INTRODUCTION

The kidneys are retroperitoneal organs

situated on the posterior wall of the abdomen on
each side of the vertebral column, at about the level
of the twelfth rib. The left kidney is lightly higher in
the abdomen than the right, due to the presence of
the liver pushing the right kidney down. The kidneys
are essentially regulatory organs which maintain the
volume and composition of body fluid by filtration of
the blood and selective reabsorption or secretion of
filtered solutes.

Chronic renal failure (CRF) is defined as a

permanent reduction in glomerular filtration rate
(GFR) sufficient to produce detectable alterations in
well-being and organ function. This usually occurs at GFR below 25 ml/min. Chronic
Renal Failure / irreversible, renal failure is progressive reduction of functioning renal
tissue such that the remaining kidney mass can no longer maintain the body’s
internal environment. It occurs when the disease or disorder damages the kidneys,
so that they are no longer capable of adequately removing fluids and wastes from
the body or maintain proper level of certain kidney-regulated chemicals in the blood
stream.

It usually occurs over a number of years as the internal structures of the

kidney are slowly damaged. In the early stages, there may be no symptoms. In fact,
progression may be so gradual that symptoms do not occur until kidney function is
less than one-tenth of normal. CRF can develop insidiously over many years, or it
may result from an episode of ARF from which the client has not recovered.

The National Kidney & Transplant Institute (NKTI) has issued a warning
against kidney diseases especially Chronic Renal Failure/ESRD, now the 7 th leading
cause of death in Philippines. According to NKTI, CRF affects 120 per 1 million
populations every year or about one individual per hour. More than 5000 individuals
with ESRD are currently on dialysis treatment.

In the United States, the incidence is 331 new cases per 1 million people. In
United Kingdom, around 32,000 kidney patients are receiving treatment for CRF,
with the number increasing each year. The National Kidney Disease Outcome
Quality Initiative* reported that end-stage renal disease has dramatically increased
in the past two decades, and estimated that close to 20 million Americans probably
have early stages of CKD. There are 400,000 people that have chronic kidney
problems requiring weekly dialysis, and 120,000 suffer acute renal failure, in which
kidney function is knocked out by toxins or infection. Dialysis extends the lives of
these patients, but it's not a cure: life expectancy for most patients is just five
years.

DEFINITION OF DISEASE

ACUTE RENAL FAILURE

Acute renal failure refers to the abrupt loss of kidney function. Over a period of
hours to a few days, the Glomerular Filtration Rate (GFR) decreases. Serum
creatinine and urea nitrogen or blood urea nitrogen (BUN) levels increase. A healthy
adult who eats a normal diet needs a minimum urine output of about 400 ml over
24 hours to excrete the body’s waste products through the kidneys. Any lower
amount indicates a decreased GFR. Oliguria refers to daily outputs of urine between
100 to 400 ml; anuria refers to urine output of less than 100ml.

RISK FACTORS/CAUSES

Pre-renal causes – interfere with renal perfusion.

 Hypovolemia  Excessive diarrhea

 Heart failure  Vomiting
 Hemorrhage  Diuresis
Intra-renal causes – related to nephrotoxicity form drugs.

 Acute tubular necrosis

Post-renal causes – arising from obstruction in the urinary tract.

 Kidney stones  Spinal cord injury

 Tumor  Benign Prostatic Hypertrophy

Causes of Chronic Renal Failure

 Acute renal failure

 Chronic glomerular disease such as glomerulonephritis
 Chronic infection such as pyelonephritis or TB
 A congenital anomaly such as polycystic kidneys
 Collagen diseases such as systemic lupus erythematous
 Endocrine disease such as diabetic nephropathy

Stages of Chronic Renal Failure:

 Reduced Renal Reserve (GFR is 40 to 70 ml/min)

 Renal Insufficiency (GFR is 20 to 40 ml/min)
 Renal Failure (GFR is 10 to 20 ml/min)
 End Stage Renal Disease (GFR is < 10 ml/min)

MANIFESTATIONS

 Anemia – decreased in erythropoietin and bleeding

 Bleeding – result form hypocalcemia and altered pH function because of
increased in BUN
 Pruritus – accumulation of waste products in the blood excreted in the skin.
 Neurologic manifestations – because of uremic encephalopathy,
hypocalcemia and elevated BUN
 Constipation – because of the use of phosphate binders, immobility, fluid
restrictions
 Fatigue – because of anemia
 Pathologic fractures – because of hypocalcemia and hyperparathyroidism
PATHOPHYSIOLOGY

Deterioration and destruction of nephrons

Reduced renal reserve

Increased BUN Decreased glomerular filtration rate Increased creatinine

Glomerular nephropathy as compensation of remaining functioning nephrons

Results to functional vasodilation and increased arterial blood pressure

Dehydration Dilute polyuria Inability of the kidney to concentrate urine loss of sodium in urine

Passage of large volume of dilute urine with large amount of sodium

Chronic increase in pressure and stretch of small arterioles and glomeruli

 Formation of sclerotic lesions or glomerulosclerosis

Further loss of kidney function and ablation of renal mass

Eventually terminates

End stage renal disease

Loss of regulatory renal function loss of excretory function

Inability of inability of inability of kidney inability of

Kidney to kidney to to synthesize 1,25 kidney to

Maintain produce dihydroxidechole- produce

Homeostasis erythropoeitin calciterol HCO3

Renal failure to produce failure to convert

Dysfunction RBC inactive forms of Calcium

anemia decreased calcium absorption

compromised excretion compromised urinary decreased Na reabsorption compromised urinary compromised urinary of
ketones excretion of H ions in the tubules excretion of nitrogeneous excretion of K

