8.

THE PATIENT AND HIS ILLNESS

a. Synthesis of the disease (Book-Centered)
CKD
Chronic Kidney disease (CKD) is usually the end result of a gradually progressive loss of
renal function: but also the occasionally the result of rapidly progressive disease of sudden
onset. Few symptoms develop until after more than 75% of the glomerular filtration in lost; then
the remaining normal parenchyma deteriorates progressively, and symptoms worsen as a renal
function decreases. If this condition continues unchecked, uremic toxins accumulate and
produce potentially fatal physiology changes in all major organ systems. If the patient can
tolerate it, dialysis of kidney transplantation can sustain life.
CKD has the classifications, according to the National Kidney Foundation Classification
of Chronic Kidney Disease: Stage 1 (at risk) kidney damage with normal GFR
(>90ml/min/1.73m
2
) ; Stage 2 ( Chronic renal insufficiency) kidney damage with mild decrease
in GFR ( 60-80 ml/min/1.73m
2
); Stage 3 (Chronic renal failure) moderate decreased in GFR
(30-59 ml/min/1.73m
2
); Stage 4 (CRF) severe decrease in GFR (15-29 ml/min/1.73m
2
); Stage
5 ( End stage renal disease ) kidney failure(<15 ml/min/1.73
2
).

A. Non- Modifiable Factors:
Race Blacks have a greater chance of acquiring hypertensive nephrosclerosis
because of the increasing incidence of hypertension and chronic kidney disease. They
also have smaller kidneys and large glomerular volume.
Gender Hypertensive nephrosclerosis is more common for males. Moreover, the
incidence of impaired renal function is greater in males than in females despite adequate
blood pressure control.
Family History of Hypertension An individual with a positive family history of
hypertension has a greater possibility of having hypertension and hypertensive
nephrosclerosis.
Age The incidence of hypertensive nephrosclerosis as a cause of Chronic Kidney
Disease is greater in patients over 65 years old. Sclerosis and hyalinosis of arterial
walls, glomerulosclerosis, atrophy of tubular epithelium and interstitial fibrosis are
common morphologic lesions in the kidneys of elderly individuals.
B. Modifiable Factors
Malignant hypertension This happens when an individual has a diastolic blood
pressure in excess of 130mm Hg. Long standing high blood pressure may damage the
kidneys by causing changes in small arteries and also by damaging the glomeruli
leading to CKD.
Pre-existing hypertension A diagnosis of hypertension from ages 25-45 is a risk
factor for developing CKD.
Urinary Tract Infection A person with a pre-existing renal disease has an increased
chance of developing urinary tract infection
Diabetes mellitus Diabetes causes about 35% of all chronic kidney disease.
Increased levels of glucose leads to alterations in renal blood vessels. If glucose levels
remain elevated, kidney function is impaired progressively.
Obesity Obesity causes hypertension and diabetes leading to chronic kidney failure.
Alcoholic drinking Alcohol causes vasoconstriction promoting hypertension leading
to chronic renal failure.
Cigarette smoking Cigarette smoking is a risk factor for progressive CKD.
Mechanisms and risk factors relevant to atherosclerosis appear to be equally relevant to
glomerulonephrosclerosis and comparably aggravated by smoking. Smoking is a risk
factor in the decline of renal function in patients with severe hypertension. Stimulation of
sympathetic nerve activity, intrarenal stimulation of endothelin-1 synthesis, disturbances
of endothelial control of vascular tone and the release of endothelial-derived relaxing
factors seem to play a role in functional changes (i.e. increase renal vascular resistance
and diminished renal plasma volume).
Diet (high fat) Dietary cholesterol supplementation accelerates glomerular injury. This
increases the chance of acquiring hypertensive nephrosclerosis. A diet high in salt
causes water retention causing increase blood volume, which can damage the kidneys,
increasing the chance of developing chronic renal failure.
Physical inactivity Physical inactivity with obesity, which is also a risk factor for
chronic kidney disease.




