ACUTE PRE-READING

Renal Disorders
1.

Compare nephritic and nephrotic syndromes.

Partial Renal Failure
o

Nephrotic Syndrome

Aetiology

Results when glomerulus is excessively permeable to plasma protein

proteinuria low plasma albumin and tissue oedema

Causes
o

Diabetes

Infections (viral, bacterial)

Drugs (NSAIDs, Heroin)

Symptoms
o
o

Hypoalbuminaemia

Generalised oedema

Hyperlipidaemia

o
o

Hypertension
Lipiduria

Blood results
o

Decreased serum albumin

Decreased total serum protein

Elevated serum cholesterol

Pathophysiology
1.
2.
3.
4.
5.

Copious amounts of proteinuria

Increases glomerular membrane permeability

Increased permeability to protein excretion of protein in urine
Decreased serum protein and subsequent oedema
Plasma oncotic pressure is diminished
Stimulation of hepatic lipoproteins synthesis hyperlipidaemia LDLs

and cholesterol triglyceride level fatty casts in urine (lipiduria)

6. Increased risk of infection
Nursing Management

Symptom management

Goals
o

Relieve oedema

Assessment

Weight patient daily

Record intake and output

Measure abdominal girth or extremity size

Medications

ACE inhibitors

NSAIDs

Loop diuretics may be needed

Diet

Low sodium (2-3 g/day)

Low- mod protein (0.5-0.6g/kg/day)

o

May increase if urine protein loss

exceeds 10g/day
Cure/control the primary disease

Hyperlipidaemia

Lipid lowering agents (colestipol/ simvastatin)

o

Moderate decrease in serum cholesterol

levels

Thrombosis

Drug therapy
o

Severe cases of nephrotic syndrome

o
o

Diabetic nephrotic syndrome

Manage diabetes

Treat oedema

Due to increased susceptibility to infection ensure patient does not

Body tissue swelling (oedema), increased BP, RBCs in urine

Caused by

Immune disorders

Infection

Symptoms

Hypertension

Haematuria

Pathophysiology
1.
2.
3.
4.
5.
6.
7.

3.

Prednisolone

interact with other infectious people.

Nephritic Syndrome

2.

Corticosteroids and cyclophosphamide

Early stages

Anticoagulant therapy for 6 months

Glomerular structure is disturbed

Reactive cellular proliferation
Decreased glomerular blood flow
Oliguria, oedema and hypertension
Damaged glomeruli leakage of red cells
Haematuria
Retention of waste products uraemia

Characterise and describe the causes and disease progression of the different types of
glomerulonephritis.
Distinguish between acute and chronic glomerulonephritis.
Glomerulonephritis inflammation of the glomeruli
o

Immunological process affecting the renal glomerulus

Affects both kidney equally

Glomerulus is PRIMARY site of inflammation, but tubular, interstitial and vascular changes

occur also
Characterised by

Extent of damage (diffused or focal)

Initial cause of disorder

Extent of changes (minimal or widespread)

Aetiology & pathophysiology

Antibody induced injury both lead to inflammation

Antibodies bind to antigens within the glomerular basement membrane

(anti-GBM antibodies)
o Immunoglobulins deposit along basement membrane
o

Release of antibodies caused by

structural alteration in GBM

OR
reaction of basement membrane with an exogenous agent
(virus)

Antibodies react with circulating non glomerular antigens and are randomly
deposited as immune complexes on GBM
o deposits appear lumpy
o

antigens dont come from glomeruli rather from either

endogenous circulating native DNA

OR
exogenous sources (bacteria, viruses)

Manifestations

Haematuria

Urinary excretion of various formed elements (RBCs, WBCs and casts

Proteinuria

Serum urea and creatinine levels increased

Types

IgA mesangioproliferative glomerulonephritis (IgAGN)

Most common in young males

Most common type

Pathophysiology
1.
2.
3.
4.
5.

