Notes on urinary disorders 1

Management of Clients
with Urinary Disorders
Mrs. Babitha K Devu, Asst. Professor, SMVDCoN

Introduction
Mrs. Babitha K Devu, Asst. Professor2
 Diseases of the kidney and urinary tract
are ‘silent killers’. Acute renal disorders
develops suddenly and nearly all can be
diagnosed easily and cured; only a few of
them leave permanent damage. Chronic
renal diseases have a slow progression
and in the early stages the signs and
symptoms are few.
 Chronic renal diseases can lead to end-
stage renal disease leading to renal failure.

Infectious And Inflammatory
Disorders of Urinary System
Urinary Tract Infection
Urethral Diverticula
Renal Tuberculosis

URINARY TRACT INFECTION
 Urinary tract infections (UTIs) are
the most common bacterial infection in
women. A urinary tract infection (UTI) is an
infection in any part of your urinary system
— your kidneys, ureters, bladder and
urethra. Most infections involve the lower
urinary tract — the bladder and the
urethra.
4 Mrs. Babitha K Devu, Asst. Professor

Definitions:
A urinary tract infection (UTI) is an infection
that affects any part of the urinary tract —
kidneys, ureters, bladder and urethra.
Symptomatic presence of microorganisms
within the urinary tract i.e., kidney, ureters,
bladder and urethra. Associated with
inflammation of urinary tract.
Cystitis, the most common type of UTI, is an
inflammation of the bladder wall.

Definitions:
Acute Pyelonephritis is an inflammation of
the renal parenchyma and collecting
system (including the renal pelvis).
Chronic Pyelonephritis is the result of
recurring infections involving the upper
urinary tract. In this the kidneys become
small, atrophic, and shrunken and lose
function due to fibrosis.
Urethritis is an inflammation of the urethra.

Epidemiology
 Seen in all age groups
 Infants up to 6 months – 2/1000
 Women – at greater risk than men (FM-8:M-
1); prevalence 40-50% in women and 0.04%
in men.
 5 - 10% women have recurrent UTI in their
life
 10 million new cases of lower UTI / year
(India)
 1 million hospitalizations / year
 Incidence of UTI increases in old age; 10%
of men and 20% of women are infected.

Classification:
 Based on location/site
 Based on complications
 Based on symptoms

Classification:
 Based on location/site
Upper UTI:
Acute pyleonephritis
Chronic pyleonephriitis
Interstitial pyleonephritis
Renal abscess
Perirenal abscess
Lower UTI:
Cystitis
Prostatitis
Urethritis

Classification:
 Based on complications
Both upper & lower UTI are further divided into
complicated and uncomplicated.
 Uncomplicated UTIs occurs without
underlying renal or neurologic disease. It
occur in an normal urinary tract and usually
involve only the bladder.
Complicated UTIs include those infections with
coexisting obstruction, stones, or catheters;
diabetes or neurologic diseases; or
pregnancy-induced changes.

Classification:
 Symptomatic presence of micro organisms
within the urinary tract. Significant
bacteriuria is the presence of at least 105
bacteria/ml of urine.
 Asymptomatic bacteriuria : bacteriuria with
no symptoms.

Classification:
 Recurrent : > 3 symptomatic UTIs within 12
months following clinical therapy.
 Reinfection: recurrent UTI caused by a
different pathogen at any time
 Relapse: recurrent UTI caused by same
species causing original UTI within 2 wks
after therapy.

Etiology:
Acute uncomplicated UTI:
 Escherichia coli – cause about 80% of
UTI
 20% of UTI caused by- Gram negative
enteric bacteria – Enterococcus,
Klebsiella, Proteus
 Gram positive cocci – Streptococcus
faecalis, Staphylococcus saprophyticus,
 S.saprophyticus – restricted to infections
in young sexually active women.

