The urinary system is responsible for the regulation of
blood volume & pressure, concentration of solutes in the blood,
extracellular fluid pH, red blood cell & Vitamin D synthesis, and most
especially waste excretion. These major functions are mostly performed by the
kidneys. These are bean-shaped organs, each about the size of tightly clenched
fists, composed of millions of nephrons. These nephrons are considered to be
the functioning unit of the kidney. Each nephron consists of a renal corpuscle,
a proximal tubule, a loop of Henle, and a distal tubule. The renal corpuscle of
a nephron consists of a Bowman’s capsule and the glomerulus. Blood filtration is concentrated here.
When this certain part of the kidney is injured, the body is
unable to excrete wastes and extra fluid in the body. This ailment is called
glomerulonephritis, and it has two types—acute and chronic. The acute form is
sudden in onset: a person may get this after a throat or skin infection. On the
other hand, the chronic form develops silently (without symptoms) over several
years: of which the cause is usually unknown. Nearly all forms of acute
glomerulonephritis have a tendency to progress to chronic glomerulonephritis.
The condition is characterized by irreversible and progressive glomerular and
tubulointerstitial fibrosis, ultimately leading to a reduction in the
glomerular filtration rate (GFR) and retention of uremic toxins.
If disease progression is not halted with therapy, the net
results are chronic kidney disease (CKD), end-stage renal disease (ESRD), and
cardiovascular disease. The diagnosis of CKD can be made without knowledge of
the specific cause. The Kidney Disease Outcomes Quality Initiative (NKF-K/DOQI)
work group has defined chronic kidney disease (CKD) as the presence of markers
of kidney damage (abnormalities in blood, urine, or imaging tests ) for ≥3
months or a glomerular filtration rate (GFR) <60 mL/minute/1.73 m2 for ≥3
months, with or without other signs of kidney damage.
I.
INCIDENCE RATE
Local Incidence rate
Kidney disease continues to be among the deadliest among
Filipinos victims, said a member of the Department of Health (DOH) 11’s Renal
Disease Control Program (Redcop) last June 1, 2013. Redcop spokesperson Dr.
Maria Theresa Lorenzo Bad-ang said the disease remains in the top ten diseases
causing mortality.
In 2010, Region 11 comprised 5.9 % of the 9,716 new cases in
the country. Other high-placing regions when it comes to kidney disease are the
National Captial Region (12.5%), Northern Luzon (11.7 %), and Western Visayas
(5.6 %). Statistics for 2011 are yet to be released by the DOH, Bad-ang said.
The prevalence of kidney/renal diseases has been in an
increasing trend, especially the end-stage renal disease (ERSD) as reported in
the Philippine Renal Disease Registry (PRDR). The rate of death due to
end-stage renal disease has been in the top ten list of the mortality of the
Department of Health (DOH).
In the past, chronic glomerulonephritis was the most common
cause of chronic renal failure. Today, diabetes mellitus and hypertension have
taken center stage in the causation of ESRD which together account for almost
60% of dialysis patients and according to the Philippine Renal Disease Registry
Annual Report in 2008, the leading cause of kidney failure in the Philippines
is diabetes (41%), followed by an inflammation of the kidneys (24%) and high
blood pressure (22%). Patients were predominantly male (57%) with a mean age of
53 years.
Worldwide Incidence Rate
Kidney diseases rank as the 7th largest killer amongst all
the diseases prevalent worldwide. What makes it more deadly is that it
encroaches silently, manifesting most of the symptoms only in the advanced
stages. Moreover as the disease strikes in the end stage, it brings along its
wake not only great physical and mental trauma but financial hardships too due
to the high cost of treatment.
http://www.hindawi.com/journals/ijn/2012/639653.fig.001.jpgFor
every patient with clinically apparent Glomerulonephritis, approximately 5 to
10 patients have undiagnosed subclinical disease. Acute Glomerulonephritis is
most common in boys ages 3-7, but it can occur at any age. Up to 95% of
children and 70% of adults recover fully: the rest especially elderly patients,
may progress to Chronic Renal Failure.
In the US and Europe, Glomerulonephritis is the third
commonest cause of end-stage renal disease (ESRD), after diabetes and HTN. But
in worldwide, Glomerulonephritis is the commonest cause of ESRD, as the result
of various infectious agents in developing countries.
