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Chronic Renal Failure

Chronic Renal Failure. OUTLINE. INTRODUCTION DEFINITION EPIDEMIOLOGY AETIOLOGY PATHOPHYSIOLOGY CLINICAL SIGNS/SYMPTOMS MANAGEMENT MEDICAL RENAL REPLACEMENT THERAPY. INTRODUCTION. Chronic Kidney Disease or CRF encompasses all degrees of decreased in Renal function

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Chronic Renal Failure

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  1. Chronic Renal Failure

  2. OUTLINE • INTRODUCTION • DEFINITION • EPIDEMIOLOGY • AETIOLOGY • PATHOPHYSIOLOGY • CLINICAL SIGNS/SYMPTOMS • MANAGEMENT • MEDICAL • RENAL REPLACEMENT THERAPY

  3. INTRODUCTION • Chronic Kidney Disease or CRF encompasses all degrees of decreased in Renal function • It’s a worldwide problem and there is a rising in incidence and prevalence of kidney failure with poor outcomes and high cost of management

  4. Definition • 3 Criteria are involved • Evidence of kidney damage or reduction in function • Duration>3months • Irrespective of the aetiology

  5. It is characterized by a progressive deterioration in renal function ultimately leading to irreversible structural damage to existing nephrons. • A substantial decline in renal function leading to azotemia.

  6. Etiology of CRF • Diabetes • Hypertension • Glomerulonephritis • Interstitial nephritis • Cystic kidney disease • Myeloma • Drugs e.g Gold , Heroin, • Chronic pyelonephritis • Congenital abnormalities • Metabolic diseases • Urinary obstruction • Renal artery stenosis • Connective tissue diseases • Hiv

  7. Pathophysiology • The presence of or exposure to the initiation risk factors (HTN,DM,PKD) result in the loss of nephron mass leading to hypertrophy of the remaining nephrons. • This results in the development of intraglomerular hypertension. • The patient remains well until so many nephrons are lost that the GFR can no longer be maintained, and the GFR progressively declines. • The patient may remain symptom less until the GFR falls as low as 15 to 20ml/min

  8. Hypertension & Diabetes • Common cause of ESRD • Diabetes –nephropathy • Hypertension is both a cause and result of CKD • HT promote renal impairment through elevated systemic pressure to glomeruli. The result is glomerular capillary hyper perfusion and hypertension leading to progressive renal damage. • Glomerular Ischemia induced by damage to preglomerular arteries and arterioles may also occur

  9. Chronic Glomerulonephritis • Common cause in adults &children • Idiopathic and Systemic disease • Trapping of immune complexes in the glomerulus and leads to inflammatory response • Responsible antigens include certain strains of Streptococci, malaria, endogenous antigens (neoplastic lesions), SLE and drugs

  10. Chronic Glomerulonephritis • Proteinuria • Haematuria • Oliguria • edema • Hypertension High Proteinuria is referred to as nephrotic syndrome, which is characterized by: • Pitting edema • Proteinuria > 3.5gm/day • Hypoalbuminaemia

  11. Interstitial Nephritis • Inflammation of the interstitium of the kidney • Drugs and toxins • Nocturia • Anemia • Renal osteodystrophy

  12. Polycystic Kidney Disease • Characterized by many bilateral renal cysts that increase renal size but reduce functioning of renal tissue • PKD is of three types 1.Autosomal dominant (adult) PKD 2.Autosomal recessive Childhood PKD 3.Congenital Polycystic kidney disease

  13. Chronic Pyelonephritis • Chronic inflammation of the renal parenchyma with scarring of the kidney. • Recurrent urine infection. • Important cause of kidney destruction in children with severe lower urinary tract infections

  14. Urinary Obstruction • This may be sudden or insidious, partial or complete, unilateral or bilateral. • Symptoms –oliguria and pain • Causes include: Prostate hypertrophy Renal calculi (stone formation) Vesicoureteric reflux indwelling urinary catheters

  15. Metabolic Diseases • Diabetes mellitus and Amyloidosis ( accumulation of glycoprotein in tissues(kidney)) are probably the most common metabolic diseases that may lead to chronic glomerular nephritis

  16. Clinical Features • Hypertension • Proteinuria • Anemia • Nocturia • Renal osteodystrophy • Myopathy • Hypophosphataemia • Neurological changes • Metabolic acidosis • Infections • Neuropathy • Uremia • Pericarditis • Encephalopathy • GIT: nausea, vomiting, diarrhea • FTT,Fatigue • Erectile dysfunction • Platelet dysfunction

  17. Clinical Features • Patients with CKD stage 1-3 are frequently asymptomatic. • Generally, the symptoms become more evident at stage 4-5.

