2. Plan
Defn
Etiology
Staging
Pathophysiology
Clinical Features
Investigations
Management
Renal Replacement
3. CHRONIC RENAL FAILURE
Def:- CRF implies long standing,
progressive deterioration in renal function.
There occurs derangement of excretory,
metabolic and endocrine functions of the
kidney and when ESRD is reached the
patient becomes dependent on renal
replacement therapy to avoid life-
threatening uraemia.
4. CHRONIC RENAL FAILURE
Uraemia – Uraemia is a clinical and
laboratory syndrome reflecting dysfunction
of all organ system as a result of untreated
or under treated acute or chronic renal
failure.
6. Pathophysiology
Initiating mechanism
Long term reduction of renal mass
Vasoactive molecules
cytokines, GF
Structural and functional hypertrophy of
surviving nephrons as an adaptive mechanism
Predispose to sclerosis of remaining viable nephrons
Progressive decline of residual nephron function.
7. Early stage, mild renal insufficiency
Kidney function is entirely normal
GFR – N or ( hyperperfusion)
Moderate renal insufficiency
GFR – 30% of normal
Asymptomatic, nocturia, mild anaemia, loss of
energy and appetite.
Urea and Creatinine
Abnormalities in calcium and phosphorous
Severe renal insufficiency
GFR < 30% of normal
Uraemic clinical manifestations
Biochemical abnormalities marked.
GFR <10 – 5% of normal
Continued survival without RRT impossible
8. Deterioration
Mild to moderate renal insufficiency
Renal function is compromised by
infections
poorly controlled HTN
Hyper or Hypovolaemia
Drugs
Contrasts
Overt Uraemia
9. Deterioration
These processes lead to –
Disturbance in water, electrolyte and acid-base
balance
Accumulation of Nitrogenous waste
azotemia
Products of protein and AA metabolism
Produce ‘Uraemic toxins’ Uraemia
10. (a) Clinical Abnormalities
(a) Fluid and electrolyte disturbances-
Volume expansion/ contraction
Hyper/ Hyponatremia
Hyper/ hypokalemia
metabolic acidosis
Hyperphosphotaemia
Hypocalcaemia
(b) Endocrine- metabolic disturbance –
Secondary Hyperparathyroidism
Vit D defi osteomalacia
Adynamic osteomalacia
Carbohydrate intolerance
Impaired gonadal function
13. Symptoms are common when Urea is > 40 mmol/L
Common symptoms-
malaise, loss of energy
loss of appetite
Insomnia
nocturia and polyuria
itching
nausea, vomiting, diarrhoea
Paraesthesia
Restless leg
Bone pain
tetany
Symptoms due to salt & water retention
Symptoms due to anaemia
Sexual dysfunction
mental slowing, clouding of consciousness, seizures coma
14. Examination:-
Few physical signs of Uraemia per se
Short stature –Bi renal failure starting in childhood
Pallor
Pigmentation
Scratch marks
Signs of fluid overload
Pericardial Friction rub
Flow murmurs
Peripheral neuropathy
Kidneys – impalpable except in polycystic disease, obstn or tumour
Physical signs of underlying disease
Cutaneous vasculitis
Retinopathy
PVD
Evidence of neurogenic bladder
15. Investigations
Urine analysis
Haematuria - GN
Proteinuria - glomerular disease
Glycosuria with normal BS
with BS
Urine microscopy
white cells – UTI, papillary necrosis, TB
Eosinophiluria – allergic tubulointerstitial nephritis
Granular casts – active renal disorder
Red cell casts – GN
Red blood cell
Urine biochemistry
24 hr Creatinine clearane,Severity of renal failure
Urinary electroytes
Urine osmolality
Serum biochemistry
Urea and creatinine
Electrolytes
-Hyperkalaemia
16. Radiological –
USG – Renal size and texture
IVU
CT – cortical scarring, retroperitoneal
fibrosis, urinary obstruction
Renal biopsy
In unexplained CRF with normal sized
kidneys
17. Complications of CRF
Anaemia
– Erythropoietin def
– Bone marrow toxins
– Bone marrow fibrosis
– Heamatenic defi – iron, B6, B12
– RBC destruction
– Blood loss
Renal osteodystrophy
Impaired renal function
Po4 Excretion 1,25 (OH)2 Cholecalciferol
Plasma Po4 Impaired mineralisation Ca
++
of bones
absorption
Stimulation of
parathyroids PTH Bone resorption Plasma Ca++
Renal osteodystrophy
High turnover – osteitis fibrosa cystica
Low turnover – osteomalacia
adynamic bone disease
24. Management-Principles
Identify and treat the underlying disease
Attempt to prevent further renal damage
Look for reversible factors which are causing
failure
Attempt to limit the adverse effect of loss of renal
functions
Institute RRT (Dialysis, transplantation)
25. RRT…..Discussed again
•Specific Therapy – Treatment should be started well before the
measurable decrease in the GFR
•Measures to mitigate the hyper filtration injury -
–Dietary proteins restriction( approx 60 gm/d)
–Pharmacological management of intraglomerular HTN
ACE Inhibitors, Diuretics, Diltiazem, Verapamil
26. RRT
Should not be initiated when totally asymptomatic
Start sufficiently early to prevent severe complications
Clear indication for initiation
– Pericarditis
– Progressive neuropathy
– Encephalopathy
– Muscle irritability
– Fluid & electrolytes imbalance refractory to conservative management
– Sr creatinine >8 mg/dl (700 mmol/l)
– Creatinine clearence <10 ml/min (<0.17ml/sec)
27. Haemodialysis
Usually for 3 – 5 hrs for 3 times a week
Continuous Ambulatory Peritoneal Dialysis (CAPD)
Permanent silastic catheter is placed in the peritoneal
cavity
Dialysis fluid is left and drained after approx 6 hrs
Renal Transplantation
– Cadaver Donor
– Live donor
– HLA matching
– Immunosuppressive therapy