The incidence of CKD is increasing most rapidly in people ages
65 and older.
Line graph showing incidence of CKD for age groups 20–64 and
65 and older.People ages 65 and older more than doubled between 2000 and 2008
and among 20- to 64-year-olds is less than 0.5 percent.
Percent with CKD among adult U.S. population by age, sex,
and race/ethnicity. Overall:14%; 20-44 years:4%; 45-64 years:12%; 65 years
+:43%; Male:11%; Female:15%; Non-Hispanic white:14%; Non-Hispanic black:12%;
Mexican American:8%According to the National Chronic Kidney Disease Fact Sheet 2010,
More than 10% of people, or more than 20 million, aged 20 years or older in the
United States have CKD.
CKD is more common among women than men. More than 35% of
people aged 20 years or older with diabetes have CKD and more than 20% of
people aged 20 years or older with hypertension have CKD
II. ANATOMY
AND PHYSIOLOGY
The urinary system, also known as the excretory system, is
concerned with the removal of water-soluble waste products from the body in the
form of urine. The various components or organs of the urinary system are
associated with the production, storage, and then expulsion of urine from the
body. At the same time, the system also takes part in several vital functions
of the body.
The basic functions are removal of waste products from the
body in the form of urine. Each part of the system is concerned with some
specific functions
The urine formed in both the kidney is carried to the
bladder by two narrow tubes, known as ureters. Ureters prevent the back flow of
urine during urination, when the bladder contracts to pass urine to the
urethra. If this function of the ureters is impaired, then diseases like,
cyctitis and kidney infection may occur. The urinary bladder is a triangular
hollow organ, which stores urine, until it is expelled from the body. It is
located in the lower abdomen region, and it has the ability to expand for
storing urine and then, contract to expel it.
Urine is expelled though the urethra, which is a tube like
structure. The sphincter muscles are circular muscles that play an important
role in keeping the urine within the bladder. In other words, they prevent the
leakage of urine, by closing tightly around the opening of the bladder. The
nerves present in the bladder controls the process of urination or micturition.
When the bladder is full and it is time urinate, the nerves of the bladder
transmit this information to the brain. The brain then, signals the bladder
muscles to contract and sphincter muscles to relax, so as to facilitate
urination.
The main components of the urinary system are two kidneys,
two ureters, a urinary bladder, two sphincter muscles and the urethra. Each of
these organs performs some specific functions, associated with the elimination
of waste products generated within our body, during the metabolic processes.
Ø MAJOR ORGANS AND
THEIR FUNCTION:
1. Kidneys
Pair of bean shaped, brownish-red structures located on the
posterior wall of the abdomen and are protected by the ribcage. The right
kidney is slightly lower than the left due to the location of the liver.It
measures 10-12 cm long, 6 cm wide and 2.5 cm thick.
They are covered by the renal capsule, which is a tough
capsule of fibrous connective tissue. Adhering to the surface of each kidney is
two layers of fat to help cushion them. There is a concaved side of the kidney
that has a depression where a renal artery enters and a renal vein and a ureter
exit the kidney.
Deep to the renal capsule is the soft, dense, vascular renal
cortex. The renal cortex is part of the kidneys containing mostly nephrons and
blood vessels. Nephrons are the basic functional units of the kidneys, with
each kidney having one million or more of these important structures.
Seven cone-shaped renal pyramids form the renal medulla deep
to the renal cortex. It is the innermost part of the kidney. The renal pyramids
are aligned with their bases facing outward toward the renal cortex and their
apexes point inward toward the center of the kidney. Each apex connects to a
minor calyx, a small hollow tube that collects urine. The minor calyces merge
to form 3 larger major calyces, which further merge to form the hollow renal
pelvis at the center of the kidney.
The renal pelvis exits the kidney at the renal hilus, where
urine drains into the ureter.
