INTRODUCTION

When the kidneys cannot remove the body’s metabolic wastes or perform their regulatory
functions renal failure occurs. The substances normally eliminated in the urine accumulate in
the body fluids as a result of impaired renal excretion, affecting 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.

PATIENT’S PROFILE

NAME- Chandan Barua

AGE-48 Years SEX- Male

BED NO- 3, REG.NO- 82239

WARD-Male Medicine I DATE OF ADMISSION-11.12.19 at 10.40 am under Unit – III.

ADDRESS – Haiderpara P.S/P.O – Siliguri , Dist – Darjeeling

INFORMANT – Wife

CHIEF COMPLAIN : Shortness of breath, edema , decrease urine output

DIAGNOSIS – Stage-V Chronic Kidney Disease (ESRD) , in a known Type II Diabetes

Mellitus, Hypertension patient.

PAST MEDICAL HISTORY – Patient is a known case of diabetes since 7 years and
hypertension since 2 years and chronic kidney failure since 1.5 year and since then was on
dialysis and medications.He was taking medicines for diabetes since 5 years anti hypertensive
since 2 years but irregular .

SURGICAL HISTORY – There is no history of surgery done in the patient .

FAMILY HISTORY – They are in a joint family Patient and his wife are there , no children
They share a common kitchen with the patient’s elder brother his wife and their son who is a
school student.

There is as such no history of kidney disease in his family but his brother is also suffering
from diabetes since 5 years.

PERSONAL HISTORY – He is a tailor and use to earn 5000 rupees a month, He has no
history of any substance abuse.

EDUCATION HISTORY- Patient has studied upto class 10th, He discontinued his studies
due to his own interest. He then started tailoring.

DIET HISTORY- They are non vegetarian, use to take meal three times a day, they are
fond of vegetables rather than non veg food, they consume less fat,less salt diet. Patient
strictly follows diabetic diet as said by his spouse.
 SOCIAL SUPPORT : They are five in their family. Decision maker is his brother in every
matter .he has a very close relation with his brother.

LIFESTYLE HISTORY- Patient’s was a sedentary type of worker since he was a tailor,
use to take large carbohydrate and fat diet before suffering from Diabetes, no physical
exercises.

DEFINITION

End-stage renal failure, also known as end-stage renal disease (ESRD), is the final,
permanent stage of chronic kidney disease, where kidney function has declined to the point
that the kidneys can no longer function on their own. A patient with end-stage renal failure
must receive dialysis or kidney transplantation in order to survive for more than a few weeks.

STAGES OF CHRONIC KIDNEY DISEASE: The stages of ESRD is classified based on

the glomerular filtration rate. According to the National Kidney Foundation ( United States)
the normal GFR range is 90 to 120 ml / min / 1.73 metre square.

Below shows the five stages of CKD and GFR for each stage:

 Stage 1 with normal or high GFR (GFR > 90 mL/min)

 Stage 2 Mild CKD (GFR = 60-89 mL/min)

 Stage 3A Moderate CKD (GFR = 45-59 mL/min)

 Stage 3B Moderate CKD (GFR = 30-44 mL/min)

 Stage 4 Severe CKD (GFR = 15-29 mL/min)

 Stage 5 End Stage CKD (GFR <15 mL/min

ETIOLOGY

IN BOOK IN PATIENT
Diabetes is a leading and the most common  Present since seven years on inj insulin
cause of renal failure. regular 22units before breakfast and 10
units before dinner
Hypertension  Present since two years
 Glomerulonephritis
 Pyelonephritis  Not present
 Polycystic kidney disease
Heriditary and congenital disorders

 Alport syndrome  Not present

 Nephrophthisis
  Polycystic kidneys
Auto immune diseases

 Lupus  Not present

 IgA nephropathy
Obstructive uropathy

 Bilateral calculi
 Bilateral Pelviureteric Junction  Not present
Obstruction Stenosis
 Posterior urethral valves

