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2. Acute renal failure (ARF) is a sudden and almost complete loss of kidney
function (decreased GFR)over a period of hours to days.
ARF manifests with oliguria, anuria, or normal urine volume.
Oliguria (less than 400 mL/day of urine) is the most common clinical
situation seen in ARF;
Anuria (less than 50 mL/day of urine) and normal urine output are not
as common.
The patient with ARF experiences rising serum creatinine and
BUN (blood urea nitrogen) levels and Retention of other metabolic waste
products (azotemia)
Normally excreted by the kidneys.
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3. Prerenal Failure
• Volume depletion
resulting from; Hemorrhage Renal losses (diuretics)
Gastrointestinal losses (vomiting, diarrhea , nasogastric suction)
• Impaired cardiac efficiency
resulting from; Myocardial infarction, Heart failure, Dysrhythmias, Cardiogenic shock.
• Prolonged renal ischemia
resulting from; Pigment nephropathy (associated with the breakdown of blood cells
containing pigments that in turn occlude kidney structures) Myoglobinuria
(trauma, burns) Hemoglobinuria (transfusion reaction, hemolytic anemia)
• Nephrotoxic agents
such as; Aminoglycoside antibiotics (gentamicin, tobramycin) Solvents and chemicals
(ethylene glycol, carbon tetrachloride, arsenic) Nonsteroidal anti-inflammatory drugs (NSAIDs)
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4. There are four clinical phases of ARF:
1; initiation, 2; oliguria, 3 diuresis, and 4;recovery
Almost every system of the body is affected when there is failure of the normal renal regulatory
mechanisms. The patient may appear critically ill, with persistent nausea, vomiting,
and diarrhea. The skin and mucous membranes are dry from dehydration,
and the breath may have the odor of urine (uremic fetor). Central nervous system
signs and symptoms include drowsiness, headache, muscle twitching, and seizures.
• Infectious processes
such as; Acute pyelonephritis, Acute glomerulonephritis, Postrenal Failure
•urinary tract obsruction
Including; Calculi (stones) Tumors Benign prostatic hyperplasia.
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5. Assessment and Diagnostic Findings
•
Urine output varies (scanty to normal volume), hematuria may be present. Patients with
intrarenal azotemia usually have urinary sodium
levels greater than 40 mcg/L.
The BUN level rises steadily at a rate dependent on the degree of catabolism (breakdown of
protein), renal perfusion, and protein intake. Serum creatinine rises in conjunction with
glomerular damage. Serum creatinine levels are useful in monitoring kidney function and
disease progression.
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6. With a decline in the GFR, the patient cannot excrete potassium normally. Patients with
oliguria and anuria are at greater risk for hyperkalaemia than those without oliguria. Protein
catabolism results in the release of cellular potassium into the body fluids, causing severe
hyperkalaemia (high serum K+ levels). Hyperkalaemia may lead to dysrhythmias and cardiac
arrest.
Patients with acute oliguria cannot eliminate the daily metabolic load of acid-type
substances produced by the normal metabolic processes. In addition, normal renal
buffering mechanisms fail. This is result a fall in the serum CO2-combining power and
blood pH. Thus, progressive metabolic acidosis accompanies renal failure.
There may be an increase in serum phosphate concentrations; serum calcium levels
may be low in response to decreased absorption of calcium from the intestine
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8. A careful history is obtained to determine whether the patient has been taking potentially
nephrotoxic antibiotic agents or has been exposed to environmental toxins. The kidneys are
especially susceptible to the adverse effects of medications because the kidneys are
repeatedly exposed to substances in the blood. They receive a large blood flow (25% of the
cardiac output at rest; the entire blood volume circulates through the kidneys about 14 times
a minute).In patients taking potentially nephrotoxic medications (aminoglycosides,
gentamicin, tobramycin ,colistimethate , polymyxin B, amphotericin B, vancomycin, amikacin,
cyclosporine), renal function should be monitored closely. Serum BUN and creatinine levels
should be obtained at baseline by 24 hours after initiation of these medications and at least
twice a week while the patient is receiving them.