Ø FUNCTIONS OF THE
KIDNEY
o Regulation of
water, electolytes excretion and waste products of metabolism
The kidneys excrete a
variety of waste products produced by metabolism. These include the nitrogenous
wastes called "urea", from protein catabolism, as well as uric acid,
from nucleic acid-metabolism. Formation of urine is also the function of the kidney. Through urine, the waste products are
excreted from the body. The kidneys also serve as the primary mechanism for
excreting drug metabolites. Regulation of the amount of water excreted is an
important function of the kidney as well. It is important to consider all fluid
gained and lost when evaluating a fluid volume status
When the kidneys are functioning normally, the volume of
electrolytes excreted per day will be equal to the amount ingested. The kidneys
are responsible for regulation of electrolyte loss and approximately 90% of the
sodium contained in the renal filtrate is reabsorbed in the renal tubules
specifically the loop of henle and proximal tubules. On the other hand,
potassium is the most abundant intracellular ion. And to maintain a normal
serum balance the kidneys are responsible for excreting more than 90% of the
total daily potassium intake. The regulation of sodium and potassium volume
excreted depends on the aldosterone, a hormone synthesized and released from
the renal cortex.
o Regulation of
acid-base balance
The organs
involved in regulation of external acid-base balance are the lungs are the
kidneys. The lungs are important for excretion of carbon dioxide (the
respiratory acid) and there is a huge amount of this to be excreted. While the
kidney performs two major functions to assists in this balance. The first is to
reabsorb and return to the body’s circulation any bicarbonate from the urinary
filtrate and the second is to excrete acid in the urine.
o Auto regulation of
blood pressure
Although the kidney cannot directly sense blood, long-term
regulation of blood pressure predominantly depends upon the kidney. This
primarily occurs through maintenance of the extracellular fluid compartment,
the size of which depends on the plasma sodium concentration.
Renin is the first in a series of important chemical
messengers that make up the renin-angiotensin system. Changes in renin
ultimately alter the output of this system, principally the hormones
angiotensin II and aldosterone. Each hormone acts via multiple mechanisms, but
both increase the kidney's sodium chloride, thereby expanding the extracellular
fluid compartment and raising blood pressure. When renin levels are elevated,
the concentrations of angiotensin II and aldosterone increase, leading to
increased sodium chloride reabsorption, expansion of the extracellular fluid
compartment, and an increase in blood pressure. Conversely, when renin levels
are low, angiotensin II and aldosterone levels decrease, contracting the
extracellular fluid compartment, and decreasing blood pressure.
o Production of
Hormones
The kidneys secrete a variety of hormones, including
erythropoietin, and the enzyme renin. Erythropoietin is released in response to
hypoxia (low levels of oxygen at tissue level) in the renal circulation. It
stimulates erythropoiesis (production of red blood cells) in the bone marrow.
Calcitriol, the activated form of vitamin D, promotes intestinal absorption of
calcium and the renal reabsorption of phosphate. Part of the
renin-angiotensin-aldosterone system, renin is an enzyme involved in the regulation
of aldosterone levels.
o Osmolality
regulation
Any significant rise in plasma osmolality is detected by the
hypothalamus, which communicates directly with the posterior pituitary gland.
An increase in osmolality causes the gland to secrete antidiuretic hormone
(ADH), resulting in water reabsorption by the kidney and an increase in urine
concentration. The two factors work together to return the plasma osmolality to
its normal levels. Urea is usually excreted as a waste product from the
kidneys. However, when plasma blood volume is low and ADH is released the
aquaporins that are opened are also permeable to urea. This allows urea to
leave the collecting duct into the medulla creating a hyper osmotic solution
that 'attracts' water. Urea can then re-enter the nephron and be excreted or
recycled again depending on whether ADH is still present or not.
i. Nephrons
Nephrons are the structures located within the renal
parenchyma that are responsible for the initial formation of the urine. It is
also the functional unit of the kidney which consists of both vacular and
tubular elements.
Its chief function is to regulate water and soluble
substances by filtering the blood, reabsorbing what is needed and excreting the
rest as urine. Nephrons eliminate wastes from the body, regulate blood volume
and pressure, control levels of electrolytes and metabolites, and regulate
blood pH. Its functions are vital to life and are regulated by the endocrine
system by hormones such as antidiuretic hormone, aldosterone, and parathyroid
hormone.The filtration begins at the renal glomerulus. The glomerular tuft
(glomerulus) contains capillaries and the beginning of the tubule system called
Bowman’s capsule. Filtrate from the glomerulus enters Bowman’s capsule and then
passes through a series of tubule segments that modify the filtrate as it
passes through the renal cortex and medulla and finally flows into the renal
calyces. A second capillary bed, the peritubular capillaries, carries the
reabsorbed water and solute back towards the vena cava.
