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Chronic Kidney Disease Case Presentation
Chronic Kidney Disease Case Presentation
2014
A Case Presentation
Prepared by:
Rose Ann A. Salunga RN
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I. INTRODUCTION
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* reference year
** External Causes of Mortality
Last Update: September 29, 2011
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The tables show that diseases of the vascular system are second to the highest
cause of morbidity and mortality in the Philippines in both male and female. It can also
be seen that males have higher rates than female. It is a must that people would
cautiously monitor their health and practice healthy living to avoid diseases that could
lead to death. And people should prioritize their health more than anything else.
B. GENERAL OBJECTIVES:
The general objective of the case study is to gain the comprehensive knowledge
about the disease to gain the practical exercise about the Adult Health Problem and
also to gain Practical experience working with a patient having chronic kidney disease
and to give holistic patient care according to their need.
Kidneys
The kidneys balance the urinary excretion of substances against the
accumulation within the body through ingestion or production. Consequently, they are
major controller of fluid and electrolyte homeostasis. The kidneys also have several
non-excretory metabolic and endocrine functions, including blood pressure regulation,
erythropoietin production, insulin degradation, prostaglandin synthesis, calcium and
phosphorus regulation and Vitamin D metabolism.
The kidneys are located retroperitoneally, in the posterior aspect of the abdomen.
On either side of the ventral column. They lie between the 12 th thoracic and third lumbar
vertebrae. The left kidney is usually positioned slightly higher than the right. Adult
kidneys are average approximately 11 cm in length, 5 to 7.5 cm in width, and 2.5 cm in
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thickness. The kidney has a characteristic curved shape, with a convex distal edge and
a concave medial boundary.
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sophisticated reprocessing machines. Every day, your kidneys process about 200
quarts of blood to sift out about 2 quarts of waste products and extra water. The waste
and extra water become urine, which flows to your bladder through tubes called ureters.
Your bladder stores urine until you go to the bathroom.
The wastes in your blood come from the normal breakdown of active tissues and from
the food you eat. Your body uses food for energy and self-repair. After your body has
taken what it needs from the food, waste is sent to the blood. If your kidneys did not
remove these wastes, the wastes would build up in the blood and damage your body.
The actual filtering occurs in tiny units inside your kidneys called nephrons. Every
kidney has about a million nephrons. In the nephron, a glomerulus—which is a tiny
blood vessel, or capillary—intertwines with a tiny urine-collecting tube called a tubule. A
complicated chemical exchange takes place, as waste materials and water leave your
blood and enter your urinary system.
At first, the tubules receive a combination of waste materials and chemicals that your
body can still use. Your kidneys measure out chemicals like sodium, phosphorus, and
potassium and release them back to the blood to return to the body. In this way, your
kidneys regulate the body’s level of these substances. The right balance is necessary
for life, but excess levels can be harmful.
The kidneys remove wastes and extra water from the blood to form urine. Urine flows
from the kidneys to the bladder through the ureters.
In addition to removing wastes, your
kidneys release three important hormones:
Erythropoietin (eh-RITH-ro-POY-
eh-tin), or EPO, which stimulates
the bone marrow to make red
blood cells
Renin (REE-nin), which regulates
blood pressure
Calcitriol (kal-suh-TRY-ul), the
active form of vitamin D, which
helps maintain calcium for bones
and for normal chemical balance in
the body
What is “renal” function?
Your health care team may talk about the
work your kidneys do as renal function. If you have two healthy kidneys, you have 100
percent of your renal function. This is more renal function than you really need. Some
people are born with only one kidney, and these people are able to lead normal, healthy
lives. Many people donate a kidney for transplantation to a family member or friend.
Small declines in renal function may not cause a problem.
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or it may result from an episode of acute renal failure from which the client has not
recovered.
Progressive loss of renal function over time; based on a gradual decline in the GFR and
creatinine clearance. The diagnosis of CKD requires the following:
1. Decline of kidney function for 3 months or more AND
2. Evidence of kidney damage (e.g. albuminuria or abnormal biopsy) OR
GFR <60 mL/min/1.73 m2
Each patient is classified into one of the following 5 stages of CKD because
management and prognosis varies according to the progression of damage.