  18. Differential Diagnosis • SLE • Renal Artery Stenosis • UTI • Acute kidney Injury • Chronic glomerulonephritis • Diabetic Nephropathy • Multiple Myeloma • Nephrosclerosis • Multiple Myeloma

  19. Investigations • Fbc • Urinalysis • Serum albumin • Lipid profile • Serium calcium and phosphate, ALP, VIT D, PTH assay • ANA, ANTI-GBM, P-ANCA • Renal USS • Retrograde pyelography • CT Scan ( renal mass, stones) • MRI ( for pxt who cant receive contrast) • Renal radionuclide scan ( renal artery stensosis) • Biopsy

  20. Renal biopsy • Indication • Management of already diagnosed condition e.g lupus • Contraindication • Small kidney • Echogenic kidneys indicative of scarring

  21. Management • Identify the underlying cause for renal disease • Attempt to prevent further renal damage • Look for reversible factors(UTI,U.obs,medications) which are making renal function worse • Attempt to limit the adverse effects of the loss of renal function • Replacement therapy-Dialysis,transplantation.

  22. Hypertension • Diuretics-loop diuretics • Beta adrenoreceptor blockers-Atenolol-renally cleared require dosage adjustment in renal failure • Calcium antagonists-Nifedipine-negative inotropic effect – reduction in cardiac workload. reduce renal vasoconstriction- Increase in RBF&GFR Headache,flushing,edema and nocturia can occur. • Vasodilators-hydralazine,prazosin and minoxidil.only used when other measures are failed

  23. Uremia • Urea is one of the toxin -Symptomatic relief when the dietary protein intake is reduced. • Nausea, vomiting and pruritis are some of the uremic symptoms • Vomiting,nausea-Ondansetron,domperidone • Pruritis-chlorpheniramine,Loratadine

  24. Anemia • Relative deficiency of erythropoietin (regulator of red cell production) • Shortened red cell survival and marrow suppression due to uremic toxins • Treatment-Recombinant human erythropoietin • Target hemoglobin between 10&12g/dl • Complication of treatment-Increased blood pressure,and Increased blood coaguility, Increased incidence of thrombosis of AV fistulae used in hemodialysis.

  25. Renal Osteodystrophy • Cholecalciferol is the precursor of active vitamin D is both absorbed in the GIT and produced in the skin • Production of 1,25-dihydroxycholecalciferol(calcitriol) requires the hydroxylation of the Cholecalciferol molecule at 1 and the 25position.1-position hydroxylation occurs in the kidney (impaired in CRF)& 25 position in the liver. • Defective mineraliation of bone and osteomalacia

  26. Renal Osteodystrophy • Hyperphosphataemia due to reduced phosphate excretion • Hypocalcaemia and a reduction in the direct suppressive action of 1,25-dihydroxycholecalciferol on the parathyroid gland results in increased secretion of PTH • Failed kidney unable to respond to PTH by increasing renal calcium absorption- the serum PTH levels remain persistently elevated, and hyperplasia of the parathyroid gland occurs-resulting in secondary hyperparathyroidism.

  27. Renal Osteodystrophy • Hyperphosphataemia-dietary restriction of foods with high phosphate (milk,cheese,egg) • Phosphate binding agents-aluminium hydroxide cap 300-600mg before each meal. • Calcium carbonate 500mg with each meal • VIT D deficiency-alfacalcidol at 0.25-microgram/day or 1,25-dihydroxycholecalciferol(calcitriol)1-2microgram/day.

  28. Neurological changes • Inability to concentrate, memory impairment, irritability • Peripheral neuropathy- demyelination of medullated fibres. (paresthesia) • Improve-once dialysis is initiated

  29. Muscle function • Muscle cramps & restless legs (legs are jumpy during the night) • Due to nutritional deficiency &electrolyte disturbances,vitamin D deficiency • Treatment- Clonazepam • Muscle cramps-quinine sulphate

  30. Edema • Result of Sodium and water retention • Hypoalbuminaemia-due to renal loss • Pulmonary and peripheral edema are best controlled with dialysis but diuretics can be useful • Salt restriction

  31. Hyperkalaemia • Potassium restricted diet • Fruits ,tender coconut, Vegetables, chocolate, Beer, instant coffee • Emergency treatment of hyperkalemia

