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CKD

CKD. Burden of CKD. Death 18 x. R educed GFR and/or Proteinuria are independent risk factors for CVD. CV events 17 x.

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CKD

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  1. CKD

  2. Burden of CKD Death 18 x • Reduced GFR and/or Proteinuria are independent risk factors for CVD CV events 17 x Age-Standardized Rates of Death from Any Cause (Panel A), Cardiovascular Events (Panel B), and Hospitalization (Panel C), According to the Estimated GFR among 1,120,295 Ambulatory Adults Hospitalization 10 x Go, A. S. et al. N Engl J Med2004;351:1296-1305

  3. An Epidemic of Kidney Disease Not enough nephrologists Prevalence CKD stages 1- 4 10% 1988-94 13% 1999-2004Coresh, JAMA 298:2038, 2007 Stage 5: GFR <15 n=300,000 Stage 4: GFR 15–29 n=400,000 Stage 3: GFR 30–59 n=7,600,000 n=5,300,000 Stage 2: GFR 60–89* n=5,900,000 Stage 1: GFR ≥90* Total=23 million USA Clinical Practice Guidelines for CKD Am J Kidney Dis. 2002;39(suppl 1):S17–S31. GFR = glomerular filtration rate (mL/min/1.73 m2); *with kidney damage

  4. Components of a Comprehensive CKD Care Plan Early detection of CKD and treatment of reversible cause Educate and Empower Patient Delay progression Prevent complications Tx comorbidities and modifiable risk factors Prepare for RRT ACE inhibitors Anemia Cardiac disease Select RRT modality BP control Malnutrition Vascular disease Mineral & Bone (MBD) Blood glucose control Diabetes Create access and initiate dialysis in a timely fashion Dyslipidemias Calcification Reduce proteinuria Smoking Evaluate for renal transplant Acidosis Dietary protein restriction Hypertension Hyperkalemia Adapted from Pereira B. Kidney Int. 2000;57:351–365.

  5. Measurement of GFR • GFR is measured by the clearance of an exogenous or endogenous filtration marker. • All clearance methods are complex so in clinical practice, GFR is estimated from the serum concentration of the endogenous filtration marker creatinine. • Cystatin C is an alternative endogenous filtration marker; other filtration markers are also under evaluation.

  6. Estimation of GFR • Modification of Diet in Renal Disease (MDRD) Formula • Estimated GFR = 1.86 (Serum Creat) -1.154 X (age) -0.203 • Multiply by 0.742 for women • Multiply by 1.21 for African Americans • CockroftGaultFormula • (140 – age) X Body Weight (Kg) 72 X Serum Creatinine (mg/dL) • Multiply by 0.85 for women

  7. CKD-EPI: CKD – Epidemiology Collaboration

  8. Estimated GFR( eGFR)

  9. CKD • CKD is defined as abnormalities of kidney structure or function, present for > 3 months, with implications for health. • CKD is classified based on Cause, GFR category, and Albuminuria category (CGA).

  10. Definition of CKD

  11. CKD : Classification : Cause - C • Assign cause of CKD based on presence or absence of systemic disease and the location within the kidneyof observed or presumed pathologic-anatomic findings

  12. CKD : Classification : Cause - C

  13. CKD : Classification : GFR - G

  14. Davidson’s 21st E

  15. CKD : Classification : Albuminuria - A

  16. CKD Progression • Defined based on one of more of the following : • Decline in GFR category (≥90 [G1], 60–89 [G2], 45–59 [G3a], 30–44 [G3b], 15–29 [G4], <15 [G5] ml/min/1.73 m2). • A certain drop in eGFR is defined as a drop in GFR category accompanied by a 25% orgreaterdrop in eGFR from baseline. • Rapid progression is defined as a sustained decline in eGFR of more than 5 ml/min/1.73 m2/yr. • The confidence in assessing progression isincreased with increasingnumber of serum creatinine measurementsand duration of follow-up.

  17. Who is at Risk for CKD? • Family history of heritable renal disease • Diabetes • Hypertension • Auto-immune disease • Old age • Prior episode of ARF • Current evidence of renal damage, even with normal or increased GFR

  18. Davidson’s 21st E

  19. Davidson’s 21st E Harrison’s 18th E

  20. Harrison’s 18th E

  21. CKD and ESRD causes USRDS 2004 • ESRD causes - USA • diabetes 43% • hypertension 26% relative with ESRD familial disease - cystic • acquired – glomerulonephritis, obstruction

  22. Monitoring of CKD • Serial measurements of • Creatinine • GFR • Albumin • Albumin-creatinine ratio in the 1st morning sample • Electrolytes including HCO3, Ca, Phos; alkaline phosphatase, iron studies, intact PTH • Renal sonogram • Renal biopsy