waste
H ions replaces Na
hyperkalemia

Metabolic acidosis in the extracellular fluid restriction diuretics uremia

 Fluid

Water retention anuria proteinuria drying of skin increased

BUN increased and

Serum creatinine

Increased circulating blood volume

Hypertension fluid shifting alteration with CNS, lung, heart function

Accelerated Increased LDL

Atherosclerosis

bipedal edema pulmonary congestion heart failure and respiratory

distress
 Rales dyspnea

DEATH
DEFINTION OF THE DISEASE

Chronic renal failure (CRF) is also called chronic kidney failure, chronic renal
insufficiency, or uremia. It is the gradual loss of the kidneys' ability to filter waste
and fluids from the blood. Chronic renal failure can range from mild dysfunction to
severe kidney failure. The kidneys serve as the body's natural filtration system,
removing waste products and fluids from the bloodstream and excreting them in
the urine. The kidneys maintain the body's salt and water balance, which is
important for regulating blood pressure. When the kidneys are damaged by
disease or inherited disorders, they no longer function properly, and lose their
ability to remove fluids and waste from the bloodstream. Fluid and waste products
building up in the body can cause many complications. Most systems in the body,
including the respiratory, circulatory, and digestive systems, are adversely
affected by chronic renal failure (CRF).

Chronic Renal Failure or Chronic Kidney Disease is irreversible and

progressive reduction of functioning renal tissue. When the remaining kidney mass
can no longer maintain the body’s internal environment, renal failure is the result.
This is labeled Stage 5 CKD and is also called End Stage Renal Disease (ESRD).
CKD can develop insidiously over many years, or it may result from an episode of
ARF from which the client has not recovered. (Black, 2009)

The incidence of ESRD or Stage 5 CKD varies widely by state and country. In
the Unites States, the incidence is 338 new cases per million people. According to
the U.S. Renal Data System, at the end of 2003 a total of 441,051 people were
being treated for end-stage renal disease (ESRD); approximately 28% have a
functioning transplant, 66% receive hemodialysis, and 5.7% are undergoing a form
of peritoneal dialysis. This pattern of treatment varies widely globally. (Black,
2009)

Synthesis of the Disease

The National Kidney Foundation (NKF) Kidney Disease Outcome Quality
Initiative (K/DOQI) defined CKD as kidney damage with a glomerular filtration rate
(GFR) of <60ml/minute/1.73m2 for more than 3 months. The NKF developed a
classification system for the stages of CKD (Table 1). Traditionally, the
classification of the type of kidney disease has been focused on pathology and
etiology. The K/DOQI classification system focuses on the GFR, but it remains
important to diagnose the cause of CKD.

There are many diseases that cause CKD; 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 extensive angiotensin II
production all contribute to the pathophysiology. In an attempt to maintain GFR,
the glomerulus hyperfiltrates; 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.

PREDISPOSING FACTOR
• Diabetes, which is the most common risk factor for chronic kidney failure in
the United States

• Age 60 or older

• Kidney disease present at birth (congenital)

• Family history of kidney disease

• Autoimmune Disorder (Lupus eryhtematosus)

• Bladder outlet obstruction (BPH and Prostitis)

• Race (Sickle cell disease)

Precipitating Factors
• Occupational Hazard (overexposure to toxins and to some medications)

• Sedentary Lifestyle (hypertension, atherosclerosis)

 • Diet (High residue diet)

Pathophysiology

Book-Centered:
Etiology: causes include glomerular disorders, tubular disorders, vascular diseases,
infectious or interstitial disorders, ureter obstruction, collagen-related diseases,
metabolic disorders, congenital disorders, and nephrotoxicity
↓
Because Vitamin Phosphorus
Renal dysfunction excretion is lowered
D cannot be
converted into its with poor renal
active form, renal excretory
calcium levels capabilities, leading
drop from poor to
Renal failure (1st stage):
absorption hyperphosphatemia
Renal function is reduced, but no
metabolic wastes accumulate
↓
nd
2 stage:
Metabolic wastes accumulate in the blood
(affected nephrons can no longer compensate)
↓
Symptoms of renal failure increases
↓
3rd stage:
Excessive amounts of metabolic wastes accumulate in the blood.
↓
Kidneys are unable to maintain homeostasis
↓
Death
Decreased renal blood flow

Primary kidney disease

Damage from Diabetes

mellitus or hypertension
 Increased
Increased BUN Decreased glomerular filtration
serum
Creatinine

Hypertrophy of remaining
nephrons

Loss of Na in
Dehydration Dilute polyuria Inability to concentrate urine Hyponatremia
urine

Further loss of nephron

function

Loss of excretory renal

Loss of nonexcretory renal function
function
 Failure to Decreased Decreased Na
produce excretion of reabsorption in
erythropoeitin nitrogenous tubule
wastes

Water retention
Anemia
Uremia
Pallor

Increased BUN Hypertension

Increased Heart Failure

Creatinine

Edema
Proteinuria

Increased Uric
acid
 Chronic renal failure is irreversible and progressive reduction of functional
renal tissue. When the remaining kidney mass can no longer maintain the body’s
internal environment, renal failure is the result.

The causes of CRF are numerous. Various injuries and disease processes may
result kidney failure like CGN, ARF, polycystic kidney disease, obstruction, repeated
episodes of pyelonephritis, and nephrotoxins. Systemic disease like DM,
hypertension, lupus erythematosus, polyarteritis, sickle cell disease, and amyloiosis,
may produce CRF. DM is the leading cause and accounts for more than 30% of
clients who receive dialysis. Hypertension is the second leading cause of CRF.

To reduce the risk of CRF, the client should be closely observed and should
receive adequate treatment to control or slow the progress of these problems
before they progress to ESRD. Some conditions like DM and lupus erythematosus
progress to kidney failure despite close treatment.