ii. Renal
Vein
The renal veins are veins that drain the kidney. They
connect the kidney to the inferior vena cava. Because the inferior vena cava is
on the right half of the body, the left renal vein is generally the longer of
the two. Unlike the right renal vein, the left renal vein often receives the
left gonadal vein (left testicular vein in males, left ovarian vein in
females). It frequently receives the left suprarenal vein as well.
ii. Renal Artery
The renal arteries normally arise off the abdominal aorta
and supply the kidneys with blood. The arterial supply of the kidneys is
variable and there may be one or more renal arteries supplying each kidney. Due
to the position of the aorta, the inferior vena cava and the kidneys in the
body, the right renal artery is normally longer than the left renal artery. The
right renal artery normally crosses posterior to the inferior vena cava. The
renal arteries carry a large portion of the total blood flow to the kidneys. Up
to a third of the total cardiac output can pass through the renal arteries to
be filtered by the kidneys.
2. Ureters
Description: The ureters are two tubes that drain urine from
the kidneys to the bladder. Each ureter is a muscular tube about 10 inches.
Muscles in the walls of the ureters send the urine in small spurts into the
bladder. ). After the urine enters the bladder from the ureters, small folds in
the bladder mucosa act like valves preventing backward flow of the urine. The
outlet of the bladder is controlled by a sphincter muscle. A full bladder
stimulates sensory nerves in the bladder wall that relax the sphincter and
allow release of the urine. However, relaxation of the sphincter is also in
part a learned response under voluntary control. The released urine enters the
urethra
3. Urinary Bladder
The urinary bladder is a hollow, muscular and distensible or
elastic organ that sits on the pelvic floor. The urinary bladder can hold
approximately 17 to 18 ounces (500 to 530 ml) of urine. When the bladder fills
with urine (about half full), stretch receptors send nerve impulses to the
spinal cord, which then sends a reflex nerve impulse back to the sphincter
(muscular valve) at th e neck of the bladder, causing it to relax and allow the
flow of urine into the urethra. The
Internal urethra l sphincter is involuntary. The ureters enter the bladder
diagonally from its dorsolateral floor in an area called the trigone. The
trigone is a triangular shaped area on the postero-inferior wall of the
bladder. The urethra exits at the lowest point of the triangle of the trigone.
The urine in the bladder also helps regulate body temperature. A bladder when
operating normally empties completely upon a complete discharge, otherwise it
is a sign that its elasticity is compromised, when it becomes completely void
of fluid, it may cause a chilling sensation due to the rapid change of body
temperature.
4. Urethra
The urethra arises from the base of the bladder. Its wall is
lined with mucous membranes and contains a relatively thick layer of smooth
muscle tissue. It also contains numerous mucous glands, called urethral glands
that secrete mucus into the urethral canal. In the human male, the urethra is
about 8 inches long and opens at the end of the head of the penis. It functions
as a urinary canal and a passageway for cells and secretions from various
reproductiveorgans. In the human female, the urethra is about 1-2 inches long
and opens in the vulva between the clitoris and the vaginal opening. Men have a
longer urethra than women.
III. ASSESSMENT
OF THE CLIENT
Ø History- Thorough
urologic health history taking is essential in diagnosing though sometimes it
is troublesome to many patients because they are uncomfortable to discuss
genitourinary illness or symptom. So it is important to have a good
communication skill and patience to make them feel comfortable when taking
history.
Urologic health history includes age, gender, race, and
ethnicity. It should also covers family history of renal problems, diabetes and
auto immune diseases like Systemic Lupus Erythematous (SLE) and Good Pasture’s
Syndrome. It also includes past medical history of any renal disease,
streptococcal infection, uncontrolled hypertension and diabetes, abdominal or
pelvic surgery that can cause denervation injury to the bladder or previous
surgery that can cause urinary incontinence and neurological diseases that may
cause abnormal bladder function. Medication history of analgesic abuse may be a
cause of renal failure and dosages of some drugs may need to be adjusted or
stopped in renal failure. Occupational history of exposure to chemical
carcinogens such as 2-naphthylamine or benzidine in the chemical or rubber
industries may induce bladder cancer many years later. Diet history is also
included. The excessive intake or omission of certain categories of foods is
noted. Information about food and fluid intake is obtained. If the client has
followed a diet for weight reduction, the details of the diet plan are pertinent.
