CONCEPT MAP: NEPHROSCLEROSIS

NCM 103.3-NB
SUBMITTED BY:
MA. ELYZA ALLENE N. PADERANGA

SUBMITTED TO:
JESUSA C. GABULE, RN, MN
MA. JESSECA P. MONSANTO, RN, MAN
DEXTER DAVE D. ORIGINES, RN, MN

July 29, 2016

A. DISEASE CONDITION
Nephrosclerosis is hardening of the walls of the small arteries and arterioles
(small arteries that convey blood from arteries to the even smaller capillaries) of the
kidney and it is often caused by blood vessel disease such as atherosclerosis,
hypertension and/or diabetes. It is usually associated with hypertension. Sclerosis of
the renal arterioles reduces blood flow that can lead to kidney failure and heart
failure.
Hypertensive Nephrosclerosis. High blood pressure, also called HBP
or hypertension has many consequences. It is the second-leading cause of kidney

failure. The kidneys and the circulatory system depend on each other for good health
the circulatory system provides nutrient-rich blood; the kidneys use the nutrients
to remove waste from the blood.
How does high blood pressure cause kidney damage?
HBP damages your kidneys in three ways:

HBP causes artery damage, and the kidneys are packed with arteries.
Kidneys are supplied with dense blood vessels, and high volumes of blood
flow through them. Over time, uncontrolled high blood pressure can cause
arteries around the kidneys to narrow, weaken or harden. These damaged
arteries are not able to deliver enough blood to the kidney tissue.

*Kidney artery aneurysm. An aneurysm is a bulge in the wall of a blood

vessel. When it occurs in an artery leading to the kidney, it's known as a
kidney (renal) artery aneurysm. Over time, high blood pressure in a
weakened artery can cause a section to enlarge and form a bulge the
aneurysm. Aneurysms can rupture and cause life-threatening internal
bleeding.

Damaged kidney arteries do not filter blood well. Kidneys have small, fingerlike nephrons that filter your blood. Each nephron receives its blood supply
through tiny hair-like capillaries, which are the smallest of all blood vessels.
When the arteries become damaged, the nephrons do not receive the
essential oxygen and nutrients. Also, the kidneys lose their ability to filter
blood and regulate the fluid, hormones, acids and salts in the body. As a
result, dangerous levels of fluid and waste can accumulate. You might
ultimately

require

dialysis

or

kidney

transplantation.

Damaged kidneys fail to regulate blood pressure. Healthy kidneys produce a

hormone to help the body regulate its own blood pressure. Kidney damage
and uncontrolled high blood pressure each contribute to a negative spiral. As
more arteries become blocked and stop functioning, the kidneys eventually
fail. This process can happen over several years, but it can be prevented.

Summary of Pathophysiology: vascular, glomerular and tubule interstitial lesions

This condition is caused by hypertension (high blood pressure). Hypertension
can be present in a person for 20 to 30 years without evidence of kidney
involvement; such persons usually die of other effects of hypertension such as
congestion of blood in the heart, hardening of the heart tissue, or cerebral (brain)
hemorrhage.
If these maladies do not occur first, there is usually some eventual renal
(kidney) involvement. Nephrosclerosis is classified as either benign or malignant.
Benign nephrosclerosis is a gradual and prolonged deterioration of the renal
arteries. First, the inner layer of the walls of smaller vessels thickens, and gradually
this thickening spreads to the whole wall, sometimes closing the central channel of
the vessel. Fat then becomes deposited in the degenerated wall tissues. The larger
arteries gain an excess of elastic tissue, which may block their channels. Both these
conditions cause the blood supply to the vital kidney areas to be blocked, and tissue
deterioration ensues.
In malignant nephrosclerosis a similar process occurs but at a much faster
rate. The disease may develop so rapidly that there is little time for gross kidney
changes to occur. The surface of the kidney, however, is nearly always covered with
large red blotches at points where bleeding has occurred. In the malignant disease
the arteriole walls thicken and may be closed off by rapid cell growth. The nuclei of
these cells die, and the elastic fibres disappear. With the loss of the elastic fibres, the
walls of the vessels become much more fragile and easily distended. Severe
ruptures and hemorrhages are frequent. The arterioles often suffer spasms that can
force blood through lesions in the vessel walls; the tissues become swollen as a
result. Malignant nephrosclerosis is accompanied by severe headache, confusion,
blurred vision, nausea, and vomitingall of which are caused by a drastic increase
in blood pressure. Unless prompt treatment can relieve the increased blood
pressure, tissue changes in the heart, culminating in heart failure, or in the brain,
leading to seizures and coma, may occur.
Benign nephrosclerosis alone hardly ever causes severe damage to the
kidney, except in susceptible populations, such as African Americans, where it may
lead to uremia and death. However, all persons with this disease usually show some