Etiology:
Complicated UTI:
 Pseudomonas aeruginosa,
Enterobacter & Serratia
 Isolated in hospital acquired infections and
catheter associated UTI.
 Viruses - Rubella, Mumps and HIV
 Fungi - Candida, Histoplasma capsulatum
 Protozoa - T. vaginalis, S. haematobium

Risk Factors:
Factors Increasing Urinary Stasis:-
 Intrinsic & extrinsic obstruction
 Urinary retention
 Renal impairment
Foreign Bodies:-
 Urinary tract calculi
 Catheters
 Urinary instrumentation

Risk Factors:
Anatomic Factors:-
 Congenital defects
 Fistula
 Shorter female urethra
 Obesity
Factors compromising Immune
response:-
 Aging
 HIV infection
 Diabetes Mellitus

Risk Factors:
Functional Disorders:-
 Constipation
 Voiding dysfunction
Other factors:-
 Pregnancy
 Hypoestrogenic state
 Multiple sex partner (women)
 Use of various contraceptive devices
 Poor personal hygiene
 Habitual delay of urination (nurse’s bladder,
teachers bladder)

Pathophysiology:
The urinary tract above the urethra is normally
sterile. Several mechanical and physiologic
defense mechanisms assists in maintaining
sterility and preventing UTIs. An alteration in
any of these defense mechanisms increases
the risk for a UTI.
 4 routes of bacterial entry to urinary tract.
1) Ascending infection
2) Blood borne spread
3) Lymphatogenous spread
4) Direct extension from other organs

Pathophysiology:
1) Ascending infection
Most common route. Organisms ascend through
urethra into bladder.
Organisms Colonize in perineal
and periurethral areas
Due to the etiological/risk factors
Entry of organisms into U.system
Ascend to urethra, bladder, &
kidneys leads to UTIs

Pathophysiology:
2) Blood borne spread/Hematogenous
spread:
 This route is rare, where blood - borne
bacteria secondarily invade the kidneys,
ureters, or bladder due to bacteraemia
from elsewhere in the body mostly S.
aureus.

Pathophysiology:
2) Blood borne
spread/Hematogen
ous spread:

Pathophysiology:
3) Lymphatogenous spread
 Men- through rectal and colonic lymphatic
vessels to prostrate and bladder.
 Women- through periuterine lymphatic to
urinary tract.

Pathophysiology:
4) Direct extension from other organs
 Pelvic inflammatory diseases
 Genito-urinary tract fistulas

Clinical Manifestations:
Lower urinary tract symptoms (LUTS) are
experienced in patients who have UTIs
of the upper urinary tract, as well as
those confined to the lower tract.
Symptoms are related to either bladder
storage or bladder emptying.

 Emptying symptoms:
Hesitancy
Intermittency
Post void dribbling
Urinary retention or incomplete emptying
Dysuria
Urine contain grossly visible blood or
sediment, giving it a cloudy appearance

 Storage symptoms:
Urinary frequency
Urgency
Incontience
Nocturia
Flank pain
Chills
Fever
Fatigue
Anorexia

27
Part affected Signs and symptoms
Kidneys (acute pyelonephritis)  Upper back and side (flank) pain
 High fever & chills
 Nausea & Vomiting
Bladder (cystitis)  Pelvic pressure
 Lower abdomen discomfort
 Frequent, painful urination
 Blood in urine
Urethra (urethritis)  Burning with urination
 Discharge

Diagnostic Studies:
 Physical Exam:
 CVA tenderness (pyelonephritis)
 Urethral discharge (urethritis)
 Tender prostate on DRE (prostatitis)
 Labs: Urinalysis
 + leukocyte esterase (indicating pyuria)
 + nitrites
 More likely gram-negative rods
 + WBCs
 + RBCs
 Positive Urine Culture = >105 CFU/mL

Diagnostic Studies:
 Labs: Urinalysis
Normal Findings Abnormal findings
•pH - 4.6 – 8.0 •pH – Alkaline (
increases)
• Appearance- clear • Appearance – cloudy
Color – pale to amber
yellow
• Color - deep amber
• Odor – aromatic • Odor – foul smelling
• Blood – none •Blood – maybe present
• Leukocyte esterase –
none
•Leukocyte esterase -
present
• WBC- absent •WBC- present
• Bacteria- absent •Bacteria- present

Diagnostic Studies:
 Imaging studies:
 IVP
 CT scan
 Renal ultrasound
 Using a scope to see inside your bladder:
Cystoscopy

Management/Collaborative Therapy:
 Symptomatic UTI- antibiotic therapy
 Asymptomatic UTI- no treatment required
except in special situations.
 Non- specific therapy:
• More water intake (6-8 oz glasses/day).
• Maintaining acidity of urine by fluids like
canberry juice and ascorbic acid.
• Sitz baths.