A high-protein intake can result in temporary renal problems. Clients
susceptible to calculi (stone) formation who ingest large amounts of
calcium-containing products or have an insufficient fluid intake may form new
stones.
Obtaining history of genitourinary pain, abnormalities
during voiding and presence or history of genital lesions are all essential.
Furthermore, Psychosexual history is also important to take though this needs
to be conducted sensitively. It requires experience, knowledge and good
clinical judgment to recognize and define underlying psychosexual problems and
differentiate them from other causes of symptoms.
Ø Physical assessment
Assessment of the kidneys, ureters, and bladder is performed
in conjunction with an abdominal assessment. Auscultation is performed before
percussion and palpation because these activities can enhance bowel sounds and
obscure abdominal vascular sounds.
Inspection
Inspect the abdomen and the flank regions with the client in
both the supine and the sitting position. The client is observed for asymmetry
(e.g., swelling) or discoloration (e.g., bruising or redness) in the flank
region. The patient is also assessed for signs of edema and changes in body
weight. Deep tendon reflex of the knee are also assessed for quality and
symmetry. This is an important part of testing for neurologic causes of bladder
dysfunction.
http://64.19.142.13/intranet.tdmu.edu.ua/data/kafedra/theacher/meds/vnm_horodeckiy/Engl/Recommendations%20for%20preparing%20practical%20classes/Assessment_of_the_Renal-Urinary_System.files/image028.jpgAuscultation
Listen for a bruit over each renal artery on the
mid-clavicular line. A bruit is an audible swishing sound produced when the
volume of blood or the diameter of the blood vessel changes. A bruit is usually
associated with blood flow through a narrowed vessel, as in renal artery
stenosis.
Palpation
Renal palpation identifies masses and areas of tenderness in
or around the kidney. The abdomen is lightly palpated in all quadrants. The
nurse asks about areas of tenderness or discomfort and examines non tender
areas first. The outline of the bladder may be seen as high as the umbilicus in
clients with severe bladder distention. Special training and practice under the
guidance of a qualified practitioner are necessary; therefore appropriate
education is essential before attempting the procedure. If tumor or aneurysm is
suspected, palpation may harm the client.
For palpation of the right kidney, the client assumes a
supine position while the nurse places one hand under the right flank and the
other hand over the abdomen below the lower right part of the rib cage. The
lower hand raises the flank, and the upper hand depresses the anterior abdomen
as the client takes a deep breath .The left kidney is deeper and rarely
palpable. A transplanted kidney is readily palpable in either the lower right
or left abdominal quadrant. The kidney should feel smooth, firm, and non tender.
Percussion
A distended bladder sounds dull when percussed. After gently
palpating to determine the general outline of the distended bladder, the nurse
begins percussion on the skin of the lower abdomen and continues in the
direction of the umbilicus until dull sounds are no longer produced.
Ø Diagnostic testing
· Urinalysis-
Urinalysis is important clinical information about kidney function and helps
diagnose other diseases
· Urine
culture- Urine culture determines whether bacteria are present in the urine as
well as their strains and concentration
· Blood Test
1. Renal Function
Test- blood test used to evaluate the status of a patient’s kidney by obtaining
serum creatinine and BUN levels in the blood.
2. ABG- Arterial
Blood Gas is a blood test that is performed by getting blood sample in an
artery. This test will measure the oxygen and carbon dioxide level in the
blood. It will also determine how well the lungs or kidney can maintain the
acid-base balance in the body.
· Imaging
Modalities
1. X-ray study
of the KUB- is a plain film of the abdomen taken without any specific client
preparation. The KUB study shows gross anatomic features and may show obvious
stones, strictures, calcifications, or obstructions in the urinary tract. This
test identifies the organs' shape, size, and relationship to other parts of the
urinary tract.
2.
Ultrasonography- noninvasive procedure that uses sound waves passed into
the body through a transducer to detect abnormalities such as fluid
accumulation, masses, congenital malformations, changes in the organ size and
obstruction.
3. CT scan- and
Magnetic Resonance Imaging- non invasive technique that provides an excellentt
cross sectional views of the kidney and urinary tract.
4. Renal
angiography/arteriography- provides an image of the renal arteries. It is used
to evaluate renal blood flow in suspected renal trauma, to differentiate renal
cysts from tumors and to evaluate hypertension.
