CRF pathophysiology and treatment

1. CHRONIC RENAL
FAILURE
Dr. ROSE VEEDON

2. DEFENITION
Chronic renal failure is a syndrome
characterised by progressive and
irreversible deterioration of renal
function due to slow destruction of
renal parenchyma , eventually
terminating in death when sufficient
number of nephrons have been
damaged

3. • Acidosis is the major problem in CRF
with development of biochemical
azotemia(high levels of nitrogen
containing compounds) and uraemia
syndrome

4. CAUSE OF CRF
• Type one and type two diabetes
• High BP
• Immune system disease (lupus nephritis)
• Inflammation of glomeruli
• Polycystic kidney disease
• Reno vascular disease (urinary obstruction
due to prostrate hypertrophy)
• Pyelonephritis (inflammation of renal
parenchyma)
• Damage to infrastructure (nephron) can result
decreased GFR

5. SYMPTOMS
• RENAL
1. Metabolic acidosis(loss of acid base balance)
increased H + ions and decreased bicarbonate
levels in the body
2. Hyperkalaemia (increased potassium ions)
3. Sodium and water imbalance (water and
sodium can not pass through bowman's
capsule and release of rennin from juxta
glomerular apparatus can also result in
sodium and water retention)
4. Hyperuricemia (increased uric acid levels in
the blood)

6. • Extra renal
1. Anaemia (decreased production of
erythropoietin from kidney leads to
decreased erythropoesis and leads to
anaemia)
2. Integumentary system (deposition of urinary
pigment such as urochome in the skin causes
yellow colour. Urea content in the sweat as
well as plasma fluids will be there and on
evaporation, urea remains on the facial skin
as powdery form)
3. CVS: Due to fluid retention excessive work
load and eventually leads to congestive heart
failure.

7. 4. RS: hypervolemia and heart failure
causes pulmonary congestion and
pulmonary oedema
5. Digestive system: mucosal ulcerations in
the lining of the stomach and intestine
(bleeding) cause anaemia
Nausea and vomiting
6. Skeletal system: renal osteodystrophy
osteomalacia osteitis
fibros
(Due to vit. D deficiency) (due to
elevated
levels of
parathormone)

8. PATHOPHYSIOLOGY
Mainly through 4 stages
1. Decreased renal reserve
2. Renal insufficiency
3. Renal failure
4. End stage kidney

9. Decreased renal reserve
• The extra capacity of kidney to function,
is required under normal condition is
termed as renal reserve
• Condition that demand additional work by
kidney cannot adequately met
• The damage to renal parenchyma is
marginal and the kidneys remain
functional
• The GFR is about 50% of the normal
• BUN and creatinine values are normal
• Patients are usually asymptomatic except
at times of stress

10. Renal insufficiency
• 75% of functional parenchyma is been
destroyed
• GFR decreased to25%
• Elevated BUN and serum creatinine
levels
• Polyuria and nocturia occur due to
tubulo interstitial damage
• Sudden stress may precipitate uremic
syndrome

11. Renal failure
• 90% of functional renal tissue has been
destroyed
• GFR is reduced to approximately 10%
• Tubular cells are non functional
• Loss of regulation of sodium and water
and results oedema, metabolic
acidosis.

12. End stage kidney
• GFR is reduced to 5% of normal
• Results in uremic syndrome with
progressive renal and extra renal
symptoms

13. COMPLICATIONS
• PULMONARY EDEMA
• CARDIAC FAILURE
• ARRHYTHMIA(hyperkalaemia)

14. DIAGNOSIS
Most of the times CRF is identified during
investigation for some other medical problems
or during routine check-up
 Family history
 Drug history
 Social history
 History of CRF usually include
 long period of polyuria, nocturia, uraemia,
lethargy, breathlessness, anorexia, nausea
Anaemia
Excruciating itch
Poor sleep patterns
Lack of concentrations
Pigmented skin

15. Serum craetinine
Urine analysis
Renal function tests

16. PATIENT COUNSELLING
POINTS
• Sodium intake should be reduced
• Potassium containing food should be
restricted
• Protein restricted diet should be
maintained
• High energy intake up to 2000-3000
kcal
• Proper carbohydrate diet

17. MEDICAL MANAGEMENT
AIMS
Reverse or arrest the process causing
renal damage (rarely possible)
Avoid condition that worsen renal
failure
Relief of symptoms
Implement regular dialysis treatment
or transplantation at the most
appropriate time

18. Reduction of BP
• As hypertension causes damage to
intrarenal vasculature and results in
thickening of the walls of arterioles ,
control of BP is essential
• This damage reduces renal perfusion
leading to stimulation of rennin -
angiotensin - aldosterone system
ACE INHIBITORS
 Ramipril 2.5 mg PO OD
 Lisinopril 5mg PO OD
 Captopril 25 mg PO TID
SIDE EFFECTS : cough, hypotension

19. BETA BLOCKERS
 Propranolol 40 mg PO BD not exceed
640mg / day
 Labetol 100 mg PO BD initially,
increased by 100 mg BD every 2-3
days
Timolol 10-30 mg PO BD not more
than 60 mg/day
SIDE EFFECTS : arrhythmia,
bradycardia, syncope, fatigue,
headache, dyspnoea

20. Reduction of oedema
• Diuretics and dialysis should be
preferred to reduce fluid retention
• Potassium sparing diuretic is
contraindicated as it may cause
hyperkalaemia
DIURETICS (Loop Diuretic)
Furosemide: 20-80 mg PO OD may be
increased by 20-40 mg BD not exceed
600 mg/day
SIDE EFFECTS : hyperuricemia,
hypokalaemia

21. Torsemide : 20 mg PO/IV OD initially ,
double the dose until the desired
diuretic effect is achieved , not exceed
200 mg
SIDE EFFECT : headache, excessive
urination

22. Vasodilation (Reduction of
vasoconstriction)
• In hypertension associated with CRF ,
vasodilators like calcium channel
blockers , alpha blockers, ACE inhibitors
can be used
• But calcium channel blockers like
verapamil and diltiazem should not be
used along with Beta blockers
• As ACE inhibitors are potassium sparing ,
k+ ion concentration should be monitored

23.  Prasozin : initial dose is 1 mg PO BD
maintenance dose is 6-15 mg PO
BD/TID
SIDE EFFECTS : Dizziness, drowsiness,
headache, weakness, nausea,
palpitation.
Amlodipine : 5mg/day PO initially; may
be increased by 2.5 mg/day every 7-
14 days ;not exceed 10 mg/day
SIDE EFFECTS : pedal oedema,
pulmonary oedema

24. Reduce GI side effects
To prevent vomiting, nausea
 Metoclopramide : 10 mg IV/IM/PO TID
30 minutes before meals and at
bedtime
CLASS : anti emetic agent
SIDE EFFECTS : fatigue, restlessness,
sedation, headache, dizziness,
somnolence

25. Ondansetron : 8 mg IV BD
CLASS : anti emetic, selctive 5HT3
antagonist
SIDE EFFECTS : Headache, malaise,
constipation
 Prochlorperazine : 5-10 mg BD/TID
CLASS : Anit emetic
SIDE EFFECTS : insomnia,
restlessness, dizziness

26. Reduction of pruritis
• In order to suppress the skin rashes
oral antihistamines can be given
 Chlorpheniramine : tablets or syrup 4
mg PO TID Not to exceed 24 mg/day
CLASS : Anti histamine
SIDE EFFECTS : dizziness, drowsiness,
muscular weakness

27.  RENAL TRANSPLANTATION