Chronic kidney disease power pt presentation.pptx

Chronic kidney disease (CKD) is a progressive condition where kidney damage prevents them from filtering waste and excess fluid from the blood, leading to their buildup in the body. Key risk factors include diabetes and high blood pressure, and while there is no cure, treatment can slow progression and manage symptoms. Symptoms, which often appear later, can include swelling, fatigue, changes in urination, and itchy skin, while treatment involves lifestyle changes, medication, dialysis, or a kidney transplant in advanced stages.

1. CRF- Kidney Failure)

2. CKD/CRF/ESRD Gradual Decline in GFR and retention of nitrogenous waste products like Urea & Creatinine. GFR is inversely proportional to Serum Creatinine.

3. Markers of Kidney Failure Blood Urea : Marker of kidney failure. It increases if kidney functions decline. It is directly proportional to Protein intake, it can be too high in catabolic stage or Infection. Serum Creatinine : It is a better marker of kidney failure, like urea it is raised if kidney functions deteriorates. It is not affected by diet. But it is directly proportional to body muscle mass.

4. Different Stages of CKD CKD I Slight impairment of GFR (90+) CKD II Mild impairment of GFR (60-90) CKDIII Mild-Moderate Impairment of GFR (30-59) CKD IV Moderate Impairment of GFR (15-29) CKD V (ESRD) Severe Impairment of GFR less than 15

5. Cockcroft- Gault formula eGFR = (140-Age) (Wt. in KG) 72 X Serum Creatinine (If pt is female, multiply by 0.85) (Normal values are 105-125 ml/min) Exact measurement of GFR can be done by DTPA scan. eGFR Calculation

6. Causes of K idney F ailure Diabetes Mellitus High Blood Pressure (Hypertension) Chronic GN Interstitial Nephritis Kidney Stones Hereditary: Polycystic kidney disease & Alports Syndrome Excessive use of Pain killers like NSAIDs Ig A Nephropathy

7. Clinical Presentation of CRF (ESRD) Majority of patients are asymptomatic initially except they are Diabetic or high BP or have Albumin in their Urine. In CKD Grade IV & V pts have Anorexia, Nausea, vomiting and hic-coughs. Investigations shows anemia, raised Urea and Creatinine . Patients may have oliguria and swelling over face and body (not all patients with CRF have oliguria and oedema). Some may have good urine out put. Patients with Chronic GN (leading to ESRD) may have small contracted kidneys in USG. Not all patients with ESRD have small contracted kidneys—Diabetics have normal sized kidneys.

8. Clinical Manifestation of Kidney Diseases Millions of Indians are living with kidney disease right now. Because kidney disease often has no symptoms, many of these people don’t even know they have it. Kidney disease puts at risk for heart attacks, strokes, and early death. Copyright 2010, John Wiley & Sons, Inc.

9. Symptoms: CKD often has no symptoms until it is in very advance stage The only way to be sure how well your kidneys are working is to get tested for serum Creatinine or eGFR. If you do have symptoms, they might include: ● Feeling sick in your stomach often ● Feeling tired or dizzy often ● Swelling in your feet, hands or face ● Back pain ● Bloody, foamy or dark-colored urine ● High blood pressure ● A change in how often you go to the bathroom (pee more or less often) Copyright 2010, J ohn Wil ey & Sons, Inc.

10. Signs May have pitting oedema & Gen Swelling Tachypneoa and SOB Crepts at base of Chest Pleural Effusion Pericardial rub Note that there can be other causes of Gen. Swelling like severe anemia and CCF Copyright 2010, John Wiley & Sons, Inc.

11. Investigations Anemia: Low Hb ( Normocytic Hypochromic ). Iron def Anemia is also common Low Calcium and high P (Renal Osteodystrophy ) Metabolic Acidosis: Reduced Bicarbonate level Gastric erosion and acid peptic disease including GI blood loss Raised Urea, Creatinine and Potassium Low Albumin (Mal Nutrition) Pericardial Effusion USG KUB: Small contracted kidneys in CKD 4-5

12. Management of Anemia in CKD There is deficiency of Human EPO which is secreted by renal tubules, generally seen in CKD III-IV and V. Because of poor intake Iron/Folic acid deficiencies are common too. Also there is platelet dysfunction & blood loss through GI Tract which is responsible for Iron def. Treatment of Iron def is mandatory before putting pt on EPO

13. Intravenous iron usage is encouraged Total Iron Saturation (TSAT) up to 30% and ferritin up to 500 ng /ml Avoid with acute infection, Do not initiate EPO therapy unless Hb < 10 g/dl Goal: to avoid Hb < 9 g/dl and Hb > 11.5 g/dl Use with great caution in patients with active malignancy or history of CVA Use of oral Iron and vitamins supplements should be given in all patients in CKD who are anemic.

