary function.
Ambulation should be initiated after 24 hours
Personal hygiene
Assist patient with maintenance of personal
hygiene and encourage them to take part in their
own care gradually upon improvement.
 A) KIDNEY CANCER: MANAGEMENT
Elimination
Monitor urine output at least every to 2 hours monitor
colour and consistency of urine
Record drainage from various catheter
Do not clamp or irrigate the catheter an less indicated
Daily weighing of PT to rule out edema using same scale
and wearing similar clothing.
Monitor bowel movements and measures to prevent
constipation.
Observe for signs of complications
Since it’s an abdominal surgery, abdominal distention is
present to some degree due to manipulation & compress of
bowel during surgery. Restrict oral intake until bowel sound
 A) KIDNEY CANCER: MANAGEMENT
Psychological support
The patient usually mourns for the loss of a vital organ. Encourage the
patient to express their concerns and respond accurately. Reassure the
patient that one kidney can effectively perform the renal functions
adequately.
Patient education and discharge
Avoid activities that increase intrabdominal pressure such as straining
on defecation, heavy lifting, sex etc for a minimum of 6 weeks.
Signs of complications that may require immediate medical attention.
Diet to promote healing and prevent constipation.
Prevention of UTI and nephrotoxins now that the patient has only one
functional kidney
Adequate fluid intake
Need for follow up and possible subsequent chemotherapy.
B) BLADDER CANCER

Most bladder tumors are papillomatous

growths within the bladder (benign)
The most common type is transitional cell
carcinoma (malignant)
Cancer of bladder is most common between
the ages of 60 and 70 years
It is three times common in men than in
women
Must bladder tumor are superficial and do
not involve bladder wall
B) BLADDER CANCER: RISK FACTORS

Cigarette smoking
Exposure to dyes used in rubber and cable
industries
Chronic abuse of phenacetin-containing analgesics
Previous chemotherapy
Previous radiotherapy especially in the treatment of
cervical cancer
Chronic lower UTIs
Prolonged use of indwelling catheter
B) BLADDER CANCER
CLINICAL FEATURES
Painless hematuria. This may be intermittent or chronic
Bladder irritability features namely dysuria, frequency and urgency
DIAGNOSTIC STUDIES
Health history
Physical examination
Urine tests
Urine for cytology to determine presence of neoplastic cells
Urine test to assess specific factor associated with bladder cancer
such as tumor antigens.
Renal ultrasound
IVP
CT scan and MRI
B) BLADDER CANCER: MANAGEMENT

1. SURGICAL MANAGEMENT
Surgical treatment the surgical procedures include:-
Transurethral resection of the bladder tumor
(electrocautery) the bladder mass is excised by
means of a bladder inserted through the
cystoscope. The remaining parts of the tumor are
cauterized.
Laser photo coagulation
Bloodless destruction of tumor cells other
advantages are minimal risk of perforation and
lack of need of a urinary catheter
B) BLADDER CANCER: SURGICAL
MANAGEMENT

Open loop resection if fulguration

Used for control bleeding for large superficial tumor
and
Cystectomy (segmental partial or radical )
This is done in case of large tumors.
Radical cystectomy involves removal of bladder,
prostate and seminal vesicles in men or removal
bladder uterus, cervix, urethra ovaries in women.
Partial cystectomy include resection of the portion
of bladder wall containing the tumor along the a
margin of normal tissue
B) BLADDER CANCER: MANAGEMENT
2. Radiotherapy
May follow cystectomy or may be used for palliative
purpose in the inoperable cancer
3. Chemotherapy
Chemotherapy may either be intravesical or systemic.
Chemotherapy may be used preoperatively or before
radiotherapy or treat distant metastases. Intravesical
chemotherapy involved instillation of chemotherapeutic
agents directly into the bladder.via urethral catheter and
retained for about 2 hours. It’s administered weekly for 6
to 12 weeks. The patient’s bladder must be empty prior to
installation. The patients position may be changed every
15 minutes for maximum contact in all areas of the
bladder
B) BLADDER CANCER: MANAGEMENT

4. Intravesical immunotherapy
Bacilli calmeter Guerin vaccine (BCG) or interferon
BCG stimulate immune system to act on the tumor
cell may be used alone or combined the interferon
NB: Nursing responsibility in intravesical radiotherapy,
chemotherapy and intravesical immunotherapy
include;
Increasing fluid intake
Advice on quiting smoking
Assessing and treating UTI
Routine urologic follow-up
B) BLADDER CANCER: MANAGEMENT
Postoperative (bladder surgical procedure)
Adequate fluid intake daily for the first one week
Avoid alcoholic beverage
Self monitor the urine output usually pink during the first
several days and clears up gradually. No bright red or
blood clots should be observed by the 10th day the urine
may be dark or rust-coloured due to scabs from the
healing tumor resection sites.
Opiod analgesic for 24-48 hrs
Stool softeness to avoid straining an defecation
B) BLADDER CANCER: MANAGEMENT

