Renal failure

1. MATERIAL ON
RENAL FAILURE
MATHEW VARGHESE V
MSN (RAK),FHNP (CMC Vellore),CPEPC
Nursing officer
AIIMS Delhi
Renal Failure and its Nursing Management

2. Anatomic and Physiologic Overview
The urinary system comprises the kidneys, ureters, bladder, and urethra. A thorough
understanding of the urinary system is necessary for assessing individuals with acute or chronic
renal dysfunction and implementing appropriate nursing care.
Kidneys
 The kidneys are a pair of brownish-red structures located retroperitoneal on the posterior
wall of the abdomen from the 12th thoracic vertebra to the 3rd lumbar vertebra in the
adult
 An adult kidney weighs 120 to 170 g (about 4.5 oz) and is 12 cm (about 4.5 inches) long,
6 cm wide, and 2.5 cm thick.
 The kidneys are well protected by the ribs, muscles, Gerota’s fascia, perirenal fat, and the
renal capsule, which surround each kidney.
 The kidney consists of two distinct regions, the renal parenchyma and the renal pelvis.
 The renal parenchyma is divided into the cortex and the medulla.
 The cortex contains the glomeruli, proximal and distal tubules, and cortical collecting
ducts and their adjacent peritubular capillaries.
 The medulla resembles conical pyramids.
 The pyramids are situated with the base facing the concave surface of the kidney and the
apex facing the hilum, or pelvis.
 Each kidney contains approximately 8 to 18 pyramids.
 The pyramids drain into 4 to 13 minor calices that, in turn, drain into 2 to 3 major calices
that open directly into the renal pelvis.
 The hilum, or pelvis, is the concave portion of the kidney through which the renal artery
enters and the renal vein exits.
 The renal artery (arising from the abdominal aorta) divides into smaller and smaller
vessels, eventually forming the afferent arteriole.

3.  The afferent arteriole branches to form the glomerulus, which is the capillary bed
responsible for glomerular filtration.
 Blood leaves the glomerulus through the efferent arteriole and flows back to the inferior
vena cava through a network of capillaries and veins.
 Each kidney contains about 1 million nephrons, the functional units of the kidney.
 Each kidney is capable of providing adequate renal function if the opposite kidney is
damaged or becomes nonfunctional.
 The nephron consists of a glomerulus containing afferent and efferent arterioles,
Bowman’s capsule, proximal tubule, loop of Henle, distal tubule, and collecting ducts
 Collecting ducts converge into papillae, which empty into the minor calices, which drain
into three major calices that open directly into the renal pelvis.
 Nephrons are structurally divided into two types: cortical and juxtamedullary.
 Cortical nephrons are found in the cortex of the kidney, and juxtamedullary nephrons sit
adjacent to the medulla.
 The juxtamedullary nephrons are distinguished by their long loops of Henle and the vasa
recta, long capillary loops that dip into the medulla of the kidney.
 The glomerulus is composed of three filtering layers: the capillary endothelium, the
basement membrane, and the epithelium.
 The glomerular membrane normally allows filtration of fluid and small molecules yet
limits passage of larger molecules, such as blood cells and albumin.
 Kidney function begins to decrease at a rate of approximately 1% each year beginning at
approximately age 30.
Physiology of Kidney and renal system
Functions of the Kidney

4.  Urine formation
 Excretion of waste products
 Regulation of electrolytes
 Regulation of acid–base balance
 Control of water balance
 Control of blood pressure
 Regulation of red blood cell production
 Synthesis of vitamin D to active form
 Secretion of prostaglandins
 Urine is formed in the nephrons in a three-step process: filtration, reabsorption, and
excretion.
 Water, electrolytes, and other substances, such as glucose and creatinine, are filtered by
the glomerulus; varying amounts of these are reabsorbed in the renal tubule, or excreted
in the urine.
 Typical normal volumes of these substances during the steps of urine formation given
above boxes. Wide variations may occur in the values depending on diet.
Autoregulation of Blood Pressure
 Regulation of blood pressure is also a function of the kidney. Specialized vessels of the
kidney called the vasa recta constantly monitor blood pressure as blood begins its passage
into the kidney.
 When the vasa recta detect a decrease in blood pressure, specialized juxtaglomerular cells
near the afferent arteriole, distal tubule, and efferent arteriole secrete the hormone renin.

5.  Renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin
II, the most powerful vasoconstrictor known.
Renal Failure
Renal failure results when the kidneys cannot remove the body’s metabolic wastes or perform
their regulatory functions. The substances normally eliminated in the urine accumulate in the
body fluids as a result of impaired renal excretion, leading to a disruption in endocrine and
metabolic functions as well as fluid, electrolyte, and acid–base disturbances. Renal failure is a
systemic disease and is a final common pathway of many different kidney and urinary tract
diseases. Each year, the number of deaths from irreversible renal failure increases
Epidemiology - Global burden (data From WHO)
 The GBD 2015 study estimated that, in 2015, 1.2 million people died from kidney failure,
an increase of 32% since 2005.
 In 2010, an estimated 2.3–7.1 million people with end-stage kidney disease died without
access to chronic dialysis.

