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Management of Chronic Kidney Disorder (CKD)

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Management of Chronic Kidney Disorder (CKD) Project

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Management of Chronic Kidney Disorder (CKD)

  1. 1. MANAGEMENT OF CHRONIC KIDNEY DISEASE (CKD) Dr Sharanya Rajan
  2. 2. AGENDA  DEFINITION  ETIOLOGY  PATHOPHYSIOLOGY  CLINICAL PRESENTATION  DIAGNOSIS  TREATMENT  COMPLICATIONS  INDICATIONS FOR DIALYSIS
  3. 3. WHAT IS CHRONIC KIDNEY DISEASE?  It is kidney damage (structurally or functionally) for ≥ 3 months with or without decrease glomerular filtration rate (GFR) OR  GFR < 60ml/min for ≥ 3 months with or without kidney damage OR  Persistent microalbuminuria/Persistent proteinuria/Persistent hematuria OR  Structural abnormalities of the kidneys (polycystic kidney disease, reflux nephropathy) proven by ultrasound
  4. 4. Causes and Incidence  Chronic renal failure occurs in approximately 1 out of 1,000 people.  Causative diseases include any type: 1. Diabetes mellitus - most common cause 2. Hypertension 3. Glomerulonephritis 4. Others  chronic pyelonephritis, PKD /polycystic kidney disease, obstructive uropathy (stones, BPH, cancer, etc), Alport syndrome, and drug-induced nephropathy
  5. 5. Estimation of GFR CrCl (ml/min)=  Cockcroft- Gault Formula ( 140 – age ) x Weight inKg 72 x Serum Creat (mg/dl)  MDRD Study Equation x ( 0.85 if female ) GFR (mil/min/1.73 m2) = 186 x (SCr) -1.154 x (age)-.203 x (0.724 if female) x (1.210 ifAfricanAmerican)
  6. 6. ETIOLOGY OF CHRONIC KIDNEY DISEASE?  Diabetes mellitus  Hypertension  Glomerulonephritis  Pyelonephritis  Renal artery stenosis  Renal calculi  Polycystic kidney disease  Congenital defects of the kidney or bladder  Secondary causes (SLE, rheumatoid arthritis, HIV, drugs- gold, heroin use etc.)  Drugs (NSAIDS, Aminoglycoside etc.)
  7. 7. PATHOPHYSIOLOGY OF CKD?
  8. 8. Symptoms INITIAL (non-specific) unintentional weight loss nausea, vomiting general ill feeling fatigue headache frequent hiccups generalized itching (pruritus) INITIAL (non-specific) increase or decrease urine output need to urinate at night anasarca easy bruising or bleeding blood in the vomit or stools breath odor (uremic fetor) muscle twitching or cramps restless legs syndrome increased skin pigmentation uremic frost decreased sensation decreased alertness/
  9. 9. Signs and Tests Blood pressure may be high Urinalysis may show protein, blood, pus or other abnormalities Creatinine and BUN levels progressively increase Creatinine clearance progressively decreases Potassium elevated Calcium low and Phosphorus high Arterial blood gas show metabolic acidosis Xray of bones may show osteodystrophy
  10. 10. Signs and Tests (cont.) Changes that indicate chronic renal failure, including both kidneys being smaller than normal, may be seen on: abdominal ultrasound plain KUB X-ray abdominal CT scan or MRI However, CKD with normal sized or enlarged kidneys: amyloidosis, diabetes multiple myeloma polycystic kidneys accelerated hypertension
  11. 11. PATHOPHYSIOLOGY OF CKD?  Regardless of the primary cause of nephron loss, some usually survive or are less severely damaged  These nephrons then adapt and enlarge, and clearance per nephron markedly increases.  The RAAS is activated causing renal hypertension  If the initiating process progress, renal failure may ensue with the rapid development of ESRD.  Focal glomerulosclerosis develops in the glomeruli, and they eventually become non-functional.  proteinuria markedly increases and systemic hypertension worsens.  Adapted nephrons enhance the ability of the kidney to postpone uremia, but ultimately the adaptation process leads to the demise of these nephrons.  Adapted nephrons have not only an enhanced GFR but also enhanced tubular functions in terms of, for example, potassium and proton secretion.
  12. 12. Classification of kidney injury RIFLE and the network criteria
  13. 13. CLINICAL PRESENTATION OF CKD?  Asymptomatic in stage 1-3 with GFR > 30ml/min  Symptomatic in stage 4-5 with GFR < 30ml/min 1. Early signs :Polyuria/oliguria, Hematuria, Edema 2. Late signs a. hypertension b. Signs of anemia (pallor) c. Signs of hyperurecemia: i. Brain ( uremic encephalopathy): low concentration, confusion, lethargy, asterixis, coma, ii. Heart: pericarditis iii. GIT: nausea & vomiting, anorexia, diarrhea iv. Reproductive system: erectile dysfunction, decreased libido, amenorrhea v. Blood system: platelet dysfunction with tendency to bleed, infections due to WBCs dysfunction vi. peripheral neuropathy: numbness, paraesthesia, restless leg syndrome vii. Skin: dry skin, pruritus, ecchymosis viii. Others: fatigue, hiccups, muscle cramps,
  14. 14. DIAGNOSIS OF CKD?  Kidney injury with or without decrease GFR for ≥ 3 months  FBC: Anemia (normochromic, normocytic), leukopenia, thrombocytopenia  Urinalysis: i. Dipstick proteinuria, if positive, do daily or 24hrs proteinuria test a. If proteinuria is ≤1g/24hrs, then consider urinary syndrome b. If proteinuria is 1 to 3g/24hrs, nephritic syndrome/ tubulointerstitial c. If proteinuria is ≥3.5g/24hrs, consider nephrotic syndrome i. RBCs, RBC casts, suggests glomerulonephritis ii. Pyuria or/and WBC casts are suggestive of interstitial nephritis/pyelonephritis  GFR evaluation; usually decreased