Any agent that reduces renal blood flow (eg , chronic analgesic use) may cause renal
insufficiency. Chronic analgesic use, particularly with NSAIDs, may cause interstitial nephritis.
Patients with heart failure or cirrhosis with ascites are at particular risk for NSAID-induced renal
failure.
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9. The kidney has a remarkable ability to recover from insult. Therefore, the objectives of
treatment of ARF are to restore normal chemical balance and prevent complications until repair
of renal tissue and restoration of renal function can take place. Any possible cause of damage is
identified, treated, and eliminated. Treatment of intrarenal azotemia is supportive, with
removal of causative agents, aggressive management of prerenal and post renal failure.
Adequate blood flow to the kidneys in patients with ARF may be restored by intravenous fluids
or blood product transfusions. If ARF is caused by hypovolemia secondary to
hypoproteinemia, an infusion of albumin may be prescribed. Dialysis may be
initiated to prevent serious complications of ARF, such as hyperkalemia,
severe metabolic acidosis, pericarditis, and pulmonary edema.
Hemodialysis, peritoneal dialysis, or
any of the new continuous renal replacement therapies may be performed.
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10. Because hyperkalemia is the most life-threatening of the fluid and electrolyte disturbances, the
patient is monitored for hyperkalemia through serial serum electrolyte levels (potassium value
more than 5.5mmol/L. The elevated potassium levels may be reduced by administering cation-
exchange (sodium polystyrene sulfonate [Kayexalate]) orally or by enema. Kayexalate works by
exchanging a sodium ion for a potassium ion in the intestinal tract. Sorbitol is often
administered in combination with Kayexalate to induce a diarrhea-type effect (it induces water
loss in the GI tract).
The nurse has an important role in caring for the patient with ARF. the nurse monitors for
complications, participates in emergency treatment of fluid and electrolyte imbalances,
assesses progress and response to treatment, and provides physical and emotional support.
Additionally, the nurse keeps family members informed about the patient’s condition, helps
them understand the treatments, and provides psychological support. Although the
development of ARF may be the most serious problem, the nurse must continue to include in
the plan of care those nursing measures indicated for the primary disorder (eg, burns, shock,
trauma, obstruction of the urinary tract).
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11. Chronic renal failure, or ESRD, is a progressive, irreversible deterioration in renal function in
which the body’s ability to maintain metabolic products, fluid and electrolyte balance fails,
resulting in uremia or azotemia (retention of urea and other nitrogenous wastes in the blood).
The incidence of ESRD has increased by almost 8% per year for the past 5 years, with more than
300,000 patients being treated in the United States . ESRD may be caused by systemic diseases,
such as diabetes mellitus (leading cause); hypertension; chronic glomerulonephritis;
pyelonephritis; obstruction of the urinary tract; hereditary lesions, as in polycystic kidney
disease; vascular disorders; infections; medications; or toxic agents
As renal function declines, the end products of protein metabolism (which are normally
excreted in urine) accumulate in the blood. Uremia develops and adversely affects every
system in the body. The greater the buildup of waste products, the more severe the
symptoms. There are three well-recognized stages of chronic renal disease:
reduced renal reserve, renal insufficiency, and ESRD10/30/2016 Dawar 11

12. The rate of decline in renal function and progression of chronic renal failure
is related to the underlying disorder,
The urinary excretion of protein, and the presence of hypertension.
The disease tends to progress more rapidly in patients
who excrete significant amounts of protein or
have elevated blood pressure than in those without these conditions.
Hypertension (due to sodium and water retention, heart failure and pulmonary edema
(due to fluid overload), and pericarditis (due to irritation of the pericardial lining by uremic
toxins) are among the cardiovascular problems manifested in ESRD. Strict fluid volume control
has been found to normalize hypertension in patients receiving peritoneal dialysis .