Stage 1: Kidney damage with normal or increased GFR (>90 mL/min/1.73 m2)
Stage 2: Mild reduction in GFR (60-89 mL/min/1.73 m2)
Stage 3: Moderate reduction in GFR (30-59 mL/min/1.73 m2)
Stage 4: Severe reduction in GFR (15-29 mL/min/1.73 m2)
Stage 5: Kidney failure (GFR <15 mL/min/1.73 m2 or dialysis)
B. Precipitating Factors
Chronic glomerular disease such as glomerunephritis
Chronic infections such as chronic pyelonephritis or tuberculosis
Congenital anomalities such as polycystic
Vascular diseases, such as renal nephrosclerosis or hypertension
Hypertension
Glomerular and vascular changes:
o Elevated systemic blood pressures cause a hypertrophic response leading
to intimal thickening of the large and the small vasculature.
o The mechanisms are compensatory at first, but later lead to glomerular
damage
Global sclerosis – ischemic injury to the nephrons causes death
Focal segmental sclerosis – glomerular enlargement for
compensation of the loss of nephrons in other areas of the kidney.
Interstitial nephritis:
o The vascular and glomerular disease lead to tubular atrophy and an
intense chronic interstitial nephritis
The intense chronic interstitial nephritis is thought be secondary to
immunologic processes against ischemia-mediated antigen changes on the
tubular epithelial cell surface.
Chronically these changes lead to tubular and glomerular loss causing nephrons
loss.
o With the death of some nephrons, less are available to maintain the GFR.
o Gradual decline in the GFR is noticed as the nephrons continue to die.
Obstructive processes such as calculi
nephrotoxic agents such as long-term aminoglycoside
endocrine diseases such as diabetic neuropathy
Such conditions gradually destroy the nephrons and eventually cause irreversible renal
failure. Similarly, acute renal failure that fails to respond to treatment becomes chronic
renal failure. Blockages
Scarring from infections or a malformed lower urinary tract system (birth defect)
can force urine to back up into the kidney and damage it. Blood clots or plaques of
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cholesterol that block the kidney’s blood vessels can reduce blood flow to the kidney
and cause damage. Repeated kidney stones can block the flow of urine from the kidney
and are another kind of obstruction that can damage the kidneys.
Overuse of Painkillers and Allergic Reactions to Antibiotics
Heavy use of painkillers containing ibuprofen (Advil®, Motrin®), naproxen (Aleve®),
or acetaminophen (Tylenol®) have been linked to interstitial nephritis, a kidney
inflammation that can lead to kidney failure. A new study suggests that ordinary use
of painkillers (e.g., one pill per day) is not harmful in men who are not at risk for
kidney disease. Allergic reactions to—or side effects of—antibiotics like penicillin
and vancomycin may also cause nephritis and kidney damage.
Drug Abuse
Use of certain nonprescription drugs, such as heroin or cocaine, can damage the
kidneys, and may lead to kidney failure and the need for dialysis.
Inflammation
Certain illnesses, like glomerulonephritis (inflammation of the filtering units of the
kidneys), can damage the kidneys, sometimes enough to cause CKD. Some
glomerulonephritis is inherited, and some may be an immune response to infections like
strep throat.
C. Predisposing Factors
Sex- both sexes are affected by chronic renal failure. But in 1998, based on United
States Renal Data System, a higher total number of males with ESRD was found
Age- CRF can be found in people of any age, from infants to the very old. The
elderly population also is the most rapidly growing ESRD population in the United
States. Note that age 30 years progressive physiological glomerulosclerosis. Aging
also results in concomitant progressive physiological decrease in muscle mass such
that daily urinary creatinine excretion also decreases.
High risk groups for chronic kidney disease (CKD) include those with a family
history of kidney disease. One inherited disease, polycystic kidney disease, causes
large, fluid-filled cysts that eventually crowd out normal kidney tissue.
