Chronic renal failure( Causes - C/P - Investigations - Treatment )

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Chronic renal failure( Causes - C/P - Investigations - Treatment )

Chronic renal failure

# Def:
It’s a gradual,s.progressive, within years irreversible deterioration of kid. Function which eventually leading to end stage renal failure.


End stage renal disease (ESRD) = GFR 10-15 ml/m

It is a stage of C.R.F. at which kidney function cannot sustain life. So replacement therapy is indicated (dialysis or transplantation)

#Causes:

1- Systemic hypertension(long duration)
2- Chronic GN (history of puffiness.)
3- Chronic pyelonephritis (history of urinary tract infection.)
4-Diabetic nephropathy (history of D.M)and diabetic triopathy
5-Lupus nephritis (young ♀ Å arthropathy.)
6- Obstr. Uropathy stones
B
7-Analgesic nephropathy (abuseof paracetamol+aspirin).
8-Cong. Polycystic Kid. F.H.
9-Gout. History of arthropathy.
10-Undermined aetiology.

Most important causes of CRF
D.M.
Hypert. In
chr. G.N the World
chr.pyelonephritis.

chr. Pyl. N. In
chr. G.N. Egypt.

#C/P

1-G.I.T.

Nausea & Vomiting persistent.
Not responding to usual ttt.
Diarrhea.
Hepatitis (blood tr.) hepatitic C, B.
Hiccough central effect.
Gastritis Urea irritant to gastric mucosa, ­­ Gastrin level.
G I T bleeding protein load
¯ Kid. Perfusion
ZAmmoniacal odour of mouth (urea excreted insaliva with splitting
by bacteri NH3).

2-Blood :
erythrobiotein deficiency.
ªAnemia¯ intake with haematinic deficiency e.g Iron
,Vit.B12 , Folate
Bleeding tendency.
¯life span of RBCs.
Blood loss during haemodialysis or througth GIT
B.M fibrosis due to hyper parathyroidism.
ACE inhibitors may decrease.
erythrobiotein release Anaemia.
ªbleeding tendencycapillary fragility.
(epistaxis) Thrombo asthenia due to toxins

ªWBCslymphocytes = B. & T.
decrease cell mediated & humoral immunity immunocomprmised
patient

. infection

3-C.V.S
Pericarditis Urea is very irritant to pericardium.it’s a feature of severe preterminal uraemia or of under dialysis,so it’s an urgent indication of dialysis.
Cardiomyopathy (toxins) affect the myocardium H.F.
Arrythmias electrolyte disturbances.
Pericardial effusion (Hgic) due to heparin use during
haemodialysis.
5-Hypertension salt & H2O retention.
Renin­.


pt e’ C.R.F. e’ Nr. Or ¯ bl. Pr.

Salt losing nephropathy Hyporeninism
e.g. tubulointerstitial disease. e.g. Diabetic nephropathy
obstr.uropathy
interest nephr.
pt e’ C.R.F. e’ no or mild anemia

= cystic kid, hypernephroma,hydronephrosis.

these kid. Secrete ­­ erythropoietin




4-Endocrine & metabolism:
insulin Resistance

-Impaired glucose tolerance and not D.M.(uremic pseudodiabetes)
-also insulin resistancemay contribute to hypertension& lipid abnormalities.
Subclinical Hypothyroidism (subclinical), it is due to sluggish TSH release
T R H

release of prolactin (also there is decrease in prolactin clearance)

Amenorrhea Impotence
glactorrhea
3-Ca ¯ 2 ry hyperparathyroidism.
4-Impaired clearanc of triglycerides,hypercholesterolemia may occur in advanced failure.
5-Bone

P­ (P mainly excreted) through kidneys. Serum Ca.
also active vit.D serum Ca .
Ca & vit.D 2ry hyper parathyroidism. leading to osteitisfibrosa cystica & osteo-sclerosis
Vit.D osteomalacia.
so vit.D & ¯ Ca 2 ry hyperparathyroidism.
Ca mobilization from bone



boney aches osteitis fibrosa
cystica
if we use
NSAID (nephrotoxic)

more deterioration of kidney function



Renal osteodystrophy


Œ osteomalacia � osteitis Ž osteosclerosis
= vit D ¯¯ fibrosa cytica (Rugger Jersey spine)
= 2ry hyperparathyroidism
Recently aluminum accumulation may vit D resist rickets
and aggravate the osteodystrophy.




6-Chest
Pneumonia ( ¯ immunity).
Acidotic breathing.

7-Neuorologisal

1- neuropathy autonomic neuropathy

motor sensory impotence gastroentritis
diarrhea
weakness Glove & &constipation orthostatic
stock.Hypothesia hypotension

Uremic myopathy.
Uremic myoclonic jerk. (myoclonus).
Convulsions.
Dysequilibruim $ due to rapid ¯¯of blood urea by intensive dialysis.
(Brain edema)
Encephalopathy.
Strokes e.g. cerebral hge, due to hypertension and bleeding tendency.
Carpal tunel $ due to amyloidosis.
Restless legs syndrome (irresistible need to move legs)
Dialysis Dementia (AL related).