 Anti-microbial therapy
• Goals of therapy:
Elimination of infection
Relief of acute symptoms
Prevention of recurrence and long term
complications
• Ideal antibiotic for UTI :
Adequate coverage over E.coli
Concentration in urine
Duration of therapy
Low resistance & Cost
Low adverse effect profile

 Principles of anti microbial therapy
• Levels of antibiotic in urine but not in blood
• Blood levels of antibiotic – important in
pyleonephritis
• Penicillins and cephalosporins – drugs of
choice for UTI with renal failure.

 Treatment Duration
• Single dose therapy
• 3 day course
• 7 day course
• 10 – 14 day course
Uncomplicated cystitis can be treated by a
short-term course of antibiotics, typically for 1
to 3 days. In contrast, complicated UTIs
require longer – term treatment, lasting 7 to 14
days or longer.

 Uncomplicated UTI
Antibiotics
Trimethoprim/Sulfamethoxazole (TMP/SMX)
Trimethoprim alone in patients with sulfa allergy
Nitrofurantoin
Fosfomycin
Ampicillin
Amoxicillin
Cephalosporins
Patient Teaching
Adequate fluid intake

 Uncomplicated UTI
Urinary analgesic
Oral phenazopyridine – to relieve discomfort
caused by dysuria. It is an azodye excreted I
urine, where it exerts a topical analgesic effect
on the urinary tract mucosa.
Dietary and hygienic management

 Recurrent, Complicated UTI
Repeated urinalysis
Urine culture and sensitivity testing
Imaging study
Antibiotics:
Trimethoprim/Sulfamethoxazole (TMP/SMX)
Sensitivity – guided antibiotic therapy:
amoxicillin, ampicillin and cephalosporin

 Recurrent, Complicated UTI
Fluoroquinolones includes ciprofloxacin,
levofloxacin, norfloxacin, ofloxacin etc.
Consider 3 to 6 months trial of suppressive or
prophylactic antibiotic regimen who have
repeated UTIs.
Consider postcoital antibiotic prophylaxis
In patients with UTIs secondary to fungi,
amhotericin or fluconazole is preferred.
Try to get rid of foley if possible!

Complications of a UTI :
 Recurrent infections, especially in women who
experience two or more UTIs in a six-month period
or four or more within a year.
 Permanent kidney damage from an acute or chronic
kidney infection (pyelonephritis) due to an untreated
UTI.
 Increased risk in pregnant women of delivering low
birth weight or premature infants.
 Urethral narrowing (stricture) in men from recurrent
urethritis, previously seen with gonococcal
urethritis.
 Sepsis, a potentially life-threatening complication of
an infection, especially if the infection works its way
up your urinary tract to your kidneys.

Conclusion:
Urinary tract infections are the 2nd most common
bacterial infections. Women are the most infected
subjects in the population. Development of
resistance to antibiotics by the bacteria result in
problems during the treatment and lead to relapse
or recurrence. Recent advances such as
development of immunologicals like intranasal
vaccines may result in life time cure of the
infection in future.

URETHRAL DIVERTICULA
 Definition:
Urethral diverticula are localized outpouchings of the
urethra. Most often they result from enlargement of
obstructed periurethral glands.
Urethral diverticulum is defined as a localized
outpouching of the urethra into the anterior vaginal
wall.
 Incidence:
In women > than men. Rare cases reported in men.
 Causes:
Urethral trauma from childbearing
Urethral instrumentation
Urethral dilation
Infection with gonococcal organisms

 Pathophysiology:
Tubuloalveolar mucous glands, known as
periurethral glands, line the urethral wall. They
are located posterolaterally in the mid and distal
third of the urethra. Most periurethral glands
drain into the distal urethra.
Urethral diverticula commonly occur in the distal
third of the urethra.