Respiratory tract infection

Deposition of IgA antibody in glomerular mesangium
Inflammation
Glomerulus permeability is affected
Haematuria, proteinuria, hypertension

Early diagnosis via a renal biopsy can lead to early intervention to slow the

process down
Acute Post-Streptococcal Glomerulonephritis (APSGN)

Most common in children and young adults

Develops 5-21 days after infection

Pathophysiology
1.

Nephrotoxic strains of group A -haemolytic streptococci

3

2.
3.

Infection of tonsils, skin or pharynx

Antibodies are produced to the streptococcal antigen antigenantibody complexes are deposited in glomeruli
Tissue injury occurs
Inflammation & filtration of metabolic waste products from
blood
Increased permeability of glomerulus to larger protein molecules
60% recovery, 40% may have persistent impaired renal function

4.
5.
6.
7.

Manifestations and complications 95% of people with APSGN recover

completely
o Generalised body oedema

Early Low-pressure tissues (around the eyes)

Later total body as ascites or peripheral oedema in legs

Hypertension

Oliguria

Haematuria with a smoky/rusty appearance

o
o

Varies with severity of disease

Fluid retention

Due to decreased glomerular filtration

Diagnosis
o

Hx and physical examination

Urinalysis

o
o
o

Reveals presense of erythrocytes in significant numbers

Serum urea, creatinine and albumin

To view extent of kidney impairment

Complement levels and ASO titre

Renal biopsy

Bleeding in upper urinary tract

Proteinuria

Due to increased extracellular fluid volume

Confirmation of disease

Management/treatment
o

Rest

reduce
Sodium and fluid restriction & diuretics

If there is an increases of nitrogenous wastes

Antibiotics

To treat severe hypertension

Adjustments of dietary protein intake

Treatment for oedema

Antihypertensive therapy

Until signs of glomerular inflammation and hypertension

Only if streptococcal infection is present

Prevention

Encourage early diagnosis and treatment of throat

4

infections and skin lesions

Must take a full course of the antibiotics prescribed

Good personal hygiene to prevent spread of cutaneous

streptococcal infections
Rapidly progressive glomerulonephritis (RPGN)

Associated with acute kidney failure

o

With rapid loss of kidney function over days and weeks

Manifestations
o

Hypertension

Oedema

Proteinuria

Haematuria

RBC casts

Occurs in a variety of situations

o

complication of inflammatory or infectious disease

complication of a multisystemic disease

as an idiopathic disease

with the use of drugs (penicillamine)

correction of fluid overload, hypertension, uraemia, and inflammatory injury

to the kidney
o dialysis is used as maintenance therapy

Chronic Glomerulonephritis

End stage of glomerular inflammatory disease

Most types can lead to this.

Characterised by
o

Proteinuria

Haematuria

Slow development of uraemia

Progresses at a slow pace over a few to 30 years

Causes

Idiopathic 20% of patients no history of renal disease

Lupus nephritis

Diabetic nephropathy

Rapidly, progressive GN

Chronic renal failure, poor prognosis

o

Uraemia and death (10 years of onset)

Long term haemodialysis

Renal transplantation, only effective treatment

Pathophysiology

o
4.

Characterise and describe the causes and complications of acute and chronic pyelonephritis.
Pyelonephritis
o

ACUTE

Inflammatory disorder affecting renal pelvis and functional portion of kidney tissue

Bacterial infection of the renal pelvis and parenchyma

Risk Factors:

Pregnancy

UTI

Blood-borne infections

Urinary calculi

Congenital malformations

Causes

Ascending infection from the lower urinary tract most common

Bloodstream spread in bacteraemic or septicemic states rare

Pathophysiology

1. Patchy areas of spread, WBC infiltration and inflammation

2. Oedema, localised abscess may form
3. Damage mainly occurs in tubules, scar tissue replacement
Complications

Acute renal failure bilateral, systemic disease

Gram-negative septicaemia severe shock, multiorgan failure.

Papillary necrosis shedding of necrotic papillae into urine, followed by

acute renal failure

Pyonephrosis pelvicalyceal system becomes distended with pus

CHRONIC

Common cause of end-stage chronic renal failure

Two forms:

Persistent bacterial infections scarring

Reflux

Underlying metabolic, chemical or immunological changes

Pathophysiology
1.
2.
3.
4.