6.  Additionally, each year, around 1.7 million people are thought to die from acute kidney
injury. Overall, therefore, an estimated 5–10 million people die annually from kidney
disease
Indian Scenario (Data from National Kidney Foundation India)
 Kidney Diseases Rank 3rd amongst Life-Threatening Diseases after Cancer & Cardiac
ailments in India
 100/million population succumb to kidney diseases
 90,000 kidney transplants per year required in India
 10,000 kidney transplant per year required in Maharashtra
 Only 22.5% of patients requiring dialysis receive treatment
 Only 2.5% of patients in kidney failure receive transplants.
 There is no renal disease registry in India
 As per their study conducted in north India the prevalence of CKD stage 3 and beyond
was found in 0.79% subjects out of 4,972 examined.
 This study also evaluated the prevalence of risk factors for CKD, like diabetes,
hypertension, renal stone disease, etc.
 While extrapolating, the authors concluded that the prevalence of ESRD in India will be
785 pmp and the incidence of ESRD will be 160 pmp.
 The commonest cause of CKD in this population-based study was diabetic nephropathy
responsible for 41% cases.
Types of Renal Failure
1. Acute Renal Failure (ARF)
2. Chronic Renal Failure (CRF)
Acute Renal Failure (ARF) OR Acute Kidney Injury (AKI)
The kidney has multiple functions and approximately one in five people admitted to emergency
will suffer from some degree of Acute Kidney Injury (AKI). AKI is viewed as a spectrum of
injury, which may result in organ failure and the need for Renal Replacement Therapy (RRT).
AKI is the sudden and almost complete loss of kidney function (decreased GFR) over a period of
hours to days. Acute kidney injury is defined as an abrupt change in serum creatinine and/or
urine output, and a majority of patients admitted to the ICU have some evidence of the disorder.
AKI is a clinical syndrome denoted by an abrupt decline in glomerular filtration rate (GFR)
sufficient to decrease the elimination of nitrogenous waste products (urea and creatinine) and
other uremic toxins. This has been traditionally referred to as Acute Renal Failure (ARF).

7. Definition
According to Acute Kidney Injury Network
AKI is a decline in kidney function over 48hrs as demonstrated by an increase in serum
creatinine of greater than 0.3mg/dl, an increase in serum creatinine of more than 50%, or the
development of oliguria.
Causes of Acute Renal Failure
Based on causes ARF can be divided in to 3
1. Prerenal Failure
 Volume depletion resulting from:
 Hemorrhage
 Renal losses (diuretics, osmotic diuresis)
 Gastrointestinal losses (vomiting, diarrhea, nasogastric suction)
 Impaired cardiac efficiency resulting from:
 Myocardial infarction
 Heart failure
 Dysrhythmias
 Cardiogenic shock
 Vasodilatation resulting from:
 Sepsis
 Anaphylaxis
 Antihypertensive medications or other medications that cause vasodilatation
2. Intrarenal Failure
 Prolonged renal ischemia resulting from:
 Pigment nephropathy (associated with the breakdown of blood cells containing
pigments that in turn occlude kidney structures)
 Myoglobinuria (trauma, crush injuries, burns)
 Hemoglobinuria (transfusion reaction, hemolytic anemia)
 Nephrotoxic agents such as:
 Aminoglycoside antibiotics (gentamicin, tobramycin)
 Radiopaque contrast agents
 Heavy metals (lead, mercury)
 Solvents and chemicals (ethylene glycol, carbon tetrachloride, arsenic)
 Nonsteroidal anti-inflammatory drugs (NSAIDs)
 Angiotensin-converting enzyme inhibitors (ACE inhibitors)
 Infectious processes such as:
 Acute pyelonephritis
 Acute glomerulonephritis

8. 3. Post renal Failure
 Urinary tract obstruction, including:
 Calculi (stones)
 Tumors
 Benign prostatic hyperplasia
 Strictures
 Blood clots
Comparison of Types of ARF
Pathophysiology
 Acute renal failure (ARF) is a sudden and almost complete loss of kidney function
(decreased GFR) over a period of hours to days.
 Although ARF is often thought of as a problem seen only in hospitalized patients, it may
occur in the outpatient setting as well.
 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.
 Regardless of the volume of urine excreted, the patient with ARF experiences rising
serum creatinine and BUN levels and retention of other metabolic waste products
(azotemia) normally excreted by the kidneys.
Pre renal Failure
 Prerenal conditions occur as a result of impaired blood flow that leads to hypoperfusion
of the kidney and a drop in the GFR.

9.  Common clinical situations are volume-depletion states (hemorrhage or GI losses),
impaired cardiac performance (myocardial infarction, heart failure, or cardiogenic shock),
and vasodilation (sepsis or anaphylaxis).
Intra renal Failure
 Intrarenal causes of ARF are the result of actual parenchymal damage to the glomeruli or
kidney tubules.
 Conditions such as burns, crush injuries, and infections, as well as nephrotoxic agents,
may lead to acute tubular necrosis and cessation of renal function.
Post renal Failure
 Post renal causes of ARF are usually the result of an obstruction somewhere distal to the
kidney. Pressure rises in the kidney tubules; eventually, the GFR decreases.
STAGES OF (AKI)
1. Initiating stage;
2. Oliguric stage;
3. Diuretic stage;
4. Recovery stage
Initiating stage:
 This occurs when the kidneys are injured and when diagnosis is made and treatment is
established it can last from hours to days.
 The initiation period begins with the initial insult and ends when Oliguria develops
Oliguric stage:
 This lasts from 5 to 15 days.
 The oliguria period is accompanied by a rise in the serum concentration of substances
usually excreted by the kidneys (urea, creatinine, uric acid, organic acids, and the
intracellular cations [potassium and magnesium]).
 The minimum amount of urine needed to rid the body of normal metabolic waste
products is 400 mL.
 In this phase uremic symptoms first appear and life-threatening conditions such as
hyperkalemia develop.
 There is decrease in erythropoietin production, tubular transport urine formation and
glomerular filtration.
 Fibrous scar tissue is formed which replaces the basement membrane. and the nephrons
are clogged with inflammatory product.
 There can be bleeding or infection during this stage.
Diuretic stage:
 In the diuresis period, the third phase, the patient experiences gradually increasing urine
output, which signals that glomerular filtration has started to recover.
 Laboratory values stop rising and eventually decrease.

