Chronic Renal Failure (UG)
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Transcript of Chronic Renal Failure (UG)
Chronic Renal Failure-UG
Lt Col (Dr)Ashutosh OjhaReader ,Internal Medicine
Plan
DefnEtiologyStagingPathophysiologyClinical FeaturesInvestigationsManagement Renal Replacement
Therapy*******Covered Separately
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.
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.
Causes of CRF:-(a) Congenital & inherited diseases
Polycystic kidney diseaseMedullary cystic diseaseTuberous sclerosisCongenital Obstructive uropathies
(b) Glomerular Diseases Primary glomerulonephropathiesSecondary 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
PathophysiologyInitiating mechanism
Long term reduction of renal massVasoactive 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.
Early stage, mild renal insufficiencyKidney function is entirely normalGFR – 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 phosphorousSevere renal insufficiency
GFR < 30% of normalUraemic clinical manifestationsBiochemical abnormalities marked.
GFR <10 – 5% of normalContinued survival without RRT impossible
Deterioration
Mild to moderate renal insufficiencyRenal function is compromised by
infectionspoorly controlled HTNHyper or HypovolaemiaDrugsContrasts
Overt Uraemia
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
(a) Clinical Abnormalities(a) Fluid and electrolyte disturbances-
Volume expansion/ contractionHyper/ HyponatremiaHyper/ hypokalemiametabolic acidosisHyperphosphotaemiaHypocalcaemia
(b) Endocrine- metabolic disturbance – Secondary Hyperparathyroidism Vit D defi osteomalacia Adynamic osteomalacia Carbohydrate intolerance Impaired gonadal function
(c) Neuromuscular disturbancesfatigue, sleep disorderslethargy, impaired mentationasterixis, peripheral neuropathy,restless leg syndrome, myoclonusseizures, myopathy, coma
(d) cardiovascular and pulmonary disturbancesHypertensionCCF, pulmonary edemaPericarditis, cardiomyophthyAccelerated atherosclerosis
(e) DermatologicalPallor, hyperpigmentationPruritus, echymosis, Uraemic frost
Clinical Features….. (f) G.I. disturbances
Anorexia, nausea, vomitingUraemic fetorPeptic ulcer, G.I BleedHepatitis, Peritonitis
(g) Haematological and Imuunnologic disturbancesAnemiaLymphocytopeniaBleeding diathesisSusceptibility to infectionHypocomplementemia
Symptoms are common when Urea is > 40 mmol/LCommon symptoms-
malaise, loss of energyloss of appetiteInsomnianocturia and polyuriaitchingnausea, vomiting, diarrhoeaParaesthesiaRestless legBone paintetanySymptoms due to salt & water retentionSymptoms due to anaemia Sexual dysfunctionmental slowing, clouding of consciousness, seizures
coma
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
InvestigationsUrine analysis
Haematuria - GNProteinuria - glomerular diseaseGlycosuria with normal BS
with BSUrine microscopy
white cells – UTI, papillary necrosis, TBEosinophiluria – allergic tubulointerstitial nephritisGranular casts – active renal disorderRed cell casts – GNRed blood cell
Urine biochemistry24 hr Creatinine clearane,Severity of renal failureUrinary electroytesUrine osmolality
Serum biochemistry Urea and creatinineElectrolytes
-Hyperkalaemia
Radiological –USG – Renal size and textureIVUCT – cortical scarring, retroperitoneal fibrosis, urinary obstruction
Renal biopsyIn unexplained CRF with normal sized kidneys
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 osteodystrophyHigh turnover – osteitis fibrosa cysticaLow turnover – osteomalacia
adynamic bone disease
Complications
Skin disordersPruritus
Retention of nitrogenous waste Hypercalcemia Hyperphosphataemia Iron deficiency
Complications
G.I. Complications– gastric emptying
reflux oesophagitis– Peptic ulceration– acute pancreatitis– Constipation
Complications
MetabolicGout Insulin requirement Lipids –
hypercholesterolaemia
Complications
Endocrine• Hyperprolactinaemia• LH• testosterone• Abnormalities of GH• Abnormal thyroid function
Complications
CNS Cerebral function Seizure thresholdDementiaPeripheral neuropathyAutonomic disturbancesMyopathy
Complications
CVS
HTN
Cardiac Hypertrophy
Myocardial fibrosis
Pericarditis
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)
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
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)
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
Thank You