Widespread scarring, glomerulosclerosis

Tubules undergo atrophy and dilate and are filled with protein casts
Hypertension, renal failure
Dialysis, renal transplant
6

5.
6.
7.
8.

Differentiate between acute renal failure and chronic kidney disease, in terms of aetiology,
clinical course and diagnostic criteria.
Outline the management of a patient with chronic kidney disease.
Discuss the difference between peritoneal dialysis and haemodialysis, in terms of indications and
nursing responsibilities.
Discuss the criteria for renal transplantation for a patient in end stage renal failure.
Acute Renal Failure
o

Characterised by:

Rapid loss of kidney function (over hours or days)

Rise in serum creatinine and/or

Reduction in urine output.

Severity ranges from small increase of serum creatinine/reduction in urine output to

development of azotaemia.
Changes to electrolytes and fluid status

Uraemia can occur, where urine is found in blood.

o
o

Oliguria is associated with Acute renal failure. people with no oliguria, have less
complications and are more likely to recover quicker
RIFLE, tool used to classify severity and outcome, as well as looking at urine output and
the increase in serum creatinine table 46-3 page 1294

Risk

Injury

Failure

Loss

End-stage kidney disease

Aetiology and pathophysiology

Causes: most common ischaemia due to hypotension or exposure to nephrotoxic

agents.

PRE-RENAL
o

Hypovolaemia

Decreased cardiac output

Anaphylaxis, neurological injury, septic shock

Decreased renovascular blood flow

Hypotension, cardiac dysrhythmias, heart failure,

myocardial infarction
Decreased peripheral vascular resistance

Dehydration, haemorrhage, GIT lossess, burns

Embolism, renal artery thrombosis

INTRA-RENAL
o

Nephrotoxic injury

Interstitial nephritis

Other

POST-RENAL
o

Benign prostatic hyperplasia

7

Bladder cancer

Calculi formation

Neuromuscular disorders

Prostate cancer

Strictures

Trauma

Spinal cord disease

Extra-renal tumours

Pre-renal
1.
2.
3.
4.

External factors reduce systemic circulation

Reduced renal blood flow
Decreased glomerular perfusion and filtration (glomerular hypoperfusion)
Decreased clearance of wastes (azotaemia). RAA system is activated
causing oliguria
5. Kidneys conserve water and sodium
6. Continued loss in perfusion
7. Loss of kidney function and intrarenal damage to renal tissues occur
8. Low urine output
Intra-renal

MOST common cause is Acute Tubular Necrosis, which is caused by

prolonged glomerular ischaemia, nephrotoxins or pigments.
o People who are more at risk of getting ATN include those who have
experienced:
Severe hypovolaemia,

Major surgery,

Trauma or burns

Development of sepsis

If ischaemia lasts longer than 2 hours, destruction occurs to the

tubular epithelium.
Nephrotoxins that are associated with ATN include:

Aminoglycoside antibiotics

Contrast media

Non-steroidal anti inflammatory drugs

Nephrotoxins cause necrosis of tubular epithelial cells -leaves the

basement membrane intact

Pathophysiology:
1.

2.
3.
4.
Post-renal
1.
2.

Nephrotoxin causing obstruction to the intra-renal structures by actual

damage or crystallisation of epithelial cells of tubules
Impaired nephron function
Haemoglobin and myoglobin release
Tubules block (renal vasoconstriction)
Flow of urine is obstructed
Urine refluxes into the renal pelvis impaired kidney function
8

1.
2.
3.
4.
o

Bilateral ureteral obstruction

Hydronephrosis, increased hydrostatic pressure and tubular blockage
Progressive decline in kidney function
Prolonged obstruction tubular atrophy irreversible kidney fibrosis

Clinical Course

Resolves quickly if no intra-renal damage has occurred

Four phases:

Initiating phase
o

Time of insult

Continues until signs and symptoms appear

Hrs to days

Maintenance phase
o

Main manifestation is oliguria, which occurs 1-7 days of causative

event
If the cause is ischaemia, oliguria may occur within 24 hours

With nephrotoxins, onset will be delayed a week

Duration of this phase is 10-14 days some cases months. the

longer the maintenance phase the poorer the prognosis.

