The Urinary System
Chronic Renal Failure
renal failure is irreversible
deterioration in renal function. It is characterised by impairment of
excretory, metabolic and endocrine functions of the kidney that leads to the
development of the clinical syndrome which is referred to as uraemia.
Chronic renal failure may be caused by any condition which destroys the normal
structure and function of the kidney. In many patients the condition
progresses insidiously over a number of years and frequently at presentation
it is impossible to determine the underlying renal disease.
Chronic renal failure can be caused by:
mellitus (the most common cause but it probably takes at least 15 years)
hypertension (very common)
(small blood vessel disease) in systemic lupus erythematosus (SLE) and
systemic sclerosis (scleroderma) caused by deposition of immune complexes in
blood vessel walls with subsequent inflammation
types of glomerulonephritis (discussed earlier), many of unknown cause
polycystic kidney disease characterised by many bilateral renal cysts that
increase renal size but reduce the volume of functioning renal tissue
pyelonephritis, especially associated with chronic vesico-ureteric reflux
nephropathy caused by long-term anti-inflammatory or analgesic treatment
(e.g., in rheumatoid arthritis)
urinary stones, especially of staghorn variety
of uraemia is not completely understood. Disturbances in water, electrolytes
and acid-base balance undoubtedly contribute to the clinical picture but the
exact pathogenesis of the clinical syndrome of uraemia is unknown. Almost any
substance present in abnormal concentration in the plasma has been suspected
of being a ‘uraemic toxin?/i>. It
is most likely that the syndrome is caused by accumulation in body fluids of a
number of substances among which must be included phosphate, urea, creatinine,
guanidine, phenols and indols. There is no satisfactory way of assessing the
biological toxicity of different substances but it must be assumed that the
uraemic toxins are substances eliminated by the normal kidney and retained in
Clinical features: < BACK TO TOP >
early stages of the disease, the patient may be asymptomatic and the existence
of renal insufficiency may be revealed by discovery of proteinuria, anaemia,
secondary hypertension or raised blood urea and creatinine during routine
not uncommon for patients to remain asymptomatic until the glomerular
filtration rate (measured by the creatinine clearance test) is 22 L/day of
symptoms and signs are referable to almost every system and many patients
present with complaints which at first sight may not suggest their renal
Generalised weakness and lack of energy, muscle aches
Breathlessness on exertion
Anorexia, nausea, vomiting and an unpleasant taste in the mouth
Disordered intestinal motility, usually
diarrhoea (direct damage of the gastrointestinal lining as well as possible
effect of hyperkalaemia) but sometimes constipation
Headaches and visual disturbances, due to associated hypertension
Pallor and pigmentation resulting in
characteristic yellow-greyish colour of the skin; some patients report
troublesome pruritus (skin itching)
rate of progression to end-stage renal failure is very variable.
the patients are free from oedema
despite reduced glomerular filtration, which is probably due to compensatory
decrease in sodium and water reabsorption to maintain normal urine volume
(there is no oliguria until late stage).
contributes to the dyspnoea and respirations are deep (hyperpnoea), later
drowsiness, confusion and coma develop.
all organs can be affected in some way:
This is common and to some extent reflects
the severity of uraemia.
Several factors contribute:
dietary intake of iron due to anorexia as well as impaired intestinal
absorption of iron due to disturbed gastrointestinal motility and mucosal
Diminished erythropoiesis due to toxic effects of uraemia on bone marrow cells
Reduced red cell survival again due to toxic effects
production of erythropoietin (EPO) in the kidneys, the hormone that normally
stimulates production of erythrocytes in the bone marrow; this is probably the
most important factor
2. Renal osteodystrophy
Metabolic bone disease consists of osteomalacia
(soft bones with abundant osteoid but
that lack minerals) and osteoporosis
(hard but brittle bones due to the loss of whole bone
The main problem appears to be failure of the
kidney to convert cholecalciferol (vitamin
D) to its active metabolite
1,25-dihydroxycholecalciferol (calcitriol) which impairs
calcium absorption from the gut. End result
is low plasma calcium levels, reduced
mineralisation of bone, and subsequent
secondary hyperparathyroidism which initiates
mobilisation of calcium from bones.
Demyelination (loss of myelin sheaths) of
fibres causing sensory neuropathy
numbness, burning feeling), motor neuropathy (muscle weakness/paralysis such
as foot drop) and autonomic neuropathy (disorders of gastro-intestinal
motility in form of constipation).
Symptoms and signs of neuropathy improve when
dialysis is started.
4. Endocrine functions
Loss of sexual drive in both sexes,
amenorrhoea in females, erectile dysfunction in males.
Uraemia is frequently mistaken for
hypothyroidism because both have very similar
5. Cardiovascular disorders
Hypertension in approximately 80% of patients
usually related to hypervolaemia and/or
activation of the
renin-angiotensin-aldosterone system as a result pf reduced glomerular
filtration; atherosclerosis is also common.
Hypertensive and/or ischaemic congestive
heart failure may later develop.
Uraemic toxic pericarditis is common in
untreated end-stage renal failure and may
present as persistent retrosternal burning
or stabbing chest pain that becomes worse on
deep breathing or swallowing
(irritation/friction on the pericardium).
6. Impairment of cellular and humoral immunity with increased susceptibility to infections.
Diagnosis: < BACK TO TOP >
analysis shows elevated urea and creatinine, sodium concentrations are usually
normal and potassium levels normal to moderately elevated (< 6 mmol/L).
clearance is always reduced, depending on the stage of the disease, reflecting
reduced glomerular filtration.
and hyperphosphataemia are found regularly and reflect deranged calcium
is usually moderate acidosis and normochromic-normocytic anaemia.
Findings on urine analysis depend on the nature of the underlying disease.
Management < BACK TO TOP >
the following measures are advisable, although they do not address the
Treatment of hypertension, urinary tract
infection, urinary tract obstruction,
sodium and water depletion (if present), nephrotoxic drugs should be
Control of diet (limit dietary protein if plasma creatinine very high, seen
Water and sodium are not restricted unless
there is visible oedema, potassium
intake doesn’t have to be reduced until end-stage renal failure.
Renal osteodystrophy is treated with
calcitriol [Calcijex, Sitriol, Rocalcitrol], a
synthetic analogue of vitamin D which doesn’t need activation in the
Human recombinant erythropoietin [Eprex]
weekly injections are given to
patients with progressive destruction of renal tissue, there comes a point
when supportive measures are required:
Haemodialysis is started usually with a
creatinine in the region of 1,000 mmol/L
and is carried
out for 4-6 hours 3 times weekly.
Continuous ambulatory peritoneal dialysis (CAPD)
uses the peritoneum as a
membrane. Dialysis fluid (around 1.5-3 L in adults) is introduced into the
through a permanent catheter (a tap in the abdominal wall) and periodically
drained and replenished 4 times/day by the patient. Peritonitis can develop as
Renal transplantation is the most effective
treatment, but tissue types must be
closely as possible and this procedure must be followed by
immunosuppressive treatment (infections and malignancies are unwanted effects).
Prognosis < BACK TO TOP >
Dr Zoran Pletikosa)
12 August 20096December 2005
speaker Mr NgThian Watt the Principal Trainer from
Napoleon Hill Associates MalaysiaDetails
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