African Americans, Hispanics, Pacific Islanders, and Native Americans are also at
increased risk.
D. Clinical Manifestations
The clinical manifestations of CRF are present throughout the body. No organ system is
spared.
Electrolyte imbalances
Electrolyte balance may be upset by impaired excretion and utilization in
the kidney. Although many clients maintain normal serum sodium level, the salt-
wasting properties of some failing kidneys, in addition to vomiting and diarrhea,
may cause hyponatremia. Because the kidneys are efficient at excreting
potassium, potassium levels usually remain within normal limits until late in the
disease.
Several mechanisms contriburte to hypocalcemia. Conversion of 25-
hydroxycholecalciferol to 1,25-dihyroxycholecalciferol (necessary to absorb
calcium) is decreased, which results in reduced intestinal absorption of calcium.
At the same time, phosphate is not excreted, which causes hyperphosphatemia.
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Because calcium and phosphate are inversely related, a high phosphate level
results in a reduced calcium level.
Metabolic changes
In advancing renal failure, BUN and serum creatinine rise as waste products
of protein metabolism accumulate in the blood. The serum creatinine level is the
most accurate measure of renal function. The proteinuria accompanying renal
disease and sometimes inadequate dietary intake of proteins cause
hypoproteinuria, which lowers the intravascular oncotic pressure. Metabolic
acidosis occurs because of the kidney’s inability to excrete hydrogen ions.
Decrease reabsorption of sodium bicarbonate and decreased formation of
dihydrogen phosphate and ammonia contribute to this problem. Acidosis
accentuates hyperkalemia and the reabsorption of calcium from the bones.
Hematologic changes
The primary hematologic effect of renal failure is anemia, usually
normochromic and normocytic. It occurs because the kidneys are unable to produce
erythropoietin, a hormone necessary for red blood cell production. Frequently, the
fatigue, weakness, and cold intolerance accompanying the anemia lead to a
diagnosis of renal failure.
Gastrointestinal changes
The entire gastrointestinal system is affected. Transient anorexia, nausea,
vomiting are almost universal. Clients often experience a constant bitter , metallic, or
salty taste, and their breath commonly smells fetid, fishy or ammonia-like. Stomatitis,
parotitis and gingivitis are common problems because of poor oral hygiene and the
formation of ammonia from salivary urea. Accumulations of gastro may be a major
cause of ulcer disease. Esophagitis, gastritis, colitis, gastrointestinal bleeding, and
diarrhea may be present. Serum amylase level may be increased, although they do
not necessarily indicate pancreatitis.
Immunologic changes
Impairment of the immune system makes the client more susceptible to
infection. Several factors are involved, including depression of humoral antibody
formation, suppression of delayed hypersensitivity and decreased chemotactic
function of leukocytes. Immunosuppression is an important part of the medical
management of renal diseaes such as glomerulonephritis.
Cardiovascular changes
The most common clinical manifestation is hypertension, produced through:
mechanism of volume overload, stimulation of the renin-angiotensin system,
sympatheically mediated vasoconstriction, absence of prostaglandins.
Respiratory changes
Some of the respiratory effects such as pulmonary edema can be attributed to
fluid overload. Metabolic acidosis causes a compensatory increase in respiratory
rate as the lungs try to eliminate excess hydrogen ions.
Musculoskeletal changes
The etiologic mechanism involves the kidney-bone-parathyroid and calcium-
phosphate-vitamin D connections. As the GRF decreases, the phosphate excretion
decreases and calcium elimination increases. Abnormal levels of calcium and
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phosphate stimulate the release of parathyroid hormone that mobilizes calcium from
the bones and facilitates phosphate excretion.
Integumentary changes
The skin is also often very dry because of atrophy of the sweat glands. Severe and
intractable pruritus may result from secondary hyperparathyroidism and calcium
deposits in the skin. The pallor of anemia is evident.