  15. 15. Diagnosis (cont.)  Biochemical blood test: i. High creatinine, high BUN ii. Electrolytes: Hyperkalemia, hyperphosphatemia, hypermagnesemia, hypocalcemia, low bicarbonate iii. pH of blood: acidosis (metabolic) iv. Hypoalbuminemia/hypoproteinemia  Plain abdominal x-ray (useful to look for radio-opaque stones or nephrocalcinosis)  Renal biopsy (reveals underlying primary cause but may be nonspecific)  Ultrasound findings: small echogenic kidneys in ESRD, hydronephrosis, polycystic kidneys
  16. 16. Ultrasound findings: small echogenic kidneys in ESRD
  17. 17. TREATMENT OF CKD?  Treatment objectives • To detect chronic kidney disease early in susceptible individuals. • To control hypertension • To control blood glucose • To treat other underlying causes • To prevent complications and further worsening of kidney function
  18. 18. Non-pharmacological treatment  Admit patient especially in stage of exacerbation  Diet: Restrict dietary protein to< 40 g/day, Restrict Na+, K+, PO4- intake, avoid potassium containing foods e.g. banana  Water and electrolyte balance: i. Daily fluid intake = previous day’s urine output + 600 ml (for insensible losses) ii. Strict fluid input and output chart  Daily weighing  General health advice e.g. smoking cessation  • Avoid nephrotoxins e.g. NSAIDs , Herbal medication
  19. 19. Pharmacological treatment  Treatment of underlying condition (diabetes, HPT, autoimmune d’ses etc.)  Treatment of fluid overload Diuretics: Furosemide, oral /IV, 40-120 mg daily  Treatment of hypertension (goal of BP<130/8OmmHg): i. ACEIs- Lisinopril, oral, 5-40 mg daily Or Ramipril, oral, 2.5-10 mg daily Or ii. ARBs- Losartan, oral, 25-100 mg daily or Valsatan, oral, 80-160 mg daily  Treatment of anemia i. Injection erythropoietin 50-100units IV/SC 3times weekly Treatment is initiated at Hb <10g/dl i. Tab. Ferrous sulphate 200mg 3times daily  Treatment of hyperkalaemia/metabolic acidosis • 10% Calcium gluconate, IV, 10-20 ml over 2-5 minutes Plus • Sodium Bicarbonate, IV, 8.4% 50mEq, over 5 minutes Plus • Regular Insulin, IV, 10 units in 50-100 ml Glucose 50%
  20. 20. Pharmacological treatment (cont.)  Treatment of hyperphosphatemia: i. Phosphate binders (calcium acetate/ calcium carbonate 2 capsules (1334mg ) orally with food)  Treatment of hypocalcemia: i. Calcium citrate 1g/day ii. Vitamin D supplement; 2 tablets (800 IU) once daily  Treatment of pruritus: Capsaicin cream or cholestyramine  Treatment of bleeding: Desmopressin 0.3 mcg/kg IV over 15-30mins
  21. 21. Renal replacement therapy (RRT)  Dialysis (hemodialysis or peritoneal dialysis)  Kidney transplant with immunosuppressant usage hemodialysis= peritoneal dialysis in terms of efficiency But hemodialysis is superior to peritoneal dialysis due to the complication (peritonitis then subsequent septic shock) associated with peritoneal dialysis Indications for dialysis are: 1. fluid overload 2. severe acidosis 3. hyperkalemia 4. pericarditis 5. encephalopathy
  22. 22. Hemodialysis: 3-4hrs, 3 times per week (Monday, Wednesday and Friday)
  23. 23. Peritoneal dialysis
  24. 24. Kidney transplant plus immunosuppressant therapy
  25. 25. Detection, Evaluation, and Management of CKD STAGE DESCRIPTION GFR EVALUATION MANAGEMENT At increased risk Test for CKD Risk factor management 1 Kidney damage with normal or  GFR >90 Diagnosis Comorbid conditions CVD and CVD risk factors Specific therapy, based on diagnosis Management of comorbid conditions Treatment of CVD and CVD risk factors 2 Kidney damage with mild  GFR 60-89 Rate of progression Slowing rate of loss of kidney function1 3 Moderate  GFR 30-59 Complications Prevention and treatment of complications 4 Severe  GFR 15-29 Preparation for kidney replacement therapy Referral to Nephrologist 5 Kidney Failure <15 Kidney replacement therapy 1Target blood pressure less than 130/80 mm Hg. Angiotension converting enzyme inhibitors (ACEI) or angiotension receptor blocker (ARB) for diabetic or non-diabetic kidney disease with spot urine total protein-to-creatinine ratio of greater than 200 mg/g.
  26. 26. Complications of CKD?  Anemia: due to lack of erythropoietin  Metabolic acidosis (severe): due to lack of NH3 production by kidneys which is involved in acid-base buffer  Hyperkalemia: due to lack of excretion  Pericarditis: due to uremia  Osteodystrophy (osteitis fibrosa cystica): due to lack of 1,25- dihydroxycholecalciferol and also Secondary hyperparathyroidism  Fluid overload (anasarca): lack of excretion and Na+ retention  Encephalopathy: due to uremia  Hypertension: due to activation of RAAS. HPT is the common cause of death due to myocardial infarction. Maintain BP <130/80  Infections: uremia prevents degranulation of the neutrophils and so myeloperoxidase can’t be released to destroy bacteria  Bleeding tendencies: due to platelets dysfunction from effects of uremia
  27. 27. Stay Healthy Always

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