When periurethral glands
become infected, they may
become obstructed.
Repeated infections lead to increasing
obstruction of the gland and result in
periurethral gland enlargement into a
suburethral cyst or an abscess cavity.
Eventually, the cavity ruptures into the
urethral lumen, creating a
communication between the urethral
lumen and the suburethral cyst.
Repeated pooling of urine into the
suburethral cyst during urination
leads to the formation of a urethral
diverticulum.

 Pathophysiology:
Pathologically, the diverticulum is a urethral
evagination that consists of mostly fibrous
tissue. Often, an epithelial lining is absent.
The chronic inflammation within the
diverticulum results in marked fibrosis and
adherence of the diverticular wall to the
neighbouring structures.
However, a severely infected urethral
diverticulum may result in spontaneous
erosion into the vagina.

 Symptoms:
 Dysuria
 Postvoid dribbling 3 D’s
 Dyspareunia
 Frequent urination (more often than every 2 hours)
 Urgency
 Suprapubic discomfort or pressure
 Feeling of incomplete bladder emptying
 Urinary incontinence
 But many women have no symptoms
 Hematuria or sediment
 Anterior vaginal wall mass on assessment, when
palapted, mass is tender and expresses purulent
discharge through the urethra.

 Diagnostic Study:
 Voiding cystourethrography (VCUG)
 USG
 MRI
 Surgical Management: Surgical correction of urethral
diverticula is indicated in patients with significant
symptoms, including recurrent urinary tract infections,
severe pain, dyspareunia, frequency, urgency, and
postvoid dribbling.
 Additional indications for surgery include urethral calculi,
urinary retention, and carcinoma.
 Transurethral incision of the diverticular neck
 Marsupialization – creation of a permanent opening of
the diverticular sac into the vagina often referred to as
a Spence procedure.
 Surgical excision
 Complication of surgery is stress urinary incontinence.

 Marsupialization

 Surgical Management:
 Surgical excision: Surgical excision is the treatment of
choice but it should be performed with caution. The
diverticular sac may be quite attached to the adjacent
urethral lumen and careless removal of the sac may
result in a large urethral defect requiring construction
of a new urethra.
 Other important considerations during surgery include
identification and closure of the diverticular neck
(connection to the urethral lumen), complete removal
of the mucosal lining of the diverticular sac to prevent
recurrence, and a multiple layered closure to prevent
postoperative urethrovaginal fistula formation
(formation of an abnormal opening between the
urethra and vagina).

Renal Tuberculosis
 Renal Tuberculosis is rarely a primary lesion. It is
usually secondary to TB of the lung. In a small
percentage of patients with pulmonary TB, the
tubercle bacilli reach the kidneys via the blood
stream.
 Onset occurs 5 to 8 years after the primary lung
infection.
 When the kidney is primarily infected, the patient is
often asymptomatic. Sometimes may have fatigue
and low grade fever. As the lesions ulcerate, and
infection descends to the bladder and other
genitourinary organs symptoms of UTI appears first.
 Tubercular skin test will be positive but have to
confirm with tubercle bacilli in the urine.
 Patient require nursing and collaborative

Immunologic Disorders of
Kidney
Glomerulonephritis
Nephrotic Syndromes

GLOMERULONEPHRITIS (Bright's Disease)
 Immunologic
processes involving
the urinary tract
predominantly
affect the renal
glomerulus. The
disease process
result in
glomerulonephritis,
which affects both
kidneys equally.

 Glomerulonephritis (GN) is inflammation of the
glomeruli, which are structures in your kidneys
that are made up of tiny blood vessels. These
knots of vessels help filter your blood and
remove excess fluids. If your glomeruli are
damaged, your kidneys will stop working
properly, and you can go into kidney failure.
 Sometimes called nephritis, GN is a serious
illness that can be life-threatening and requires
immediate treatment. GN can be both acute, or
sudden, and chronic, or long-term. This condition
used to be known as Bright's disease.