14. Renal Osteodystrophy Kidney failure disrupts systemic calcium and phosphate homeostasis and affects the bone, GIT and parathyroid glands. In kidney failure there is decreased renal excretion of phosphate and diminished production of calcitriol (1,25-dihydroxyvitamin D) Calitriol increases serum calcium levels The increased phosphate and reduced calcium, lead to secondary hyperparathyroidism , where PTH can be normal or raised, metabolic bone disease, soft tissue calcifications and other metabolic abnormalities

15. Secondary hyperparathyroidism In renal failure driven by Hypocalcaemia Decreased vitamin D hyperphosphataemia

16. Hyperparathyroidism Increase PTH is hallmark of secondary hyperparathyroidism The major factors leading to it’s increase are; Decreased production of Vit D3 (calcitriol) Decreased serum calcium Increased serum phosphorous

17. GFR(Low) 1,25 DHCC (Low) Ca (Low) PTH (High) Calcitriol PO4 (High)

18. Treatment of CKD bone disease Various Rx for secondary hyper PTH and hyperphosphataemia include; Dietary phosphorous restriction Calcium and non-Ca phosphate binders Calcitriol or other Vit D analogues Calcimimetics Parathyroidectomy

19. Uraemic Secondary Hyperparathyroidism Cause PO 4 retention Low 1,25 Vit D synthesis Effects Proximal weakness, Bone pain (late) Alk Phos (High), bone erosions Rx Diet, PO 4 binders Calcitriol , PTHx (usually for 3 o )

20. Calcitriol 1,25-(OH)2 Vitamin D3 or other analogues bind to receptor on PT tissue and suppress PTH production

21. Phosphate Binders Calcium-based phosphate binders Calcium carbonate ( Cal-Sup/ Shelcal ) Only Cal-Sup Varies, eg . 1 BD, 1-4 TDS Must be chewed with food to maximize binding of ingested phosphorous.

22. Phosphate Binders Non-calcium phos binder Sevelamer HCl Often used in conjunction with Cal-sup Has replaced calcium carbonate Sevelamer Carbonate ( Sevcar ) 400-800 mg TDS is better that all other Phosphate binders

23. Phosphate Binders Aluminium -containing phos binders Alu -tabs/ aluminium hydroxide Most effective, but not in use any more, Sevalamer carbonate has replaced all other phosphate binders. Systemic absorption with subsequent neurological, haematological and bone toxicity.

24. Calcimimetics Calcium receptor-sensing agonists Act on PT gland and increase sensitivity of receptor to calcium Cinacalcet ( Sensipar or PTH) Significant decrease PTH, w/o  Ca or phos binders Avoids calcification

25. Parathyroidectomy Last option Considered when other methods fail to ↓ PTH Either total or sub-total Used to re-implant in forearm.

26. Hormonal Problems in CKD pts. Impotency in Male Abnormal menstrual cycle in female: Amenorrhea or excessive bleeding. Mid term abortion Infertility in both male and female

27. Management of CKD sec. to DM Commonest cause of Chronic kidney Failure is Diabetes Mellitus. Following guidelines should be followed for saving kidneys for those having Diabetes ; Early detection of Microalbuminuria (Urinary albumin excretion) Good control of blood sugars to keep their HbA1C 7.0-7.5 Maintain Normal Blood pressure (120/80) with Angiotensin Converting enzyme (ACE) Inhibitors or Angiotensin Receptor Blockers(ARB ) Those who are diabetics should see Nephrologist every 6 months.

28. Management of CKD sec. to high Blood Pressure Aim to keep Blood Pressure of 140/80 for those who are on medication Reduction of Salt intake Patients may require 2-3 or more antihypertensive medications to control BP Modification of life style Those who have high BP should consult Nephrologists to make sure their kidneys are not affected.

29. Hypertension & CKD In patients with CKD 1-3 the first line of antihypertensives are ACE-Inhibitor or ARB Those who are diabetic or having proteinuria (CKD 1-3) first line of antihypertensives are ACE-I or ARB But ACE-I or ARB should be avoided in CKD 4-5 or ESRD patients who are on dialysis because severe hyperkalemia can occur with its usage. Sudden fall in GFR and rise in creatinine has been seen in CKD 3,4&5 patients with the use of ACE-I or ARB.

30. Dietary Restriction – Good Vs Bad Protein Restriction in CKD III – CKD V There is a big controversy regarding protein restriction in CKD. Though protein restriction decreases blood urea and symptoms of CRF but too much restriction leads to Malnourishment, which leads to lowering of Hb and lowering of serum albumin. Pt becomes very weak and susceptible to infection. Protein should be restricted to 1 gm per Kgm body weight only in CKD III – CKD V patients. Patients on Dialysis require more protein especially those on CAPD.

31. Renal Replacement Therapy Dialysis Hemodialysis including SLEDD and CRRT Peritoneal Dialysis Acute PD CAPD APD Renal Transplant

32. Hemodialysis Diffusion of smaller particles through semi permeable membrane. Urea, Creatinine, Potassium and other nitrogenous substances are diffused and filtered out. Substances which are useful to the patients like Bicarbonate and Calcium are added to the blood. Ultrafiltration of excess fluid is done by applying negative pressure to the membrane.

33. Cont…

34. Peritoneal Dialysis

35. Renal Transplantation

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