The pathogenesis of CRF involves deterioration and destruction of nephrons

with progressive loss of renal function. As the total GRF decreases and clearance is
reduced, serum urea nitrogen and Creatinine levels increase. Remaining functioning
nephrons hypertrophy as they filter a larger load solutes. A consequence is that the
kidneys lose their ability to concentrate urine adequately. To continue excreting the
solutes, a large volume of dilute urine may be passed, which makes the client
susceptible to fluid depletion. The tubules gradually loose their ability to reabsorb
electrolytes. Occasionally, the result is salt wasting, in which urine contains large
amounts of Sodium, which leads to more polyuria.

As renal damage advances and the number of functioning nephrons declines,

the total GFR decreases further. Thus, the body becomes unable to rid itself of
excess water salt and other waste products through the kidneys. When the GFR is
less than 10-20 ml/min, the effect of uremic toxins on the body becomes evident. If
the disease is not treated by dialysis or transplantation, the outcome of CRF is
uremia and death.
 The clinical manifestations of the early stages of renal failure depend on the
disease process and contributing factors. As nephron destruction progresses, the
manifestations are described as uremic syndrome. The clinical manifestations of
CRF are present throughout the body. No organ system is spared. Renal alterations
include the inability of the kidney to concentrate urine and regulate electrolyte
excretion. Polyuria progresses to anuria, and the client loses normal diurnal
patterns of voiding. In addition, all normal functions of the kidney, such as
regulation of acid-base balance, regulation of BP, biogenesis of erythropoietin are
impaired.

Electrolyte balance may be upset by impaired excretion and utilization in the

kidney. Although many clients maintain a normal serum sodium level, the salt-
wasting properties of some failing kidneys, in addition to vomiting and diarrhea,
may cause hyponatremia. Apparent hyponatremia may be a dilutional effect of
water retention often contributes to edema, hypertension and heart failure.

The primary hematologic effect of renal failure is anemia, usually normocytic

and normochromic. It occurs because the kidneys are unable to produce
erythropoietin, a hormone necessary for red blood cell production. If it is left
untreated, hematocrit levels can decrease to less than 20%. Frequently, the fatigue,
weakness, and cold intolerance accompanying the anemia lead to a diagnosis of
renal failure. The mild anemia found in the early stages is usually due to reduced
production of the hormone erythropoietin, which results in decreased production of
red blood cells. Later, hemolysis, GI losses, and clotting abnormalities contribute to
the severity of the condition. Occasionally, the client has iron or folate depletion
because of nutritional deficiencies. Bleeding tendencies become apparent as the
disease progresses. Platelet defects are the primary defect responsible for bleeding
in the uremic client. The accumulation of uremic toxins interferes with platelet
adhesiveness.
Signs and Symptoms
Chronic renal failure (CRF) usually produces symptoms when renal function —
which is measured as the glomerular filtration rate (GFR) — falls below 30 milliliters
per minute (< 30 mL/min). This is approximately 30% of the normal value. When
the glomerular filtration rate (GFR) slows to below 30 mL/min, signs of uremia (high
blood level of protein by-products, such as urea) may become noticeable. When the
GFR falls below 15 mL/min most people become increasingly symptomatic.

Systemic Manifestations:

• Neurological system - cognitive impairment, personality change, asterixis

(motor disturbance that affects groups of muscles), seizures (rare)

• Gastrointestinal system - nausea, vomiting, food distaste (often described

as bland, metallic, "like cardboard")

• Blood-forming system - anemia due to erythropoetin deficiency, easy

bruising and bleeding due to abnormal platelets

• Pulmonary system - fluid in the lungs, with breathing difficulties

• Cardiovascular system - chest pain due to inflammation of the sac

surrounding the heart (pericarditis) and pericardial effusion (fluid
accumulation around the heart)

• Skin - generalized itching

Four stages of decreased renal function:

 • Reduced Renal Reserve – (GFR up to 50 ml/min) a state in which BUN is
high-normal but the client has no clinical manifestations. Normal functioning
is evident as long as the client is not exposed to unusual physiologic or
psychosocial stress.

• Renal insufficiency – (GFR 25 to 50 ml/min) reflects a more advanced

pathologic process with mild azotemia when the client is receiving a general
diet. Impaired urine concentration, nocturia (excessive urination at night),
and mild anemia are common findings.

• Renal failure – (GFR 5 to 25 ml/min) indicated by severe azotemia, acidosis,

impaired urine dilution, severe anemia, and a number of electrolyte
imbalances, such as hypernatremia, hyperkalemia, and hyperphosphatemia

• ESRD – (GFR less than 5 ml/min) characterized by 2 groups of clinical

manifestations: deranged excretory and regulatory mechanisms and a
distinctive grouping of GI, cardiovascular, neuromascular, hematologic,
integumentary, skeletal, and hormonal manifestations. The kidneys can no
longer maintain homeostasis.

Initially it is without specific symptoms and can only be detected as an increase

in serum creatinine or protein in the urine. As the kidney function decreases:

• Blood pressure is increased due to fluid overload and production of

vasoactive hormones leading to hypertension and congestive heart failure

• Urea accumulates, leading to azotemia and ultimately uremia (symptoms

ranging from lethargy to pericarditis and encephalopathy). Urea is excreted
by sweating and crystallizes on skin (uremic frost).

• Potassium accumulates in the blood (known as hyperkalemia with symptoms

ranging from malaise to fatal cardiac arrhythmias)

• Erythropoietin synthesis is decreased (leading to anemia causing fatigue)

• Fluid volume overload - symptoms may range from mild edema to life-
threatening pulmonary edema

• Hyperphosphatemia - due to reduced phosphate excretion, associated with

hypocalcemia. Later this progresses to tertiary hyperparathyroidism, with
hypercalcemia, renal osteodystrophy and vascular calcification

• Metabolic acidosis, due to decreased generation of bicarbonate by the

kidney, is one of the most life threatening consequences of renal failure.
Causes altered enzyme activity by excess acid acting on enzymes and also
depression of the CNS by excess acid interfering with neuronal excitability

• Renal and Urologic: Initially, salt-wasting and consequent hyponatremia

produce hypotension, dry mouth, loss of skin turgor, listlessness, fatigue, and
nausea; later, somnolence and confusion develop. As the number of
functioning nephrons decreases, so does the kidneys’ capacity to excrete
sodium, resulting in salt retention and overload. Accumulation of potassium
causes muscle irritability, then muscle weakness as the potassium levels
arise.