10.  Although the volume of urinary output may reach normal or elevated levels, renal
function may still be markedly abnormal. Because uremic symptoms may still be present
and the need for expert medical and nursing management continues.
 The patient must be observed closely for dehydration during this phase; if dehydration
occurs, the uremic symptoms are likely to increase
Recovery stage:
 The recovery period signals the improvement of renal function and may take 3 to 12
months.
 Laboratory values return to the patient’s normal level. Although a permanent 1% to 3%
reduction in the GFR is common, it is not clinically significant.
Signs and symptoms of acute kidney fail
 Decreased urine output, although occasionally urine output remains normal
 Fluid retention, causing swelling in your legs, ankles or feet

11.  Shortness of breath
 Fatigue
 Confusion
 Nausea
 Weakness
 Irregular heartbeat
 Chest pain or pressure
 Seizures or coma in severe cases
Assessment and Diagnostic Findings
CHANGES IN URINE
 Urine output varies (scanty to normal volume)
 Hematuria maybe present
 Urine has a low specific gravity (1.010 or less, compared with a normal value of 1.015 to
1.025).
 Patients with prerenal azotemia have a decreased amount of sodium in the urine (below
20 mEq/L) and normal urinary sediment.
 Patients with intrarenal azotemia usually have urinary sodium levels greater than 40
mEq/L with casts and other cellular debris.
 Urinary casts are mucoproteins secreted by the renal tubules whenever inflammation is
present.
CHANGE IN KIDNEY CONTOUR
 Ultrasonography is a critical component of the evaluation of both acute and chronic renal
failure.
 Although many sonographic findings are nonspecific, their diagnostic utility is greatly
enhanced by a familiarity with the clinical presentation and a thorough understanding of
renal pathophysiology
INCREASED BUN AND CREATININE LEVELS (AZOTEMIA)
 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 kidneyfunction and disease progression.
HYPERKALEMIA
 With a decline in the GFR, the patient cannot excrete potassium normally.

12.  Patients with oliguria and anuria are at greater risk for hyperkalemia than those without
oliguria.
 Protein catabolism results in the release of cellular potassium into the body fluids,
causing severe hyperkalemia (high serum K+ levels).
 Hyperkalemia may lead to dysrhythmias and cardiac arrest.
METABOLIC ACIDOSIS
 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 reflected by a fall in the serum CO2-combining power and blood pH.
 Thus, progressive metabolic acidosis accompanies renal failure.
CALCIUM AND PHOSPHORUS ABNORMALITIES
 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 and as a
compensatory mechanism for the elevated serum phosphate levels.
ANEMIA
 Anemia inevitably accompanies ARF due to reduced erythropoietinproduction, uremic GI
lesions, reduced RBC life span, and blood loss, usually from the GI tract.
 With use of the parenteral form of erythropoietin (Epogen), anemia is not the major
problem it once was.
DIAGNOSTIC APPROACH TO AKI
Assessment
1. History
History of present illness
 Onset and duration
 Changes in urine volume,
 Hematuria
 Urine sediments
 Anemia
Past history: H/o of Hypovolemia, septic shock, major surgery
Recent exposure to nephrotoxic medications, radiocontrast agents, endogenous toxins
Social history: drug abuse, occupational exposure
Family history of renal disease

13. 2. Physical assessment:
General appearance: patient is usually well with mild disease, advanced disease manifests as
uremic symptoms, pallor from anemia and yellow discoloration from deposition of urochromes,
Vital signs
Tachycardia, commonly high B.P. low B.P: poor renal perfusion, volume depletion, cardiogenic
shock and sepsis.
3. Lab investigations:
 Urinalysis & Urine microscopy
Protein: acute tubular necrosis
blood, crystals, infection
Anuria suggests complete urinary tract obstruction
 Elevated Serum creatinine & BUN (azotemia)
 Hyper kalmia
 Hyperphosphatemia
 Hypocalcemia
 Hyperuricemia >15mg/dl
4. For localization of obstruction: Renal sonogram, Plane x ray, CT or MRI, Retrograde or
anterograde pyelography
5. For suspected vascular obstruction: Magnetic resonance angiography, Doppler
ultrasound, CT based angiography
6. Renal Biopsy is reserved for patients in whom prerenal and postrenal AKI have been
excluded and the cause of intrinsic AKI is unclear.
 Glomerulonephritis
 vasculitis
 Allergic interstitial nephritis.