functional impairment, such as loss of concentration or a variably diminished GFR. A

mild degree of proteinuria is a frequent finding.
Aldosterone

produces

vascular

and

perivascular

inflammation.

The

inflammatory process results in the thickening and fibrosis of renal arteries and
arterioles which lose their normal compliance leading to significant alteration in renal
dynamics (nephrosclerosis). The loss of the normal structure of the renal arteries
and arterioles extends to the glomeruli which leading to massive increase in
intraglomeruli pressure which destroy the glomeruli. The capillaries may rupture due
to the severe hemodynamic alteration in the kidneys leading to the leakage of protein
and blood, clot formation and scarring (a process called glomerulosclerosis, the
characteristic lesion of nephrosclerosis). In addition, the areas of focal perivascular
inflammation affects adjacent nephrons traversing nearby resulting to damage to
adjacent renal tubules
Role of renin-angiotensin system (RAS) in diabetic renal disease and CVD.
Considerable evidence suggests that components of the RAS exert similar
pathological effects on the renal glomerulus as in the systemic and cerebral
vasculature. Thus, interruption of the system would be anticipated to produce parallel
improvement in renal and CVD outcome.
Heart failure is growing in this country because of our aging population,
because more persons are surviving their myocardial infarctions, and because of the
increasing prevalence of diabetes, particularly in our elderly population. There is also
accumulating evidence that RAS activation is an important contributor to
development of heart failure. Data from several recent intervention trials also
suggest that treatment strategies that reduce the RAS can impact stroke incidence,
severity, and recurrence in patients with type 2 diabetes mellitus. Recent studies
have shown the benefits of angiotensin receptor blockers and an ACE/diuretic
combination in reduction of primary and secondary strokes in high-risk patients,
including patients with diabetes.
Aldosterone effects on the vasculature. In addition to decreasing endothelial
cell NO production, aldosterone contributes to vascular growth and remodeling.
These effects of aldosterone are mediated by both genomic and nongenomic effects
of this hormone. The genomic effects on the vasculature include increases in protein

synthesis, inflammation, and fibrosis. Aldosterone also causes water to be

reabsorbed along with sodium; this increases blood volume and therefore blood
pressure. Thus, aldosterone indirectly regulates blood levels of electrolytes (sodium,
potassium and hydrogen) and helps to maintain the blood pH. Some effects are
mediated by the interaction of aldosterone and other growth factors such as
Angiotensin II. Many of the vascular actions of aldosterone are similar to those
promoted by hyperglycemia and other metabolic abnormalities associated with
diabetes.
Data from several trials support the recent guidelines of a goal blood pressure
of less than 130/80 mm Hg with therapy that includes an ACE or ARB in patients with
diabetes and hypertension. Accumulating evidence indicates that strategies that
interrupt the RAS provide special benefits in reducing CVD, stroke, renal disease,
and eye disease in diabetic persons. The diabetes substudy of the HOPE showed
that at similar blood pressures, therapy with ramipril not only reduced CVD event, but
also resulted in a 24% greater decrease in the rate of progression to overt
nephropathy