Differentiating between pre-renal oliguria and intra-renal oliguria

Pre-renal

No damage to renal tissue

Caused by decreased circulating blood volume

Reversible, with IV fluids

Volume resuscitation can correct pre-renal

conditions caused by hypovolaemia.

Hypoperfusion due to low cardiac output and low

renal perfusion pressure cant be corrected with
volume resuscitation.

Charecterised by urine with a high specific

gravity (>1.010), and low sodium concentration

(<10-20 mmol/L)
Intra-renal

Characterised by urine with a normal specific

gravity (1.010) and a high sodium concentration
(>40mmol/L)

Injured tubules cannot respond to autoregulatory

mechanisms

Intra-renal oliguria caused by ATN = presence of

tubular RBC and WBC casts in the urine.

Urinary changes

Decreased urine output <400mL per 24 hours

Urinalysis may show casts, RBCs, WBCs. A specific

gravity fixed at 1.010 and urine osmolarity of 300
9

dysfunction
Fluid volume excess

Neck veins may become distended with a bounding pulse

Oedema and hypertension may develop

Fluid overload can eventually lead to HF, pulmonary

oedema, and pericardial and pleural effusions

Metabolic acidosis

Kidneys cant excrete acid products of metabolisms OR

synthesise ammonia, needed for hydrogen ion excretion.

Serum bicarbonate decreases due to bicarbonate being in

buffering hydrogen ions

Defective reabsorption and regeneration of bicarbonate

occurs.
Severe acidosis = Kussmal respirations (rapid deep

respirations) by increasing exhalation of carbon dioxide in

order to compensate.
Lethargy and stupor occurs later if no treatment

Sodium balance

Damaged tubules cant conserve sodium

Urinary excretion of sodium increases = below normal

levels of serum sodium

Avoid high sodium diet intake can cause volume

expansion, HF and hypertension

Potassium excess

mmol/kg.
Proteinuria may be present glomerular membrane

Due to impaired function of the kidneys serum potassium

levels increases
Haematological disorders

Anaemia renal failures causes impaired production of

erythropoietin
WBCs are altered causing numerous systemic and local

infections
Calcium deficit and phosphate excess

Waste product accumulation

Neurological disorders

Diuretic Phase
o

Begins with gradual increase in daily urine output to 1-3L/day and

can reach up to 3-5L/day or more

High urine output is caused by osmotic dieresis - due to high urea
concentration in glomerular filtrate and tubules inability to
concentrate urine

Recovery Phase
o

Begins GFR (glomerular filtration rate) increases allowing

10

creatinine and serum urea levels to decrease

Tubular cells repair and regenerate

Major improvements occur in first 1-2 weeks. Kidney function can

take up to 12 months
The outcome of Acute Kidney Disease is influenced by

o
o

Patients overall health

Severity of kidney failure

Number and type of complications

Can progress to Chronic Renal Failure if not fully recovered

Diagnostic Studies

Client history

Pre-renal causes considered when there is a hx of dehydration, blood loss or

severe heart disease.

Intra-renal causes considered if the patient has been taking nephrotoxic

agents or has a recent hx of prolonged hypotension or hypovolaemia.

Post-renal is suggested with a hx of changes in urinary stream, stones,

benign prostatic hyperplasia or cancer of the bladder or prostate.

Urinalysis

Urine sediment containing abundant cells, casts or protein suggests intrarenal disorders

Urine osmolarity, sodium content and specific gravity differentiates causes.

Haematuria, pyuria and crystals may be seen in post-renal.

Serum creatinine and urea

Evaluates kidney function

Serum creatinine levels increase rapidly within 24-48 hours.