C. Signs and Symptoms with Rationale

Increased BUN - There is increased levels of BUN because of waste products of protein
metabolism accumulate in the blood.
Increased Serum Creatinine - The increased level of serum creatinine is due to the
waste products of protein metabolism accumulating in the blood.
Dilute polyuria The kidney is unable to concentrate urine because of the hypertrophy
of the remaining nephrons
Hyponatremia - vomiting and diarrhea may cause hyponatremia.
Dehydration - vomiting, diarrhea and polyuria causes dehydration.
Decreased Libido - there is decreased libido because there is disturbances in
reproduction possibly from both physiologic and psychological factors.
Infertility - infertility is because of the disturbances in reproduction from physiologic and
psychological factors.
Delayed wound healing Because of immune disturbances brought about the loss of
non-excretory renal functions
Infection - impairment of the immune system makes the client more susceptible to
infection.
Erratic blood glucose level - this is because of the impaired insulin secretion.
Anemia and pallor - it occurs because the kidneys are unable to produce
erythropoietin, a hormone necessary for red blood cell production.
Osteodystrophy - is a result of decreased calcium absorption because of the failure to
convert inactive forms of calcium
Metabolic Acidosis - Metabolic acidosis occurs because of the kidneys inability to
excrete hydrogen ions. Decreased absorption of sodium bicarbonate and decreased
formation of dihydrogen phosphate and ammonia contribute to this problem.
Hyperphosphatemia - There is hyperphosphatemia because of the decreased
phosphate excretion.
Hypocalcemia - Hypocalcemia occurs because conversion of 25-hydroxycholecalciferol
to 1,25-dihydroxycholecalciferol which is necessary of calcium absorption is decreased.
Hyperkalemia - Catabolism, potassium containing medications, trauma, blood
transfusions, and acidosis contribute to potassium excess.
Hypertension Is caused by water retention due to the decreased sodium reabsorption
in tubules
Heart Failure - Heart failure may result from anemia, vascular access, complications of
coronary artery disease, electrolyte imbalance, acidosis, myocardial infarction and
thiamine depletion.
Edema - Is caused by water retention due to the decreased sodium reabsorption in
tubules
Increased uric acid Because of uremia due to the decreased excretion of nitrogenous
wastes
Proteinuria - Because of uremia due to the decreased excretion of nitrogenous wastes
Peripheral nerve changes - Because of uremia due to the decreased excretion of
nitrogenous wastes
Pericarditis- Pericarditis is usually related to the accumulation of uremic toxins.
CNS changes - Because of uremia due to the decreased excretion of nitrogenous
wastes
Pruritus - Pruritus may result from secondary hyperparathyroidism and calcium deposits
in the skin.
Bleeding Tendencies - Platelet abnormalities are the primary defect that is responsible
for bleeding in the uremic client.
Altered Taste - The entire gastrointestinal system is affected. Clients often experience a
constant bitter, metallic or salty taste.


MODIFIABLE FACTORS
Malignant hypertension
Pre-existing hypertension
Urinary tract infection
Diabetes Mellitus
Obesity
Alcohol drinking
Cigarette smoking
Diet (High fat, High salt)
Physical inactivity
Decreased renal blood flow
Decreased glomerular filtration
Hypertrophy of remaining nephrons
Inability to concentrate urine
Further loss of nephron functions
Dilute polyuria
Dehydration
Loss of sodium
in urine
Hyponatremia
Loss of excretory
renal function
b. Schematic diagram (Book-Centered)

NON-MODIFIABLE
FACTORS
Race (Black)
Gender (Male)
Family History of
Hypertension
Age (65 & above)
A
Loss of non-excretory function
Disturbances in
reproduction
Immune
disturbance
s
Increased
production
of lipids
Failure to
produce
erythropoietin
Failure to convert
inactive forms of
calcium
Impaired
insulin action
Decreased
libido
Infertility
Delayed
wound
healing
Infection
Advanced
atherosclerosis
Erratic blood
glucose levels
Anemia,
Pallor
Decreased
calcium
absorption
Osteodystroph
y
Hypocalcemia





Decreased
phosphate
excretion
Decreased
potassium
excretion
Decreased
excretion of
nitrogenous
waste
Decreased sodium
reabsorption in
tubule
Hyperkalemia Water
retention
Hypertension Heart
failure
Edema
Decreased
calcium absorption
Hyperphosphatemia
Hypocalcemia
Hyperparathyroidism
Decreased
potassium excretion
Hyperkalemia
Uremia

A
Decreased
hydrogen
secretion and
decreased
bicarbonate
reabsorption
Metabolic
acidosis
Increased
BUN
Increased
uric acid
Increased
creatinine
Proteinuria
Peripheral nerve
changes
Pericarditis
CNS changes
Pruritus
Bleeding
tendencies
Altered
taste
Respiratory
changes
c. Synthesis of the disease (Book-Centered)
Chronic Kidney Disease (CKD) is usually the end result of a gradually progressive loss
of renal function: but also the occasionally the result of rapidly progressive disease of sudden
onset. Few symptoms develop until after more than 75% of the glomerular filtration in lost; then
the remaining normal parenchyma deteriorates progressively, and symptoms worsen as a renal
function decreases. If this condition continues unchecked, uremic toxins accumulate and
produce potentially fatal physiology changes in all major organ systems. If the patient can
tolerate it, dialysis of kidney transplantation can sustain life.
A. Non- Modifiable Factors
Family History of Hypertension The clients mother died due to a heart attack. The
three other siblings presently all have hypertension.
Age Client is 78 years old. Older clients are at risk for CKD because of reduced
cardiac contractile function, vascular compliance, renal plasma flow, and renal mass.
The older adult has more difficulty maintaining a homeostatic fluid balance. The ability
to retain sodium declines with age, as does the ability to concentrate urine. Older clients
are also more likely to have pre-existing renal damage from such diseases as
hypertension.