8-Skin

itching parath. Hr. ­­ hyper calcaemia.
Hyper phosphatemia.
Colour (earthy look), it is a mixture of 3 colours

yellow pallor hyperpigmentation

urochrome pigment Hb
Recurrent pyogenic infection.
Urea frost whitish powder on the skin surface.
Bronze colour due to haemochromatosis.



9-Acid base & electrolytes

Ca ¯ - P ­ - Al ­ (excreted through kid.).
SK ­ (excreted through kid.)
PH ¯ = metabolic acidosis due to H+ retension.
Na retention.

10-Urinary manifestation

-Manifestation of the cause as UTI, renal stones some cases early give polyurea ,nocturia& then oliguria.

# Investigations

to prove renal failure:

Urea ­, Cr­, PH¯, K

To prove chronicity

(¯ Ca, ­P, ¯ Hb) as these changes take a time.
These changes may occur with acute renal failure.
Broad casts in urine.
Granular cast and low fixed sp. G (1010) = Isothenuria.
Sonar Shrunken kidney.
(most important) Advanced hydronephrosis
Polycystic kidney
Poor differentiation between cortex &
medulla=parenchymaldisease.
Remember that in Diabetic nephropathy& amyloidosis,the kid. Size is usually normal or enlarged.

Causes( to control any reversible factors)
Urine infection, RBCs casts
Plain x - ray stone.
Sonar cystic kid.
Bl. Sugar diabetic nephropathy.
Markers for S.L.E.

Reversible factors in uremia= (aggravating factors)
1-Hypertension 4-Urinary tract obstruction.
2-Reduced kid perfusion
3- UTI 5-Nephrotoxic drugs

# ttt of C.R.F.

A-Conservative (medical ttt)

Indication:.
Fair general condition
= Minimal symptoms
= Stable C.R.F.
S. Cr. < 8mg% .
Blood urea < 200 mg %.
( the above 3 indications must be fulfilled together)

Lines of medical ttt :

Diet· Low protein diet £ 40 gm ( small piece of meat)
i.e 0.6gm/kg
·­ CHO source of E (250 gm/d)
·¯ K diet e.g fruits & citrus fruits.
· Na
Na losing Salt
retention
Na supplements
Restriction of sodium
· Fluid chart 500 C.C. + (volume of urine in the previous day).
· Avoid nephrotoxic drugs.


Prolonged dietary protein restriction should be avoided. It is preferable to start dialysis therapy little earlier than to cause malnutrition.

G I T:

Vomiting metacolopramide or domperidone.
Hiccough metacolopramide or domperidone.
µ Gastritis we can use H2 blockers or proton pump inhibitor.

Phosphate chelators:

Oral Ca carbonate acts as a Calcium supplement & also reduces absorption of Diatery Phosphorus.500mg tab.TDS before meals. Also Ca acetate can be used.

Endocrine:

¶Ca supply Ca tablets.
Vit D (one alpha) It is a synthestic.
analogue of vit D (alfacalcidole)

tab. 0.25 Ug or 1 Ug/Day.
¶ Anabolic steroids improve bone disease & ¯protein catabolism
¶­ prolactin parlodel.

Blood:

­ Anemia Iron therapy.
blood transfusion.
erythropoietin injection S.C or I.V(genetically made).

CVS:

Hypert B.Blockers.
ACE inhibitors.
Ca channel blocker.
Pericarditis Dialysis
NSAID (nephrotoxic)
Steroids.
Hr. failure ttt (see C.V.S.).
Arrythmia ttt (see C.V.S.).
Acid base:

acidosis ( rise Na HCO3)
­ k (glucose insulin)
also Ion exchange resins to remove potasium from GIT.
·ttt of U. T.I.
Stone surgery.
D.M. control
S L E ttt
Hypert ttt.
Å follow up monthly with periodic investigations e.g
creatinine, urea, Na and K, Hb ,Ca ,P.

B-Dialysis:

Indication:.

bad G. condition. One indication is enough
S. Cr. > 8 and > 6 in D.M. to start Dialysis.
Bl. Urea > 200.

Haemodialysis:

Adv. Less invasive than peritoneal Dialysis.
Rapid action.
vDisadv. Infection Hepatitis C, B
bleeding (heparin) A I D S
Contraindic. Bleeding tendency.
Hypotension.

Q: uses of haemodialysis machine:
1- Acute &chronic renal failure 2- K.+↑Ca 3- Drug toxicity. (Salicylates,Barbiturate&Alchol )
4- Ultra filtration & reinfusion Ascites.
5- Ultrafiltration to treat pulm. Oedema.

Peritoneal dialysis