Sitzs bath 2-3 times a day for 15-20 minutes

this promote muscle relaxation and reduce
risk of urinary retention
Psychological care
Pt education
Regular follow up and need for follow up
cystoscopies every 3-6 months for 3 years
and at least yearly. Thereafter renal and
Ureteral surgery.
C) WILM’S TUMOR

Renal tumor of infants and children

About 40% are inherited as an autosomal dominant
gene
Clinical features
Abdominal swelling /distant
Pain
Fever
Hematuria
Hypertension
C) WILM’S TUMOR

Diagnosis
Health history and physical assessment
Laboratory tests (urinalysis and blood tests)
Renal ultrasound
Renal arteriography

Management
Surgical – removal of the affected kidney
Radiotherapy- used as primary RX or postoperative
Chemotherapy
RENAL FAILURE
RENAL FAILURE

Renal failure is partial or complete impairment of

kidney function resulting in an inability to excrete
metabolic waste products and water.
This causes functional disturbances of all body
systems.
Renal failure can be acute or chronic
I) ACUTE RENAL FAILURE (ARF)

ARF is a clinical syndrome characterized by rapid

loss of renal function with progressive azotemia.
Azotemia is an accumulation of nitrogenous
wastes products such as nitrogen, urea, and
creatinine in the blood. ARF has a rapid onset. It
may develop over hours or days with progressive
elevation of BUN, creatinine and potassium with or
without oliguria. It’s potentially reversible but also
associated with high mortality of about 50%.
Most commonly ARF follows severe prolonged
hypotension/hypovolemia or exposure to
nephrotoxic agents.
I) ACUTE RENAL FAILURE (ARF)
A) Pre-renal causes ( accounts for 60-70% of ARF)
These are factors external to the kidneys that reduce renal
blood flow and lead to decreased glomerular perfusion
and filtration. The pre-renal causes are;
Hypovolemia secondary to dehydration, hemorrhage,
excessive dieresis, hypoalbuminemia, burns and GIT
loses (diarrhea and vomiting)
Decreased cardiac output secondary to cardiogenic
shock, heart failure, myocardial infarction and cardiac
arrhythmias.
I) ACUTE RENAL FAILURE (ARF)

Decreased peripheral vascular resistance

secondary to anaphylaxis, neurologic injury and
septic shock.
Vascular obstruction secondary to embolism,
hepatorenal syndrome, renal artery syndrome and
bilateral renal vein thrombosis

NB; DISCUSS THE PATHOPHYSIOLOY

I) ACUTE RENAL FAILURE (ARF)

B) Intrarenal causes (account for 20-30% 0f all causes of ARF)

These are conditions that cause direct damage to the renal tissue
(parenchyma) hence causing impaired renal function. The
Intrarenal causes are;
Prolonged prerenal causes.
Primary renal diseases namely acute glomerulonephritis, acute
pyelonephritis
Nephrotoxic injury secondary to;
Drugs such as aminoglycosides, amphotericin B
Radiographic contract agents
Hemolytic blood transfusion reaction- hemoglobin blocks the renal
tubules.
Severe crush injury- necrotic muscle cells release myoglobin which
block the renal tubules
I) ACUTE RENAL FAILURE (ARF)
INTRARENAL CAUSES CONT;
Toxemia in pregnancy (eclampsia)
Malignant hypertension
Systemic lupus erythematosus
Interstitial nephritis as a result of;
Allergy to antibiotics, NSAIDS and ACE inhibitors.
Infection which may be bacterial, viral or fungal

NB; DISCUSS PATHOPHYSIOLOGY

I) ACUTE RENAL FAILURE (ARF)

C) Post renal causes (account for less than 5% of all

ARF)
Post renal causes involve mechanical obstruction
of urinary outflow, which results in urine reflux into
the renal pelvis and subsequent renal failure. These
causes are almost treatable and azotemia can be
reversed if the underlying cause is treated before
kidney damage occurs. They include;
Prostate cancer
Benign prostatic hyperplasia
Calculi
Trauma
I) CLINICAL COURSE OFACUTE RENAL
FAILURE (ARF)

Clinically, ARF progress through 4 phases;

