Quick Renal Notes
By Dr A McLeod
The ureter enters the kidney at the hilum where it forms the renal
pelvis (lined with transitional cells). This divides into two or three
major calyces, which further divide into minor calyces. Also entering
the kidney via the hilum are the renal artery and vein, nerves and
• The renal arteries come directly from the
descending aorta in the region of L1-L2.
• The renal veins drain directly into the IVC.
• Lymphatic drainage is to the para-aortic nodes.
• Innervation is mainly via the coeliac plexus
the kidney the blood vessels
are arranged into interlobar arteries and
veins that run through the medulla to the boundary of cortex and
medulla where arcuate vessels run at the cortico-medullary junction to
join them up.
Interlobular vessels run from the arcuate vessels to
supply the cortex. It is from these arcuate vessels that the afferent
artery runs into the corpsucle.
Blood leaves the corpuscle by the
arterioles which pass though one of two types of capillary network
(peritubular in cortical nephrons, vasa recta in juxtamedullary
nephrons) and into the various levels (interlobular, arcuate,
interlobar) of veins.
Larger version of picture here
Microanatomy of the kidney
corpuscle: Made up of a glomerulus and a capsule. The glomerulus
‘ball’ of capillaries that invaginates into a saucer shaped
about 200 μm across, called Bowmans capsule.
The glomerulus exists to
produce a protein free filtrate of blood. Fluid is filtered through
three negatively charged layers (capillary endothelium, basement
membrane, capsule epithelium). Molecules with a MW of 70 kDa or above,
or which carry a positive charge do not penetrate this filter to a high
Hydrostatic forces push fluid into the glomerular capsule while oncotic
pressure and a smaller hydrostatic force oppose this. The net flow is
into the capsule.
Note the narrower efferent vessel - this is what
maintains the high outwards pressure.
The Nephron: the glomerular
capsule leads into the nephron. Approximately six nephrons connect to a
single collecting duct. Two of these ducts become a duct of Bellini and
this drains urine through the apices of the renal pyramids into the
renal pelvis via the minor and major calyces.
There are about 1-1.5 million nephrons in the kidney, divided into two
types – each has a renal corpuscle and a tubule. They are 5-7cm
85% of nephrons are cortical. The corpuscle lies in the outer
cortex and there is a short loop of Henle that barely penetrates the
medulla. These nephrons are responsible for most of the reabsorption
that occurs within the kidney. The remaining 15% of nephrons are
juxtamedullary and have their corpuscles within the inner 1/3rd of the
cortex. They have long loops of Henle that reach well into the medulla.
These nephrons are involved in urine concentration.
Mnemonic: Cells Not
Removed - Just Clean Urine = Cortical Nephrons Reabsorb, Juxtamedullary
The blood supply for the two types of nephron is slightly different:
- In both nephron types the afferent arteriole of the glomerulus
branches from the interlobular artery.
- In the cortical nephrons, the efferent arteriole taking blood
away from the glomerulus enters a capillary network (the peritubular
capillaries) and from here enters the interlobular veins.
- In the juxtamedullary nephrons, the efferent arteriole taking
blood away from the glomerulus follows the loop of Henle down into the
medulla in a set of long loops (vasa recta) that rejoin at the
interlobular vein. This mechanism is necessary for the generation of
90% of blood entering the kidney perfuses the cortex and cortical
nephrons while only 10% perfuses medulla and juxtamedullary glomeruli.
Enzymes produced by the kidney
Produced in granular cells contained within the tunica media of the
afferent arteriole of the juxtaglomerular apparatus. This enzyme
converts angiotensinogen to angiotensin I within the liver.
produced in the peritubular interstitium and inner cortex cells.
Stimulates erythrocyte stem cells in the bone marrow to produce more
produced in the tubular cells. Hydroxylates 25-hydroxyvitamin D3 to
1,25 hydroxyvitamin D3. This is the active form needed for calcium
When empty the bladder lies in the pelvis and rests upon symphysis
pubis and the pubic floor. When filled it enlarges into the abdominal
cavity. The neck region is relatively immobile and is held by the
puboprostatic and lateral vesicle ligaments.