5. Cystoscopic
examination- aka cystoscopy is a term used to describe an internal examination
of the bladder. This procedure can also examine urethra or urinary channel and,
in men, the prostate. Additionally, the two ureters - which are the small tubes
that move urine from the kidneys to bladder - can be examined during this
procedure.
· Kidney
biopsy- procedure in which a small sample of tissue is removed from a part of
the body. The sample is looked at under a microscope, or tested in other ways.
VI. GLOMERULONEPHRITIS
Glomerulonephritis encompasses a variety of diseases most of which are
caused by an immunologic reaction that result in proliferative and inflammatory
changes in the glomerular structure that can lead damage to the basement
membrane, mesangium or capillary endothelium.
Acute glomerulonephritis is defined as the sudden onset of
hematuria, proteinuria, and red blood cell (RBC) casts. This clinical picture
is often accompanied by hypertension, edema, azotemia (ie, decreased glomerular
filtration rate [GFR]), and renal salt and water retention. Acute GN can be due
to a primary renal disease or to a systemic disease.
Chronic glomerulonephritis is the advanced stage of a group
of kidney disorders, resulting in inflammation and slowly worsening destruction
of internal kidney structures called glomeruli. All forms of acute
glomerulonephritis have a tendency to progress to chronic glomerulonephritis.
The condition is characterized by irreversible and progressive glomerular and
tubulointerstitial fibrosis, ultimately leading to a reduction in the
glomerular filtration rate (GFR) and retention of uremic toxins. If disease
progression is not halted with therapy, the net results are chronic kidney
disease (CKD)
VI.1 ASSESSMENT OF
THE CLIENT WITH DIFFERENT PATHOLOGICAL CONDITION
· HISTORY
Patients suspected of Glomerulonephritis should obtain
medical history of streptococcal infection, recent upper respiratory infection,
family history of renal disease and an autoimmune disorder
Most of the time the
patient is male ages 3-7 years old that suddenly develops periorbital edema and
change in color of the urine.
Also, ask about the onset and duration of the illness. The
onset is usually abrupt. In the setting of acute postinfectious glomerulonephritis
(GN), a latent period of up to 3 weeks occurs before onset of symptoms. The
onset of nephritis within 1-4 days of streptococcal infection suggests
preexisting renal disease.
Inquire about the symptom of possible flank pain secondary
to stretching of the renal capsule, scanty dark colored urine, decreased urine
output, periorbital and facial edema and hypertension.
· PHYSICAL
ASSESSMENT
The physical examination begins with a careful assessment of
vital signs, particularly blood pressure to check for hypertension,
tachycardia, orthopnea and dyspnea due to symptomatic fluid overload. Careful
abdominal examination for ascites is also important. Periorbital and facial
edema from salt and water retention is seen in glomerulonephritis. Assessment
for alteration in mental status due to malignant hypertension or hypertensive
encephalopathy is also essential and demand prompt attention.
· DIAGNOSTIC
TESTING
Urinalysis usually provides the information necessary for
diagnosis of glomerulonephritis. It shows a fixed specific gravity, small
amounts of WBCs, proteinuria exept
during exacerbation and consistent hematuria. Gross hematuria and proteinuria
are the cardinal findings. The urine usually has a dark, smoky, cola-colored or
red brown hue. The proteinuria produces persistent and excessive foam.
Blood test for Serum BUN and Creatinine levels in the blood
may be elevated and C-reactive proteins and antistreptolysin O titer are
usually elevated in post streptococcal glomerulonephritis.
Kidney biopsy is the definitive diagnosis for
glomerulonephritis
VI.2 PATHOLOGY OF DISEASE CONDITION
· INCIDENCE
RATE
Glomerulonephritis represents 10-15% of glomerular diseases.
Despite sporadic outbreaks, the incidence of Acute Glomerulonephritis has
fallen over the past few decades. Factors responsible for this decline may
include better health care delivery and improved socioeconomic conditions.
Acute Glomerulonephritis predominantly affects males (2:1 male-to-female ratio)
and only 10% occur in patients older than 40 years old. Acute
Glomerulonephritis has no predilection for any racial or ethnic group. A higher
incidence (related to poor hygiene) may be observed in some socioeconomic
groups.