Initiating phase
Oliguric phase
Diuretic phase
Recovery phase

NB: In some cases, recovery does not occur and

consequently ARF progresses to chronic renal
failure with eventual dialysis or renal transplant
I) CLINICAL COURSE OF ACUTE RENAL
FAILURE (ARF)
1. Initiating phase
Begins at the time of insult and continues until the
sign and symptoms become apparent. This phase
can last for hours to days.
2. Oliguric phase
The key feature in this phase is oliguria, which
occurs within 1-7 days of the causative event. The
phase lasts for few days to several weeks or
several months, with an average duration of 10-14
days.
The longer the oliguric phase, the poorer the
prognosis for complete recovery of renal function.
I) ACUTE RENAL FAILURE (ARF): OLIGURIC
PHASE
Other features of oliguric phase include fluid and
electrolytes abnormalities and uremia as follows;
i. Urinary changes
Urinary output decreases to less than 400ml per 24 hours.
Bloody urine
Urinalysis shows casts, RBCs, WBCs, a specific gravity
fixed at 1.010, and urine osmolality at 300mmol/Kg. this
is the same specific gravity and osmolality of the plasma,
reflecting tubular damage with loss of kidney’s ability to
concentrate urine.
Proteinuria if renal failure is related to glomerular
membrane dysfunction.
I) ACUTE RENAL FAILURE (ARF): OLIGURIC
PHASE

ii) Fluid volume excess (fluid retention)

Distended neck veins
Bounding pulse
Edema
Hypertension
May complicate to congestive cardiac failure,
pulmonary edema, an pericardial and pleural
effusion.
I) ACUTE RENAL FAILURE (ARF): OLIGURIC
PHASE

iii) Metabolic acidosis

Kidneys cannot synthesize ammonia, which is
needed for hydrogen ion excretion.
Kidneys cannot excrete acidic products of
metabolism.
The serum bicarbonate level decreases because
bicarbonate is used up in buffering hydrogen ions.
Defective reabsorption and regeneration of
bicarbonate occurs.
Kussmaul breathing (deep, rapid respirations) to
increase excretion of carbondioxide.
I) ACUTE RENAL FAILURE (ARF): OLIGURIC
PHASE

iv) Sodium balance

Increased excretion of sodium by the damaged tubules
Uncontrolled Hyponatremia (low serum sodium)
v. Potassium excess (hyperkalemia)
Hyperkalemia (elevated serum potassium) due to
inability of the damage kidneys to excrete potassium.
Hyperkalemia worsens in presence of massive tissue
injury and blood transfusion because the damaged cells
release more potassium into the extracellular fluid.
Acidosis worsens Hyperkalemia because as hydrogen
ions enter the cells, potassium is driven out of the cells
I) ACUTE RENAL FAILURE (ARF): OLIGURIC
PHASE

vi) Hematologic disorders

Anemia because renal failure impairs erythropoietin
production
Thrombocytopenia hence bleeding tendencies due
to impaired platelet production
Luekopenia due to altered WBC production hence
immunodeficiency. The patient is therefore
susceptible to infections, which is one of the major
cause of death in patients with ARF.
I) ACUTE RENAL FAILURE (ARF): OLIGURIC
PHASE

vii) Calcium deficit and phosphate excess

Hypocalcaemia due to decreased absorption of
calcium in the GIT. Absorption of Calcium requires
activated vitamin D.
Activation of vitamin D is done by the kidneys.
Low calcium levels stimulates secretion of parathyroid
hormone by the parathyroid gland.
The hormone causes release of calcium from the
bones, a process that is accompanied by release of
phosphate hence hyperphosphatemia.
Hyperphosphatemia is worsened by decreased
I) ACUTE RENAL FAILURE (ARF): OLIGURIC
PHASE

viii. Waste product accumulation

Elevated BUN
Elevated creatinine 
ix. Neurologic changes
Occurs due to accumulation of nitrogenous waste
products in the brain and other nervous tissue. The
features include fatigue, memory impairment,
impaired concentration, lethargy, stupor and coma
 
I) ACUTE RENAL FAILURE (ARF):
3) Diuretic phase
Begins with a gradual increase in daily urine output of
1-3 L/day, but may reach 3-5 L/day and may last for 1-3
weeks.
The increased urine output is caused by the osmotic
diuresis from high urea concentration in the glomerular
filtrate and the inability of the tubules to concentrate
the urine.
In this phase the kidneys’ have resumed their ability to
excrete waste but not concentrate urine
Therefore hypotension, hypovolemia and electrolytes
imbalances may follow the massive fluid loss. The
I) ACUTE RENAL FAILURE (ARF):

DIURETIC PHASE CONT;

However, the BUN and Creatinine levels are
elevated and uremic signs and symptoms are still
persistent.
By the end of the phase, the patient’s acid-base,
electrolytes and wastes product values begin to
normalize.
4) Recovery phase
Begins when the GFR increases, with gradual
decrease in BUN and Creatinine levels. Major
improvements occur in the first 1-2 weeks. However,