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Forth stage
Medicine
Lec-4
د.عماد البدراني
31/10/2015
Chronic Renal failure
Definition:
Is an irreversible deterioration in renal function which classically develops over period of
years . Initially manifested only as biochemical abnormality, eventually loss of excretory,
metabolic, and endocrine function of the kidney lead to development of clinical symptoms
and signs of renal failure which is referred to as uremia
Etiology
1) Pre-renal
Include long standing R.A.S
2) Renal causes
Include chronic G.N chronic interstitial nephritis, D.M hypertension, C.T disease (S.L.E)
myeloma, amyloidosis, radiation nephritis, and neoplasia
3) Post-renal causes
Due to long standing urinary obstruction
Pathogenesis:
Disturbances in water, electrolytes and acid-base balance, contribute to clinical picture in
patient with chronic renal failure but the exact pathogenesis of clinical syndrome of uremia
is unknown. And many substances present in abnormal concentration in the plasma have
been suspected of beinguremic toxins
Clinical feature
In early CRF the patient is often asymptomatic,
Renal failure may present as raised urea and creatinine found during routine
examination, often accompanied by H.T proteinuria or anemia
Symptoms usually develop when G.F.R reach 20ml/min.And nocturia
(Due loss of concentration ability and osmotic load).
Is often early symptoms and then because of wide spread effect of renal failure,
symptoms and signs develop related to almost every body system.
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1-Anemia : anemia is common and usually correlate with the severity of CRF and contribute
to many of the non-specific symptoms of CRF.
Causes:
1) relative deficiency of erythropoietin
2) diminishederythropoiesis due to the toxic effects of uremia on bone marrow
3) reduced red cell survival
4) increased blood loss due to capillary fragility and poor platelet function
5) reduced dietary intake and absorption of iron and other hematocrits
They found in the cystic disease of kidney the anemia is rare,while in the interstitial
nephritis the anemia is so sever.
Anemia can be treated by synthetic human erythropoietin {Eprex} and it is effective in
treat anemia. Butit cause side effect like tingling sensation and S.T convulsion and lead
to uncontrolled hypertension, failure of erythropoietin therapy is due to iron deficiency
or active inflammation or malignancy or aluminum over load
2-Renal- osteo dystrophy:
The metabolic bone disease accompanied CRF consist of admixture of:
1) Osteomalcica: (due to decrease activity od 1-alph hydroxylase enzyme of vit. D)
which lead to decrease intestinal absorption of calcium and lead to hypocalcaemia
and reduce calcification of osteoid
2) Oestitis fibrosis: Cystic decalcified lesion in bone due to secondary hyper
parathyroidwhich is stimulated by low plasma calcium and by hypophosphatemia. In
some patient tertiary or autonomous hyper parathyroid with hypocalcaemia
develops
3) Osteoporosis: occur in many patient possibly related to malnutrition
4) Osteosclerosis: is seen mainly in the sacral area at the base of the skull
And in the vertebrae, the cause is unknown.
3- Myopathy:
Generalized myopathy is due to:
A) Poor nutrition
b) Hyperthyroidism
c) Vit. D deficiency
d) Electrolyte disturbances
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Muscle cramps is common can be treated by quinine sulphate
restless leg patient legs are jumpy during night maybe trouble treated by clonazepam
4-Neuropathy:
There is demyelination of modulated fiberLead to:
A) Sensory neuropathy present as parenthesis
B) Motor neuropathy present as foot drop
C) Autonomic neuropathy present as delayed gastric empty, diarrhea ,postural
hypotension
The clinical manifestations of neuropathy appear late in in curse of CRF
5- Endocrine function:
Number of hormonal abnormities may be present like:
A) Hyperprolactinemia
B) Hyperparathyroid
C) In femaleamenorrhea is common
D) In both sexes there is loss of libido and sexual function
E) Half-life of insulin is prolonged.
6-Cardiocascular disease:
a. hypertension develops in 80% of patient with CRF due to Na retention, increase
rennin and increase aldosterone ( hypertension should be well controlled )
b. atherosclerosis is common and may be accelerated by hypertension
c. vascular calcification may develops
d. pericarditis is common in untreated or inadequate Rx and it may lead to pericardial
tamponade and late constructive pericarditis
7-Acidosis : due to decline renal function and this acidosis usually asymptomatic and lead
to proton buffered in bone in place of calcium, this aggravating metabolic bone disease
8-infection: cellular and humoral immunity are impaired with increased susceptibility to
infection ( infection is the most common cause of death in dialysis patients after
cardiovascular diseases )
9-GIT disturbance : very common and presented as anorexia, nausea, vomiting and
abnormal bowel motion, also CRF patients are vulnerable to gastric and duodenal
ulceration
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Management of CRF
there are several aspects:
1. identify the underlying disorder by history, physical examination, biochemical tests,
immunology, radiology and renal biopsy ( in some cases the cause may be amenable
ti specific therapy e.g. immunosuppression in some types of GN )
2. search for reversible factors and the correction of which may result in improvement
in renal function, like:
I.
hypertension
II.
decrease renal perfusion ( renal artery stenosis, decrease BP due to drugs, Na and
water depletion, poor cardiac function )
III.
UT obstruction
IV.
UTI
V.
other infection
VI.
nephrotoxic medication
progression of CRF
a plot of reciprocal serum creatinine concentration against time allows good follow up,
when patient need dialysis and detect any worsening of renal function
Factors of progression of CRF
1- control of BP : good control of BP is beneficial especially in disease affecting the
glomerulus and may retard deterioration of CRF and diabetic and with heavy proteinemia.
ACE-I is more effective in diabetic nephropathy
2-Diet : in experimental studies, progression of renal failure can be retarded by dietary
manipulation mostly by restriction of dietary protein.
in human studies results have been less clear cut for most patients living in areas where
renal replacement therapy is available severe protein restriction is not generally
recommended. moderate restriction (60g/day) should be accompanied by adequate
calories to prevent malnutrition. anorexia and muscle loss may indicate a need to start
dialysis Rx.
3-lipid : hypercholesterolemia is almost universal in patients with proteinuria and increase
Triglyceride level is common is patient with CRF, these accelerate development of vascular
diseases and accelerate progression of CRF. should be treated.
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4-electrolytes and fluid : in CRF, kidney cannot concentrate urine, so high volume of urine
is needed to excrete products of metabolism and fluid intake of 3 liters per day is desirable,
some patients with "salt-wasting" may require high sodium and water intake ( these seen in
patient with cystic diseases, obstruction,reflux nephropathy and other tubulointerstitial
diseases but not seen in glomerular diseases ), limitation of potassium intake to
70mmol/day is required
5-Osteodystrophy:
plasma calcium and phosphate should be kept as near to normal as possible,
hypocalcaemia is controlled by giving 1-alpha-Vit D ( synthetic analogue of Vit D )
hyperphosphatemia is controlled by dietary restriction of food with high phosphate
content as milk ,cheese and eggs. use of phosphate-binding drugs as calcium
carbonate tablet 500mg 1*3, aluminum OH is also a phosphate binder 300-600 mg
before meal, side effects are constipation and aluminum toxicity
hyperparathyroidism is controlled with these measures, rarely the patient needs
parathyroidectomy
Renal replacement therapy in CRF
1. Haemodialysis : should be started when despite adequate medical Rx, the patient
with advanced renal failure and before developing serious complication, this occur
when serum creatinine 800 mircomol (9mg). vascular access is needed and in
emergency state a central venous catheter is needed. hemodialysis is for 3-5 hours
3times/week
2. CAPD "Continuous Ambulatory Peritoneal Dialysis"
3. Renal transplantation