Chronic kidney disease.pptx

Chronic kidney disease by pg

1. Chronic kidney disease Dr .B.Mounika Dept of General Medicine

2. Introduction Etiology Pathogenesis Diagnosis Complications Management

3. Chronic kidney disease (CKD ) : CKD is a progressive, irreversible deterioration in renal function in which the body’s unable to maintain metabolic And fluid and electrolyte balance resulting in uremia or azotemia . Other names-CRF,CRD.. Azotemia : It is biochemical abnormality i.e elevation of blood urea nitrogen(BUN) and serum creatinine . Uremia :Syndrome that incorporates all signs and symptoms seen in various systems throughout the body caused by raised BUN,Cr,Acute /chronic Renal failure.

4. ETIOLOGY AND RISK FACTORS Decreased renal blood flow Systemic diseases Diabetes mellitus Hypertension SLE Polyarteritis Sickle cell disease Amyloidosis C\c giomerulonephritis Pyelonephritis Arf

5. Obstruction of the urinary tract Hereditary lesions Polycystic kidney disease Infections Vascular diseases Medication or toxic agents Environmental or occupational agents Lead Cadmium Mercury Chromium

6. Most common causes: Diabetes Hypertension Glomerular diseases Systemic diseeases Interstitial diseases Unknown

7. Pathogenesis:

8. Clinical manifestations: Urinary symptoms: Polyuria results from inability of kidneys to concentrate urine,Occurs most often at night Oliguria, Anuria Occurs as CKD worsens

9. Alterations in fluids and electrolytes: Sodium & Water retention- PITTING EDEMA in the lower extremity Fluid accumulation -Pulmonary edema and loss of air space- Ventilation-perfusion mismatch – SOB Hyperkalemia -Malaise, palpitations, arrhythmias.. Hyperphosphatemia Hypocalcemia Altered CHO metabolism Elevated triglycerides Waste products accumulation-BUN ↑ and serum creatinine levels ↑ as GFR ↓

10. Metabolicacidosis : Impaired H+ secretion from the body leads to anion-gap metabolic acidosis. In tubulo -interstitial disease or diabetic nephropathy causes Non-anion-gap renal tubular acidosis. Protein energy malnutrition – WT LOSS

11. Hematologic system: Anemia: Fatigue , reduced exercise capacity, and pallor Bleeding tendencies: Defect in platelet function. Infection: Changes in leukocyte function Altered immune response and function Diminished inflammatory response

12. Renalosteodystrophy : Increased risk of fractures Hypocalcemia : Early stages due to hyperphosphatemia Later stages due to decreased synthesis of 1 α- hydroxylase vitD Sec/ Ter HyperPT : Occurs due hyperphosphatemia … Osteoporosis,Osteomalacia,Calcium deposition in soft tissue Complications of uremia : Urea and other toxins accumulate in the blood and cause life threatening issues Uremia -induced platelet dysfunction-Increased tendency to bleed and ecchymosis, GI bleeding Uremic pericarditis-Chest pain, malaise, Pericardial friction rub Uremic encephalopathy-Headaches, confusion, coma

13. CVS : Hypertension,Heart failure,Left ventricular hypertrophy,Peripheral edema,Dysrhythmias,Uremic pericarditis. CNS : Altered mental ability,Seizures and Coma. Dialysis encephalopathy,Peripheral neuropathy. GIT: N/V ,Mucosal ulcerationsStomatitis Uremic fetor ( urinous odor of the breath)GI bleedingAnorexia . RS: Kussmaul respiration,DyspneaPulmonary edema,Uremic pleuritis,Pleural effusionPredisposition to respiratory infections,Depressed cough reflex,“Uremic lung.

14. Stages and Complications of CKD

15. Investigations : History and physical examination Routine lab measurements BUN Serum Creatinine Serum Electrolytes Hematocrit and Hb levels Urine Analysis Urine Culture Identification of Reversible Renal Disease Renal Ultrasound Renal Scan CT Scan Renal Biopsy

16. Usg findings in CKD: Increased parenchymal echogenecity Loss of corticomedullary differentiation Bilateral small kidney <10cm

17. Treatment: Aim of treatment Prevention of further deterioration Treatment of complications Controlling Blood Pressure,Sugar,Proteinuria are key elements in the reduction of CKD progression.