• Cardiovascular: Renal failure leads to hypertension, arrhythmias (including

life-threatening ventricular tachycardia or fibrillation), cardiomyopathy,
uremic pericarditis, pericardial effusion, with possible cardiac tamponade,
heart failure, and periorbital and peripheral edema.

• Respiratory: Pulmonary changes include reduced pulmonary macrophage

activity with increased susceptibility to infection, pulmonary edema, pleuritic
pain, pleural friction rub and effusions, crackles, thick sputum, uremic
pleuritis and uremic lung, dyspnea due to heart failure, and Kussmaul’s
respirations as a result of acidosis.

• GI: Inflammation and ulceration of GI mucosa cause stomatitis, gum

ulceration and bleeding and, possibly, parotitis, esophagitis, gastritis,
duodenal ulcers, lesions on the small and large bowel, uremic colitis,
pancreatitis and proctitis. Other GI symptoms include a metallic taste in the
 mouth, uremic fetor (ammonia smell to breath), anorexia, nausea and
vomiting.

• Cutaneous: Typically, the skin is pallid, yellowish, bronze, dry, and scaly.
Other cutaneous symptoms include severe itching; purpura, ecchymoses,
petechiae; uremic frost (most often in critically ill or terminal illness); thin,
brittle fingernails with characteristic lines, and dry, brittle hair that may
change color and fall out easily.

• Neurologic: Restless leg syndrome, one of the first signs of peripheral

neuropathy, causes pain, burning, and itching in the legs and feet, which may
be relieved by voluntary shaking, moving, or rocking them. Eventually, this
condition progresses to paresthesia and motor nerve dysfunction (usually
bilateral footdrop) unless dialysis is initiated. Other signs and symptoms
include muscle cramping and twitching, shortened memory and attention
span, apathy, drowsiness, irritability, confusion, coma and seizures. EEG
changes indicate metabolic encephalopathy.

• Endocrine: Common endocrine abnormalities include stunted growth patterns

in children (even with elevated growth hormone levels), infertility and
decreased libido in all sexes, amenorrhea and cessation of menses in
females, and impotence, decreased sperm production, and testicular atrophy
in males. Increased aldosterone secretion (related to increased renin
production) and impaired carbohydrate metabolism (increased blood glucose
levels similar to diabetes mellitus) may also occur.

• Hematopoietic: Anemia, decreased red blood cell (RBC) survival time, blood
loss from dialysis and GI bleeding, mild thrombocytopenia, and platelet
defects can occur. Other problems include increased bleeding and clotting
disorders; demonstrated by purpura, hemorrhage from body orifices, easy
bruising, ecchymoses, and petechiae.

• Skeletal: Calcium-phosphorus imbalance and consequent parathyroid

hormone imbalances cause muscle and bone pain, skeletal demineralization,
pathologic fractures, and calcifications in the brain, eyes, gums, joints,
 myocardium, and blood vessels. Arterial calcification may produce coronary
artery disease. In children, renal osteodystrophy (renal rickets) may develop.

DIAGNOSTIC PROCEDURES

In addition to a physical examination and complete medical history,

diagnostic procedures for renal failure may include the following:

Urine tests

A urinalysis may show protein or other abnormalities. An abnormal urinalysis

may occur 6 months to 10 or more years before symptoms appear.

• Creatinine levels progressively increase

• BUN is progressively increased

• Creatinine clearance progressively decreases

• Potassium test may show elevated levels

• Arterial blood gas and blood chemistry analysis may show metabolic acidosis

Twenty–four–hour urine tests: This test requires you to collect all of your urine
for 24 consecutive hours. The urine may be analyzed for protein and waste products
(urea nitrogen and creatinine). The presence of protein in the urine indicates kidney
damage. The amount of creatinine and urea excreted in the urine can be used to
calculate the level of kidney function and the glomerular filtration rate (GFR).

Glomerular filtration rate (GFR): The GFR is a standard means of expressing

overall kidney function. As kidney disease progresses, GFR falls. The normal GFR is
about 100–140 mL/min in men and 85–115 mL/min in women. It decreases in most
people with age. The GFR may be calculated from the amount of waste products in
the 24–hour urine or by using special markers administered intravenously. Patients
are divided into five stages of chronic kidney disease based on their GFR.

URINE SPECIFIC GRAVITY - This is a measure of how concentrated a urine sample

is. Water has a specific gravity of 1.000. A dilute urine sample has a specific gravity
less that 1.020 (often less than 1.010). A concentrated urine sample would have a
specific gravity over 1.030 or 1.040

Blood tests- to determine blood cell counts, electrolyte levels, and kidney function.

The following abnormalities found in the blood may signal CRF:

• Anemia (low red blood cell count)

• High level of parathyroid hormone

• Hypocalcemia (low blood level of calcium)

• Hyperphosphatemia (high blood level of phosphate)

• Hyperkalemia (high blood level of potassium)

• Hyponatremia (low blood level of sodium)

• Low blood level of bicarbonate

• Low plasma pH (blood acidity)

Blood tests

Creatinine and urea (BUN) in the blood: Blood urea nitrogen and serum
creatinine are the most commonly used blood tests to screen for, and monitor renal
disease. Creatinine is a breakdown product of normal muscle breakdown. Urea is
the waste product of breakdown of protein. The level of these substances rises in
the blood as kidney function worsens.
Electrolyte levels and acid–base balance: Kidney dysfunction causes
imbalances in electrolytes, especially potassium, phosphorus, and calcium. High
potassium (hyperkalemia) is a particular concern. The acid–base balance of the
blood is usually disrupted as well.