B. Modifiable Factors
Malignant hypertension Client has a history of hypertension, which is an underlying
cause to CKD. The clinical syndrome consists of slowly progressive renal failure, low
grade proteinuria and bland urine sediment. Kidney disease can also cause new
hypertension or exacerbate pre-existing hypertension. High blood pressure puts more
stress on blood vessels throughout the body, including the kidney filters (nephrons).
Hypertension is the number two cause of kidney failure.
Diet (high fat) The client is fond of eating foods high in sodium, such as processed
foods, junk foods such as chips, and fast food like Jollibee. Her diet may be a
contributing factor to her longstanding hypertension.



C. Signs and symptoms with rationale
Decreased production of RBC Erythropoietin normally stimulates precursor cells in
the bone marrow to produce RBCs. However, there is a decreased production of the
hormone erythropoietin by the kidneys caused by the decreased of functioning renal
tubular cells.
Decreased hematocrit - it occurs because the kidneys are unable to produce
erythropoietin, a hormone necessary for red blood cell production.
Decreased hemoglobin - it occurs because the kidneys are unable to produce
erythropoietin, a hormone necessary for red blood cell production.
Pallor - it occurs because the kidneys are unable to produce erythropoietin, a hormone
necessary for red blood cell production.
Fatigue, weakness, and shortness of breath - (11/08/13 and 11/12/13) Decreased
hemoglobin impairs oxygenation, causing weakness. Due to decreased oxygen supply
by the blood secondary to anemia.
Dizziness - (11/07/13) Compromise of left ventricular forward function may result in
symptoms of poor systemic circulation such as dizziness because of decrease cerebral
tissue perfusion.
Increased BUN - There is increased levels of BUN because of waste products of protein
metabolism accumulate in the blood.
Increased creatinine - The increased level of serum creatinine is due to the waste
products of protein metabolism accumulating in the blood.
Metabolic and respiratory alkalosis Dialysis, which removes nitrogenous wastes,
may result to alkalosis.
Hypertension - Is caused by water retention due to the decreased sodium reabsorption
in tubules
Decreased cardiac output - (11/08-12/13) Lack of oxygen causes left ventricle to
enlarge with stretched tissues and compensate thus decreasing cardiac output.
Increased Troponin I - (11/07/13) An increased troponin I, a cardiac enzyme, is an
indicator of unstable angina pectoris which elevates after an attack. An increase in the
troponin level means that there may have either been damage to the heart or there is a
loss of membrane integrity due to impaired renal excretion. In the case of the client,
increased troponin levels may also be due to: high blood pressure or weakening of the
heart muscle 2* to CKD.
Chest pain Decreased in blood flow to the heart may lead to myocardial necrosis and
eventually myocardial infarction. In the presence of MI, troponin I increases which
causes chest pain.



MODIFIABLE FACTORS

Malignant Hypertension:
Diagnosed for about 10 years

Diet: High in fats & sodium,
processed, fast food

Decreased renal blood flow
Decreased glomerular filtration
Hypertrophy of remaining nephrons
Inability to concentrate urine
Further loss of nephron functions
Loss of excretory
renal function
d. Schematic diagram (Client-Centered)

NON-MODIFIABLE
FACTORS
Age: 78

Family History: Mother passed
away d/t heart attack, 3 other
siblings have hypertension

A
Loss of non-excretory function




Failure to
produce
erythropoietin
Pallor: (11/8, 12, 13/13)
Fatigue: (11/ 8, 12, 13/13)
Weakness: (11/ 8, 12, 13/13)
Shortness of breath: (11/7, 8, 12, 13/13)
Dizziness: (11/7/13)
Decreased
production of
RBC (11/8/13)
Anemia
Decreased
production
of RBC
Decreased
hemoglobin (120g/L)
and hematocrit (0.35)
(11/8/13)

A
Decreased
excretion of
nitrogenous
waste
Decreased sodium
reabsorption in
tubule
Water
retention
Hypertension
BP Readings:
11/07 160/90
11/08 140/90
11/09 140/90
11/10 140/80
11/11 130/80
11/12 160/90

Decreased
cardiac
output
(11/8 - 12/13)
Increased
Troponin I
(11/8/13)
Chest pain
(11/7/13)
Decreased
blood flow to
heart
Myocardial
necrosis
Myocardial
infarction/
ACS
Metabolic and
respiratory alkalosis
(11/7/13)
Increased BUN (as
verbalized by SO
Increased
creatinine (as
verbalized by SO)
Dialysis