Chronic Renal Failure (UG)

Chronic Renal Failure-UG

Lt Col (Dr)Ashutosh OjhaReader ,Internal Medicine

Plan

DefnEtiologyStagingPathophysiologyClinical FeaturesInvestigationsManagement Renal Replacement

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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

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