Decreased production of the active form of vitamin D can cause low levels of
calcium in the blood. Inability to excrete phosphorus by failing kidneys causes its
levels in the blood to rise. Testicular or ovarian hormone levels may also be
abnormal.

Blood cell counts: Because kidney disease disrupts blood cell production and
shortens the survival of red cells, the red blood cell count and hemoglobin may be
low (anemia). Some patients may also have iron deficiency due to blood loss in their
gastrointestinal system. Other nutritional deficiencies may also impair the
production of red cells.

Other Tests

Plain abdominal x-ray - Particularly useful to look for radio-opaque stones or

nephrocalcinosis

Renal ultrasound - a non-invasive test in which a transducer is passed over the

kidney producing sound waves which bounce off the kidney, transmitting a picture
of the organ on a video screen. The test is use to determine the size and shape of
the kidney, and to detect a mass, kidney stone, cyst, or other obstruction or
abnormalities. Ultrasound may show that the kidneys are small in size and
echogenic (a sign of renal scarring), signs that supports a diagnosis of CRF. Kidneys
in CRF are usually smaller (< 9 cm) than normal kidneys with notable exceptions
such as in diabetic nephropathy and polycystic kidney disease.
Renal radionuclide scan - Useful to screen for renal artery stenosis when
performed with captopril administration but is unreliable for GFR of less than 30
cc/min; also quantitates differential renal contribution to total GFR

CT scan - CT scan is useful to better define renal masses and cysts usually noted
on ultrasound. Also, it is the most sensitive test for identifying renal stones. IV
contrast-enhanced CT scans should be avoided in patients with renal impairment to
avoid acute renal failure; this risk significantly increases in patients with moderate-
to-severe CKD. Dehydration also markedly increases this risk.

MRI - is very useful in patients who require a CT scan but who cannot receive
intravenous contrast. It is reliable in the diagnosis of renal vein thrombosis, as are
CT scan and renal venography. Magnetic resonance angiography also is becoming
more useful for diagnosis of renal artery stenosis, although renal arteriography
remains the criterion standard.

Voiding cystourethrogram (VCUG) - Criterion standard for diagnosis of

vesicoureteral reflux

Kidney biopsy - a procedure in which tissue samples are removed (with a needle
or during surgery) from the body for examination under a microscope; to determine
if cancer or other abnormal cells are present.

MEDICAL MANAGEMENT

The goal of therapy is to slow down or halt the otherwise relentless progression
of CRF to ESRD.

1. Control of blood pressure and treatment of the original disease, whenever

feasible, are the broad principles of management. Generally, angiotensin
converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists
(ARBs) are used, as they have been found to slow the progression to ESRD.
 2. Replacement of erythropoietin and vitamin D3, two hormones processed by
the kidney, is usually necessary, as is calcium.
3. Phosphate binders are used to control the serum phosphate levels, which are
usually elevated in chronic renal failure.
4. After ESRD occurs, renal replacement therapy is required, in the form of
either dialysis or a transplant

Preparation for renal replacement therapy (RRT)

Early preparation is important. The health care team educates the patient about the
different procedures involved in RRT, which include the following:

• Hemodialysis- removal of toxic elements from the blood, which is filtered

through a membrane while circulated outside of the body
• Peritoneal dialysis- filtration through the lining membrane of the abdominal
cavity; fluid is instilled into the peritoneal space, then drained
• kidney transplantation

It is important to place an arteriovenous fistula (AVF),a passage between an

artery and a vein that provides a suitable blood vessel for repeated dialysis at least
3 months prior to beginning hemodialysis, because an AVF requires 3 months to
mature before it can be used. The health care team can address the patient's fears
and anxieties about treatment and can clarify the financial, emotional, and social
concerns of RRT.

I. Promote Fluid and Electrolyte and Acid Base Balance

A. Fluid Balance

• Monitor fluid volume status

 Weight – most accurate indicator (daily)
 Input and Output monitoring
 Assessment of skin turgor and mucous membrane
Fluid restrictions
Amount of fluids to be taken per day (400 ml (insensible fluid loss) + previous
 days urine output.

Moisten the lips, give ice chips

Diuretic therapy
Furosemide and Mannitol are often use

B. Electrolyte Balance

1. Hyperkalemia – impaired potassium excretion; indication for dialysis;

result

from metabolic acidosis

 If there is Emergency Hyperkalemia – give 50% dextrose and regular insulin

 Can give sodium bicarbonate – for acidosis
 Client can be given with Sodium Polystyrene Sulfonate (Kayexalate) – can
be given with Sorbitol to promote evacuation; can be given orally or rectally

 Avoid salt substitutes

2. Hyponatremia – restriction of fluids

 Fluid restrictions
3. Hypocalcemia – decreased activation of Vit. D; hyperphosphatemia

 Calcium Carbonate, Calcium Lactate and Vitamin D

 Emergency Hypocalcemia – give Calcium Gluconate IV
4. Hyperphosphatemia – impaired excretion of Phosphate by the kidneys in

the urine

 Phosphate binders – they bind phosphate in the GI tract for excretion

• Aluminum hydroxide – cause constipation so stool softener maybe given
• Aluminum Carbonate – if use for a long period, this can caused dementia
Calcium base phosphate binders – excrete phosphorus but increased Ca.
Calcium Carbonate
Calcium Acetate
 5. Hypermagnesemia – impaired excretion of Magnesium by the kidneys