· RISK FACTORS
AND ETIOLOGY
The definite cause of the glomerulonephritis remains
unknown. But two classification of Glomerulonephritis based on etiology were
formulated. The Primary Glomerulonephritis are disorders in which the
glomerulus is the predominant or the sole tissue involved and if there’s immune
response to pathogens. If it is caused
by another disease or if it’s related to a systemic disease, such as diabetes
or lupus, infection, autoimmune disorder or drugs it is called Secondary
Glomerulonephritis.
PATHOPHYSIOLOGY
Acute glomerulonephritis results from antigen-antibody
complexes trapped in the glomerular capillary membrane produced by an infection
in the body.
The source of antigens is either exogenous or endogenous.
These antigens will stimulate immune response producing antigen-antibody
complexes circulating in the general system. The circulating complexes and the
other live antigens will lodge to the glomerular capillaries of the kidney.
Activation of the biochemical mediators of inflammation will then start by
releasing CHEMOKINES. Chemokines attracts t-cells, leukocytes and neutrophils
which release lysosomal enzymes that can damage the glomerular cell walls
causing t-cell mediated injury. Since there’s membrane damage, it will lead to
platelet aggregation and activation of the coagulation system which will cause
the fibrin to deposit in the bowman’s space. The result of these events will
cause changes in the glomerular structure (crescent formation and thickening of
the glomerular filtration membrane) that will eventually lead to glomerular
damage. The changes in the glomerular structure (crescent formation and
thickening of the glomerular filtration membrane) will cause decrease in GFR
that will also cause decreased urine output fluid retention, facial and
periorbital edema, pulmonary edema and hypertension. The glomerular damage will
cause proteinuria and hematuria in the urine.
If this condition is left untreated and episodes of acute
glomerulonephritis still occurs, further loss and damage to the structures of
the kidney will happen it will progress to chronic glomerulonephritis. If
disease is not halted with treatment and the damage becomes irreversible, it
may lead to Chronic Kidney Disease.
CLINICAL MANIFESTATION
Classic manifestations of sudden onset include hematuria
and proteinuria caused by the damaged in the glomerulus.
Generalized edema, particularly facial and peri orbital swelling is a typical
finding caused by the fluid volume excess in the body. The client may have
ascites, dyspnea and orthopnea and crackles upon lung auscultation due to
pulmonary edema. The client is likely to have headache and moderate to severe
hypertension. Decreased urine output or oliguria may ba present for several
days: the longer it persist, the more irreversible the kidney damage.
CHRONIC KIDNEY DISEASE
Chronic kidney disease (CKD) is an important source of
long-term morbidity and mortality. It has been estimated that CKD affects more
than 20 million people in the United States. Given that most patients are
asymptomatic until the disease has significantly progressed, they remain
unaware of the condition. Renal failure is the ninth leading cause of death
among Filipinos according to the survey conducted by the Philippine Information
Agency dated June 4, 2012.
CKD is a worldwide public health problem. It is recognized
as a common condition that is associated with an increased risk of
cardiovascular disease and chronic renal failure (CRF). In the United States,
there is a rising incidence and prevalence of kidney failure, with poor outcomes
and high cost. On the other hand, in the country, the National Kidney and
Transplant Institute (NKTI) Executive Director, Dr. Aileen Reigo-Javier said
based on the Philippine Renal Disease Registry (PRDR), the top causes of kidney
failure in the country is diabetes (44.6%), followed by the high blood pressure
(23%) and inflammation of the kidneys (19.3%).
Chronic kidney disease, also known as chronic renal disease,
is a progressive loss in renal function over a period of months or years. The
symptoms of worsening kidney function are unspecific, and might include feeling
generally unwell and experiencing a reduced appetite. Often, chronic kidney
disease is diagnosed as a result of screening of people known to be at risk of
kidney problems, such as those with high blood pressure or diabetes and those
with a blood relative with chronic kidney disease
CKD is classified into five stages. Stage I is the mildest,
usually causing few symptoms like slightly diminished function; kidney damage
with normal or relatively high GFR of ≥90 mL/min/1.73 m2. On the other hand,
stage 5 is established kidney failure of GFR <15 mL/min/1.73 m2 and
permanent renal replacement therapy. (Kidney Disease Outcome Quality
Initiative, 2009) Stage V is also referred to as “established” CKD, also called
End-Stage Renal Disease (ESRD), Chronic Kidney Failure and Chronic Renal
Failure. The prevalence of kidney disease has been an increasing trend,
especially the End-Stage Renal Disease as reported in the Philippine Renal
Disease Registry.