14. Management of AKI
Medical Management
 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.
 Prerenal azotemia is treated by optimizing renal perfusion, whereas postrenal failure is
treated by relieving the obstruction. Treatment of intrarenal azotemia is supportive, with
removal of causative agents, aggressive management of prerenal and postrenal failure,
and avoidance of associated risk factors. Shock and infection, if present, are treated
promptly.
Overall, medical management includes
1. Maintaining fluid balance
2. Avoiding fluid excesses
3. Performing dialysis
1. Maintenance of fluid balance
 It is based on daily body weight, serial measurements of central venous pressure,
serum and urine concentrations, fluid losses, blood pressure, and the clinical
status of the patient.
 The Parenteral and oral intake and the output of urine, gastric drainage, stools,
wound drainage, and perspiration are calculated and are used as the basis for fluid
replacement.
 The insensible fluid lost through the skin and lungs and produced through the
normal metabolic processes is also considered in fluid management.
 Adequate blood flow to the kidneys in patients with Prerenal causes of ARF may
be restored by intravenous fluids or bloodproduct transfusions.
 If ARF is caused by hypovolemia secondary to hypoproteinemia, an infusion of
albumin may be prescribed.
2. Avoiding fluid excesses
 Fluid excesses can be detected by the clinical findings of dyspnea,tachycardia,
and distended neck veins.
 The lungs are auscultated for moist crackles. Because pulmonary edema may be
caused by excessive administration of parenteral fluids, extreme caution must be
used to prevent fluid overload.
 The development of generalized edema is assessed by examining the presacral
and pre tibialareas several times daily.
 Mannitol, furosemide, or ethacrynicacid may be prescribed to initiate a diuresis
and prevent or minimize subsequent renal failure.
3. Performing dialysis
Dialysis may be initiated to prevent serious complications of ARF, such as hyperkalemia, severe
metabolic acidosis, pericarditis and pulmonary edema. Dialysis corrects many biochemical

15. abnormalities; allows for liberalization of fluid, protein, and sodium intake; diminishes bleeding
tendencies; and may help wound healing. Hemodialysis, peritoneal dialysis, or any of the new
continuous renal replacement therapies may be performed.
Pharmacologic Therapy
Management of hyperkalemia
 Hyperkalemia is the most life-threatening of the fluid andelectrolyte disturbances, the
patient is monitored for hyperkalemiathrough serial serum electrolyte levels (potassium
valuemore than 5.5 mEq/L [5.5 mmol/L]), electrocardiogram changes (tall, tented, or
peaked T waves), and changes in clinical status.
 The elevated potassium levels may be reduced by administering cation-exchange resins
(sodium polystyrene sulfonate [Kayexalate]) orally or by retention enema.
 Kayexalate works by exchanging asodium 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).
 If a retention enema is administered (the colon is the major site for potassium exchange),
a rectal catheter with a balloon maybe used to facilitate retention if necessary.
 The patient should retain the resin 30 to 45 minutes to promote potassium removal.
 Afterward, a cleansing enema may be prescribed to remove the Kayexalate resin as a
precaution against fecal impaction.
 All external sources of potassium (foods, saltsubstitutes, medications) are eliminated or reduced.
 Sodium bicarbonate may be administered to elevate the plasma pH.
 Sodium bicarbonate increases the pH, which causes potassium to move into the cell, and
the result is lowering of the serum potassium level.
 This is short-term therapy and is used with other long-term measures, such as dietary
restriction and dialysis.
Adjustment of drug dose
Because many medications are eliminated through the kidneys,medication dosages must be
reduced when a patient has ARF. Examples of commonly used medications that require
adjustment are antibiotic agents (especially aminoglycosides), digoxin, ACE inhibitors, and
medications containing magnesium.
Diuretics
Diuretic agents are often used to control fluid volume, but they have not been shown to hasten
the recovery from ARF.
Dopamine
Low-dose dopamine (1 to 3 mg/kg) is often used to dilate the renal arteries through stimulation
of dopaminergic receptors; however, research has not definitely demonstrated that dopamine
prevents ARF or improves outcome in patients with established renal failure.
ANP
Atrial natriuretic peptide (ANP), an endogenous hormone synthesized by the cardiac atria, has
been shown to improve renal function in multiple animal models of ARF. It has also decreased
the need for dialysis in patients with oliguric acute tubular necrosis in a multisite clinical trial of
patients.

16. NaHCo3 and Phosphate Binders
In patients with severe acidosis, the arterial blood gases or serum bicarbonate levels (CO2-
combining power) must be monitored ,because the patient may require sodium bicarbonate
therapy or dialysis. If respiratory problems develop, appropriate ventilator measures must be
instituted. The elevated serum phosphate level may be controlled with phosphate-binding agents
(aluminum hydroxide). These agents help prevent a continuing rise in serum phosphate levels by
decreasing the absorption of phosphate from the intestinal tract.
Nutritional Therapy
 ARF causes severe nutritional imbalances (because nausea and vomiting contribute to
inadequate dietary intake), impaired glucose use and protein synthesis, and increased
tissue catabolism.
 The patient is weighed daily and can be expected to lose 0.2 to0.5 kg (0.5 to 1 lb) daily. If
the nitrogen balance is negative (ie, the patient’s caloric intake falls below caloric
requirements). If the patient gains or does not lose weight or develops hypertension, fluid
retention should be suspected.
 Dietary proteins are limited to about 1 g/kg during the Oliguric phase to minimize protein
breakdown and to prevent accumulation of toxic end products. Caloric requirements are
met with high-carbohydrate meals because carbohydrates have a protein sparing effect
(ie, in a high-carbohydrate diet, protein is not used for meeting energy requirements but is
“spared” for growth and tissue healing).
 Foods and fluids containing potassium or phosphorus (bananas, citrus fruits and juices,
coffee) are restricted.
 Potassium intake is usually restricted to 40 to 60 mEq/day, and sodium is usually
restricted to 2 g/day.
 The patient may require parenteral nutrition.
 Blood chemistry evaluations are made to determine the amounts of sodium, potassium,
and water needed for replacement, along with assessment for over hydration or under
hydration.
 After the diuretic phase, the patient is placed on a high-protein, high-calorie diet and is
encouraged to resume activities gradually.
Nursing Management
 The nurse has an important role in caring for the patient with ARF.
 In addition to directing attention to the patient’s primary disorder, 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, and obstruction of the urinary tract).
 The major nurses responsibilities are as follows