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13. Cardiovascular disease is the predominant cause of death in patients with ESRD. In chronic
hemodialysis patients, approximately 45% of overall mortality is attributable to cardiac
disease, and about 20% of these cardiac deaths are due to acute myocardial infarction
Severe itching (pruritus) is common. Uremic frost, the deposit of urea crystals on the
skin, is uncommon today because of early and aggressive treatment of ESRD with
dialysis.
GI signs and symptoms are common and include anorexia, nausea, vomiting, and hiccups.
Neurologic changes, including altered levels of consciousness, inability to concentrate,
muscle twitching, and seizures, have been observed. The precise mechanisms for many of
these signs and symptoms have not been identified. It is generally thought, however, that
the accumulation of uremic waste products is the probable cause.
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14. Reduced renal reserve , characterized by a 40% to 75% loss of nephron function. The patient
usually does not have symptoms because the remaining nephrons are able to carry out the
normal functions of the kidney.
Renal insufficiency occurs when 75% to 90% of nephron function is lost. At this point, the serum
creatinine and blood urea nitrogen rise, the kidney loses its ability to concentrate urine and
anemia develops. The patient may report polyuria and nocturia.
End-stage renal disease (ESRD), the final stage of chronic renal failure, occurs when there is less
than 10% nephron function remaining. All of the normal regulatory, excretory, and hormonal
functions of the kidney are severely impaired. CRD is evidenced by elevated creatinine and
blood urea nitrogen levels as well as electrolyte imbalances. Once the patient reaches this point,
dialysis is usually indicated. Many of the symptoms of uremia are reversible with dialysis.10/30/2016 Dawar 14

15. Weakness and fatigue; confusion; inability to concentrate; disorientation; tremors; seizures;
asterixis; restlessness of legs; burning of soles of feet; behavior changes
Gray-bronze skin color; dry, flaky skin; pruritus; ecchymosis; purpura; thin, brittle nails;
coarse, thinning hair
Hypertension; pitting edema (feet, hands, sacrum); periorbital edema; pericardial friction
rub;engorged neck veins; pericarditis; pericardial effusion; pericardial tamponade;
hyperkalemia; hyperlipidemia
Crackles; thick, tenacious sputum; depressed cough reflex; pleuritic pain; shortness of breath;
tachypnea; Kussmaul-type respirations; uremic pneumonitis; “uremic lung”
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16. Anemia; thrombocytopenia, Amenorrhea; testicular atrophy; infertility;
decreased libido
Muscle cramps; loss of muscle strength; renal osteodystrophy; bone pain; bone fractures;
foot drop
Ammonia odor to breath (“uremic fetor”); metallic taste; mouth ulcerations and bleeding;
anorexia, nausea, and vomiting; hiccups; constipation or diarrhea; bleeding from
gastrointestinal tract
With advanced renal disease, metabolic acidosis occurs because the kidney cannot excrete
increased loads of acid. Decreased acid secretion primarily results from inability of the kidney
tubules to excrete ammonia (NH3 −) and to reabsorb sodium bicarbonate (HCO3 −). There is
also decreased excretion of phosphates and other organic acids.10/30/2016 Dawar 16

17. Decreased GFR can be detected by obtaining a 24-hour
urinalysis for creatinine clearance. As glomerular filtration decreases (due to nonfunctioning
glomeruli), the creatinine clearance value decreases, whereas the serum creatinine and BUN
levels increase. Serum creatinine is the more sensitive indicator of renal function because of its
constant production in the body. The BUN is affected not only by renal disease but also by
protein intake in the diet, catabolism (tissue and RBC breakdown), parenteral nutrition, and
medications such as corticosteroids.
The kidney cannot concentrate or dilute the urine normally in ESRD. Appropriate responses by
the kidney to changes in the daily intake of water and electrolytes, therefore, do not occur.
Some patients retain sodium and water, increasing the risk for edema, heart failure, and
hypertension. Hypertension may also result from activation of the renin–angiotensin–
aldosterone axis and the concomitant increased aldosterone secretion. Other patients have a
tendency to lose salt and run the risk of developing hypotension and hypovolemia. Episodes of
vomiting and diarrhea may produce sodium and water depletion, which worsens the uremic
state.