The blood supply is via the superior vesicular and inferior vesicular
arteries which branch from the internal iliac artery. Drainage is via
the vesicular plexus and the prostatic venous plexus. Lymph flows to
the para aortic node.
The wall of the bladder is yellow and contains many folds that allow it
to expand in the range from 100-400 ml with very little increase in
internal pressure. Capacity is much higher that this (>1 L) but
sensations of fullness become pain as the bladder becomes more ful.
The ureters enter into the back of the bladder through the ureteric
orifices that form two corners of the trigone (along with the urethral
meatus) which is reddish in colour and lies in the base of the bladder.
This is less mobile / distensible than the rest of the bladder and is
more sensitive to pain.
Histologically the bladder is lined by smooth muscle in three layers
commonly described as two layers of longituginal sandwiching a circular
layer. In reality all three layers are helices. The bladder has an
internal smooth muscle (involuntary) sphincter at the neck of the
bladder. An external skeletal muscle (voluntary) sphincter lies distal
to this within the urethra.
|The Male Urethra
This is about 20 cm long and is divided into three sections:
prostatic urethra is surrounded by the prostate gland and is where
prostatic secretions and contents of the ejaculatory duct enter.
membranous urethra is the section that passes through the pelvic floor
– this is where the skeletal muscle (voluntary) sphincter is
- The spongy urethra is the section travelling within the
the male urethra is lined by:
The muscular wall is a
continuation of the wall of the bladder and its lamina propria contains
many vascular channels and a few mucus-secreting glands.
- transitional epithelium proximally
- with stratified squamous at the external
meatus merging with the skin of the glans penis.
||The Female Urethra
about 4-5 cm long and is simpler as it only serves one function. There
is a voluntary (skeletal muscle) sphincter along its length at the
level at which it passes through the pelvic floor.
the female urethra is lined by:
wall is a continuation of the wall of the bladder and its lamina
propria contains many vascular channels and a few mucus-secreting
- transitional epithelium proximally
stratified squamous epithelium along most of its length.
Urine is formed in the kidney and transported via the collecting ducts
and ducts of Bellini to the renal pelvis – as urine collects this
dilates. Action potentials are generated in the pacemaker region of the
renal pelvis and these generate contractions in the ureters that help
the movement of urine into the bladder through the ureteric orifices in
The Nephrotic and Nephritic syndromes
These confuse many students - if you are one do not worry too much. You
are not alone!
Both syndromes are caused by the
formation of soluble complexes of antigens after an insufficient
clearing from the immune system. The difference in the syndromes is
that in nephrotic syndrome there is fixation of immune system
complement and in nephritic syndrome there is not.
activation of complement, Nephri
activation of complement!
Soluble antigen/antibody complexes are deposited within the slit pores
(between opposing podocyte foot processes) or within the mesangial
Damage to the glomerular basement membrane leads to an increased pore
size and number. Together with a decrease in the negative charge of the
basement membrane, this allows a heavy urinary protein loss (>3.5g /
day). This leads to hyopalbuminaemia, which in turn leads to oedema as
the oncotic force within the blood vessels (from albumin) decreases.
The loss of blood volume and pressure in the afferent glomerular
arteries stimulates the release of renin. This increases levels of
aldosterone and increases the retention of Na+ and water so increasing
the tendency towards oedema.
As with nephrotic syndrome, antigen/antibody complexes are deposited
within the slit pores or within the mesangial artery, but in nephritic
syndrome, these complexes evoke a complement based response.
Podocyte and slit pore
both nephrotic and nephritic syndromes:
- Albumin and cholesterol leak into urine
- Oncotic pressure falls
- Widespread oedema results
|Complement activation in
- Release of histamine (mast cells and platelets)
- Dilatation of blood vessels
- Influx of leucocytes
|Nephrotic syndrome symptoms:
- High levels proteinuria
|Nephritic syndrome symptoms:
- Lower proteinuria
- Oedema (peri-orbital, leg, sacral)
- 24 hour urine: proteinuria (>3.5g / l in nephrotic)
- Protein creatinine ratio is an alternative
- Serum albumin (<30g / l in nephrotic)
- Urine microscopy: haematuria, haemoglobinuria, red cell casts
- Renal function: Serum urea, creatinine and endogenous creatinine
- Most hospitals now calculate estimated GFR (eGFR) from age,
race and creatinine.