in

patients

with

type

diabetes

and

normalbuminuria

or

microalbuminuria. Six other small trials, involving a total of 352 patients with type 2
diabetes and overt nephropathy, showed that ACE inhibitors were more efficacious
than other antihypertensive drugs (Ang II-receptor antagonists excluded) in reducing
proteinuria. In the UKPDS, there was a striking reduction in diabetic retinopathy and
blindness in those who were more vigorously treated with either captopril or atenolol,
pharmacological agents that reduce RAS activity.
Pathophysiological role of aldosterone in diabetic renal disease and CVD.
Aldosterone is a steroid hormone that is primarily produced in the zona glomerulosa,
the outer layer of the adrenal cortex. Classical effects of aldosterone are to promote
sodium retention and potassium loss by the kidney, although it exerts similar but
lesser effects on the colon, sweat, and salivary glands. The three principal factors
that regulate aldosterone secretion are Ang II, ACTH, and potassium. Changes in
aldosterone secretion in response to changes in volume status or alteration in salt
intake are mediated primarily by Ang II. Most patients with type 2 diabetes have
normal Ang II regulation of aldosterone and normal circulating level of this hormone.
However, in diabetic patients with dysautonomia, usually associated with longstanding diabetes, there may be impaired conversion of the precursor of renin,

prorenin, to renin by the diabetic kidney. This defect in the processing of renin may
ultimately result in the syndrome of hyporenin-hypoaldosteronism, in which high
levels of circulating prorenin are associated with unstimulatable renin, resulting in
low aldosterone levels and a propensity to hyperkalemia. In these patients, the use
of an ACE inhibitor or an ARB as an aldosterone antagonist should be exercised with
caution to avoid hyperkalemia.
Aldosterone and hypertension in diabetic patients. Hypertension in diabetes is
characterized by reduced nitric oxide (NO)-mediated vasorelaxation, reduced
baroreflex sensitivity, and enhanced sympathetic activity, abnormalities that are
promoted by aldosterone. Aldosterone appears to have effects on the brain, the
heart, vasculature, and kidneys that lead to elevated blood pressure. These changes
include

enhanced

sympathetic

nervous

system

activity,

reduced

vascular

compliance, and endothelial-derived vasorelaxation, increases in volume expansion

and reduced serum potassium, and increases in left ventricular mass and cardiac
output. Aldosterone antagonists have been shown to substantially reduce blood
pressure in patients as well as in animal models with hypertension. Aldosterone
antagonists also appear to have considerable potential in treating the diabetic patient
with hypertension. There are data in the stroke-prone spontaneously hypertensive
rats (SHRSP), suggesting that aldosterone antagonists may also reduce strokes
However, there are no extant studies demonstrating the ability of aldosterone
antagonists to prevent stroke in men.
Aldosterone,

albuminuria,

and

diabetic

nephrosclerosis.

The

pathophysiological alterations that characterize glomerulosclerosis parallel those of

atherosclerosis and include mesangial cell proliferation/hypertrophy, foam cell
accumulation, build-up of extracellular matrix and amorphous debris, inflammation
and evolving sclerosis. All of these changes lead to matrix expansion, basement
membrane abnormalities, and loss of basement membrane permoselectivity, which
in turn leads to proteinuria. There is considerable experimental evidence that
aldosterone contributes to the development of nephrosclerosis and renal fibrosis in
models of diabetes and hypertension.

B. PREDISPOSING/PRECIPITATING FACTORS

PREDISPOSING FACTORS

Age. As you get older, your risk for type 2 diabetes, heart disease, and
stroke goes up. Blood pressure tends to rise with age. About 65
percent of Americans age 60 or older have high blood pressure.
However, the risk for prehypertension and high blood pressure is
increasing for children and teens, possibly due to the rise in the

number of overweight children and teens.

Gender. In relation to Diabetes and heart problems, whether you're
male or female also affects how likely you are to develop heart
disease. Men are more likely to develop heart disease. But once a
woman reaches menopause, her risk for heart disease goes up. But
even then, women still aren't as likely as men. In relation to
hypertension, before age 55, men are more likely than women to
develop high blood pressure. After age 55, women are more likely than

men to develop high blood pressure.

Overweight.
Lifestyle. Unhealthy lifestyle habits can raise your risk for high blood
pressure, and they include too much sodium or too little potassium,

lack of physical activity, drinking too much alcohol and stress

Race (Blacks, African Americans). This is partly because these
populations are more likely to be overweight, have high blood pressure
and have type 2 diabetes. Compared with these ethnic groups, African
Americans tend to get high blood pressure earlier in life, often, on
average, have higher blood pressure numbers, are less likely to

achieve target blood pressure goals with treatment.

Family History.