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18. Potential complications of chronic renal failure that concern the nurse
and that necessitate collaborative approach to care include the following:
• Hyperkalemia due to decreased excretion, metabolic acidosis, catabolism,
and excessive intake (diet, medications, fluids)
• Pericarditis, pericardial effusion, and pericardial tamponade due to retention of
uremic waste products and inadequate dialysis
• Hypertension due to sodium and water retention and malfunction of
the renin–angiotensin– aldosterone system
• Anemia due to decreased erythropoietin production, decreased RBC life span
bleeding in the GI tract from irritating toxins, and blood loss during hemodialysis
• Bone disease and metastatic calcifications due to retention of phosphorus,
low serum calcium levels, abnormal vitamin D metabolism, and elevated aluminum levels
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19. The goal of management is to maintain kidney function and homeostasis for as long as
possible. All factors that contribute to ESRD and all factors that are reversible (eg,
obstruction) are identified and treated. Management is accomplished primarily with
medications and diet therapy, although dialysis may also be needed to decrease the level of
uremic waste products in the blood.
Complications can be prevented or delayed by administering prescribed
antihypertensives, erythropoietin (Epogen), iron supplements, phosphate-binding
agents, and calcium supplements.
Hyperphosphatemia and hypocalcemia are treated with aluminum-based antacids that bind
dietary phosphorus in the GI tract.
Hypertension is managed by intravascular volume control and a variety of
antihypertensive agents. Heart failure and pulmonary edema may also require treatment
with fluid restriction, low-sodium diets, diuretic agents, inotropic agents such as digitalis
or dobutamine, and dialysis.10/30/2016 Dawar 19

20. Anemia associated with chronic renal failure is treated with recombinant human
erythropoietin (Epogen). Anemic patients (hematocrit less than 30%) present with
nonspecific symptoms, such as malaise, general fatigability, and decreased activity tolerance.
Epogen therapy is initiated to achieve a hematocrit of 33% to 38%, which generally alleviates
the symptoms of anemia. Epogen is administered either intravenously or subcutaneously
three times a week.
Hyperkalemia is usually prevented by ensuring adequate dialysis treatments with
potassium removal and careful monitoring of all medications, both oral and intravenous,
for their potassium content. The patient is placed on a potassium-restricted diet.
Occasionally, Kayexalate, a cation-exchange resin, administered orally, may be needed.
The patient with increasing symptoms of chronic renal failure is referred to a dialysis and
transplantation center early in the course of progressive renal disease. Dialysis is usually
initiated when the patient cannot maintain a reasonable lifestyle with conservative
treatment.10/30/2016 Dawar 20

21. Dialysis is used to remove fluid and uremic waste products from the body when the kidneys
cannot do so. It may also be used to treat patients with edema that does not respond to
treatment, hepatic coma, hyperkalemia, hypercalcemia, hypertension, and uremia.
Hemodialysis is the most commonly used method of dialysis: more than 300,000 Americans
currently receive hemodialysis
It is used for patients who are acutely ill and require short-term dialysis (days to weeks) and
for patients with ESRD who require long-term or permanent therapy. A dialyzer (once
referred to as an artificial kidney) serves as a synthetic semipermeable membrane, replacing
the renal glomeruli and tubules as the filter for the impaired kidneys. For patients with
chronic renal failure, hemodialysis prevents death,
Treatments usually occur three times a week for at least 3 to 4 hours per treatment (some
patients undergo short-daily hemodialysis;
There are two types Dialysis,
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22. The objectives of hemodialysis are to extract toxic nitrogenous substances from the blood
and to remove excess water. In hemodialysis, the blood, laden with toxins and nitrogenous
wastes, is diverted from the patient to a machine, a dialyzer, in which the blood is cleansed
and then returned to the patient
Diffusion, osmosis, and ultrafiltration are the principles on which hemodialysis is based. The
toxins and wastes in the blood are removed by diffusion—that is, they move from an area of
higher concentration in the blood to an area of lower concentration in the dialysate. The
dialysate is a solution made up of all the important electrolytes in their ideal extracellular
concentrations. The electrolyte level in the patient’s blood can be brought under control by
properly adjusting the dialysate bath. The semipermeable membrane impedes the diffusion
of large molecules, such as red blood cells and proteins
Ultrafiltration is defined as water moving under high pressure to an area of lower pressure.
