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Chronic kidney disease

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Chronic kidney disease

  1. 1. THUSHARA C 1ST YEAR. M PHARM PHARMACY PRACTICE
  2. 2. CONTENTS 1.DEFINITION 2.STAGES OF CKD 3.ETIOPATHOGENESIS 4.CLINICAL FEATURES 5.DIAGNOSTIC TEST RESULTS 6.THERAPY
  3. 3. DEFINITION Chronic renal failure is a syndrome characterized by progressive and irreversible deterioration of renal function due to slow destruction of renal parenchyma, eventually terminating in death when sufficient number of nephrons have been damaged. Acidosis is the major problem in CRF with development of biochemical azotaemia and clinical uraemia syndrome.
  4. 4. CKD is categorized by the level of kidney function, based on glomerular filtration rate (GFR), into stages 1 to 5, with each increasing number indicating a more advanced stage of the disease, as defined by a declining GFR. This classification system from the National Kidney Foundation’s Kidney Dialysis Outcomes and Quality Initiative (K/DOQI) also accounts for structural evidence of kidney damage.
  5. 5. STAGES OF CKD STAGE GFR DESCRIPTION TREATMENT 1 90+ Normal kidney function, but urine findings or structural abnormalities or genetic trait point to kidney disease Observation, control of blood pressure. 2 60-89 Mildly reduced kidney function, and other findings (as for stage 1) point to kidney disease Observation, control of blood pressure and risk factors.
  6. 6. 3A 3B 45-59 30-44 Moderately reduced kidney function Observation, control of blood pressure and risk factors 4 15-29 Severely reduced kidney function Planning for end stage renal failure 5 <15 or on dialysis Very severe, or end stage kidney failure (sometimes call established renal failure) Treatment choices.
  7. 7. ETIOPATHOGENESIS  The diseases leading to CRF can generally be classified into two major groups: those causing glomerular pathology, and those causing tubulointerstitial pathology. DISEASE CAUSING GLOMERULAR PATHOLOGY 1. Primary glomerular pathology : Glomerulonephritis, membranous glomerulonephritis, membranoproliferative glomerulonepritis and anti-glomerular basement membrane nephritis.
  8. 8. 2. SYSTEMIC GLOMERULAR PATHOLOGY: Systemic lupus erythematosus, serum sickness nephritis and diabetic nephropathy DISEASE CAUSING TUBULOINTERSTITIAL PATHOLOGY 1. Vascular causes: Long-standing primary or essential hypertension produces characteristic changes in renal arteries and arterioles referred to as nephrosclerosis . Nephrosclerosis causes progressive renal vascular occlusion terminating in ischaemia and necrosis of renal tissue. 2. Infectious causes: Chronic pyelonephritis
  9. 9. 3.Toxic causes:The most common example is intake of high doses of analgesics such as phenacetin, aspirin and acetaminophen (chronic analgesicnephritis). Other substances that can cause CRF after prolonged exposure are lead, cadmium and uranium.  4. Obstructive causes: Chronic obstruction in the urinary tract leads to progressive damage to the nephron due to fluid backpressure. The examples of this type of chronic injury are stones, blood clots, tumours, strictures and enlarged prostate. Regardless of the initiating cause, CRF evolves progressively through 4 stages:  Decreased renal reserve  Renal insufficiency  Renal failure  End stage kidney
  10. 10. CLINICAL FEATURES  Clinical manifestations of fullblown CRF culminating in uraemic syndrome are described under 2 main headings: primary (renal) uraemic manifestations and secondary (systemic or extra-renal) uraemic manifestations. • Primary uraemic manifestations: 1. Metabolic acidosis 2. Hperkalaemia 3. Sodium water imbalance 4. Hyperuricaemia 5. Azotaemia
  11. 11. • Secondary uraemic (extra renal) manifestations: 1. Anaemia 2. Integumentary system: Deposit of urinary pigment such as urochrome in the skin causes sallow-yellow colour. The urea content in the sweat as well as in the plasma rises. On evaporation of the perspiration, urea remains on the facial skin as powdery ‘uraemic frost’. 3. Cardiovascular system: Hypervolaemia and eventually CHF 4. Respiratory system: Hypervolaemia and heart failure cause pulmonary congestion and pulmonary oedemato back pressure.