Renal cancers  Not present

MISCELLANEOUS CAUSES

 Renal vein thrombosis

 Renal cortical necrosis
 Not present
 Renal tuberculosis
 Reflux nephropathy

PATHOPHYSIOLOGY
Damage of nephron result in hypertrophy and hyperplasia of remaining nephron, leading to
decreased function of nephron to excrete effectively.
Due to low renal perfusion renin-angiotensin system is activated and secretion of aldosterone
cause sodium and water retension. This leads to hypertension, increased vascular volume,
edema and heart failure.
There is potassium imbalance ( Hyperkalemia) due decreased renal excretion of potassium,
rapid administration of potassium and movement of potassium from ICF compartment to
ECF compartment. This occurs due to acidosis when hydrogen ions enter the cells to buffer
the pH of the ECF, the potassium moves out of the cell.
As the nephrons fail to excrete effectively, the ends products of protein metabolism
( normally excreted in urine) accumulate in blood. As a result the blood urea nitrogen (BUN)
and creatinine increase and uremia develops. Uremia adversely affects every system in the
body and results in skin disorders, gastro-intestinal manifestations, neurologic manifestations,
sexual dysfunction and may also cause pericarditis. Uremia also contribute to blood
coagulopathies.
Disturbance in erythropoietin synthesis occurs and result in anaemia. Mild hemolysis and
bleeding ( coagulopathies due to uremia) also cause anaemia.
The kidneys fail to regulate the acid base balance due to decreased excretion of metabolically
produced acid and loss of bicarbonate ( HCO3). So there is accumulation of non-volatile
acids and cause metabolic acidosis.
Due to decreased GFR, there is decreased phosphate elimination and increase in serum
phosphate level ( hyperphosphatemia). This result in decreased serum calcium level
( hypocalcemia). As a compensatory mechanism there is a increased secretion of
parathormone from parathyroid gland which causes calcium resorption and calcium leaves
bone and finally bone changes and bone diseases like osteomalacia occurs.
The kidneys are responsible for the final conversion of the inactive Vit- D to its active form
i .e.1, 25 Dihydroxycholecalciferol. But in renal failure this process is disturbed and thus
causes renal rickets and osteodystrophy.
Therefore overall renal failure leads to metabolic, endocrinal disturbances and disturbances
of internal homeostasis equilibrium.

CLINICAL MANIFESTATION

The clinical manifestation are a result of retained substances including urea, creatinine,
electrolytes, hormones,and many other substances. Uremia is a syndrome that incorporates all
sign and symptoms seen in various systems throughout the body.

In book In patient
Gastrointestinal
 Ammonia odour to breath “uremic fetor”
 Metallic taste  Anorexia
 Anorexia, nausea and vomiting  Nausea
 Mouth ulcerations and bleeding  Hiccups
 Hiccups  Constipation
 Gastritis present
 Peptic ulcer
 Constipation or diarrhoea
 Bleeding from gastro-intestinal tract

Musculoskeletal
 Muscle cramps
 Loss of muscle strength  Bone
  Renal osteodystrophy pain
 Bone pain present
 Bone fractures
 Foot drop

Cardiovascular  Hypertension
 Hypertension present
 Pitting edema ( feet, hands, sacrum)  Periorbital
 Periorbital edema edema
 Engorged neck veins  Pitting edema
 Atherosclerotic heart disease Over feet hands
 Myocardiopathy
 Pericarditis
 Pericardial effusion
 Heart failure

Ocular symptoms
 Hypertensive retinopathy  Not present

Pulmonary
 Thick, tenacious sputum  Shortness
 Crackles of breath
 Depressed cough reflex  Crackles
 Shortness of breath due to Pulmonary edema Present
 Tachypnea
 Kussmaul type respirations ( very deep respirations )
 Uremic pnemonitis
Psychologic
 Denial  Anxiety present
 Anxiety
 Depression
 Psychosis
 Behaviour changes