As
aforementioned in the above paragraphs, Diabetes and Hypertension individually
aggravates the risk of developing chronic kidney disease. But in the case of
patient EVG, she possesses both the co-morbidity thereby increasing her risk
two-folds. As critical care nurses, our interest rocketed and our desire to
understand and explore this scenario jolted us to choose the case of the
patient.
PATHOPHYSIOLOGY
There are many diseases that cause CKD like diabetes mellitus, because
when you have DM, there’s too much glucose in your blood. High levels of
glucose are toxic to the tiny, fragile capillaries in the kidneys’ glomeruli.
Holes form in the capillary walls and the glomeruli lose their ability to
filter blood. Another cause of CKD is Hypertension, because high blood pressure
damages both arteries leading to kidneys and tiny capillaries inside them.
Larger vessels stiffen and narrow so that the kidneys don’t get enough blood.
Capillaries inside the glomeruli become brittle and develop holes. Eventually,
the glomeruli shrink and are replaced by scar tissue.
Another is Obstruction in the Urinary Tract, cystic kidney
disease, Glomerulonephritis, and recurrent urinary infection; each has its own
pathophysiology. However, there are common mechanisms for disease progression.
Pathologic features include fibrosis, loss of renal cells, and infiltration of
renal tissue by monocytes and macrophages. Proteinuria, hypoxia, and excessive
angiotensin II production all contribute to the pathophysiology. In an attempt
to maintain glomerular filtration rate (GFR), the glomerulus hyper filtrates;
this results in endothelial injury. Proteinuria results from increased
glomerular permeability and increased capillary pressure. Hypoxia also
contributes to disease progression angiotensin II increases glomerular
hypertension, which further damages the kidney.
Proteinuria is one of the strongest predictors of
progression of CKD, proteinuria occurs due to damage capillary walls in the kidney due to hypertension or
diabetes. As the glomerular filtration rate(GFR) declines, clients may show not
only proteinuria but also hypertension as a compensatory mechanism because of
decrease oxygen in the blood because of this event the heart will pump faster
to circulate oxygenated blood and because of the workload the heart is prone to
cardiomegaly. A wide range of lab abnormalities, and manifestation resulting
from disorders in the organs. Like anemia, the hormone EPO is produced in the
kidney, EPO travels to the bone marrow to meet stem cells, EPO signals the stem
cells to produce 2 million red blood cells (RBC) each second. In CKD damaged
kidney tissue can’t produce enough EPO to stimulate the creation of adequate
numbers of red blood cells, resulting in anemia, and a lack of RBC in the
blood, leads to a shortage of oxygen in the body’s tissues. When the heart
pumps harder to try to make up for the lack of oxygen. It can become enlarged
and damaged from overwork. Bone disease, protein energy malnutrition, and
neuropathy; alterations in health status.
FORMULATION OF
APPROPRIATE NURSING DIAGNOSIS
· Fluid volume
excess related to failure of regulatory mechanism and fluid retention as
evidenced by edema and blood pressure changes
· Disturbed
body image related to visible facial and periorbital swelling
· Ineffective
tissue perfusion related to vasoconstriction as manifested by fatigue and
headache
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Hawks JH. (2009). Medical-Surgical Nursing, Clinical Management for Positive
Outcomes 8th Edition. Elsevier PTE LTD.
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(2002). Medical-Surgical Nursing: Concepts and Clinical Application: A
Reference Book and Study Guide. Manila: Educational Pub. House.
· Smeltzer
S.H., et.al (2008). Brunner and Suddarth’s Textbook of Medical Surgical Nursing
11th Edition. Lippincott Williams and Wilkins.
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(2007). Essentials of Pathophysiology, Concepts of Altered Health States 2nd
Edition. Lippincott Williams and Wilkins.
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S.M. (2006). Lippincott Manual of Nursing Practice, 8th Edition. USAL:
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(2007). Anatomy and Physiology, The Unit of Form and Function 4th Edition.
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of Anatomy & Physiology, Sixth Ed., Seeley Et Al., McGraw-Hill
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