1. Changes in Urination
Because your kidneys are tasked with making urine, and thereby eliminating waste, any
changes in the frequency, color, or appearance of urine should be taken seriously.
Some common types of changes include:
Urinating more frequently during the night or in greater amounts
Urinating less often or in smaller amounts
Having foamy or bubbly urine or blood in your urine
Difficulty urinating
2. Swelling
If your kidneys are unable to remove extra fluid from your body, you will likely
experience swelling in your legs, ankles, feet, face, or hands. Water retention due to a
loss of GFR leading to sodium and fluid retention. Fluid moves into the extravascular
space, due to increased hydrostatic pressure, causing pitting edema in the lower
extremity (fluid movement could also be due to hypoalbuminemia, in some diseases,
leading to a low oncotic pressure).
3. Skin Rash / Itching
If your kidneys are unable to remove waste from the bloodstream, the buildup can
cause rashes and severe itching.
4. Leg, Back or Side Pain
Kidney problems can lead to pain in the back, side or even in the leg. Kidney cysts
(large, fluid-filled sacs) resulting from polycystic kidney disease that form on kidneys
and occasionally on the liver can also cause back and leg pain.
5. Metallic Taste in Mouth/Ammonia Breath
When waste builds up in the bloodstream, it can cause bad breath, a metallic taste in
the mouth, and affect how food tastes. You may also have a change in appetite that
results in weight loss.
6. Nausea and Vomiting
Waste buildup in the blood can also cause nausea and vomiting.
7. Feeling Cold
Healthy kidneys make the hormone known as erythropoietin, which prompts the body to
make oxygen-carrying red blood cells. Kidney disease can interrupt the healthy
production of this hormone and cause a decrease in red blood cells, a condition known
as anemia. Anemia and kidney disease can result in a variety of symptoms, including
constantly feeling cold and shortness of breath.
8. Shortness of Breath
Kidney disease can cause extra fluid to build up in the lungs, leading to shortness of
breath. Anemia, a common side-effect of kidney disease which starves your body of
oxygen, can also cause you to feel winded or short of breath. Fluid accumulation
causes pulmonary edema and loss of air space causing ventilation-perfusion mismatch.
This leaves less area for oxygen diffusion form the blood vessels.
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9. Dizziness and Trouble Concentrating
When you suffer from anemia related to kidney failure, both your body and your brain
will be lacking the proper amount of oxygen. The result can be dizziness, trouble with
concentration, and memory-related issues.
10. Fatigue
When kidneys fail, and side effects like anemia set in, you may experience tired
muscles, weakness, and overall fatigue. Erythropoietin (EPO), the major erythropoiesis
stimulator, is released from the kidneys; with renal failure, there is loss of EPO release
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V. MEDICAL MANAGEMENT
The goal of management is to maintain kidney function and homeostasis for as long as
possible. Because of the great deterioration of renal function, the duration of
management may vary from months to years. Nothing can be done to prevent or delay
the fatal outcome.
Control of urinary volume: fluids are forced since kidney has lessened ability
to concentrate solids. more fluids about 2litres is needed to excrete waste.
Sometimes frusemide may be required to increase urine production.
Control of nausea and vomiting: anorexia, nausea and vomiting tend to
develop when the cretinine clearance falls below 5ml/min. so reduction in protein
is required to improve nausea. Blood: 0.8-1.4 mg/dL is the normal. Due to
impaired kidney function, creatinine in the blood elevates.
Creatinine clearance rate was 10.g mg/dl on 4/2, 8.5 mg/dl on 068/4/6, 9.7mg/dl
on 068/4/9.
Antiseizure agents
Antihypertensive agents: hypertension is managed by intravascular volume
control and a variety of anti- hypertensive agents.
Control of hyperkalaemia will be treated with I/V glucose and insulin in a ratio of 3
gm Glucose to 1 unit soluble insulin.
Control of anemia: blood transfusion are frequently required.
Accurate record of input and output chart should be maintained
Other therapy: dialysis
It is usually initiated when the patient cannot maintain a reasonable
lifestyle with conservative treatment.