- Renal imaging – excretion urography
- Renal biopsy
- Not for children with selective protein leak, no casts / RBC,
no hypertension – likely to be minimal change.
- Not for long standing IDDM with retinopathy / neuropathy.
- Not if a possible drug induced cause is found – stop this
- Blood glucose: for DM
- Throat swab: for streptococcus
- Antinuclear antibody: for SLE (if positive then do dsDNA antibody
It is estimated that 2% of the population have renal or vesicular
(bladder) calculi at any one time. 50% of these will develop another
stone within ten years. Males are overall twice as likely to suffer
from this disease than females.
Major Causes: These are those that either decrease urine volume
(dehydration), reduce the levels inhibitors of nucleation, or
supersaturate (calcium, oxalate, uric acid)
Dehydration: Working in hot environments, living in hot countries
Hypercalcaemia (increased serum
If the GFR is normal, this invariably leads to hypercalciuria and an increased risk
of stone formation.
• Primary hyperparathyroidism (signalling for
calcium release from bone)
• Excess vitamin D ingestion
Hypercalciuria (increased urine
The danger level has been reported to be >7.5 mmol. / L for men and
>6.25 mmol. / L for women.
• Excess calcium ingestion
• Excessive bone resorption e.g. in disuse as in
immobilised patients or from bony metastases
oxalate levels in the urine)
• GI disease such as Crohn’s
• Excess oxalate ingestion (spinach, rhubarb,
• Calcium restriction – increases the
absorption of oxalate
• Errors in glyoxylate metabolism – more
oxylate is synthesised leading to renal failure in the teens –
twenties. Liver transplant corrects.
Hyperuricaemia (increased serum
uric acid levels) and hyperuricocuria (increased urine uric acid levels)
• Can be caused by idiopathic gout
Urinary tract infection (UTI)
These can result in the formation of struvite stones – often big
enough to form a ‘cast’ of the collecting system –
these are called staghorn calculi. Mucoprotins from the bacterium make
an organic matrix upon which the stone forms.
• The most common infectious cause is Proteus
mirabilis, which hydrolyses urea to ammonium hydroxide. Ammonium ions
and alkalinity favour stone formation.
These can work in one of three ways
Promote calcium stone formation (e.g. loop diuretics, antacids,
Promote uric acid stone formation (e.g. thiazides, salicylates,
Drug can precipitate into stones
Calcium stones are radio-opaque and form 80% of stones. 60% contain
Non-calcium stones are radiolucent and form the remaining 20%
Most stone are asymptomatic but some cause a very intense pain. This
can be constant, intermittent or colicky and may be sharp or dull. If
there is an obstruction present then the pain will be made worse by
either copious fluid intake or by diuretics including alcohol. Physical
movement may also result in pain (and haematuria) as the stone moves.
Ureteric colic is one of the most severe pains known. It generally runs
from th eflank to the iliac fossa and testis or labia. The patient will
be pale, sweating and restless – changing position to try to
relieve the pain. The patient may vomit and there may be haematuria.
If bladder calculi are present with a bladder bacteriuria the following
will be seen: frequency, dysuria, haematuria and a severe pain if
trigonitis is present.
An obstruction of the bladder neck or urethra will result in anuria and
painful bladder extension.
May present as acute renal failure or acute on chronic renal failure.
The history may reveal: dehydration, excess vitamin D consumption,
Mid-stream urine: MC&S, U+E, Ca2+, oxalate, urate, pH (acid =
urate, alk = infec.)
Bloods: creatinine, Ca2+
KUB: for stag-horn and other calculi
Stone analysis can help with rarer causes
Stones smaller that 0.5cm usually pass on their own while those larger
than 1 cm usually require further intervention (see below). Other
indications for intervention include: UTI, complete obstruction /
anuria, and persistent or frequent pain.