  12. 12. 5. Digestive system: Azotaemia directly induces mucosalr ulcerations in the lining of the stomach and intestines. Subsequent bleeding can aggravate the existing anaemia. Gastrointestinal irritation may cause nausea, vomiting and diarrhoea. 6. Skeletal system: The skeletal manifestations of renal failure are referred to as renal osteodystrophy . i. Osteomalacia ii. Osteitis fibrosa
  13. 13. DIAGNOSTIC TEST RESULTS  a. Creatinine clearance may range from 0 to 90 mL/min, reflecting renal impairment.  b. Blood tests typically show  (1) Elevated BUN and serum creatinine concentration.  (2) Reduced arterial pH and bicarbonate concentration.  (3) Reduced serum calcium level.  (4) Increased serum potassium and phosphate levels.  (5) Possible reduction in the serum sodium level.  (6) Normochromic, normocytic anemia (hematocrit 20% to 30%).
  14. 14.  c. Urinalysis may reveal glycosuria, proteinuria, erythrocytes, leukocytes, and casts. Specific gravity is fixed at 1.010.  d. Radiographic findings. Kidney, ureter, and bladder radiography, IV pyelography, renal scan, renal arteriography, and nephrotomography may be performed. Typically, these tests reveals mall kidneys (less than 8 cm in length).
  15. 15.  Structural assessments of the kidney may be performed using a number of imaging procedures, including:  • ultrasonography  • intravenous urography (IVU)  • plain abdominal radiography • computed tomography (CT), magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA).
  16. 16. TREATMENT • Treatment objectives:  1. Improve patient comfort and prolong life.  2. Treat systemic manifestations of CKD.  3. Correct body chemistry abnormalities.  NONPHARMACOLOGIC THERAPY  • A low-protein diet (0.6 to 0.75 g/kg/day) can delay progression of CKD in patients with or without diabetes, although the benefit is relatively small. Management of the CKD patient is generally conservative. Dietary measures and fluid restriction relieve some symptoms of CKD and may increase patient comfort and prolong life until dialysis or renal transplantation is required or available.
  17. 17.  PHARMACOLOGICAL TREATMENT 1. Treatment of edema: Angiotensin-converting enzyme (ACE) inhibitors and diuretics: may be given to manage edema and CHF and to increase urine output. a. ACE inhibitors—captopril, enalapril , lisinopril ,fosinopril b. (1) Osmotic and loop diuretics (2) Thiazide-like diuretics. Metolazone is the most commonly used thiazide diuretic in CKD.
  18. 18.  2. Treatment of hypertension.: Antihypertensive agents may be needed if blood pressure becomes dangerously high as a result of edema and the high renin levels that occur in CKD.  a. ACE inhibitors—captopril, enalapril, lisinopril, fosinopril  b. calcium-channel blockers, including amlodipine and felodipine , have similar eff ects and may be used instead of ACE inhibitors.  c. βAdrenergic blockers, including propranolol and atenolol , reduce blood pressure through various mechanisms.  d. Other antihypertensive agents are sometimes used in the treatment of CKD, including (-adrenergic drugs, clonidine , and vasodilators, such as hydralazine .
  19. 19.  3. Treatment of hyperphosphatemia :involves administration of a phosphate binder, such as aluminum hydroxide or calcium carbonate.  4. Treatment of hypocalcemia:  a. Oral calcium salts.  b. Vitamin D  Choice of agent: For the treatment of hypocalcemia in CKD and other renal disorders, calcitriol (vitamin D3, the active form of vitamin D) is the preferred vitamin D supplement because of its greater efficacy and relatively short duration of action. Other single- entity preparations include dihydrotachysterol, ergocalciferol , doxercalciferol and paricalcitol .
  20. 20.  5. Treatment of other systemic manifestations of CKD  a. Treatment of anemia includes administration of iron (e.g., ferrous sulfate), folate supplements, and epoetin alfa.  (1) Severe anemia may warrant transfusion with packed red blood cells.  (2) Epoetin alfa stimulates the production of red cell progenitors and the production of hemoglobin. It also accelerates the release of reticulocytes from the bone marrow.  (3) Darbepoetin is an epoetin alfa analogue  (4) Intravenous iron products may be given to replete iron stores. Iron dextran is commonly used. Newer iron products include sodium ferric gluconate and iron sucrose, which are better tolerated and can be infused more rapidly compared to iron dextran.