This process is much more efficient at water removal than osmosis. Ultrafiltration is
accomplished by applying negative pressure or a suctioning force to the dialysis membrane.
Because patients with renal disease usually cannot excrete water, this force is necessary to
remove fluid to achieve fluid balance10/30/2016 Dawar 22

23. The anticoagulant heparin is administered to keep blood from clotting in the dialysis circuit
Dialyzers or artificial kidneys, are either flat-plate dialyzers or hollow-fiber that contain
thousands of tiny cellophane tubules that act as semipermeable membranes. The blood flows
through the tubules, while a solution (the dialysate) circulates around the tubules. The
exchange of wastes from the blood to the dialysate occurs through the semipermeable
membrane of the tubules
The patient is subject to a number of problems and complications. One leading complication
of patients undergoing maintenance hemodialysis is atherosclerotic cardiovascular disease.
Disturbances of lipid metabolism (hypertriglyceridemia. Heart failure, coronary heart
disease and anginal pain, stroke, . Anemia and fatigue contribute to diminished physical and
emotional well-being, lack of energy and loss of interest, Gastric ulcers and other
gastrointestinal problems occur from the physiologic stress of chronic illness, Disturbed
calcium metabolism leads to renal osteodystrophy that produces bone pain and fractures
other problems include fluid overload associated with heart failure, malnutrition, infection,
neuropathy, and pruritus.10/30/2016 Dawar 23

24. The goals of peritoneal dialysis are to remove toxic substances and metabolic wastes and to
re-establish normal fluid and electrolyte balance. Peritoneal dialysis may be the treatment of
choice for patients with renal failure who are unable or unwilling to undergo hemodialysis or
renal transplantation. Patients who are susceptible to the rapid fluid, electrolyte, and
metabolic changes that occur during hemodialysis experience fewer of these problems with
the slower rate of peritoneal dialysis. Therefore, patients with diabetes or cardiovascular
disease, many older patients, and those who may be at risk for adverse effects of systemic
heparin are likely candidates for peritoneal dialysis
Additionally severe hypertension, heart failure, and pulmonary edema not responsive to
usual treatment with peritoneal dialysis
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25. In peritoneal dialysis, the peritoneum, a serous membrane that covers the abdominal organs
and lines the abdominal wall, serves as the semipermeable membrane. The surface of the
peritoneum constitutes a body surface area of about 22,000 cm2. Sterile dialysate fluid is
introduced into the peritoneal cavity through an abdominal catheter at intervals .
Urea and creatinine, metabolic end products normally excreted by the kidneys,
are cleared from the blood by diffusion and ossmosis as waste product move
from an area of higher concentration (the peritoneal blood supply) to an area of lower
concentration (the peritoneal cavity) across a semipermeable membrane (the peritoneal
membrane). Urea is cleared at a rate of 15 to 20 mL/min, whereas creatinine is removed at a
slower rate. It usually takes 36 to 48 hours . Ultrafiltration (water removal) occurs in
peritoneal dialysis through an osmotic gradient created by using a dialysate fluid with a higher
glucose concentration.
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26. Peritoneal dialysis is not without complications. Most are minor, but several, if unattended,
can have serious consequences.
PERITONITIS (inflammation of the peritoneum) is the most common and most serious
complication of peritoneal dialysis
LEAKAGE of dialysate through the catheter site may occur immediately after the catheter is
inserted. Hypertriglyceridemia is common in patients undergoing long-term peritoneal
dialysis.
Other complications that may occur with long-term peritoneal dialysis include abdominal
hernias (incisional, inguinal, diaphragmatic, and umbilical), probably resulting from
continuously increased intra-abdominal pressure.
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