  32. Acidosis • Reduction in serum bicarbonate • Sodium bicarbonate 1-6g/day

  33. Infection • Cellular and humoral immunity is impaired with increased susceptibility to infection • Infections are the second common death in dialysis patients after the cardiovascular deaths

  34. Treatment • Dialysis • Hemodialysis • Peritoneal dialysis • Haemofiltration • Transplantation with immunosuppressive agents

  35. Dialysis • The movement of fluid and molecules across a semi permeable membrane from one compartment to another. • Dialysis does not correct renal dysfunction • Dialysis helps to replace renal function when kidneys have failed • Correct fluid/electrolyte imbalances • Remove waste products

  36. Dialysis • When initiated? • When uremia can no longer be managed conservatively. • Immediately when: • Unresponsive to diuretics (fluid overload) • Pericarditis present • Uncontrolled hypertension • Neurologic manifestations • Unresponsive hyperkalemia • GFR less than 15 ml/minute

  37. Dialysate • A balanced mix of electrolytes and water • Closely resembles human plasma • Need not be sterile in hemodialysis, but sterile with peritoneal dailysis

  38. Dialysate Solutions • Common electrolytes included: • Potassium • Sodium chloride • Magnesium • Calcium • Glucose: added to increase filtration of fluid • Bicarbonate or acetate added to buffer (stabilize any existing metabolic acidosis)

  39. Dialysis: General Principles • Diffusion • Movement of solutes from an area of greater concentration to lesser concentration • Osmosis • Movement of fluid from an area of lesser to an area of greater concentration of solutes.

  40. Dialysis: General Principles • Ultrafiltration (water & fluid removal) • Movement of fluid across a semi permeable membrane as a result of an artificially created pressure gradient.

  41. Types of Dialysis • Hemodialysis • Peritoneal Dialysis • Hemofiltration/Continuous Renal Replacement Therapy (CRRT)

  42. Hemodialysis • Uses a machine and an artificial kidney to remove excess fluid and waste products from the blood • Does not regulate BP or other renal functions (hormonal control) • Preferred method when quick removal of water and toxins is indicated

  43. Hemodialysis • Blood pumped out of client via the vascular access • Passes through a filter (dialyzer) • Semi-permeable pores allows small substances to pass through (creatinine, urea, water) does not allow passage of blood, protein, bacteria • Blood returned to client once filtered

  44. Duration & Frequency • Dependent on: • Amount of metabolic waste to be cleared • Clearance capacity of dialysis machine • The amount of fluid to be removed • 12 hours per week, divided into three 4 hour treatments • Restricts activity level of client

  45. Anticoagulation • Heparin used to inhibit tendency of blood to clot when in contact with foreign surfaces (dialyzer membrane) • Clients receiving erythropoietin may need more heparin • Risk for hemorrhage during and immediately after treatment

  46. Hemodialysis Complications • Hypotension-100-200ml of NS • Headache-Paracetamol • Nausea/vomiting-ondansetron • Malaise • Dizziness • Muscle cramps • Blood Loss • Sepsis • Disequilibrium syndrome • Dialysis encephalopathy • Itching –Diphenhydramine 25-50mg

  47. Hemodialysis Complications • Disequilibrium syndrome • Due to rapid changes in the composition of the extracellular fluid. • Solutes (BUN) removed more rapidly from the blood than from the CSF and brain • Creates a high osmotic gradient in the brain resulting in a shift of fluid into the brain = Cerebral edema • Confusion • Decreased level of consciousness • Restlessness • Headache • seizures

  48. Advantages maximum solute clearance best tx for severe hyper-K+ ready availability limited anti-coagulation time bedside vascular access Disadvantages hemodynamic instability hypoxemia rapid fluid + solute shifts complex equipment specialized personnel Costly Hemodialysis

  49. Peritoneal Dialysis • After placement of peritoneal dialysis catheter-usually PD is not initiated until 7-14 days to allow for proper sealing of the catheter. • Three phases are present in peritoneal dialysis • Inflow(fill)-a prescribed amount of dialysate solution is inserted usually 2 liters in an adult over about 10-15 minutes(based on client comfort) • Dwell(equilibration)-diffusion and osmosis occur between the patients blood and the peritoneal cavity. The duration of the dwell time can last 20-30 minutes to 8 hours or more. • Drain-draining of the peritoneal fluid takes approximately 20-30 minutes and may be facilitated by gently massaging the abdomen

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