PRECIPITATING FACTORS

Kidney Disease
Heart problem
Diabetes Mellitus
Prolonged/ frequent Hypertension

C. CLINICAL MANIFESTATIONS

Progressive

increase

in

BUN/Cr

in

chronic

HPN

patient.

The ratio of BUN to creatinine is usually between 10:1 and 20:1. An

increased ratiomay be due to a condition that causes a decrease in the flow

of blood to the kidneys, such as congestive heart failure or dehydration.

Mild/increasing proteinuria usually <1 gm/day (non-nephrotic range). People
with proteinuria have urine containing an abnormal amount of protein. The
condition is often a sign of kidney disease.Healthy kidneys do not allow a
significant amount of protein to pass through their filters. But filters damaged
by kidney disease may let proteins such as albumin leak from the blood into

the urine.
The symptoms of nephrosclerosis include impaired vision, blood in the urine,
loss of weight, and the accumulation of urea and other nitrogenous waste

products in the blood, a condition known as uremia.

Symptoms of chronic kidney disease, such as loss of appetite, nausea,
vomiting, itching, sleepiness or confusion, weight loss, and an unpleasant
taste in the mouth, may develop.

D. DIAGNOSTIC STUDIES (relevance to the condition)

Urinalysis.
BUN and Creatinine. The determination of serum blood urea nitrogen
currently is the most widely used screening test for the evaluation of kidney
function. The test is frequently requested along with the serum creatinine test
since simultaneous determination of these 2 compounds appears to aid in the
differential diagnosis of prerenal, renal and postrenal hyperuremia. Increased
blood urea nitrogen (BUN) may be due to prerenal causes (cardiac
decompensation, water depletion due to decreased intake and excessive loss,
increased protein catabolism, and high protein diet), renal causes (acute
glomerulonephritis,

chronic

nephritis,

polycystic

kidney

disease,

nephrosclerosis, and tubular necrosis) and postrenal causes (eg, all types of
obstruction of the urinary tract, such as stones, enlarged prostate gland,
tumors). Males: 1-17 years: 7-20 mg/dL and > or =18 years: 8-24 mg/dL.
Females: 1-17 years: 7-20 mg/dL and > or =18 years: 6-21 mg/dL. Reference
values have not been established for patients who are <12 months of age.
Serum blood urea nitrogen (BUN) determinations are considerably less
sensitive than BUN clearance (and creatinine clearance) tests, and levels may

not be abnormal until the BUN clearance has diminished to <50%. Clinicians
frequently calculate a convenient relationship, the urea nitrogen/creatinine
ratio: serum bun in mg/dL/serum creatinine in mg/dL. For a normal individual
on a normal diet, the reference interval for the ratio ranges between 12 and
20, with most individuals being between 12 and 16. Significantly lower ratios
denote acute tubular necrosis, low protein intake, starvation or severe liver
disease. High ratios with normal creatinine levels may be noted with catabolic
states of tissue breakdown, prerenal azotemia, high protein intake, etc. High
ratios associated with high creatinine concentrations may denote either
postrenal obstruction or prerenal azotemia superimposed on renal disease.
Because of the variability of both the BUN and creatinine assays, the ratio is
only a rough guide to the nature of the underlying abnormality. Its magnitude
is not tightly regulated in health or disease and should not be considered an
exact quantity.
Blood Glucose Tesing.
Echocardiogram. May be required to assess left ventricular size
Renal imaging with either an ultrasound or an intravenous pyelogram reveals
that kidney size is usually symmetric and may be normal or modestly reduced.
E. MEDICAL AND SURGICAL MANAGEMENT
MEDICAL MANAGEMENT

Treatment involves strict blood pressure control. Most people need to take a
combination of drugs, including an angiotensin II receptor blocker or an
angiotensin converting enzyme (ACE) inhibitor, and possibly calcium channel

blockers, thiazide diuretics, or beta-blockers..

antihypertensive drugs. Effective treatment of the hypertension (diastolic <90)

usually slows the progression of renal injury

It is not clear whether ACE inhibitors and angiotensin II receptor blockers,
which are the drugs of choice for renal protection in patients with proteinuric
chronic

renal

failiure,

are

also

protective

in

patients

with

benign

nephrosclerosis without proteinuria

*There is accumulating evidence for the role of aldosterone as a risk factor for
cardiovascular and renal disease in type 2 diabetes, above and beyond that of
Angiotensin II. Preliminary evidence suggests favorable cardiovascular and renal

effects of blocking aldosterone actions. Further studies are needed to assess the
potential benefits of a combination of ACE/ARB and aldosterone antagonists in
reducing the burden of CVD and renal disease in such a high-risk patient population