Magnesium – mainly excreted in the urine; seen in antacids or enemas

 Diuretic therapy
 Avoid magnesium containing antacids or enemas
 Emergence Hypermagnesemia – Give Calcium Gluconate

C. Acid Base Balance

Metabolic Acidosis

• Impaired hydrogen ion excretion

• Increased excretion of bicarbonate
• Accumulation of urea, creatinine and uric acid
• Hyperkalemia
 Give Sodium Bicarbonate – alkalinic meds
 Give Sodium Lactate – alkalinic meds
 Give Shohl’s solution – treatment of metabolic acidosis; caused stomatitis

II. Reserve Renal Function

 Dopamine Hydrochloride – to dilate renal arteries promoting renal perfusion

 Control of hypertension with the use of ACE inhibitors, diet and weight control

III. Optimal Nutrition

 High CHO diet – to spare CHON metabolism

 Low CHON diet but with essential amino acids (50 proteins); 50 mg/day
 Serve foods in small amount – because of nausea, anorexia and stomatitis

IV. Improve Body Chemistry

 Dialysis – method used to remove toxic substances like urea, creatinine, uric
acid

and excess fluid from the blood.

2 methods:

1. Hemodialysis

2. Peritoneal Dialysis

4 Goals of Dialysis

1. Excretion of by products of CHON metabolism.

2. Maintenance of a safe concentration of serum electrolytes.

3. Correction of acidosis and normalization of bicarbonate level.

4. Removal of excess fluid from the blood.

Hemodialysis – arterial blood that is loaded with toxic substances and excess
fluids

and electrolytes flows into a dialyzer and goes back into the venous circulation.

 The procedure may take for 3 – 4 hours, 3 times a day

 AV fistula – due to repeated venipuncture and to prevent blood vessel damage

Nursing Considerations:

1. Strict asepsis should be observed during the procedure.

2. Watch out for signs of hemorrhage.

3. Prothamine sulfate – should be at the bedside – in case of overdose of heparin.

4. Monitor effectiveness of hemodialysis

  Weight loss – indicates effectiveness; weigh client before and after dialysis.
 Monitor serum electrolytes, BUN, Crea and uric acid, blood pH and
bicarbonate level
5. Vital signs monitoring during the procedure.

6. Watch out for hypertension.

7. Watch out for signs of dialysis disequilibrium syndrome – results form imbalance
solute concentration among compartments.
 Seizures, Altered LOC
 Confusion
 Irritability
 8. Watch out for complications:

1. Anemia – because of residual blood loss left in the dialyzer.

2. Bacteremia or infection at the site of AV fistula

3. Hemorrhage and blood clotting.

Peritoneal Dialysis – makes use of the peritoneal cavity as the dialyzer and peritoneal
membrane as the dialysis membrane.

 The fluid is instill into the peritoneal cavity

 3 – 5 cm below the umbilicus, cathteter is inserted to prevent bacterial invasion
 1.5 – 3 liters – dialysate fluid amount.

• Continuous Ambulatory Peritoneal Dialysis – most common type

 1.5 – 3 liters of dialysate fluid is instilled into the peritoneal cavity.
 After emptying, fold the bag and placed it into the pocket.
 Dwell time is 4-6 hours; allow the fluid to stay in the peritoneal cavity for 4 – 6
hours.
 After the dwell time, unfold the bag and placed it below the peritoneal cavity – to
allow the fluid to drain by gravity.
 Infused another dialysate fluid as the process continues.
 Their must be 4 dialysis cycles per day including an 8 hour dwell overnight.

Nursing Considerations:

1. Strict asepsis should be observed throughout the procedure because peritonitis is of a

major concern.

2. Prevent catheter obstruction – results to low dialysate output.

 It there is a decreased dialysate output, instruct client to move side to side.

3. Watch out for signs of complications of dialysis.

1. Hernia – give hernial output.

2. Back muscle exercise for low back pain.

3. Promote effective oxygenation because of limited diaphragmatic expansion.

4. Adequate dietary intake of CHON if with peritonitis.

 5. Hypotension may be occurring due to inadequate dialysate output.

6. Over hydration may develop due to inadequate dialysate output.

7. If there is scarring of the peritoneal membrane, the client is expected to shift to

hemodialysis.

8. Clearance of blood slower than hemodialysis.

IV. Renal Transplantation – surgical implantation of human kidney from a compatible

donor to a recipient.

Post-operative Considerations:

1. Monitor fluid balance

 I and O every 30 – 60 minutes

 Daily weight monitoring
2. Watch out for signs of graft rejections

Signs and symptoms of graft rejection

 Fever
 Tenderness at the site of attachment
 Body malaise
 Anemia
3. Placed an immunosuppressive therapy – to prevent graft rejection

 Cyclophosphamide
4. Monitor serum electrolytes, BUN and Crea, hgb and hct.

5. Allow the client to incorporate the new kidney as a part of the body

6. Vital signs monitoring

Surgical Management

Arteriovenous Fistula
 An AV fistula requires advance planning because a fistula takes a while after
surgery to develop (in rare cases, as long as 24 months). But a properly formed fistula is
less likely than other kinds of vascular accesses to form clots or become infected. Also,
fistulas tend to last many years, longer than any other kind of vascular access.

A surgeon creates an AV fistula by connecting an artery directly to a vein, usually

in the forearm. Connecting the artery to the vein causes more blood flow into the vein.
As a result, the vein grows larger and stronger, making repeated insertions for
hemodialysis treatment easier. For the surgery, you will be given a local anesthetic. In
most cases, the procedure can be performed on an outpatient basis.