 Types of glomerulonephritis:
Acute glomerulonephritis - begins
suddenly.
With this type, symptoms come on
suddenly and may be temporary or
reversible.
Eg: Acute poststreptococcal
glomerulonephritis
Chronic glomerulonephritis - develops
gradually over several years. It is slowly
progressive generally leading to

 What are the causes of GN?
The causes of GN depend on whether it’s acute
or chronic.
Acute GN can be a response to an infection such as strep
throat or an abscessed tooth. It may be due to problems
with your immune system overreacting to the infection.
Certain illnesses are known to trigger acute GN, including:
Infections
Post streptococcal throat infection or impetigo
Infective endocarditis
Viral infections like HIV and Hepatitis B & C

Immune Diseases
Systemic Lupus Erythematosus (SLE)
Scleroderma
Goodpasture syndrome
IgA nephropathy
Vasculitis
Polyarteritis
Wegener’s granulomatosis

Conditions causing scarring of Glomeruli
Diabetic Nephropathy
Hypertension
Focal segmental glomerulosclerosis
Other causes
Amyloidosis
Illegal drug use

The chronic form of GN can develop over several
years with no or very few symptoms.
 Chronic GN doesn’t always have a clear cause. A
genetic disease can sometimes cause chronic GN.
Hereditary nephritis (Alport syndrome) occurs in
young men with poor vision and poor hearing. Other
possible causes include:
 certain immune diseases
 a history of cancer
 exposure to some hydrocarbon solvents
 As well, having the acute form of GN may make you more
likely to develop chronic GN later on.

 Pathology

 Pathology
 Glomerulonephritis are triggered by immune mediated
injury.
• The cellular immune response contributes to the
infiltration of glomeruli by circulating mononuclear
inflammatory cells (lymphocytes and macrophages)
and crescent formation in the absence of antibody
deposition.
• The humoral immune response leads to immune
deposit formation and complement activation in
glomeruli.
• Antibodies can be deposited within the glomerulus
when circulating antibodies react with intrinsic or
with extrinsic antigens that have been trapped
within the glomerulus.

 Pathology
• Injury usually occurs as a consequence of the
activation and release of a variety of
inflammatory mediators.
• Haemodynamic, and toxic stresses can also
induce glomerular injury.
• A few glomerular diseases are due to hereditary
defects resulting in deformity of the glomerular
basement membrane

 What are the symptoms of GN?

• Kidney pain normally happens in the
“flank” region, which is just below the
bottom of rib cage.

• Cola-colored or diluted, iced tea- colored urine from
red blood cells in your urine (hematuria)
• Foamy/bubbly urine due to excess protein
(proteinuria)
• Urinating less often in acute GN & frequent nighttime
urination in chronic GN

 What are the symptoms of
GN?
• High blood pressure
(hypertension)
• Fluid retention (edema) with
swelling evident in your face,
hands, feet and abdomen
• Fatigue/SOB from anemia or
kidney failure.
• Extra fluid in your lungs,
causing coughing

 How is GN diagnosed?
Urinalysis test: Blood and protein in urine are
important markers for the disease.
More urine testing may be necessary to check for
important signs of kidney health, including:
 creatinine clearance
 total protein in the urine
 urine concentration
 urine specific gravity
 urine red blood cells
 urine osmolality

Blood tests may show:
 anemia, which is a low level of red blood
cells
 abnormal albumin levels
 abnormal blood urea nitrogen
 high creatinine levels

Immunology testing to check for:
 antiglomerular basement membrane
antibodies
 antineutrophil cytoplasmic antibodies
 antinuclear antibodies
 complement levels
Results of this testing may show your
immune system is damaging your kidneys.