Analgesia should be given e.g. intramuscular morphine and a high fluid
level and increased levels of exercise should be encouraged.
• Extracorporeal shockwave lithotripsy
• Percutaneous (through unbroken skin)
nephrolithotomy with endoscopic removal of stone.
• Open surgery
/ Histology of the Ureters
The ureters are hollow muscular tubes between 25-35 cm long they run
retroperitoneally over the posterior abdominal wall in front of the
external iliac artery and down to the pelvic brim.
|The ureters are divided into
The ureters have constrictions along their
length dividing these sections – these narrowings are the most
natural places at which
stones may get stuck producing an acute colicky pain.
- the renal pelvis
- the abdominal
- the pelvic ureter
- intramural ureter (that part within
the wall of the bladder).
This pain characteristically starts in the
groin and radiates to either the scrotum in men of the labia majora in
The blood supply to the ureters is as follows:
Drainage is by corresponding veins and lymph nodes drain to the para
- Renal arteries
- Lumbar segmental
- Common Iliac
- Internal iliac
- Superior vesicular arteries
Sensory innervation is via T11-L2 and S2-S4
Bladder outlet obstruction
This may result in acute renal failure
Causes of bladder outlet obstruction can be divided into three
- Phimosis (Narrowness of opening of prepuce, preventing it
being drawn back over the glans)
- Benign - BPH most common cause of outflow obstruction
– 1 in 3 men over 50 has LUTS due to BPH.
- Bladder neck
Sympathetic smooth muscle tone – mediated by alpha-1 receptors
- Upper motor neurone dis. leads to high pressure detrusor
contractions and poor coordination with sphincters – detrusor sphincter dyssynergia
- Lower motor neurone dis. (S2, 3 , 4) leads to a low
detrusor pressure with a large residual urine volume.
|There are two sets
of symptoms that may suggest BOO:
- Urge incontinence
- Poor flow
- Straining to void
- Post micturition drbbling
- Feeling of incomplete bladder emptying
|When these are present a full exam
should be made and investigations ordered:
suprapubic area for palpable bladder / suprapubic tenderness
Digital rectal exam:
prostate for size, shape, consistency and abnormalities suggestive of
Bloods: U+Es inc
Urine: U+E's, dipstick,
If renal impairment suspected
Urinary flow rate (noninvasive)
Urodynamics (invasive) if flow rate equivocal, problem is neurological,
or if LUTS persistant or recurrent post surgery for outlet obstruction.
Pharmaceuticals (for BPH)
- Uro-selective α-blockers
- 5-alpha reductase inhibitors (6 months to work but more
effect in larger prostates)
- TransUrethral Resection of Prostate (TURP)
- Balloon dilatation
Blood in the urine, either macroscopic 'frank' (visibly red
or smoky urine) or microscopic (2-5 RBCs per high power field in spun
urine, dependent on lab).
One mnemonic for most common causes is GOBSHITE
- Arterfactual ie not blood e.g. beetroot, rifampicin,
- Wegeners granulomatosis
- tumours of the bladder / prostate
- tuberculosis of the bladder or prostate
- stone / foreign body
- cystitis: acute, radiation, chronic interstitial
cystitis (Hunner's ulcer)
systemic e.g. sickle cell
structural lesions e.g. UPJ obstruction, polycystic kidney
– pylonephritis, cystitis, prostitis, urethritis
immunological - PSGN, IgA nephropathy, endocarditis
iatrogenic – anticoagulants, cyclophosphamide drug
tumour: anywhere in urinary system e.g. kidney, bladder, prostate etc.