These fistulas require up to 6 weeks to mature before they can be used, which
makes this approach inappropriate for immediate hemodialysis. Peritoneal dialysis or
large venous access catheters may be used while the fistula is maturing. External
arteriovenous shunts are rarely used.
 Assessment Nursing Scientific Planning Interventions Rationale Expected
Diagnosis Explanation Outcome

Decreased This happens After 6 hours of >monitor VS >provides Patient’s cardiac

S> cardiac output when the renin nursing baseline data output shall
r/t vascular in the kidney is interventions, >review >for early have improved
O>patient may resistance stimulated to patient will be impending prevention of
manifest: release able to improve failure or shock cardiac
>pale palpebra Angiotensin I. cardiac output tamponade
conjunctiva and Angiotensin I will as evidenced by >monitor >to note Patient shall
lips, be converted to decrease in cardiac rhythm effectiveness of have an
>fatigue Angiotensin II by paleness and medication increased in
>cold clammy ACE. activity >position head >to enhance cardiac output
skin Angiotensin II tolerance of bed or keep venous return as evidence by
>prolonged acts on the trunk horizontal stable vital signs
capillary refill adrenal cortex, while raising
>unstable VS causing it to After 24 hours of legs >to assess fluid
secrete nursing >monitor I&O overload
aldosterone. interventions, >to conserve
Because patient will be >promote energy
aldosterone is a able to manifest adequate rest >to reduce of
potent increase cardiac >encourage anxiety
vasoconstrictor, output as relaxation
it will cause evidenced by technique >to prevent
 vasoconstriction stable vital signs >avoid strenous excessive
on the blood activities workload of the
vessels which heart
increases blood >to promote
resistance. >change circulation
position every 2 >to reduce
hours anxiety
>encourage
verbalization of >to prevent
feelings fluid retention
>maintain IVF
regulation
>monitor
patient’s
response to
activities

Assessment Nursing Scientific Planning Interventions Rationale Expected

Diagnosis Explanation Outcome
S> Altered tissue Because the After 6 hours of >monitor vital >to have a Patient shall
O>patient may perfusion r/t kidney is nursing signs. baseline data have improved
manifest: inability of the damage, one of interventions, tissue perfusion
>easy kidney to its functions is patient will be >monitor intake >to assess fluid
fatigability produce not properly able to improve and output status
>pallor, cold erythropoietin carried out. One tissue perfusion
clammy skin of these as evidenced by >weigh daily >to asses for
> elevation in functions is to decrease in fluid overload
creatinine produce paleness.
>oliguria, erythropoietin, >emphasize diet >protein helps
>Weak capillary which are After 24 hours of restriction limit BUN Patient shall
refill >3 secs., needed for the nursing have maintained
>weak pulse production of interventions, >elevate head >to promote an increase
>decrease Hgb RBC. Thus, the patient will be of bed circulation tissue perfusion
count in the different body able maintain
blood parts are not perfusion as >encourage >conserves
oxygenated evidence of quiet and calm energy
properly absence of environment
paleness and
report of easy >Provide >to reduce
fatigability adequate rest oxygen demand
 >encourage >enhances
early ambulation venous return

>encourage >to decrease

relaxation tension level
techniques

Assessment Nursing Scientific Planning Interventions Rationale Expected

Diagnosis Explanation Outcome

Activity This happens After 6 hours of >monitor vital >to have a Patient shalll
S> intolerance r/t because the nursing signs baseline data have been able
decrease kidney is not interventions, to attain
O>patient may hemoglobin in releasing patient will be >evaluate >to provide improvement in
manifest: the blood erythropoietin to able to improve current comparative activity
>easy be able to activity limitations data tolerance
fatigability, pale produce tolerance as >for early
conjunctiva and adequate RBC. evidence by >assess detection of
lips, With decrease decrease in cardiopulmonary possible adverse Patient shall
>decrease RBC circulating fatigability to physical reaction to the have been able
hemoglobin in the body it activity activity to use identified
count in the will cause After 24 hours of techniques to
blood inadequate nursing >to decrease enhance activity
>altered vital oxygenation interventions, >provide oxygen tolerance
signs leading to patient will be adequate rest consumption
decrease able to use
insufficient identified >to conserve
energy to techniques to >increase energy
endure or enhance activity activity levels
complete tolerance gradually
activities >helps to
>provide minimize
positive frustration
atmosphere >to reduce
stress
>encourage
verbalization of
feelings
>to protect
 >assist patient patient from
wit the activities injury
>to enhance
>promote participation
comfort
measure

Assessment Nursing Scientific Planning Interventions Rationale Expected

Diagnosis Explanation Outcome

S> Fluid volume Because of After 6 hours of >monitor vital >to have a Patient shall
excess r/t damage nursing signs baseline data have been able
O>patient may impaired renal nephrons, the interventions, to improve
manifest: function kidney’s ability patient will be >auscultate >to determine hydration status
>edema, to filter sodium able to improve breath sounds presence of
oliguria, excretion is hydration status crackles Patient shall
>changes in diminished as evidence by have been able
respiratory resulting in decrease in >measure >it may indicate to attain stable
pattern, water retention edema and abdominal girth increasing fluid vital signs,
>BP changes, because sodium normal vital retention decrease signs
specific gravity is reabsorbed in signs of edema
changes, large amount. >record I&O >to assess fluid
decreased Hct Edema will After 24 hours of accurately status
and Hgb, altered result due to nursing
electrolytes, retention of interventions, >weigh daily on >provides a
bibasal rales, sodium and patient will have regular schedule comparative
difficulty of water. a stabilize fluid data
breathing volume as >evaluate
evidenced by edematous >to reduce
balanced I&O, extremities, tissue pressure
vital signs within change position and risk of skin
normal limits, frequently breakdown
and decrease
signs of edema >place in semi-
fowler’s position
 >to facilitate
movement of
diaphragm
improving
>suggest respiratory
interventions effort
such as frequent
oral care >to reduce
discomforts of
fluid restriction

