CHRONIC RENAL FAILURE CRFالدكتور خلدون ذنون- كلية طب نينوى- المرحلة الرابعة
Pay attention to the following:
1. Causes of CRF.
2. Various symptoms and signs of CRF.
3. Management of each disorder in CRF.
4. Dialysis in CRF; haemodialysis and peritoneal dialysis.
5. Kidney transplant in CRF.
DefinitionIrreversible deterioration in renal function which occurs over a period of years. At the start there is only biochemical abnormalities & features of uraemia appear later. End stage renal failure (ESRF) is the final event where death is likely.
AetiologyDiabetes mellitus 30% most common cause of ESRF.
Glomerular diseases 15%.
Interstitial diseases 10%.
Renal artery stenosis 5%.
Congenital & inherited 5% e.g polycystic kidney disease, Alports syndrome.
Systemic inflammatory diseases 5% e.g SLE, vasculitis.
PathogenesisWater, electrolytes & acid-base disturbance.
Accumulation of uraemic toxins & intermediary products of
Clinical featuresMay present as (B.urea&(S.creatinine often with hypertension, proteinuria or anaemia.
Symptoms begin when GFR is(30ml/min.N:80-120ml/min
Nocturia is an early symptom.
Tiredness & breathlessness.
ESRF creatinine clearance <5ml/min.patient is ill & anaemic, Na & water retention, Kussmauls respiration, anorexia, nausea, hiccough, pruritis, vomiting, muscle twiching, fits, drowsiness & coma.
Physical signsYellow complexion & palor.
Pulsus paradoxus (pericardial tamponade).
Pericardial friction rub.
Itching marks & Skin bruises.
Brown line nail pigmentation.
Peripheral neuropathy: parasthesia, (sensation, restless legs, absent reflexes.
AV fistulae, peritoneal or central venous catheters, transplanted kidney in iliac fossae with skin scar.
Anaemia common, due to:- Relative (erythropoietin .
- Uraemic toxins affecting bone marrow.
- (RBC survival.
- Bleeding due to capillary fragility&platelet dysfunction.
- Reduced dietary intake & absorption of iron & other haematinics.
- Polycystic kidney disease: anaemia is less severe or absent.
- Interstitial kidney disease: anaemia is severe for the degree of
CRF. Both may be due to effect on interstitial fibroblast that
Renal osteodystrophy- Osteomalacia :(activity of renal 1( hydroxylase enzyme.
(1,25DHC( (intestinal Ca absorption, hypocalcaemia &
( osteoid calcification.
- Secondary hyperparathyroidism (osteitis fibrosa)
(Ca&(PO4((PTH. Some develop hypercalcaemia due to
tertiary or autonomous hyperparathyroidism.
- Osteoporosis due to malnutrition.
- Osteosclerosis in sacral area, base of skull, vertebrae.
MyopathyDue to malnutrition, hyperparathyroidism, (vit.D, electrolyte
disturbance, muscle cramp (treated by quinine sulfate), restless leg
syndrome at night (treated by clonazepam).
NeuropathyDemyelination of medullated fibres, sensory neuropathy, motor
neuropathy e.g foot drop., autonomic neuropathy e.g delayed
gastric emptying, diarrhoea, postural hypotension. Neuropathy
occur late & improved by dialysis.
Endocrine dysfunction- Hyperprolactinaemia( amenorrhea & galactorrhea in females,
loss of libido & sexual function in both sexes; treated by
- T1/2 of insulin is prolonged due to reduced tubular metabolism
((dose of insulin in D.M with ESRF), post receptor defect in
insulin action(relative insulin resistance which is improved by
Cardiovascular disorder- Hypertension in 80% due to: (Na retention, (renin&angiotensinII
- Atherosclerosis is common.Vascular calcification lead to limb
- Pericarditis is common in ESRF(Pericardial tamponade &
( AcidosisAffect bone: protons are buffered in bone in place of calcium(
bone disease. Acidosis((renal function &(tissue catabolism.
( InfectionDepressed cellular & humoral immunity. Infection is the second
most common cause of death in CRF after CV disease.
( Bleeding(bleeding tendency(skin ecchymoses & mucosal bleeds. Platelet
dysfunction(( bleeding time, partially corrected by dialysis.
( GIT disorderAnorexia, nausea &vomiting,(incidence of peptic ulcer disease.
InvestigationsUrea, creatinine, electrolytes, calcium and phosphate, serum albumin, full blood count and clotting screen, urine analysis, urine microscopy, Blood glucose and serum lipids, renal U/S, culture of urine and blood, chest X-ray, serology for HIV and viral hepatitis before dialysis, ECG. PTH estimation, ferritin, folate and B12.