17. 1. Monitoring Fluid And Electrolyte Balance
 Because of the serious fluid and electrolyte imbalances that can occur with ARF, the
nurse monitors the patient’s serum electrolyte levels and physical indicators of these
complications during all phases of the disorder.
 Hyperkalemia is the most immediate life threatening imbalance seen in ARF.
 Parenteral fluids, all oral intake, and all medications are screened carefully to ensure that
hidden sources of potassium are not inadvertently administered or consumed.
 Intravenous solutions must be carefully selected according to the patient’s fluid and
electrolyte status.
 The patient’s cardiac function and musculoskeletal status are monitored closely for signs
of hyperkalemia.
 The nurse monitors fluid status by paying careful attention to fluid intake (intravenous
medications should be administered in the smallest volume possible), urine output,
apparent edema, distention of the jugular veins, alterations in heart sounds and breath
sounds, and increasing difficulty in breathing.
 Accurate daily weights, as well as intake and output records, are essential. Indicators of
deteriorating fluid and electrolyte status are reported immediately to the physician, and
preparation is made for emergency treatment.
 Hyperkalemia is treated with glucose and insulin, calcium gluconate, cation-exchange
resins (Kayexalate),or dialysis.
 Fluid and other electrolyte disturbances are often treated with hemodialysis, peritoneal
dialysis, or other continuous renal replacement therapies.
2. Reducing Metabolic Rate
 The nurse also directs attention to reducing the patient’s metabolic rate during the acute
stage of renal failure to reduce catabolismand the subsequent release of potassium and
accumulation of endogenous waste products (urea and creatinine).
 Bed rest may be indicated to reduce exertion and the metabolic rate during the most acute
stage of the disorder.
 Fever and infection, both of which increase the metabolic rate and catabolism, are
prevented or treated promptly.
3. Promoting Pulmonary Function
 Attention is given to pulmonary function, and the patient is assisted to turn, cough, and
take deep breaths frequently to prevent atelectasis and respiratory tract infection.
 Drowsiness and lethargy may prevent the patient from moving and turning without
encouragement and assistance.
4. Preventing Infection
 Asepsis is essential with invasive lines and catheters to minimize the risk of infection and
increased metabolism.
 An indwelling urinary catheter is avoided whenever possible because of the high risk for
UTI associated with its use.
5. Providing Skin Care
 The skin may be dry or susceptible to breakdown as a result of edema; therefore,
meticulous skin care is important.
 Additionally, excoriation and itching of the skin may result from the deposit of irritating
toxins in the patient’s tissues.

18.  Massaging bony prominences, turning the patient frequently, and bathing the patient with
cool water are often comforting and prevent skin breakdown.
6. Providing Support
 The patient with ARF requires treatment with hemodialysis, peritoneal dialysis, or
continuous renal replacement therapies to prevent serious complications.
 The patient and family need assistance, explanation, and support during this time. The
purpose and rationale of the treatments are explained to the patient and family by the
physician.
 High levels of anxiety and fear, however, may necessitate repeated explanation and
clarification by the nurse.
 The family members may initially be afraid to touch and talk to the patient during the
procedure but should be encouraged and assisted to do so.
 Although many of the nurse’s functions are devoted to the technical aspects of the
procedure, the psychological needs and concerns of the patient and family cannot be
ignored.
 Continued assessment of the patient for complications of ARF and of its precipitating
cause is essential.
Prevention of Acute Renal Failure
1. Provide adequate hydration to patients at risk for dehydration:
 Surgical patients before, during, and after surgery
 Patients undergoing intensive diagnostic studies requiring fluid restriction and
contrast agents (eg, barium enema, intravenous pyelograms), especially elderly
patients who may not have adequate renal reserve
 Patients with neoplastic disorders or disorders of metabolism (ie, gout) and those
receiving chemotherapy
2. Prevent and treat shock promptly with blood and fluid replacement.
3. Monitor central venous and arterial pressures and hourly urine output of critically ill
patients to detect the onset of renal failure as early as possible.
4. Treat hypotension promptly.
5. Continually assess renal function (urine output, laboratory values) when appropriate.
6. Take precautions to ensure that the appropriate blood is administered to the correct
patient in order to avoid severe transfusion reactions, which can precipitate renal failure.
7. Prevent and treat infections promptly. Infections can produce progressive renal damage
8. Pay special attention to wounds, burns, and other precursors of sepsis.
9. Give meticulous care to patients with indwelling catheters to prevent infections from
ascending in the urinary tract. Remove catheters as soon as possible.
10. To prevent toxic drug effects, closely monitor dosage, duration of use, and blood levels
of all medications metabolized or excreted by the kidneys.
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19. CHRONIC RENAL FAILURE (END-STAGE RENAL DISEASE)
CRF is defined as irreversible deterioration in renal function which classically develops over a period of
year. Also known as Chronic Kidney disease (CKD)
Definition – CKD
Chronic renal failure, or ESRD, is a progressive, irreversible deterioration in renal function in
which the body’s ability to maintain metabolic and fluid and electrolyte balance fails, resulting in
uremia or azotemia (retention of urea and other nitrogenous wastes in the blood).
Causes and Risk Factors
 Diabetes mellitus
 Hypertension
 Autoimmune disease
 Older age
 African ancestry
 A family history of renal disease,
 A previous episode of acute renal failure
 Structural abnormalities of the urinary tract
 Primary glomerular diseases
 Hereditary nephropathies,
Stages of CRF