Assessment Nursing Scientific Planning Interventions Rationale Expected

Diagnosis Explanation Outcome

Fatigue r/t This happens After 6 hours of >monitor vital >to provide a Patient shall
S>verbalization presence of because there nursing signs comparative have reported
of an anemia decrease interventions, data improve sense
unremitting and hemoglobin in patient will be >note daily of energy
overwhelming the blood due to able to report energy patterns >helpful in
lack of energy inability of the improve sense determining Patient shall
kidney to of energy pattern/timing of have performed
O>patient may produce a >accept reality activity activities within
manifest, hormone that is of patient >to promote level of ability
>decrease necessary in the After 24 hours of reports of participation
hemoglobin production of nursing fatigue and do
level, easy RBC. With interventions, not
fatigability, cold decrease patient will be underestimate
clammy skin, hemoglobin able to perform effect on quality
pallor, appears circulating in the activities of daily of life
weak and tired body, there is living and >enhances
poor participate in >establish commitment to
oxygenation. desired realistic activity promote optimal
With poor activities at goals with the outcomes
oxygenation, the level of ability patient >to promote
body is not sense of well-
properly >encourage being
energized thus patient to do
leading to whatever
insufficient or possible >indicate the
decrease in need to alter the
capacity for >monitor activity
physical and patient’s
mental work at response to
usual level activity
ASSESSMENT NURSING SCIENTIFIC OBJECTIVES INTERVENTIO RATIONALE EXPECTED
DIAGNOSIS EXPLANATIO NS OUTCOME
N

S: Impaired Skin Due to the loss Short term: Short term:

Integrity r/t of excretory >monitor vital >serves as

O: Patient may possible renal function, After 4 hours signs baseline data The patient

manifest: accumulation there is of nursing shall have

interventions, >assess skin >chronic fluid verbalized
>pruritus of excretory decreased
> scratches waste excretion of
and wounds products in nitrogenous the patient will integrity for excess can understanding

on upper the skin 20 substances, be able to pitting of result in skin of individual

extremities CKD which may verbalize extremities on breakdown causative/risk

>poor skin result to understanding manipulation, factors.

turgor accumulation of individual and

>pale skin of excretory causative/risk demarcation

>dry and scaly waste factors. of clothing and

skin products in shoes on

Long term: patient’s body
>uremic frost the skin Long term:
>this results
leading to After 5 days of >assess for in changes in The patient’s
pruritus. NI, patient’s presence of sensation such optimal skin
Itching may optimal skin peripheral as integrity shall
lead to integrity will neuropathy paresthesia, be maintained
impaired skin maintain as
weakness and as evidenced
integrity as evidenced by
twitching by the
wounds and the absence of
absence of
scratches may scratches and
scratches and
appear. The wounds.
>assess for wounds.
client’s skin >uremic skin
dry, scaling
may also be does not have
skin
dry and scaly the usual
brought about amount of oil
by uremic
frost, a because of

symptom of decreased

CKD which sweat and oil

promotes urea glands

excretion in
the skin in a >assess for
form of sweat. pruritus >pruritus can
be caused by
dry skin and/or
calcium
phosphate
>instruct precipitation
patient to
wear loose- >restrictive

fitting clothing clothing can

when edema increase risk

is present of skin
breakdown
>stress
importance of
not scratching
>scratching
skin and
can cause
 keeping lesions and
fingernails open sores
short

>suggest use
of tepid water >cold water

for bathing may increase

the itch

ASSESSMENT NURSING SCIENTIFIC OBJECTIVES INTERVENTIO RATIONALE EXPECTED

DIAGNOSIS EXPLANATIO NS OUTCOME
N

S: Ø Risk for Injury Accumulation Short term: >establish > to gain the Short term:
O: Patient may r/t body of BUN due to rapport trust of the
manifest: weakness 20 CKD causes After 4 hours patient The patient

> limited ROM disease inadequate of nursing >monitor vital >serves as and his SO

>generalized condition. removal of interventions, baseline data shall have

weakness catabolic
>slowed waste the patient signs >provides verbalized

movements products from and her SO will baseline data understanding

be able to >evaluate of the factors
>difficulty the tissues.
verbalize knowledge of that can
turning Generalized
understanding safety needs contribute to
>postural weakness >serves as
of the factors and injury the possibility
instability results when baseline data
that can prevention of injury and
during energy levels of the extent
performance is used up by contribute to will take action
>assess range of an activity
of ADLs the body the possibility to protect one
of motion that the
>altered faster than it of injury and self.
activities patient can
mentation can be will take action
tolerate and
>inability to produced in to protect one
give
concentrate the muscle self.
precautions to
fibers and prevent injury
Long term:
waste Long term:
products After 3 days of
The patient
builds up nursing >make the
>to prevent shall be free
faster than it interventions, necessary
injury and from possible
can be patient will be things within
keep patient harm like falls
removed. It free from the reach of
away from or trauma.
can also be a possible harm the patient
hazard
result of poor like falls or and protect
 peripheral trauma.
perfusion from fall by

creating raising side

decreased rails or putting

oxygen supply pillows

to most body
>provide
tissue. >to get the
information
participation
regarding
of the patient
disease
and SO in the
condition that
plan of care
may result in
increase risk
of injury

>assist with
ADL like >to prevent
changing of injury
clothing and
position
changes

Bibliography:
Book:

Black, Joyce M. and Hawks, Jane Hokanson (2005), Medical Surgical Nursing. 7th edition, Elsevier Saunders.

Internet Sites:

• http://www.emedicine.com/rc/rc/pimages/i14/renal.htm

• http://www.nlm.nih.gov/medlineplus/ency/article/003107.htm

• http://www.sciencedaily.com/releases/2007/03/070319114512.htm

• http://www.nephrologychannel.com/cfr/#pre

• http://www.technologyreview.com/read_article.aspx?id=17740&ch=biotech&sc=&pg=2