These could also be divided into pre-renal, renal, and post-renal if
you prefer to think of them that way
- dipstick testing - to exclude other causes of a red urine
- mid stream urine for microscopy culture and sensitivity
- 24-hour urine creatine clearance and urinary protein excretion -
this is used to detect mild degrees of renal impairment
- urea and electrolytes - to assess renal impairment
- full blood count
- plain film of kidney, ureters and bladder
- intravenous urography
- ultrasound scan - instead of, or in addition to, IVU
Further investigations may include:
- cystoscopy and retrograde pyelogram - for structural
abnormalities and tumours
- CT scan
- renal biopsy - if histological diagnosis is indicated
- renal arteriography - but not generally indicated
Causes of Proteinuria
Mnemonic: SNOT DUO
||Systemic e.g. CCF,
diabetes mellitus, fever, effects of excessive exercise.
||Nephrotic syndrome -
renal disorder: proteinuria, hypoalbuminaemia, oedema.
–absent from early morning samples (usually benign)
||Tubular proteinuria -
failure of tubules to reabsorb some plasma
proteins (glomeruli normal)
||Drugs - e.g. gold, other
heavy metals, penicillin, NSAIDs, solvents
|| Urinary system
contamination: UTI, vaginal mucus, ejaculate.
– extra-renal causes of excess plasma proteins, overwhelm system
These could also be divided into pre-renal, renal, and post-renal if
you prefer to think of them that way
- diabetes mellitus
- effects of excessive exercise
- Drugs including:
- Heavy metals
- Orthostatic/postural proteinuria – absent from early
morning samples (usually beingn)
- Overflow proteinuria – extra-renal causes of excess plasma
proteins, overwhelm system
- amylase in acute pancreatitis
- Bence-Jones protein in multiple myeloma
- Waldenstrom's macroglobulinaemia
- light chain disease
- haemoglobin in intravascular haemolysis
- myoglobin following crush injury
- lysozyme in myelomonocytic leukaemia / M4 acute myeloid
- Nephrotic syndrome - renal disorder: proteinuria,
- Primary causes
- Minimal change glomerulonephritis
- Membranous glmoerulonephritis
- Focal segmental glomerulonephritis
- Secondary causes:
- Diabetes mellitus
- Amyloid deposition (primary or secondary to myeloma/chronic
inflammatory disease (eg SLE, RA))
- Tubular proteinuria - failure of tubules to reabsorb some plasma
proteins (the glomeruli are normal)
- chronic pyelonephritis
- acute tubular necrosis
- renal tubular acidosis
- heavy metal poisoning
- renal transplantation
- Urinary system contamination
- vaginal mucus
Key History Points
About the symptoms:
- Urine discoloured, red, frothy
- Leg swelling/SOB/orthopneoa (Oedema)
- Itching, cramps, headaches, numbness, tired, weak, difficulty
- Progresion of symtoms over time
- Recent sore throat
About the patient:
- Ethnic origin
- African – sickle, malaria, hypertension
- Chinese – HbsAG
- Indian – diabetes, TB, atherosclerosis
- Balkan – interstitial nephritis
- Tropical – stones
- IV drugs – infections, bacterial endocarditis
- Heavy metal/solvent exposure
- Travel (malaria, bilharzia)
- Personal history of renal disease/recurrent UTIs/ skin disease
- Family history renal disease
- Occupational history
Key Examination Points
- features of nephrotic syndrome
- heart failure
- enlarged kidneys
- postural proteinuria (negative early morning sample)
- Dipstick urinanalysis - highly specific detection of glomerular
proteinuria (albuminuria>300 mg/d)
- Will not detect microalbuminuria in early diabetic nephropathy
- Will not detect Bence Jones protein
Next, need to determine:
- Whether the proteinuria is persistent?
- The amount of protein excretion
- 24-hour urine collection - indicated if there is persistent
proteinuria (three postive samples).
- Urine microscopy - help identify proteinuria, microscopic
- Dipstick urinalysis: persistent proteinuria in 3 samples
- 24 hour urine collection, as the best method of quantifying
- creatinine clearance
- differential protein clearance
- Or: urinary albumin:creatinine ratio in early morning sample.
(Should be < 0.1).