24 hour urine collection

Renal scan

Assesses renal blood flow and the integrity of the collecting system

CT scan and MRI

Best test of kidney function

Identifies lesions and masses, collections, obstructions and vascular

abnormalities
Renal ultrasound

First test done

Provides imaging without exposure to potentially nephrotoxic contrast

agents

Evaluates possible kidney disease and obstruction of urinary collecting

system
Multidisciplinary care

GOAL

To eliminate the cause

Manage the signs and symptoms

Prevent complications while kidneys recover

11

Assessment

Differentiate between pre-renal, intra-renal, post-renal.

Determine if there is adequate intravascular volume and cardiac output to

ensure adequate kidney perfusion

Volume resuscitation for pre-renal (crystalloids Normal Saline)

Chronic Renal Failure

o

Involves

Progressive, irreversible loss of kidney function

Decreased glomerular filtration rate

Kidney damage

Pathological abnormalities or markers of damge including abnormalities in blood and

urine samples

GFR

Normal is 125mL/min/1.73m2

Stages

Stage 1 = 90

Stage 2 = 60-80

Stage 3 = 30-59

Stage 4 = 15-29

Stage 5 = <15 (or dialysis)

Causes

Diabetes mellitus

Glomerulonephritis

Hypertension

Aetiology and pathophysiology

Early stages

Polyuria occurs due to decreased ability of kidneys to concentrate urine

(Mostly occurring at night nocturia)

Stage 3

50% of nephron function is destroyed

Hypertension, anamia, elevated urea and creatinine levels

Stage 4

Stage 5

Complications occur at late stage 3 early stage 4 phase

Oedema, worsening electrolyte imbalance, metabolic acidosis and

multisystem effects due to uraemia.

Risk factors:

Age

Male

Ethnicity

Behavioural factors
o

Smoking

12

Biomedical factors
o

High BP, obesity

Clinical Manifestations

Uraemia

Psychological

Neurological
o

Cardiovascular
o

Anaemia, infection, bleeding

Peripheral neuropathy
o

Hyperlipidaemia, gout etc

Haematological
o

Dry skin, pruritis, pigmentation changes etc

Metabolic
o

Thyroid abnormalities, infertility, sexual dysfunction etc

Integumentary
o

Anorexia, nausea, peptic ulcer, gastritis etc

Endocrine/reproductive
o

Oedema, dyspnoea. Pneumonia etc

Gastrointestinal
o

Hypertensive retinopathy

Pulmonary
o

Hypertension, HF, Atherosclerosis etc

Ocular
o

Headaches, seizures, lethargy, fatigue etc

Motor weakness, restless leg syndrome

Urinary system

Polyuria - nocturia

Specific gravity of urine is fixed at 1.010

Fluid retention as CKF progresses oliguria

Proteinuria, casts, pyuria and haematuria depending on cause

Metabolic disturbances

Waste product accumulation

o

Serum urea and creatinine levels increased

Altered carbohydrate metabolism

o

Due to impaired glucose use resulting from insensitivity to the

normal action of insulin

Elevated triglycerides
o

Hepatic production of triglycerides in due to hyperinsulinaemia

Hyperlipidaemia with VLDLs, normal or LDLs, HDLs

Electrolyte and acid-base imbalances

Potassium
o

Hyperkalaemia

13

Fatal arrhythmias when K reaches 7-8mmol/L

Due to excretion by kidneys

Sodium
o

Normal low

Sodium retention can lead to oedema, hypertension and HF

Calcium and phosphate

Magnesium

Metabolic acidosis
o

Due to impaired ability of kidneys to excrete acid load and from

defective reabsorption and regeneration of bicarbonate

Haematological system

Anaemia
o

Decreased production of erythropoietin by kidneys

Bleeding tendencies
o

Qualitative defect in platelet function caused by impaired platelet

aggregation and impaired release of platelet factor 3

Infection
o

Diminished inflammatory response because of altered chemotactic

response by neutrophils and monocytes

Increased incidence of cancer

o

Lung, breast, uterus , colon, prostate and skin malignancies are

commonly found

Cardiovascular

Cardiovascular disease most common cause of death in pts with CKF

Long term dialysis = myocardial infarction, ischaemic heart disease,

peripheral arterial disease etc

Hyperkalaemia, hypocalcaemia = cardiac arrhythmias

Hypertension = retinopathy, encephalopathy and nephropathy

Respiratory

Kussmaul respirations. Dyspnoea from fluid overload. Pulmonary oedema.