 A biopsy of your kidneys may be necessary to
confirm the diagnosis. This involves analyzing a
small sample of kidney tissue taken by a needle.
 To learn more about your condition, you may also
have imaging tests such as the following:
 CT scan
 kidney ultrasound
 chest X-ray
 intravenous pyelogram

 What treatments are available for GN?
Treatment options depend on the type of GN
you’re experiencing, the severity of disease
and its cause.
 Control high blood pressure, especially if
that’s the underlying cause of the GN.
 Angiotensin-converting enzyme inhibitors,
or ACE inhibitors, such as:
captopril
lisinopril (Zestril)
perindopril (Aceon)

 Control high blood pressure, especially if
that’s the underlying cause of the GN.
 Your doctor may also prescribe angiotensin
receptor blockers, or ARBs, such as:
losartan (Cozaar)
irbesartan (Avapro)
valsartan (Diovan)

 Immunosuppression
 Corticosteroids like prednisolone
 Cytotoxic agents like cyclophoshamide,
azathioprine may also be used if your immune
system is attacking your kidneys. They reduce
the immune response.
 Plasmapheresis. This process removes the
fluid part of your blood, called plasma, and
replaces it with intravenous fluids or donated
plasma that contains no antibodies.
 Antibiotics in case of APSGN, only if infection
persist.

 Symptomatic management
 Diuretics
 Statins for treating high cholesterol levels
 Treating flu like symptoms if present
Dietary Management
 reduce the amount of protein, salt, and
potassium in your diet. Additionally, you must
watch how much liquid you drink. Calcium
supplements may be recommended.

 If your condition becomes advanced and
you develop kidney failure, you may need
to have dialysis. In this procedure, a
machine filters your blood. Eventually, you
may need a kidney transplant

 What are the complications associated with GN?
 GN can lead to nephrotic syndrome, which causes you to
lose large amounts of protein in your urine. This can end in
ESRD.
 The following conditions can also occur due to GN:
 acute kidney failure
 chronic kidney disease
 electrolyte imbalances, such as high levels of sodium or
potassium
 chronic urinary tract infections
 congestive heart failure due to retained fluid or fluid overload
 pulmonary edema due to retained fluid or fluid overload
 high blood pressure
 malignant hypertension, which is rapidly increasing high
blood pressure

The following are positive steps to recover from
GN and prevent future episodes:
•Maintain a healthy weight.
•Restrict salt in your diet.
•Restrict protein in your diet.
•Restrict potassium in your diet.
•Quit smoking.

 Definition:
Nephrotic syndrome results when the
glomerulus is excessively permeable to plasma
protein, causing proteinuria that leads to low
plasma albumin and tissue edema.
Nephrotic syndrome refers to a set of clinical
manifestations that includes hematuria and at
least one of the following:
 Oliguria (< 400ml/24 hour)
 HTN
 Increased BUN or decreased GFR
NEPHROTIC SNDROME

 Definition:
Nephrotic syndrome is a collection of
symptoms that indicate kidney damage.
Nephrotic syndrome includes the following:
 Albuminuria—large amounts of protein in the
urine (> 3.5 g/day)
 hyperlipidemia—higher than normal fat and
cholesterol levels in the blood
 edema, or swelling, usually in the legs, feet, or
ankles and less often in the hands or face
 hypoalbuminia—low levels of albumin in the
blood
NEPHROTIC SNDROME

NEPHROTIC SNDROME
 Incidence
 People of all ages, genders and
ethnicities can get nephrotic syndrome,
but is slightly more common in men than
in women. In children, it happens most
often between the ages of 2 and 6.

NEPHROTIC SNDROME
 Causes
 Primary Glomerular
Disease
 Various types of GN
like inherited,
membranous, focal
 Primary Nephrotic
syndrome
 External causes
 SLE, DM,
Amyloidosis, Bacterial,
Viral, Protozoal
 Causes
 Neoplasms
 Hodgkin’s lymphoma
 Solid tumors of
lungs, colon, breast
 Leukemia's
 Allergens
 Bee sting, Pollen
 Drugs
 Penicillamine
 NSAIDs
 Captopril
 Heroin

NEPHROTIC SNDROME

NEPHROTIC SNDROME
 Pathophysiology
 Albumin is a protein that acts like a sponge,
drawing extra fluid from the body into the
bloodstream where it remains until removed by
the kidneys. When albumin leaks into the urine,
the blood loses its capacity to absorb extra fluid
from the body, causing edema.
 Nephrotic syndrome results from a problem
with the kidneys’ filters, called glomeruli.
Glomeruli are tiny blood vessels in the kidneys
that remove wastes and excess fluids from the
blood and send them to the bladder as urine.