- Mid stream urine:
- microscopic haematuria
- urinary tract infection
- urinary sugar
- Bence Jones protein
- Bloods and renal biochemistry:
- urea and electrolytes, creatinine clearance
- blood glucose
- serum cholesterol
- serum proteins
- immunological tests (autoantibodies, ANCA, complement, serum
- abdominal X-ray/ultrasound - provides information on renal size
- IVU - assess structural abnormalities – (NB dangerous in
myeloma or renal failure)
- Renal biopsy (if abnormal imaging, proteinuria > 1g/24 hours,
haematuria, or ↓ renal function)
Summary of some important diseases:
Minimal Change Glomerulonephritis
- Damage to podocytes
- Nephrotic range
- Responds to steroids
- Variable glomerular changes
- IgA immune complex deposits
- Any age
- Presents with haematuria
- Many progress to renal failure
- Commonest cause, probably autoimmune
- May be secondary to systemic disease (SLE, infection, neoplasia,
- Capillary loop immune complex deposits
- 1/3 get better/ 1/3 continue, 1/3 get renal failure
Acute Renal failure (ARF)
Also known as Acute Kidney Injury (AKI) or Acute Kidney Disease (AKD)
- A clinical syndrome - not a diagnosis
- Rapid decline in excretory function occurring over a period of
hours or day. Suspect if:
- >1.5-fold rise in serum creatinine concentration
- fall in estimated GFR of >25% (assume baseline eGFR 75
ml/min/1.73 m2 if true value not known)
- oliguria (defined as urine output <0.5 ml/kg/h), in the
context of an acute illness
The principal differential diagnosis of ARF is dehydration which is important as it
is easily correctable. Suggested by:
Other causes include:
- normal sized kidneys
- urine sodium concentration < 20 mM
- urine osmolality / plasma osmolality > 1.5
Really Good Drink Does Most To Offer Some Help
on chronic failure
- muscle pain e.g. heroin abuse
syndrome (acute glomeruplonephritis) - dyspnoea and haemoptysis
- Cytotoxics such as cisplatin or streptozotocin
- Aminoglycosides such as gentamicin
- retinal changes
hypertension - retinal changes
disease e.g. ischaemic acute tubular necrosis
causes - postrenal e.g. stones, prostatic hypertrophy,
congenital obstructive disorders
- burns, trauma, shock, heart failure
failure - jaundice and stigmata of liver disease
As always, differentials can also be arranged into pre-renal, renal and
- hypovolaemia, for example acute haemorrhage, burns
- circulatory failure - heart failure or shock
- acute tubular nephropathy, for example ischaemic acute tubular
- acute interstitial nephropathy, for example in ascending urinary
- acute glomerulonephritis - Goodpasture's syndrome
- haemolytic uraemic syndrome
- drugs - cytotoxics such as cisplatin or streptozotocin,
aminoglycosides such as gentamicin, tetracyclines, NSAIDs,
- malignant hypertension
- following blood transfusion
- multiple myeloma
- hepatorenal syndrome
Post renal causes:
- obstructive lesions like stones, prostatic hypertrophy,
congenital obstructive disorders
- dipstick:blood and protein, signs of UTI
- microscopy, culture and sensitivity
- sodium, urea, creatinine and osmolality
- FBC, ESR, urea and electrolytes, creatinine, LFTs, CRP, CK
- ECG - may reveal changes associated with hyperkalaemia
- CXR - ?evidence of pulmonary oedema
- renal ultrasound - assess renal size ?evidence of obstruction
- renal biopsy might be indicated
- daily weights
Have a very low threshold for immediate specialist referral if
- suspected ARF
- ARF superimposed on chronic kidney disease (CKD)
- newly detected ERF (GFR < 15 mL/min/1.73 m2)
The two most immediate aspects of management are
- treatment of any hyperkalaemia (danger of arrhythmias)
- treatment of fluid overload (danger of pulmonary oedema).
The overall management of a patient with acute renal failure is divided
into various management objectives:
- treatment of cause of acute renal failure
- management of fluid balance
- management of electrolyte balance
- management of uraemia
- control of acidosis
- control of infection - choice of drugs must take into account
decreased renal function
Renal replacement therapy (RRT)
This is required when the kidneys are functioning at less than
10–15%. RRT is accomplished in one of the following ways:
- Cadaver donated
- Living-relative donated
People with advanced chronic renal failure (CRF) who have progressed to
end-stage renal disease (ESRD) usually require dialysis.