ACE inhibitors. Reduce proteinuria, specific renal protective effect both in

diabetic and nondiabetic renal impairment, reduce morbidity and mortality
rates in congestive heart failure, monotherapy less effective in older patients
(>50 y), larger doses required in black patients, innhibit or blunt all adverse
metabolic effects of thiazides, reduce left ventricular hypertrophy and thirst,

dose reduction required in renal failure

Angiotensin II receptor antagonists. Reduce proteinuria, indicated in patients
intolerant of ACE inhibitors, do not cause cough, reduce left ventricular
hypertrophy and thirst similarly to ACE inhibitors, do not interfere with
breakdown of bradykinin

F. NURSING DIAGNOSIS & INTERVENTION

Weight loss, exercise, and salt and water restriction also help control blood pressure.
1.
2.
3.
4.
5.
6.
7.
8.

Risk for Decreased Cardiac Output

Risk for Ineffective Protection
Disturbed Thought Process
Risk for Impaired Skin Integrity
Risk for Impaired Oral Mucous Membrane
Knowledge Deficit
Fluid Volume excesscompromised regulatory mechanism.
Fatiguedecreased metabolic energy production/dietary restriction, anemia,

increased energy requirements, e.g., fever/

9. inflammation, tissue regeneration.
10. Therapeutic Regimen: ineffective managementcomplexity of therapeutic
regimen, decisional conflicts: patient value system; health beliefs, cultural
influences; powerlessness; economic difficulties; family conflict; lack of/refusal
of support systems.
11. Hopelessnessdeteriorating physiological condition, long-term stress,
prolonged activity limitations.

G. BIBLIOGRAPHY:
1. Brunner, Lillian Sholtis., Doris Smith. Suddarth, and Suzanne C. O'Connell.
Smeltzer. "Nephrosclerosis" Brunner & Suddarth's Textbook of Medical-

surgical Nursing. 12th ed. Vol. 1. Philadelphia: Lippincott Williams & Wilkins,
2008. 818-20. Print.
2. Nephrosclerosis. Shaw Science Partners. https://vimeo.com/123838471.
3. High blood pressure dangers: Hypertension's effects on your body. Mayo
Clinic Staff. Retrieved on August 29, 2016 at
http://www.mayoclinic.org/diseases-conditions/high-blood-pressure/indepth/high-blood-pressure/art-20045868
4. Kidney Damage and High Blood Pressure. Updated: June 29 ,2016 retrieved
on August 28 2016 at
http://www.heart.org/HEARTORG/Conditions/HighBloodPressure/WhyBloodPr
essureMatters/Kidney-Damage-and-High-Blood5.
6.
7.
8.

Pressure_UCM_301825_Article.jsp
http://www.rightdiagnosis.com/n/nephrosclerosis/intro.htm
http://www.rightdiagnosis.com/n/nephrosclerosis/video.htm
http://emedicine.medscape.com/article/244342-treatment
Nephron (1999). 82:193198 (DOI:10.1159/000045402) Vol. 82, No. 3, 1999.
Editorial Review Risk Factors Associated with Hypertensive Nephrosclerosis.
Bleyer A.J., Appel R.G. Section on Nephrology, Wake Forest University

School of Medicine, Winston-Salem, N.C., USA

9. (2008, June) Rogers, K. Retrieved on August 25, 2016 at
https://www.britannica.com/science/nephrosclerosis. The Editors of
Encyclopdia Britannica
10. http://www.diabetes.org/are-you-at-risk/lower-your-risk/nonmodifiables.html
11. http://www.nhlbi.nih.gov/health/health-topics/topics/hbp/atrisk
12. http://www.ncbi.nlm.nih.gov/pubmed/823063
13. http://nurseslabs.com/6-chronic-renal-failure-nursing-care-plans/2/
14. http://www.sjkdt.org/article.asp?issn=13192442;year=1999;volume=10;issue=3;spage=267;epage=274;aulast=Meyrier