18. Hypertension : Target BP (120-140SBP/70-90DBP)depends on GFR,Proteinuria Antihypertensive drugs: First-line Agents- ACEI,ARB Second-line Agents- Diuretics (thiazide OR furosemide) Third-line Agents- CCB ( diltiazem , verapamil, amlodipine, diltiazem ), BB (labetalol ) Sodium restriction-Diets vary from 2 to 4 g depending on degree of edema and hypertension

19. Proteinuria: ACEI,ARB should be advised to all patients with diabetic nephropathy and patients with CKD and proteinuria, irrespective of whether or not hypertension is present. ACEI,ARB reduces proteinuria by reducing BP, glomerular perfusion pressure and GFR Protein restriction: 0.6 to 0.75 gm /kg of ideal body weight/day 1.2 to 1.3 gm /kg of ideal body weight/day once the patient starts dialysis

20. Hyperkalemia : For mild hyperkalemia - K binding agents : Zirconium cyclosilicate and Patiromer For severe- IV insulin and glucose IV 10% calcium gluconate Sodium bicarbonate-Shift potassium into cells,Correct acidosis Sodium polystyrene sulfonate Avoid high-potassium foods -Oranges, Bananas,figs , avocados,Tomatoes,Green vegetables , milk,yoghurt,chocoliate,baked,fries,salt substitutes. Avoid drugs which cause hyperK -ACEI,ARB,K-sparing diuretic .

21. Anemia : Erythropoietin:Epoetin alfa Administered IV or subcutaneously Increases hemoglobin and hematocrit in 2 to 3 weeks. Starting dosage 50-150 units/kg per week IV or SC, 1-3 times per wK Side effect: Hypertension Iron supplements: If plasma ferritin <100 ng /ml Folic acid supplements: Needed for RBC formation Avoid blood transfusions

22. Renal osteodystrophy : Phosphate intake restricted to<1000 mg/day Phosphate binders 1.Calcium carbonate-Bind phosphate in bowel and excreted 2.Sevelamer hydrochloride-Lowers cholesterol and LDLs Phosphate binders Should be administered with each meal. Phosphate restriction:1000 mg/day ,Foods high in phosphate Dairy products Supplementing vitamin D - Ergocalciferol (D2) Cholecalciferol (D3) Controle secondary hyperparathyroidism with Calcimimetic agents - Cinacalcet ( Sensipar ) ↑ Sensitivity of calcium receptors in parathyroid glands,decrease plasma PTH Vitamin D analogs Calcium based phosphate binders-Calcium acetate,Calcium carbonate Subtotal parathyroidectomy

23. Metabolic acidosis: plasma bicarbonate concentrations should be maintained above 22 mmol /L Sodium bicarbonate supplements given-starting dose of1 g 8-hourly OR NaHCO3 0.5–1.0 mEq /kg daily There is some evidence that correcting acidosis may reduce the rate of decline in renal function.

24. Oral hypoglycemic drugs in CKD: Contraindications: 1-Biguanide: Metformin if SCr1.5 mg/ dLin men, 1.4 mg/ dLin women”or GFR 30 mL/min/1.73 m2 2-sulfonylureas Tolazamide , Tolbutamide , Acetohexamide and Glyburide.Chlorpropamide if GFR 50 mL/min/1.73 m2. 3-Alpha-glucosidaseinhibitors Acarbose if GFR 30 mL/min/1.73 m2 Miglitilol GFR 25 mL/min/1.73 m2 Safe drugs ,can be used in dialysis pts –DPP4 inhibitors Drugs need dose reduction in dialysis pts-Meglitinides

25. ESRD: End-stage renal disease (ESRD) occurs when GFR <15ml/min Renal Replacement Therapy (RRT) required when the kidneys are functioning at less than 10–15%. RRT is accomplished in one of the following ways: 1-Dialysis Hemodialysis Peritoneal dialysis 2-Kidney transplant

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