  21. 21.  b. Treatment of GI disturbances  (1) Antiemetics help control nausea and vomiting.  c. Treatment of skin problems. An antipruritic agent, such as diphenhydramine, may be used to alleviate itching.
  22. 22. DIALYSIS  a. Hemodialysis: is the preferred dialysis method for patients with a reduced peritoneal membrane, hypercatabolism, or acute hyperkalemia.  (1) This technique involves shunting of the patient’s blood through a dialysis membrane containing unit for diffusion, osmosis, and ultrafiltration. The blood is then returned to the patient’s circulation.  (2) Vascular access may be obtained via an arteriovenous fistula or an external shunt.  (3) The procedure takes only 3 to 8 hrs; most patients need three treatments a week. With proper training, patients can perform hemodialysis at home
  23. 23.  (4) The patient receives heparin during hemodialysis to prevent clotting.  (5) Various complications may arise, including clotting of the hemofilter, hemorrhage, hepatitis, anemia, septicemia, cardiovascular problems, air embolism, rapid shift s in fluid and electrolyte balance, itching, nausea, vomiting, headache, seizures, and aluminum osteodystrophy. 
  24. 24.  b. Peritoneal dialysis is the preferred dialysis method for patients with bleeding disorders and cardiovascular disease.  (1) The peritoneum is used as a semipermeable membrane. A plastic catheter inserted in to the peritoneum provides access for the dialysate, which draws fluids, wastes, and electrolytes across the peritoneal membrane by osmosis and diffusion.  (2) Peritoneal dialysis can be carried out in three different modes.  (a) Intermittent peritoneal dialysis :Is an automatic cycling mode lasting 8 to 10 hrs, performed three times a week. This mode allows night time treatment and is appropriate for working patients.
  25. 25.  (b) Continuous ambulatory peritoneal dialysis : is performed daily for 24 hrs with four exchanges daily. The patient can remain active during the treatment.  (c) Continuous cyclic peritoneal dialysis : may be used if the other two modes fail to improve creatinine clearance. Dialysis takes place at night; the last exchange is retained in the peritoneal cavity during the day, then drained that evening.  (3) Advantages of peritoneal dialysis include a lack of serious complications, retention of normal fluid and electrolyte balance, simplicity, reduced cost, patient independence, and a reduced need (or no need) for heparin administration.
  26. 26.  (4) Complications of peritoneal dialysis include hyperglycemia, constipation, and inflammation or infection at the catheter site. Also, this method carries a high risk of peritonitis.
  27. 27. This surgical procedure allows some patients with end- stage renal disease to live normal and, in many cases, longer lives.  a. Histocompatibility must be tested to minimize the risk of transplant rejection and failure. Human leukocyte antigen (HLA) type, mixed lymphocyte reactivity, and blood group types are determined to asses histocompatibility.  b. Renal transplant material may be obtained from a living donor or a cadaver. Renal transplantation:
  28. 28.  c. Three types of graft rejection can occur. (1) Hyperacute (immediate) rejection results in graft loss within minutes to hours after transplantation.  (a) Acute urine flow cessation and bluish or mottled kidney discoloration are intraoperative signs of hyperacute rejection.  (b) Postoperative manifestations include kidney enlargement, fever, anuria, local pain, sodium retention, and hypertension.  (c) Treatment for hyperacute rejection is immediate nephrectomy.  (2) Acute rejection may occur 4 to 60 days after transplantation.
  29. 29.  (3) Chronic rejection occurs more than 60 days after transplantation.  (a) Signs and symptoms include low-grade fever, increased proteinuria, azotemia, hypertension, oliguria, weight gain, and edema.  (b) Treatment may include alkylating agents, cyclosporine, antilymphocyte globulin, and corticosteroids. In some cases, nephrectomy is necessary
  30. 30.  d. Complications include  (1) infection,diabetes, hepatitis, and leukopenia, resulting from immunosuppressive therapy.  (2) hypertension, resulting from various causes.  (3) cancer (e.g., lymphoma, cutaneous malignancies, head and neck cancer, leukemia, colon cancer). (4) pancreatitis and mental and emotional disorders (e.g., suicidal tendencies, severe depression, brought on by steroid therapy).

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