Chronic renal failure (CRF) is a progressive decline in kidney function leading to end-stage renal disease (ESRD), requiring renal replacement therapy to prevent life-threatening uremia. Causes of CRF include congenital diseases, glomerular and vascular disorders, and urinary tract obstructions, with symptoms becoming pronounced as kidney function deteriorates. Management involves addressing underlying causes, implementing dietary and pharmacological strategies, and considering renal replacement therapies like dialysis and transplantation when appropriate.

1. Chronic Renal Failure-UG
Lt Col (Dr)Ashutosh Ojha
Reader ,Internal Medicine

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.

5.  Causes of CRF:-
(a) Congenital & inherited diseases
Polycystic kidney disease
Medullary cystic disease
Tuberous sclerosis
Congenital Obstructive uropathies
(b) Glomerular Diseases
Primary glomerulonephropathies
Secondary glomerular diseases
SLE, DM, HTN, TTP etc
(c) Vascular disease
Atherosclerotic renal vascular disease
(d) Tubulointerstitial disease
Tubulointertitial nephritis
( idiopalnic, drugs)
Reflux nephropathy-
TB, MM
(e) Urinary Tract obstruction – calculus, tumour, prostate

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

11. (c) Neuromuscular disturbances
fatigue, sleep disorders
lethargy, impaired mentation
asterixis, peripheral neuropathy,
restless leg syndrome, myoclonus
seizures, myopathy, coma
(d) cardiovascular and pulmonary disturbances
Hypertension
CCF, pulmonary edema
Pericarditis, cardiomyophthy
Accelerated atherosclerosis
(e) Dermatological
Pallor, hyperpigmentation
Pruritus, echymosis, Uraemic frost

12. Clinical Features…..
(f) G.I. disturbances
Anorexia, nausea, vomiting
Uraemic fetor
Peptic ulcer, G.I Bleed
Hepatitis, Peritonitis
(g) Haematological and Imuunnologic disturbances
Anemia
Lymphocytopenia
Bleeding diathesis
Susceptibility to infection
Hypocomplementemia

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

18. Complications
Skin disorders
Pruritus
 Retention of nitrogenous waste
 Hypercalcemia
 Hyperphosphataemia
 Iron deficiency

19. Complications
G.I. Complications
– gastric emptying
reflux oesophagitis
– Peptic ulceration
– acute pancreatitis
– Constipation

20. Complications
Metabolic
Gout
Insulin requirement
Lipids –
hypercholesterolaemia

21. Complications
Endocrine
• Hyperprolactinaemia
• LH
• testosterone
• Abnormalities of GH
• Abnormal thyroid function

22. Complications
CNS
Cerebral function
Seizure threshold
Dementia
Peripheral neuropathy
Autonomic disturbances
Myopathy

23. Complications
CVS
 HTN
 Cardiac Hypertrophy
 Myocardial fibrosis
 Pericarditis

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

28. Thank You