Neurologic
 Weakness and fatigue  Weakness
 Headache and fatigue
 Sleep disturbances  Sleep
 Inability to concentrate disturbances
 Disorientation  Headache
 Tremors Present
 Confusion’
 Seizures
 Asterixis-hand flapping tremor
 Burning soles of feet
 Hematologic
 Anaemia  Anaemia present
 Thrombocytopenia
 Bleeding

Metabolic
 Carbohydrate intolerance  Nutritional
 Hyperlipidemia deficiency
 Nutritional deficiencies present
 Gout

Reproductive
 Amenorrhea
 Decreased libido  Not present
 Sexual dysfunction
 Infertility/ azoospermia
 Testicular atrophy

Endocrine
 Hyperparathyroidism
 Thyroid abnormalities  Not present

LABORATORY VALUES IN CHRONIC RENAL FAILURE

IN BOOK IN PATIENT
Specific gravity of urine: The specific gravity of urine Urine RE/ME Done
remains low and fixed and is similar to that of glomerular Protein- trace , Sugar-nil,Color-pale
filtrate i.e. about 1.010. Normal specific gravity of urine is yellow,Epithelial cell-1-2/LPF,Pus cell-
1.020 to 1.030 1-2/HPF,Caste ,crystal,RBC,bacteria-nil
Blood urea nitrogen: Serum creatinine and BUN increases.
Serum creatinine is more sensitive indicator of renal function Urea-154mg/dl,creatinine-8.48mg/dl,
than blood urea nitrogen, as BUN is affected not only by
renal disease but also by protein intake.
Elevated triglyceride: Hyperinsulinemia stimulates hepatic
production of triglycerides. Almost all patient with uremia Not done
develop hyperlipidemia, with elevated very low density
lipoproteins, normal or decreased low density lipoproteins
(LDLs) and decreased high density lipoproteins
Hyperkalemia: Hyperkalemia is due to decreased excretion K+ --5.44mmol/lt
of potassium from the kidneys and excessive intake of
potassium in diet, medicatios and fluids. When serum
potassium level reaches 7-8 m mol/ litre fatal dysrhythmias
can occur. Normal K value is 3.5-5.5 m mol/ litre
Sodium: It may be normal or low in CRF. Normal Na value Na+ --139.6mmol/lt
is 2.5-5.5 mg/dl
Hyperphosphatemia and hypocalcemia: Usually the Not done
phosphate level is raised and blood calcium level decreases
as calcium and phosphorus are inversely related. The normal
range of calcium is 4.5-5.5 m Eq/litre. Normal range of
phosphate is 2.8 – 4.5 m Eq /litre.
Magnesium: Magnesium is primarily excreted by kidneys Not done
and hypermagnesemia is not a problem. Normal range is
from 1.3 – 2.1 m Eq / litre.
Decreased RBC count: The RBC count decreases due to RBC-3.6X106/mm3 HB-10.4gm/dl,
inadequate erythropoietin production and shortened life span HCT-32.5L%, MCV-91 mm3
of RBCs. MCH-28.8pg, MCHC-31.8g/dl,
Plasma bicarbonate: The average adult produces 80-90 m RDWCV-13.5%, RDWSd-44mm3,
Eq/ litre of acid per day. This acid is normally buffered by PLT-379103/mm3, MPV-10.6mm3,
bicarbonate. In renal failure plasma bicarbonate level, which PCT-0.403%, PDW-20.3H%
is an indirect measure of acidosis, usually falls to a new
steady state of around 16-20 mEq / litre Not done
Parathormone: Decreased serum calcium level causes
increased secretion of parathormone from parathyroid
glands. Not done

OTHER DIAGNOSTIC EVALUATION

Liver function test done.
Arterial blood gas analysis: ABG levels show low blood Totalbilirubin0.33mg/dl,Directbilirubin-
Ph. Low carbon dioxide and low bicarbonate. 0.14mg/dl,SGOT-82.4U/lt,SGPT-3.5
U/lt, Total protein-7.12gm/dl, albumin-
ECG changes: There is tall tented T waves and widened 3.9gm/dl, alkaline phosphate-191U/lt
QRS which indicate hyperkalemia

MEDICAL MANAGEMENT

Conservative therapy to preserve existing renal function.Medical management is

accomplished primarily with medication and diet therapy, although dialysis may be needed to
decrease the level of uremic waste imbalance.