Uraemic pleuritis. Pleural effusion
o Thick sputum
o

Cough reflex is depressed

Gastrointestinal

Diarrhoea = hyperkalaemia and altered calcium metabolism

Constipation = ingestion of iron salts and/or calcium containing phosphate

binders

Stomatitis

Anorexia, nausea, vomiting = irritation of GIT by waste products

Mucosal ulcerations = ammonia produced by bacterial breakdown of urea

Neurological

Musculoskeletal

GFR = impaired excretion of urinary phosphate = serum phosphate

14

Failure to activate vitamin D = impaired calcium absorption = serum

calcium

serum phosphate + serum calcium = release of PTH = serum calcium

and phosphate, which bind together and deposit into muscles, lungs, skin
and subcutaneous tissues, GIT, eyes.
Integumentary

Decreased oil and sweat gland activity = dry scaly skin

Anaemia = pale skin

Stages 4 and 5 = yellow-grey discolouration of skine due to absorption and

retention of urinary pigments that give urine its colour

Dry skin, calcium phosphate deposition in skin and sensory neuropathy =

pruritis.
Reproductive

Women
o

Decreased oestrogen, progesterone and leutinising hormone levels

no ovulation and no period

After dialysis mense and ovulation may return

Men
o

Loss of testicular consistency, decreased testosterone levels and

low sperm counts.

Decreased libido, infertility

Sexual dysfunction due to anaemia

Endocrine

Both sexes

hypothyroidism

Psychological

Diagnosis

Urinalysis

To see if protein is in urine. Due to proteinuria being the first indication of

kidney damage

assessment with blood and urine tests

Urine test

Person with1+ proteinuria shown 2-3 times in 3 months should have further

For albumin-to-creatinine ratio (ACR) or protein-to-creatinine ratio (PCR)

o

Provides accurate estimate of the excretion rate of albumin or

protein
ACR of >300mg of albumin per 1g creatinine - CKF

GFR

Better than serum creatinine alone. Serum creatining could be the same for

two patients but then their GFR are completely different

Renal U/S

CT Scan

Renal Biopsy

15

Haemotocrit and haemoglobin levels

Management

Conservative therapy

GOAL
o

Preserve existing kidney function

Treat clinical manifestations

Prevent complications

Provide patient comfort

Control of:
o

Hyperkalaemia

Drug therapy

ACUTE
o

IV glucose and insulin OR

IV 10% calcium gluconate

Stage 4
o

Sodium OR calcium polystyrene

sulfonate is used to lower potassium
levels
Patients should be checked for
sodium and water retention
because it exchanges sodium
ions for potassium ions

Dietary/nutritional

Restriction of high potassium foods and drugs

Hypertension

Target BP is 130/80

Drug therapy

Antihypertensive drugs
o

Diuretics (frusemide)

Beta blockers (atenolol)

o
o
o

ACE inhibitors (ramipril)

Angiotensin receptor blockers (losartan)
Calcium channel blockers
(amylodipine)

To monitor the effects of these drugs pts BP

should be checked in supine, sitting and standing

positions.
Lifestyle/nutritional

Weight loss (if obese)

Exercise, smoking cessation, avoid alcohol.

DASH diet

Hyperparathyroidism

Anaemia

16

Haemoglobin levels should be 110-120g/L and

haematocrit should be 39% for patient with CKF

Using DNA technology an erythropoietin-stimulating agen
can be made to be used for anaemia