20. Warning Signs or Early Signs of CRF

21. Signs and Symptoms of Chronic Renal Failure
1. Neurologic
 Weakness and fatigue
 Confusion
 Inability to concentrate
 Disorientation
 Tremors
 Seizures
 Asterixis
 Restlessness of legs
 Burning of soles of feet
 Behavior changes
2. Integumentary
 Gray-bronze skin color
 Dry, flaky skin
 Pruritus
 Ecchymosis
 Purpura
 Thin, brittle nails
 Coarse, thinning hair
3. Cardiovascular
 Hypertension
 Pitting edema (feet, hands, sacrum)
 Periorbital edema
 Pericardial friction rub
 Engorged neck vein
 Pericarditis
 Pericardial effusion
 Pericardial tamponade
 Hyperkalemia
 Hyperlipidemia
4. Pulmonary
 Crackles
 Thick
 Tenacious sputum
 Depressed cough reflex
 Pleuritic pain
 Shortness of breath
 Tachypnea
 Kussmaul-type respirations
 Uremic pneumonitis; “uremic lung”

22. 5. Gastrointestinal
 Ammonia odor to breath (“uremic fetor”)
 Metallic taste
 Mouth ulcerations and bleeding
 Anorexia
 Nausea and vomiting
 Hiccups
 Constipation or diarrhea
 Bleeding from gastrointestinal tract
6. Hematologic
 Anemia
 Thrombocytopenia
7. Reproductive
 Amenorrhea
 Testicular atrophy
 Infertility;
 Decreased libido
8. Musculoskeletal
 Muscle cramps
 Loss of muscle strength;
 Renal osteodystrophy
 Bone pain
 Bone fractures
 Foot drop
Diagnosis of CRF
Urinetests:
 Urinalysis: dipstick test, urine albumin &creatinine.
 Twenty-four-hour urine tests
 Glomerular filtration rate
Blood tests:
 Creatinine and urea Electrolyte
 Blood cell counts, Erythropoietin, PTH, Acidosis, ABG analysis ,hemoglobin,Calcium
and phosphorus imbalance, albumin-to-creatinine ratio in a spot first-morning urine
sample
Other tests:
 Abdominal ultrasound, Renal Biopsy, Abdominal CT scan, Abdominal MRI, Renal scan,
Bone density test
Complications
Potential complications of chronic renal failure that concern the nurse and that necessitate a
collaborative approach to care includethe following:

23. 1. Hyperkalemia due to decreased excretion, metabolic acidosis, catabolism, and excessive
intake (diet, medications, fluids)
2. Pericarditis, pericardial effusion, and pericardial tamponade due to retention of uremic
waste products and inadequate dialysis
3. Hypertension due to sodium and water retention and malfunction of the renin–
angiotensin–aldosterone system
4. Anemia due to decreased erythropoietin production, decreased RBC life span, bleeding in
the GI tract from irritating toxins, and blood loss during hemodialysis
5. Bone disease and metastatic calcifications due to retention of phosphorus, low serum
calcium levels, abnormal vitamin D metabolism, and elevated aluminum levels
Medical Management
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
Pharmacologic Therapy
1. Antacids. Hyperphosphatemia and hypocalcemia are treated with aluminum-based
antacids that bind dietary phosphorus in the GI tract.
2. Antihypertensive and Cardiovascular Agents. 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.
3. Antiseizure Agents. Neurologic abnormalities may occur, so the patient must be
observed for early evidence of slight twitching,headache, delirium, or seizure activity. If
seizures occur, the onsetof the seizure is recorded along with the type, duration, and
general effect on the patient. The physician is notified immediately. Intravenous
diazepam (Valium) or phenytoin (Dilantin) is usually administered to control seizures.
The side rails of the bed should be padded to protect the patient.
4. Erythropoietin. Anemia associated with chronic renal failure is treated with recombinant
human erythropoietin (Epogen). The patient receiving Epogen may experience influenza-
like symptoms with initiation of therapy; these tend to subside with repeated doses.
Management
DIALYSIS
Dialysis performs the function of the kidneys if they’ve failed. According to the National Kidney
Foundation, end-stage kidney failure occurs when the kidneys are performing at only 10 to 15
percent of their normal function.Dialysis is a treatment that filters and purifies the blood using a
machine. This helps keep your fluids and electrolytes in balance when the kidneys can’t do their
job.Dialysis has been used since the 1940s to treat people with kidney problems.

24. Types of dialysis
There are three different types of dialysis.
A. Hemodialysis
Hemodialysis is the most common type of dialysis. This process uses an artificial kidney
(hemodialyzer) to remove waste and extra fluid from the blood. The blood is removed from the
body and filtered through the artificial kidney. The filtered blood is then returned to the body
with the help of a dialysis machine.
To get the blood to flow to the artificial kidney, your doctor will perform surgery to create an
entrance point (vascular access) into your blood vessels. The three types of entrance points are:
 Arteriovenous (AV) fistula. This type connects an artery and a vein. It’s the preferred
option.
 AV graft. This type is a looped tube.
 Vascular access catheter. This may be inserted into the large vein in your neck.