VI. Nursing Management:
Nursing care is directed toward assessing fluid status and identifying potential source of
imbalance
Implement a dietary program to ensure proper nutritional intake within the limits of the
treatment regimen.
Promote positive feelings by encouraging increased self care
Provide explanations and information to the patient and family concerning ESRD,
treatment options and potential complications
Nurse must be familiar with various drugs and their side effects
Provide emotional support to the patient and his family because of the numerous
changes experienced.
Cardiovascular disease (CVD)is the leading cause of death in patients with
CKD.
o Reducing risk factors for development of CVD is beneficial.
E.g. treatment of hyperlipidemia, lifestyle and dietary changes
Tight blood pressure control:
o Reducing damage due to the end organ effects of hypertension on the
kidney as well as the heart.
o Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II
receptor blockers(ARBs) block the effects of angiotensin II on (i) sodium and
fluid retention, (ii) vasoconstriction, (iii) stimulating ADH release, (iv) stimulating
aldosterone release, and (v) inducing a sympathetic response.
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ACEIs and ARBs also slow down progression of proteinuria in
patients with diabetic CKD.
Diabetes management:
o Tight glucose management slows the progression of vascular and heart
disease.
Avoidance of IV contrast, NSAIDs, and nephrotoxic drugs:
o These agents can potentially induce an acute kidney injury (AKI) on the
underlying kidney disease and therefore exacerbate the baseline CKD.
Diet:
o Mixed evidence exists whether dietary protein restriction is beneficial in
slowing disease progression.
o Proteins affect the renal hemodynamics, raising the GFR, in hypothesized
2 ways.
Hormonal effects – proteins cause secretion of glucagon, IGF-1
and kinins, all of which have been shown to raise the GFR.
Tubuloglomerular effects – high amino acid (AA) filtration leads to
increased AA and hence the sodium uptake in the proximal convoluted
tubule. A decreased sodium delivery to the distal convoluted tubule leads to
the rennin-angiotensin system activation via the macula densa and these
work to raise the GFR (mechanisms above)
o Controlling hyperphosphatemia: Protein restriction also limits phosphorus
consumption. Hyperphosphatemia plays a major role in the progression of renal
osteodystrophy. Phosphate binders are used to reduce phosphate absorption
through the GI tract.
VII. Surgical Management
Kidney transplantation: it involves transplanting a kidney from a living donor to a
recipient who has ESRD. The success rate increases if kidney transplantation from
a living donor is performed before dialysis is initiated.
VIII. REFERENCES
1. Coresh J, Selvin E, Stevens LA, et al. Prevalence of chronic kidney disease in
the United States. 2007.
2. Collins AJ, Foley RN, Chavers B, et al. U.S. renal data system 2011 annual data
report. Am J Kidney Dis. 2012.
3. Matsushita K, van der Velde M, Astor BC, et al. Association of estimated
glomerular filtration rate and albuminuria with all-cause and cardiovascular
mortality in general population cohorts: a collaborative meta-analysis. Lancet.
2010.
4. Rashidi A, Sehgal AR, Rahman M, O'Connor AS. The case for chronic kidney
disease, diabetes mellitus, and myocardial infarction being equivalent risk factors
for cardiovascular mortality inpatients older than 65 years. Am J Cardiol. 2008.
5. Rao MV, Qiu Y, Wang C, Bakris G. Hypertension and CKD: Kidney Early
Evaluation Program (KEEP) and National Health and Nutrition Examination
Survey (NHANES), 1999–2004. Am J Kidney Dis. 2008.
6. Botdorf J, Chaudhary K, Whaley-Connell A. Hypertension in cardiovascular and
kidney disease. Cardiorenal Med. 2011.
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7. Segura J, Ruilope L. Hypertension in moderate-to-severe nondiabetic CKD
patients. Adv Chronic Kidney Dis. 2011.
8. Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the Joint
National Committee on Prevention, Detection, Evaluation, and Treatment of High
Blood Pressure. 2003.