IN BOOK IN PATIENT

HYPERKALEMIA: Hyperkalemia may provoke life threatening

dysrhythmias. It is prevented by ensuring adequate dialysis Diet low in potassium
treatments with potassium removal and careful monitoring of
medications and fluids for their K- content. Sodium polystyrene Inj Lasix 2amp TDS
sulphonate ( Kayexalate) a cation- exchange resin, may be needed
for acute hyperkalemia.
HYPERPHOSPHATEMIA AND HYPOCALCEMIA: It may Phosphate intake less than
cause renal osteodystrophy. Phosphate intake is generally restricted 1000mg/day
to less than 100 mg / day, but dietary control alone is usually
inadequate. Calcium based phosphate binders such as calcium Tab CaCO3 500mg bd as
carbonate ( os-cal) or calcium phosphate are prescribed which help calcium based phosphate
to bind phosphate in bowel and is then excreted in stool but there is binder
a risk of hypercalcemia. If calcium is high or the calcium
phosphorus product exceed 55 mg/dl, a polymeric phosphate binder
such as sevelamer (Renagel) may be prescribed. Tab Calcium and Vitamin
HYPOCALCEMIA is often a problem. Then serum phosphate D 1 tab od
level is lowered and supplemental calcium is provided along with
active form of vitamin D. Tab Arkamin 100mg Tds
HYPERTENSION: Treatment of hypertension includes: Tab Metoprolol Xl 50mg
 Weight loss ( if obese ) Od
 Therapeutic lifestyle changes Tab Amlo 5mg odac
 Diet recommendations
 Administration of antihypertensive drugs
 It is recommended that target BP be less than 130/80
mm of Hg Nebulisation with duolin
HEART FAILURE AND PULMONARY EDEMA: These and budecort 4 hourly
conditions require low sodium diets, diuretic agents, inotropic Tab NaHCO3 5OOmg tds
agents such as digoxin or dobutamine and dialysis. to avoid acidosis
ANEMIA: The most important cause of anemia is decreased
production of erythropoietin due to the decrease in the number of Tab IFA bdac
functioning renal tubular cells. Blood transfusions should be Inj erythropoietin 4000iu
avoided unless the patient experiences an acute blood loss or has sc once a 2 week.
symptomatic anaemia. Erythropoietin is administered intravenously Inj ceftriaxone 1gm iv bd
or subcutaneously three times a week in ESRD and it may take 2 to To prevent infection
6 weeks for the hematocrit to increase. Supplemental iron, vitamin Inj pantoprazole 40mg iv
B 12 and folic acid are usually administered as well. od
DYSLIPIDEMIA: Recommendations for patients with ESRD Inj ondem 4mg iv tds
include a goal of low LDLs below 100 mg/ dl ( 2.6 m mol/ litre) and
maintaining a triglyceride level below 200 mg/dl (2.25 m mol/litre)
NEUROLOGIC ABNORMALITIES: Neurologic disorders may
occur so the patient must be observed for early evidence of slight Not given
twitching, headache, delirium or seizure activity. IV Diazepam or
phenytoin is usually administered to control seizures. The side rails
of the bed should be raised and padded to protect the patient.

DIETARY MANAGEMENT

Dietary intervention is necessary with the deterioration of renal function and includes careful
regulation of protein intake, fluid intake to balance fluid losses, sodium intake to balance
sodium losses, and some restriction of potassium. At the same time, adequate caloric intake
and vitamin supplementation must be ensured. Protein is restricted because urea, uric acid,
and organic acids- the break down products of dietary and tissue protein –accumulate rapidly
in the blood when there is impaired renal clearance. The allowed protein must be of high
biological value ( dairy products, eggs, meats).High biologic value protein are complete
proteins and supply essential amino acids for growth and repair. High calorie diet is adviced
to prevent wasting. Vitamin supplementation is necessary because protein restricted diet does
not provide the necessary complement of vitamins.