25. Both the AV fistula and AV graft are designed for long-term dialysis treatments. People who
receive AV fistulas are healed and ready to begin hemodialysis two to three months after their
surgery. People who receive AV grafts are ready in two to three weeks. Catheters are designed
for short-term or temporary use.
Hemodialysis treatments usually last three to five hours and are performed three times per week.
However, hemodialysis treatment can also be completed in shorter, more frequent sessions.
Most hemodialysis treatments are performed at a hospital, doctor’s office, or dialysis center. The
length of treatment depends on your body size, the amount of waste in your body, and the current
state of your health.
After you’ve been on hemodialysis for an extended period of time, your doctor may feel that
you’re ready to give yourself dialysis treatments at home. This option is more common for
people who need long-term treatment.
B. Peritoneal dialysis
Peritoneal dialysis involves surgery to implant a peritoneal dialysis (PD) catheter into
your abdomen. The catheter helps filter your blood through the peritoneum, a membrane in your
abdomen. During treatment, a special fluid called dialysate flows into the peritoneum. The
dialysate absorbs waste. Once the dialysate draws waste out of the bloodstream, it’s drained from
your abdomen.
This process takes a few hours and needs to be repeated four to six times per day. However, the
exchange of fluids can be performed while you’re sleeping or awake.
There are numerous different types of peritoneal dialysis. The main ones are:
 Continuous ambulatory peritoneal dialysis (CAPD). In CAPD, your abdomen is filled
and drained multiple times each day. This method doesn’t require a machine and must be
performed while awake.
 Continuous cycling peritoneal dialysis (CCPD). CCPD uses a machine to cycle the
fluid in and out of your abdomen. It’s usually done at night while you sleep.
 Intermittent peritoneal dialysis (IPD). This treatment is usually performed in the
hospital, though it may be performed at home. It uses the same machine as CCPD, but the

26. process takes longer.
C. Continuous renal replacement therapy (CRRT)
This therapy is used primarily in the intensive care unit for people with acute kidney failure. It’s
also known as hemofiltration. A machine passes the blood through tubing. A filter then removes
waste products and water. The blood is returned to the body, along with replacement fluid. This
procedure is performed 12 to 24 hours a day, generally every day.
Risks associated with hemodialysis
Hemodialysis risks include:
 low blood pressure
 anemia, or not having enough red blood cells
 muscle cramping
 difficulty sleeping
 itching
 high blood potassium levels

27.  pericarditis, an inflammation of the membrane around the heart
 sepsis
 bacteremia, or a bloodstream infection
 irregular heartbeat
 sudden cardiac death, the leading cause of death in people undergoing dialysis
Risks associated with peritoneal dialysis
Peritoneal dialysis is associated with an increased risk for infections in or around the catheter site
in the abdominal cavity. For example, after catheter implantation, a person can
experience peritonitis. Peritonitis is an infection of the membrane lining the abdominal wall.
Other risks include:
 abdominal muscle weakening
 high blood sugar due to the dextrose in the dialysate
 weight gain
 hernia
 fever
 stomach pain
Risks associated with CRRT
The risks associated with CRRT include:
 infection
 hypothermia
 low blood pressure
 electrolyte disturbances
 bleeding
 delayed renal recovery
 weakening of bones
 anaphylaxis

28. Kidney Transplantation
Kidney transplantation has become the treatment of choice formost patients with ESRD. Kidney
transplantation involves transplanting a kidney from a living donor or human cadaver to a
recipient who has ESRD Kidney transplants from well-matched living donorswho are related to
the patient (those with compatible ABO andHLA antigens) are slightly more successful than
those from cadaverdonors. The success rate increases if kidney transplantationfrom a living
donor is performed before dialysis is initiated A nephrectomy of the patient’s own native kidneys
may b eperformed before transplantation. The transplanted kidney isplaced in the patient’s iliac
fossa anterior to the iliac crest. The ureter of the newly transplanted kidney is transplanted into
the bladder or anastomosed to the ureter of the recipient
Nursing management
Nursing Diagnosis: Excess fluid volume related to decreased urine output, dietary excesses, and
retention of sodium and water
Goal: Maintenance of ideal body weight without excess fluid
1. Assess fluid status:
 Daily weight
 Intake and output balance
 Skin turgor and presence of edema
 Distention of neck veins
 Blood pressure, pulse rate, and rhythm
 Respiratory rate and effort
2. Limit fluid intake to prescribed volume.
3. Identify potential sources of fluid:
 Medications and fluids used to take medications: oral and intravenous
 Foods
4. Explain to patient and family rationale for restriction.