IV iron supplements

Administered IV or SC
If plasma ferritin concentrations fall below 100

ng/mL
Blood transfusions should be avoided

Hyperglycaemia

Dyslipidaemia

Lowering LDLs below 2.6mmol/L and maintaining

triglyceride level below 2.25mmol/L

Statins used to lower LDLs

Fibrates (fibric acid derivatives) used to lower

triglycerides

Nutritional therapy
o

Protein restriction

Water restriction

Sodium and potassium restriction

deep-green and yellow vegetables, beans and legumes

Phosphate restriction

Oranges, bananas, melons, tomatoes, prunes, raisins,

Dairy products and foods containing dairy products

Dialysis
o

Indications

Conservative treatments can no longer manage uraemia

GFR < 15mL/min

Complications hyperkalaemia, neuropathies,

encephalopathy, pericarditis, hypertension

Types of Dialysis

Hemodialysis

Requires vascular access via:

o

Temporary venous catheter eg vascath

inserted into the internal jugular vein or

the femoral vein
Semipermanent tunnelled catheter

inserted into the internal or external

jugular vein
Arterio-venous fistula is surgically
created about at least 3 months prior to
the patient requiring dialysis. Why?
this increases blood flow to
accommodate dialysis
17

the vein dilates and becomes

tough for repeated cannulation

the vein is accessed using 2

large bore cannulas

a graft can be used if native
vessels are unsuitable

Catheters have 2 lumens

o

Red lumen withdraws blood

Blue lumen returns blood

Process:
o

Machine is set up with a circuit which is

primed with normal saline

Venous access is obtained

Machine is started and withdraws blood

from the patient into the circuit and

pushes it through a filter which
removes:
wastes urea, creatinine

Excess electrolytes potassium

Excess water

The clean blood is then returned to the

patient
Haemodialysis takes approx 4 hours and
is required 3 times per week

Complications of dialysis
o

Hypotension

Muscle cramps

Blood loss

Sepsis

Disequilibrium syndrome

Nursing Responsibilites
o

Avoid taking blood pressure on the arm

with a fistula
Observation of fistula thrill and bruit

Vital signs

Monitoring blood results

Fluid balance, weight

Observe for complications

Peritoneal dialysis

Involves instilling a solution containing glucose,

dextrose or amino acids into the peritoneal cavity
which filters metabolic wastes and removes
water via the blood vessels contained in the
18

visceral and parietal peritoneum

Benefits
o

Preserves residual renal function

Delays the need for vascular access

Can be done at home

Contraindications
o

Abdominal conditions eg pancreatitis,

diverticulitis
History of multiple abdominal surgeries

Hernias

Obesity

Chronic back problems

Severe obstructive pulmonary disease

Catheter
o

Requires the insertion of a catheter into

the peritoneal cavity via the anterior

abdominal wall utilizing a surgical or
nonsurgical technique
Catheters are approx 60cm long with 2

dacron cuffs to anchor the catheter in

place
Catheter is tunnelled under the skin to

minimize bacterial invasion into the

peritoneal cavity
Catheter is taped to the skin and dressed

Exchange
o

PD can commence 7 14 days after

catheter insertion, when tissue has

grown around the dacron cuffs sealing
the sites
An exchange takes approx 45 minutes

and involves
Inflow approx 2L over 10 minutes

Dwell 20-30 minutes

Drain 15 minutes

Types
o

Continuous ambulatory PD performed

manually by patient 3 4 times during

the day
Automated PD utilizes a machine for
8 10 hours overnight while the patient
sleeps.

Complications
o

Perforation of bladder, bowel, blood

19

vessel during catheter insertion

Site infection

Peritonitis

abdominal pain

Outflow problems

Hernias

Lower back problems

Bleeding

Pulmonary complications

Protein loss

Carbohydrate and lipid abnormalities

Encapsulating, sclerosing peritonitis

Nursing Responsibities
o

Inspection and care of PDC insertion

site -application of antiseptic and

dressing
Aseptic technique for catheter and

solution connection and disconnection

Vital signs

Monitoring blood results

Fluid balance, weight

Education of patients

Renal Transplant

Exclusion criteria

Age

Co-morbidities

smoking

Obesity

Drug & alcohol abuse

Not taking medications while on dialysis

Process

Patients are referred for transplant by a renal

dialysis unit

Review by transplant physician/surgeon

Borderline patients are reviewed by more

specialists

Patients are reassessed annually for suitability

20