Calorie intake-30-35 kcal/kg,Protein-0.6-1.0g/kg, based on GFR, urinary protein

losses,and creatinine clearance.Sodium-1-3g/day, HD-2-3 g/day
Potassium –as per lab values, HD-2-3 g/day,Phosphorus -8-12 mg/kg HD<17
mg/kg,Calcium 1000-1500mg/day for HD and ESRD Patients,Vitamin C-
100MG/Day.Hemodialysis patients urine output+500ml=1000ml intake

Usually the fluid allowance per day is 500 ml to 600 ml more than the previous day’s 24 hour
urine output. For this patient -Renal diet,TOFR-intake +200ml as recommended by Doctor

Some foods with high potassium contents should be avoided eg. Oranges, bananas, melons,
tomatoes, prunes, deep green and yellow vegetables ,beans and legumes.

Foods containing high phosphorus content like yogurt, milk, cheese should be avoided.

RENAL REPLACEMENT THERAPIES

The main renal replacement therapies include the various types of dialysis and kidney
transplantation.

DIALYSIS Types of dialysis include hemodialysis and peritoneal dialysis .Dialysis is

technique in which substances move from the blood through a semipermeable membrance
into a dialysis solution(dialysate) and to remove the waste products in renal failure.

Dialysis is begun when the patient’s uremia can no longer be adequately managed
.Generally dialysis is initiated when GFR or creatine clearance is less than 15ml/min. But
this criterion can vary in different clinical situation and the physician will determine when to
start dialysis based on the patients clinical status.

Patient’s dialysis is to be done on 14.12.19 for the first time

SURGICAL MANAGEMENT

A Patient with ESRD finally needs the treatment with kidney transplantation .During the past
40 years more than 400000 kidney transplantations have been performed world wide.

Kidney transplantation involves transplanting a kidney from a living donor or

deceased donor to a recipient who has no renal function. Transplantation from well matched
living donors who are related to patient (those with compatible ABO and human leukocyte
antigen) is slightly more successful than from cadaver donors.

For the donor kidney laboratory studies include 24 hour urine study for creatinine
clearance and total protein ,CBC and electrolyte profiles .Hepatitis B and C ,HIV and
cytomegalo virus are done to assess for the presence of any transmissible diseases.

The donor patient has to undergo ECG and chest X ray , renal ultrasound and renal
arteriogram or three dimensional CT are done to ensure that the blood vessels supplying each
kidney are adequate and there are no anomalies and to determine which kidney will be
removed.

Kidneys are removed and can be preserved up to 72 hours but most transplant surgeons
prefer to transplant kidneys before 24 hours of removal.

PREOPERATIVE MANAGEMENT
A complete physical examination is performed to detect any conditions that would cause
complications after transplantation.

The patient is evaluated for any infections including gingival (gum) disease and dental
carries

Diagnostic tests includes

i) Tissue typing

ii) Blood typing

iii) Antibody screening

iv) Study of lower urinary tract to assess bladder neck function and to detect urethral reflux,

If routine dialysis has been established hemodialysis is often performed the day before
transplantation to optimize the patients physical status.

A psychological evaluation is conducted to assess the patients ability to adjust to the

transplant copying styles, social history ,social support available and financial resources.

PREOPERATIVE NURSING MANAGEMENT

Patient teaching should address to post operative pulmonary hygiene ,pain management
options, dietary restrictions ,IV and arterial lines ,tubes and early ambulation .Patient may be
concerned about the donor and anxious about the outcome of surgery.

Helping the patients to deal with these concerns is part of the nurse’s role.

POST OPERATIVE MEDICAL MANAGEMENT

The goal of care is to maintain homeostasis until the transplanted kidney is functioning well.