29. 5. Assist patient to cope with the discomforts resulting from fluid restriction.
6. Provide or encourage frequent oral hygiene
Nursing Diagnosis: Imbalanced nutrition; less than body requirements related to anorexia,
nausea, vomiting,dietary restrictions, and altered oral mucous membranes
Goal: Maintenance of adequate nutritional intake
1. Assess nutritional status:
 Weight changes
 Laboratory values (serum electrolyte,BUN, creatinine, protein, transferrin,and iron
levels)
2. Assess patient’s nutritional dietary patterns:
 Diet history
 Food preferences
 Calorie counts
3. Assess for factors contributing to altered nutritional intake:
 Anorexia, nausea, or vomiting
 Diet unpalatable to patient
 Depression
 Lack of understanding of dietary restrictions
 Stomatitis
4. Provide patient’s food preferences within dietary restrictions.
5. Promote intake of high biologic value protein foods: eggs, dairy products, meats.
6. Encourage high-calorie, low-protein, low-sodium, and low-potassium snacks between meals.
7. Alter schedule of medications so that they are not given immediately before meals.
8. Explain rationale for dietary restrictions and relationship to kidney disease and increased urea
and creatinine levels.
9. Provide written lists of foods allowed and suggestions for improving their taste without use of
sodium or potassium.
10. Provide pleasant surroundings at meal-times.
11. Weigh patient daily.
12. Assess for evidence of inadequate protein intake:
 Edema formation
 Delayed healing
 Decreased serum albumin levels
Nursing Diagnosis: Deficient knowledge regarding condition and treatment
Goal: Increased knowledge about condition and related treatment
1. Assess understanding of cause of renal failure, consequences of renal failure, and its
treatment:
 Cause of patient’s renal failure
 Meaning of renal failure
 Understanding of renal function
 Relationship of fluid and dietary restrictions to renal failure
 Rationale for treatment (hemodialysis, peritoneal dialysis, transplantation)

30. 2. Provide explanation of renal function and consequences of renal failure at patient’s level of
understanding and guided by patient’s readiness to learn.
3. Assist patient to identify ways to incorporate changes related to illness and its treatment into
lifestyle.
4. Provide oral and written information as appropriate about:
 Renal function and failure
 Fluid and dietary restrictions
 Medications
 Reportable problems, signs, andsymptoms
 Follow-up schedule
 Community resources
 Treatment options
Nursing Diagnosis: Activity intolerance related to fatigue, anemia, retention of waste products,
and dialysis procedure
Goal: Participation in activity within tolerance
1. Assess factors contributing to fatigue:
 Anemia
 Fluid and electrolyte imbalances
 Retention of waste products
 Depression
2. Promote independence in self-care activities as tolerated; assist if fatigued.
3. Encourage alternating activity with rest.
4. Encourage patient to rest after dialysis treatments.
Nursing Diagnosis: Disturbed self-esteem related to dependency, role changes, change in body
image, and change in sexual function
Goal: Improved self-concept
1. Assess patient’s and family’s responses and reactions to illness and treatment.
2. Assess relationship of patient and significant family members.
3. Assess usual coping patterns of patient and family members.
4. Encourage open discussion of concerns about changes produced by disease and treatment:
 Role changes
 Changes in lifestyle
 Changes in occupation
 Sexual changes
 Dependence on health care team
5. Explore alternate ways of sexual expression other than sexual intercourse.
6. Discuss role of giving and receiving love, warmth, and affection.
Nursing Diagnosis: Risk for complications Hyperkalemia; pericarditis, pericardial effusion,
and pericardial tamponade; hypertension;anemia; bone disease and metastatic calcifications
Goal: Patient experiences an absence of complications

31. A. Hyperkalemia
1. Monitor serum potassium levels and notify physician if level greater than 5.5 mEq/L.
2. Assess patient for muscle weakness, diarrhea,ECG changes (tall-tented T waves and widened
QRS).
B. Pericarditis, Pericardial Effusion, and Pericardial Tamponade
Assess patient for fever, chest pain, anda pericardial friction rub (signs of pericarditis)and, if
present, notify physician.
2. If patient has pericarditis, assess for thefollowing every 4 hours:
 Paradoxical pulse > 10 mm Hg
 Extreme hypotension
 Weak or absent peripheral pulses
 Altered level of consciousness
 Bulging neck veins
3. Prepare patient for cardiac ultrasound to aid in diagnosis of pericardial effusion and cardiac
tamponade.
4. If cardiac tamponade develops, prepare patient for emergency pericardiocentesis
C. Hypertension
1. Monitor and record blood pressure as indicated.
2. Administer antihypertensive medications as prescribed.
3. Encourage compliance with dietary and fluid restriction therapy.
4. Teach patient to report signs of fluid overload, vision changes, headaches, edema, or seizures.
D. Anemia
1. Monitor RBC count, hemoglobin, and hematocrit levels as indicated.
2. Administer medications as prescribed, including iron and folic acid supplements, Epogen, and
multivitamins.
3. Avoid drawing unnecessary blood specimens.
4. Teach patient to prevent bleeding: avoid vigorous nose blowing and contact sports, and use a
soft toothbrush.
5. Administer blood component therapy as indicated.
E. Bone Disease and Metastatic Calcifications
1. Administer the following medications as prescribed: phosphate binders, calcium supplements,
vitamin D supplements.
2. Monitor serum lab values as indicated (calcium, phosphorus, aluminum levels) and report
abnormal findings to physician.
3. Assist patient with an exercise program.
Reference
 Nicola Thomas, Renal nursing, 2 Nd edition, Page no105-117
 Harrison’s Principles of internal medicine ,18th
edition page no28647-2879
 Roger Gabriel. Practical Renal Medicine, page no: 81-92
 "Definition of Acute Kidney Injury (Acute Renal Failure)". Uptodate.com. N.p, 2016. Web. 18 Aug. 2016.
 www.healthline.com/health/glomerulonephritis
 www.mayoclinic.org/diseases-conditions/glomerulonephritis/home/ovc-20307753
 https:/www.kidney.org/atoz/content/glomerul
 emedicine.medscape.com/article/239278-overvie