Management of CRFTreat the underlying disease e.g D.M, hypertension, stones,
2. Control of B.PControl of B.P may retard the rate of deterioration of GFR especially in diabetic nephropathy& heavy proteinuria.
Target B.P in CRF is 130/80, proteinuria(1gm/day 125/75.
B.P control also prevent or retard LV hypertrophy, heart failure & occlusive vascular diseases.
ACE inhibitors retard progression of renal failure & reduce proteinuria, it is more effective than other therapies.Angiotensin II receptor antagonists give the same effect also certain Ca antagonist. ACE inhibitors( (glomerular perfusion pressure by dilating the efferent arteriole( (GFR.
3. DietDietary protein restriction retards deterioration in renal function, 0.3-0.8gm/kg (difficult to adhere to & may cause malnutrition).
Moderate restriction of protein 60gm/day with adequate intake of calories to prevent malnutrition, severe restriction of protein is not advised when renal replacement therapy is available.
Anorexia & muscle loss needs dialysis.
4. LipidsHypercholesterolaemia occurs with proteinuria.
(triglyceride is common in CRF.
(Lipids enhance development of vascular disease & may accelerate progression of CRF. HMG CoA reductase inhibitors are used.
5. Electrolytes & fluidsLimit Na intake to 100mmol/day, may be required in late CRF.
Use loop diuretic for edema
Salt wasting occurs in: renal cystic disease, obstructive uropathy, reflux nephropathy, tubulo-interstitial diseases; they need 5-10gm salt/day/mouth.
Limit K+ intake to 70mmol/day, Avoid potassium sparing diuretics, ACEI, ARB, if there is hyperkalemia.
6. AcidosisPlasma bicarbonate should be >22mmol/L, give calcium carbonate 3gms/day which also binds excess phosphate in intestine.
7. AnaemiaRecombinant human erythropoietin (EP) is effective, target HB is 10-12gm/dl, given SC, complication: (B.P, (blood coagulability, (incidence of thrombosis of the AV fistulae which is reduced by slow correction of anaemia. Effect of EP is diminished in: iron deficiency, active inflammation, malignancy, aluminium overload.
Iron supplement is needed with EP to keep ferritin > 100(g/L & transferrin saturation >20%.
8. OsteodystrophyHypocalcaemia is corrected by 1- (-hydroxylated synthetic analogue of vit.D
Hyperphosphataemia is corrected by dietary restriction of e.g milk, cheese, eggs & phosphate binding drugs e.g calcium carbonate 500mg with each meal & AL hydroxide binds phosphate; to prevent aluminium toxicity minimum dose is given & administered immediately before meals.
Secondary hyperparathyroidism is controlled by above measures; and by calcimimetic agents that reduce PTH, parathyroidectomy may be needed in autonomous hyperparathyroidism.
9. Renal replacement therapy RRTPreparation should begin 12 month before start of RRT.
Psychological and social support.
Planning for hemodialysis or peritoneal dialysis.
Screen for hepatitis B, C, and HIV virus.
Indicated for symptomatic advanced kidney disease, cr.>600- 800(mol/L, GFR 8-10ml/min.
( Haemodialysis:Standard therapy in ESRF.
needs AV fistula-forearm, 3-5hrs/3times weekly. Survival(20y is
Complications: hypotension, arrhythmias, bleeding, air embolism, dialysis hypersensitivity, pulmonary edema and sepsis in between treatment.
Continuous ambulatory peritoneal dialysis CAPD.- Permanent Silastic catheter in to the peritoneal cavity. 2L of
sterile isotonic dialysis fluid introduced to peritoneal cavity &
left for 6hours, repeated 4times daily, during which patient is
- Useful in: young children, elderly with cardiovascular
Instability & D.M.
- Can be used for more than 10 years.
- Complication: peritonitis, sclerosis and failure of peritoneal
Automated peritoneal dialysis: mechanical device, exchange fluid at night, leaving the patient free during the day or with only a single exchange to perform during the day.
Renal transplantation- Corrects all the metabolic abnormality.
- Donor: cadaver, living relative.
- ABO compatibility & HLA matching are essential.
- Graft rejection is the major cause of failure.
- 3y graft survival 80%, 3y patient survival is 90%.
- Long term immunosuppressive therapy is required, combination
of prednisolone with ciclosporin A or azathioprine. Ciclosporin is
- Immunosuppression ( (infection,(malignancy especially of
Skin (50% of white patient develop skin malignancy by 15y.),
lymphoma due to Epstein Barr virus is rare.