After a kidney transplantation rejection and failure can occur within 24hours within 3 to 14
days or after many years .Since the body’s immune response views the transplanted kidney as
foreign it continually works to reject it to overcome or minimise the body’s defense
mechanism immunosuppressive agents are administered.

POST OPERATIVE NURSING MANAGEMENT

Nursing management includes:

1)Assessing the patient for transplant rejection by monitoring blood pressure ,weight
,assessing oliguria and edema ,fever ,swelling or tenderness over the transplanted kidney or
graft.

2) Preventing infection by maintaining aspetic technique during procedures such as dressings,

catheterization etc .Patient must be protected from exposure to infection by hospital staff
,visitors and others patients with active infection .Attention to hand hygiene and use of mask
is important.

3) Monitoring urinary function

4) Addressing psychological concerns

5) Monitoring and managing potential complications e.g. gastro intestinal ulceration and
corticosteroid induced bleeding, fungal colonization e.g. GI tract and urinary bladder
secondary to corticosteroid and antibiotic therapy.

6) Teaching patients self care and

7) Continuing care

COLLABORATIVE CARE

Collaborative care for Chronic Renal Failure comprises of the following

1. Drug Therapy

2. Nutritional therapy

3. Dialysis and

4. Surgical intervention i.e kidney transplantation

5. Home and community based care

The patients must be provided with ongoing education. The patient must be taught how to
check the vascular access device for patency and appropriate precautions such as avoiding
venipuncture and blood pressure measurements.

The patients and family need to know what problems to report to the health care provider
,These include the following

1) Worsening signs and symptoms of renal failure (nausea vomiting ,change in usual urine
output ,ammonia odour on breath.

2) signs and symptoms of hyperkalemia(muscle weakness,diarrhoea,abdominal cramps)

3) signs and symptoms of access problems (clotted fistula or graft ,infection)

NURSING ASSESSMENT

HISTORY TAKING

The complete history of existing renal disease in family was taken .History of diabetes
mellitus, hypertension ,drug history ,diet history, educational status and occupational history.
History of past illness and treatments ,dialysis etc.

PHYSICAL EXAMINATION

Nurse must perform thorough physical examination including vital signs, cardiovascular
,pulmonary ,GI, neurologic ,dermatologic and muscutoskeletal systems.

PHYSICAL ASSESSMENT: systemwise;

 AREAS OF ASSESSMENT DATE OF ASSESSMENT: 12.12.2019

EMOTIONAL STATE
Calm and co-operative
Anxious/ Calm / Angry / Cooperative /
Fearful / Restless / Withdrawn

CENTRAL NERVOUS SYSTEM

Level of consciousness Conscious, alert

Alert/ drowsy/ confused/ semiconscious/
comatose

Oriented to Time Present

Place Present
Person Present

Speech ( Relevant / irregular / slurred / Relevant

aphasia)

Sleep Adequate with oxygen inhalation

( Adequate / disturbed )

RESPIRATORY SYSTEM
Chest movement Bilaterally equal
(Unilateral / Bilateral / Absent )

Respiratory pattern
(Normal / dyspnea /Orthopoea/ dyspnoea
Tachypnoea/ Bradypnoea /Paroxysmal
nocturnal dyspnoea

Respiratory rate 28b/min

Air entry
Bilaterally equal / diminished specify Diminished right lung
(R) (L) lung

Breathe sounds
(Normal / rales / rhonchi / wheeze) Ronchi with coarse crepts

Cough Occasional

Oxygen on flow 5l/min through face mask

CARDIOVASCULAR SYSTEM

Heart rate 80b/min

 Blood pressure 160/90 mm of Hg

Heart sounds S1,S2 Audible

SpO2 96% with oxygen

Neck vein distension Absent

Normotension / Hypertension / Hypertension

Hypotension

Chest pain Absent

GASTRO INTESTINAL SYSTEM

Mouth Clean , normal

(Clean / Sordes / Halitosis)