NEPHROTIC SNDROME
 Pathophysiology
 As blood passes through healthy kidneys, the
glomeruli filter out the waste products and
allow the blood to retain cells and proteins the
body needs. However, proteins from the blood,
such as albumin, can leak into the urine when
the glomeruli are damaged. In nephrotic
syndrome, damaged glomeruli allow 3 grams
or more of protein to leak into the urine when
measured over a 24-hour period, which is more
than 20 times the amount that healthy
glomeruli allow.

NEPHROTIC SNDROME
 Pathophysiology
 Abnormal permeability of the GBM results in
proteinuria. This cause hypoalbuminemia
which alters oncotic pressure in the vascular
tree
 Fluid shift into the interstitial spaces, causing
edema
 Stimulates plasma renin activity and augments
aldosterone production
 Retention of sodium, water by kidney leading to

NEPHROTIC SNDROME
 Pathophysiology
 Due to hypoalbuminia & diminished plasma oncotic
pressure
 Stimulates hepatic lipoprotein synthesis
 Hyperlipidemia
Immune responses, both humoral & cellular, are
altered. As a result, infection is a primary cause of
morbidity and mortality.
Calcium and skeletal abnormalities due to blunt
calcium responses.
Hypercoagulability results from the urinary loss of
anticoagulant proteins.

NEPHROTIC SNDROME
 Signs and Symptoms
 In addition to albuminuria, hyperlipidemia,
edema, and hypoalbumina, people with nephrotic
syndrome may experience
 Weight gain
 Fatigue
 Foamy/bubbly urine
 Loss of appetite
 Due to edema skin assumes waxy pallor
 Malaise
 Abnormal or absent menses
 Hypertension

NEPHROTIC SNDROME
 Laboratory Findings
 Urine Test
 Presence of albumin and blood
 Dipstick test
 Creatinine clearance test
 Specific gravity & osmolality
 Blood test
 Serum albumin, total serum protein, serum
cholesterol, Triglycerides
 Check for systemic diseases
 Kidney biopsy

NEPHROTIC SNDROME
 COMPLICATIONS
 Blood clots/thromboembolism
 Increased risk of infections include pneumonia, a
lung infection; cellulites, a skin infection;
peritonitis, an abdominal infection; and
meningitis, a brain and spine infection.
 Hypothyroidism
 Anemia
 Coronary artery disease
 High blood pressure
 Acute kidney injury—sudden and temporary loss
of kidney function

NEPHROTIC SNDROME
 Management
 Aims:
 Heal the leaking GBM
 Stop the loss of protein in client’s urine
 Break the cycle of edema
 Interventions include:-
 Fluid & electrolyte balance
 inflammation
 Prevent thrombosis
 Minimizing protein loss

NEPHROTIC SNDROME
 Management
 Maintain Fluid & Electrolyte balance
 Monitor the fluid balance via weights, girth
measurements, I/O charts
 Loop diuretics
 Plasma volume expanders such as albumin,
plasma and dextran
 Restrict potassium and sodium
 Skin care – good hygiene, massage, position
change & special mattresses

NEPHROTIC SNDROME
 Management
 Reduce inflammation & thrombosis
 Steroid therapy
 Cytotoxic drugs
 Anticoagulants
 Antiplatelets
 Minimize protein loss
 Protein intake of 1 to 1.5g/kg/day with more
than 35 kcal/kg/day to prevent protein
breakdown.
 Dietary salt restrictions

Notes on urinary disorders 1

More Related Content

What's hot (20)

Similar to Notes on urinary disorders 1 (20)

More from Babitha Devu (20)

Recently uploaded (20)

Notes on urinary disorders 1