  23. Pathophysiology of CKD Involves 2 broad sets of mechanisms of damage: • Initiating mechanisms specific to the underlying etiology: E.g., • Genetically determined abnormalities in kidney development or integrity, • Immune complex deposition and inflammation in certain types of glomerulonephritis, • Or, Toxin exposure in certain diseases of the renal tubules and interstitium & Harrison’s 18th E

  24. Pathophysiology of CKD (2): A set of Progressive mechanisms: involving hyperfiltration and hypertrophy of the remaining viable nephrons, common consequence following long-term reduction of renal mass, irrespective of underlying etiology. Harrison’s 18th E

  25. Pathophysiology of CKD The responses to reduction in nephron number are mediated by vasoactive hormones, cytokines, and growth factors. Eventually, these short-term adaptations of hypertrophy and hyperfiltration become maladaptiveas the increased pressure and flow predisposes to distortion of glomerular architecture, associated with sclerosis and dropout of the remaining nephrons (Fig.) Increased intrarenal activity of the renin-angiotensin axisappears to contribute both to the initial adaptive hyperfiltration and to the subsequent maladaptive hypertrophy and sclerosis, the latter, in part, owing to the stimulation of transforming growth factor β (TGF-β). This process explains why a reduction in renal mass from an isolated insult may lead to a progressive decline in renal function over many years. Harrison’s 18th E

  26. Chronic kidney disease progression • initiating factors • nephron size, number, hyperfiltration diabetes, metabolic syndrome • cardiovascular disease age, family history • nephrotoxins primary kidney disease - hereditary or acquired • progression factorshypertension, cardiovascular disease, proteinuria diabetes, hyperlipidemia, inflammation, smoking, obesity, sedentary lifestyles, protein intake ? phosphate, PTH, FGF23, vitamin D lack • acute kidney injury Kronenberg Nature Reviews Nephology 5:677-89,2009

  27. Harrison’s 18th E

  28. Structural/ Functional Hypertrophy of remnant nephrons Loss of Nephron Mass Sclerosis of remnant nephrons Pathophysiology of CKD • Final Common Pathway is loss of nephron mass Diabetes Hypertension Chronic GN Cystic Disease Tubulointerstitial disease Mediated by vasoactive molecules, cytokines and growth factors, renin angiotensin axis

  29. Harrison’s 18th E

  30. Symptoms of CKD • Stage 1 and 2 • Asymptomatic, Hypertension • Stage 3 and 4 • Anemia – loss of energy • Decreasing appetite; Poor nutrition • Abnormalities in Calcium, Phosphorus metabolism • Sodium, water, potassium and acid base abnormalities • Stage 5 • All of the above – accentuated; eventually overt Uremia

  31. Common Causes and Presentation

  32. Clinical Features of Diabetic CKD

  33. Clinical Features of Non-Diabetic CKD

  34. Pathophysiology of the ‘Uremic syndrome’ Can be divided into manifestations in 3 spheres of dysfunction: • (1) Those consequent to the accumulation of toxins that normally undergo renal excretion, including products of protein metabolism • (2) Those consequent to the loss of other renal functions, such as fluid and electrolyte homeostasis and hormone regulation • (3) Progressive systemic inflammation and its vascular and nutritional consequences. Harrison’s 18th E

  35. Pathophysiology of Uremia • Azotemia – refers to the retention of nitrogenous waste products. Uremia – advanced stages of azotemia with end organ dysfunction • Accumulation of products of protein metabolism • Urea – anorexia, malaise, vomiting and headaches • Loss of other renal functions • Erythropoietin deficiency – anemia • Metabolic bone disease; Endocrine abnormalities • Fluid, electrolyte and acid base disorders

  36. Sodium and Water Imbalance • Glomerulotubular feedback is disrupted – sodium retention, contributes to hypertension; hyponatremia is unusual. • Higher than usual doses for diuretics. In situations with volume depletion – can be severe, because of inadequate sodium retention. • Treatment: Salt restriction; high doses of diuretics

  37. Potassium Imbalance • Potassium • GI excretion is augmented • Constipation, dietary intake, protein catabolism, hemolysis, hemorrhage, transfusion of stored blood, metabolic acidosis, • Drugs: ACE inhibitors, ARBs, B blockers, K sparing diuretics and NSAIDs • Hyporeninemichypoaldosteronism: Diabetes, sickle cell disease

  38. Symptoms of Uremia

  39. Acid Base Imbalance • Damaged kidneys are unable to excrete the 1 mEq/kg/d of acid generated by metabolism of dietary proteins. • NH3 production is limited because of loss of nephron mass • Decreased filtration of titrable acids – sulfates, phosphates • Decreased proximal tubular bicarb reabsorption, decreased positive H ion secretion • Arterial pH: 7.33 - 7.37; serum HCO3 rarely below 15 – buffering offered by bone calcium carbonate and phosphate • Should be maintained over 21 • Treatment: Sodium bicarbonate, calcium carbonate, sodium citrate

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