Teeth ( Clean / Plague / loose) Plague

Nausea/ Vomitting Present

Tongue (Clean / coated) Dry, coated

Oral ulcers Absent

Nutrition route Oral

Peristalsis Present

Constipation / diarrhoea / malena Constipation

Abdominal distension Present

INTEGUMENTARY SYSTEM

Skin ( intact / break down / rash / Dark

blister/ infection / specify site)

Cyanosis Absent

Capillary refill ( < 3 sec ) Present

Peripheries ( Warm / Cold ) Cold

 Oedema ( site) Generalized

Nails clubbing Absent

Icterus Absent

Temperature
Febrile / afebrile Afebrile 98.6’F

Scalp Clean

Eyes Normal

Nose Normal

Ear Normal

MUSCULOSKELETAL SYSTEM

Joints ( mobile / stiff / painful / Mobile

contracture)

Ambulant Ambulant

GENITOURINARY SYSTEM

Voids freely / catheter Voids freely

Haematuria / Retention / Incontinence / Normal

Sediments

Burning micturation Absent

DATA ANALYSIS

Laboratory values (serum electrolyte, BUN, creatinine, protein, transferrin and iron
levels)must be assessed.

Blood glucose levels ,RBC count ,ECG changes ,bold pressure and weight recordings must
be assessed.

NURSING DIAGNOSIS
1)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

NURSING INTERVENTION RATIONALE

1.Assess fluid status by: Assessment provides baseline and ongoing database
a)Daily weight checking for monitoring changes ans evaluating interventions.
b)Intake and output balance
c)observing distension of neck veins
d)monitoring blood pressure ,pulse rate
and rhythmn
e)Respiratory rate and effort

To prevent fluid overload.

2.Limit fluid intake to prescribed volume
Understanding promotes patient and family
3.Explain to patient and family rationale cooperation with fluid restriction.
for fluid restriction.

4.Administer diuretics as prescribed

2)Imbalance nutrition less than body requirements related to anorexia ,nausea and
vomiting ,dietary restrictions and altered oral mucous membranes
 NURSING INTERVENTION RATIONAL

1.Assess nutritional status by monitoring Gives baseline data for monitoring changes
weight changes and laboratory values. and evaluating effectiveness of intervention.

2.Assess the patients diet history and food Past and present dietary patterns are
preferences . considered in planning meals.

3.Assess for anorexia ,nausea ,vomiting To promote adequate dietary intake by

,depression,stomatitis and lack of elimination of problems related to feeding.
understanding of dietary restrictions.

4.Provide patients food preferences within Increased dietary intake is encouraged.

dietary restrictions.
Complete proteins are provided for positive
5.Promote intake of high biologic value protein nitrogen balance needed growth and healing.
foods, eggs, dairy products, meat.
Reduce source of restricted foods and
6.Encourage high calorie ,low protein,low proteins and provides calories for energy
sodium and low potassium snacks between ,sparing protein for tissue growth and
meals healing.

Unpleasant factors that contribute to patients

7.Provide pleasant surroundings at meal times anorexia are eliminated.
GOAL: Maintenance of adequate nutritional intake.

3)Activity intolerance related to fatigue ,anemia,retention of waste products and dialysis

procedure.

GOAL-Participation in activity within tolerance.

NURSING INTERVENTION RATIONALE

1)Assess factors contributing to activity Indicates factors contributing to severity of
intolerance fatigue
a)fatigue b)anemia c)fluid and electrolyte
imbalances d)Retention of waste products
e)Depression
2)Promote independence in self care Promotes improved self esteem
activities as tolerated assist if fatigued
3)Encourage alternating activity with rest Promotes activity and exercise within limits
4)Encourage patient to rest after dialysis and adequate rest.
treatments

4)Impaired skin integrity related to uremic frost and changes in oil and sweat glands

GOAL-Skin will remain intact and patient will feel comfortable

NURSING INTERVENTIONS

1.Keep the skin clean while relieving itching and dryness .Use soap such as basis soup

2.Add bath oil to bath water to maintain moisture and softness

3.Apply prescribed ointments or creams to relieve itching

4.Keep the patients nail short and trimmed to prevent excoriation

5.Keep hair clean and moisturised.