Indicators that dialysis is required include:
eGFR at most 15 and often 10 or below.
Pericarditis associated with end-atsge renal failure
- Blood is removed intravenously, passes though a dialysis machine
and returns to the body into the bloodstream.
- In the dialysis machine the blood is passed over a membrane that
filters waste and fluid into a dialysate solution. The dialysate is
then pumped out to a disposal tank and new dialysate is pumped in. The
process of removing excess fluid is known as ultrafiltration.
There are three methods of accessing the bloodstream:
- Arteriovenous fistula (AVF)
- A surgically created join between a vein and an artery in the
wrist, forearm or upper arm.
- Created 2-12 months before use to allow time to
‘mature’. At this point a palpable thrill can be felt under
the skin indicating that the fistula has gained th strength needed to
be put to use.
- Pros: lowest risk of
infection and malfunction; longest lasting option.
- Cons: No always
possible in th elederly, obese patients or those with certain medical
- Arteriovenous graft (AVG)
- A vein and artery are connected by way of a plastic tube. The
tube accepts the dialysis needles.
- Pros: The AVG only
requires 10 to 14 days to heal before it can be used
- Cons: frequently
malfunctions, causes infection, and has a shorter life span than the
- Temporary venous dialysis catheter
- A Y shaped connector with a needle penetrating into a large
vein such as internal jugular, subclavian or femoral. The two exterior
ports connect to and from the dialysis machine.
- Pros: can be used
temporarily in patients who do not have an AVF or AVG but who need
hemodialysis urgently. Can be used long-term in patients who cannot
tolerate either of the other two options.
- Cons: It poses
significant risk for infection and failure and must be replaced often.
The list of potential complications is very long. Some of the more
important ones are:
- Hypotension (20%)
- Light-headness (25% - 55%)
- Nausea and vomiting (15%)
- Leg cramps (5%–20%)
- Back pain (5%)
- Chest pain (5%)
- Headache (5%)
- Itching (5%)
- Fever, chills (rare)
- Acute anaphylaxis
- Acute haemolysis
- Air embolism
- Access problems (e.g., clotting, infection, malfunction)
- Peritoneal dialysis uses the peritoneal membrane
- Dialysate is injected into the peritoneal space in the
a two-way catheter (the Tenckhoff catheter).
- The membrane that lines
the abdomen (the peritoneum) allows waste and fluid to pass from the
blood into the dialysate over the course of several hours. The
made up mostly of salts and sugar (glucose), encourages ultrafiltration
through the peritoneum.
- The dialysate is which is pumped out.
- The cycle starts again.
There are two types of
- Continuous ambulatory peritoneal dialysis (CAPD)
- One cycle every 4-6 hours
- Approx two litres of fluid exchanged each cycle.
- Person remains active and mobile except when physically
changing the dialysate.
- Continuous Cyclic Peritoneal Dialysis (CCPD)
- The abdominal catheter is connected to the machine at
- Over an
8 to 12 hour night, the machine exchanges fluid four to eight times.
- About 10 liters are exchanged during the night.
- The fluid lasts throughout the day with some patients
require a mid-day exchange.
Complications of peritoneal dialysis include the following:
- Abdominal infection
- Amyloidosis (stiffening of kidney due to protein deposit)
- Diabetes (requires blood sugar monitoring)
- Infected catheter
- Peritonitis (caused by bacterial infection of peritonium or
- Vitamin and mineral deficiencies
- Live donor (usually a relative)
- Cadaveric donor
- Procedure performed under general anesthesia typically
taking 2 to 3 hours.
- The failed kidneys are left in place
- Transplantedkidney placed below them in the abdomen.
- Blood vessels are attached to the blood vessels of the legs
- ureter is attached to the bladder with a small plastic
- Kidney usually starts to work after about a day.
- Lifelong immunosuppressant medications needed.
- Rise in creatinine or new proteinuria may indicate
- Sudden rise (esp in first year) consistent with acute
- Slow rise consistent with chronc rejection.
Created February 2010