6.Administer prescribed antihistamines for relief of itching.

5)Constipation related to fluid restrictions and ingestion of phosphate binding agents

GOAL-Patient will be relieved of constipation

NURSING INTERVENTIONS

1.Be aware that phosphate binders cause constipation that cannot be managed with usual
interventions.
2.Encourage high fiber diet,bearing in mind the potassium content of some fruits and
vegetables .

3.Use stool softners as prescribed and use of commercial fiber supplements may be done.

4.Avoid laxatives and catharites that cause electrolyte toxicities (compound containing
magnesium or phosphorous.

5.Increase activity of the client as tolerated.

6)Risk of injury while ambulating related to potential fractures and muscle cramps due
to calcium deficiency

GOAL-Patient will be ensured a safe level of activity.

NURSING INTERVENTION

1)Inspect patients gait,range of motion and muscle strength .

2)Monitor serum calcium and phosphate levels watch for hypocalcemia or hypercalcemia and
treat if needed.

3)Administer analgesics as ordered and provide massage for severe muscle cramps.

4)Monitor x rays and bone scan results for fractures bone demineralization and joint deposits.

5)Calcium supplements to be given between meals to increase serum calcium.

6)Vit D supplemented to increase absorption and utilization of calcium.

7)Increase activity as tolerated avoid immobilisation because it increases bone

demineralization.

7)Knowledge deficit regarding conditions and treatment.

GOAL-Increased knowledge about condition and related treatment.

NURSING INTERVENTION

1.Provide explanation of renal function and consequences of renal failure at patients level of
understanding and guided by patients readiness to learn.

2.Provide aral and written information as appropriate about

a)Renal function and failure.

b)Fluid and dietary rectrictions

c)Medications
d)Reportable problems sign and symptoms

e)follow up schedule

f)community resources and

g)treatment options

POTENTIAL NURSING PROBLEMS

1.Hyperkalemia due to decreased excretion ,metabolism, acidosis, catabolism and excessive

intake(diet, medications ,fluids)

2. Pericarditis pericardial effusion and pericardial tamponade due to retention of urenine

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 lifespan ,bleeding in

the GI tract from irritating toxins and ulcer formation and blood loss during hemodialysis.

5.Bone disease and metastatic and vascular calcifications due to retention of phosphorous low
serum calcium levels ,abnormal vit D metabolism and elevated aluminium levels.

PROGNOSIS

The prognosis of the ESRD depends upon the conservative management provided to the
patient including dialysis and the availability and success of kidney transplantation.

Kidney transplantation was first done in 1954 in Boston between identical twins .Kidney
transplantation is extremely successful with 1 year graft of about 90% for deceased donor
transplants and 95% for live donor transplants.

A patient has already sustained enough kidney damage when he had moved into the fifth
stage of CKD therefore appropriate conservative therapy with renal transplantation can
prolong the life .Otherwise the outcome of the disease is seen usually poor.

BIBLIOGRAPHY

1)Suzzane C Smeltzer etal ;Brunner and Suddharths Text Book of medical surgical
Nursing ;Wolters Kluwer Publication ;Fourth Indian Reprint 2012.Pg no 1325 to 1333 ,Pg no
1351 to 1354

2)Chintamani,Lewis Medical Surgical Nursing .Elsevier Reprint ,2011,Pg No 1207 to

1215 .Pg no 1223-1226

3)Prof PV Ramachandran ,etal ;Lippincott Manual of Nursing Practice;9 th Edition;Wolters

Kluwen India Pvt Ltd Ch21;pg no 804 to 806

4)Anne Waugh .Allison Grant;Ross and Wilson Anatomy and Physiology in Health and
Illness Elsevier reprint 2005;Ch13pg no 354