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Chronic Kidney Disease - Chronic Renal Insufficiency

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Chronic Kidney Disease - Chronic Renal Insufficiency

  1. 1. Chronic Kidney Disease Darrell Gray, II MD Internal Medicine Tenwek Hospital
  2. 2. Definitions <ul><li>CKD = > 3 months of ↓ glomerular filtration rate (GFR) +/- kidney damage as evidenced by serology, imaging or pathology </li></ul><ul><li>GFR= (140 – age) x LBW (kg) x Constant </li></ul><ul><li>serum Creat (in µmol/L) </li></ul><ul><li>Constant: 1.23 for men; 1.04 for women </li></ul>
  3. 3. How do we apply GFR? . . . in Staging
  4. 4. How does CKD develop? <ul><li>Common pathway </li></ul>Initial Pathologic Insult Reduced Nephron Mass Glomerular Injury Growth Promoters Acting on Intact Glomeruli End-Stage Kidney Glomerular Hypertrophy on intact Glomeruli
  5. 5. Ok, but what are the clinical features? <ul><li>General </li></ul><ul><ul><li>Malaise, nausea, anorexia, pruritis, metallic taste, uremic fetor (fishy breath), coma </li></ul></ul><ul><li>By system </li></ul><ul><ul><li>Skin: White crystals in and on skin (uremic frost), dry scaly skin, easy bruising </li></ul></ul><ul><ul><li>Neurologic: encephalopathy, neuropathy, seizures </li></ul></ul><ul><ul><li>Cardiovascular: HTN, HL, CHF, pericarditis, friction rub </li></ul></ul><ul><ul><li>GI: gastritis, ulcers, AVMs, pancreatitis </li></ul></ul>
  6. 6. More clinical features <ul><ul><li>Metabolic: Acidosis, ↑K+, ↑PO4, ↓Ca, ↑PTH </li></ul></ul><ul><ul><ul><li>Acidosis and hyperkalemia can become profound when GFR< 20 </li></ul></ul></ul><ul><ul><li>Hematologic: Anemia, bleeding </li></ul></ul><ul><ul><ul><li>Typically when GFR <30 </li></ul></ul></ul><ul><ul><li>Musculoskeletal: Osteomalacia, adynamic bone disease, metastatic calcifications, mixed bone disease </li></ul></ul><ul><ul><li>Endocrine: Insulin resistance, growth retardation, hypogonadism, impotence, infertility </li></ul></ul>
  7. 7. More about metabolic signs <ul><li>Hyperphosphatemia, Hypocalcemia and Hypermagnesemia. </li></ul><ul><ul><li>Decreased production of 1,25-dihydroxy vitamin D3 results in decrease GI Ca ++ absorption. </li></ul></ul><ul><ul><li>Decreased ability of the kidney to excrete PO 4 - . </li></ul></ul><ul><ul><li>These result in a decrease in serum Ca ++ which leads to an increase in PTH which results in increased bone reabsorbtion of Ca ++ in an attempt to normalize free Ca ++ levels and leads to renal bone disease. </li></ul></ul>
  8. 8. <ul><li>Hyperkalemia </li></ul><ul><ul><li>Gradual decrease in tubular handling of K + can result in hyperkalemia. </li></ul></ul><ul><ul><li>Usually occurs when GFR severely reduced (<10 ml/min). </li></ul></ul><ul><ul><li>K + restriction often needed. </li></ul></ul><ul><ul><li>Diabetics with Type IV RTA / Hyporeninemic Hypoaldosteroneism can develop hyperkalemia without a severely depressed GFR. </li></ul></ul>
  9. 9. Stop replcmnt Excessive Ca/VitD replcmnt ↓ variable ↑ Phos binders and Vit D Severe 2 º hyperPTH ↑↑↑ ↑ ↓ Phos Binders 2 º hyperPTH ↑ ↑ ↓ 1,25 OH Vit D Vit D def ↑ ↓ ↓ Treatment Process PTH Phos Calcium
  10. 10. So my pt presents with concerning Hx and PE. What studies to do I need?? <ul><li>Labs </li></ul><ul><ul><li>K+, Creatinine, Ca++, Mg, Phos </li></ul></ul><ul><ul><li>Urinalysis </li></ul></ul><ul><ul><li>Strict I/O </li></ul></ul><ul><ul><li>Daily weight </li></ul></ul><ul><li>Imaging </li></ul><ul><ul><li>Kidney ultrasound </li></ul></ul><ul><ul><ul><li>Small kidneys bilaterally </li></ul></ul></ul>
  11. 11. But don’t forget !! <ul><li>Medications </li></ul><ul><ul><li>Renally dose medications such as antibiotics/antiretrovirals, ranitidine, atenolol </li></ul></ul><ul><ul><li>Be extremely cautious with starting an ACEI or ARB. Talk with consultant. </li></ul></ul><ul><ul><li>Avoid using Morphine as toxic metabolites build up. </li></ul></ul><ul><ul><li>If diuresis is necessary, use lasix if patient has hyponatremia, and thiazide if pt has hypernatremia </li></ul></ul><ul><ul><ul><li>However, thiazides are not effective when GFR <30 </li></ul></ul></ul>
  12. 12. Causes of Chronic Renal Failure <ul><li>Glomerulonephritis </li></ul><ul><li>HTN </li></ul><ul><li>Diabetic nephropathy </li></ul><ul><li>Pulmonary-renal syndromes </li></ul><ul><li>Systemic diseases </li></ul><ul><li>Urinary tract pathology </li></ul><ul><li>Congenital </li></ul>
  13. 13. Glomerulonephritides <ul><li>Idiopathic Membranous Glomerulonephritis. </li></ul><ul><li>Focal and Segmental Glomerulonephritis (FSGS) </li></ul><ul><ul><li>Associated with HIV </li></ul></ul><ul><li>IgA Nephropathy (Berger’s Disease). </li></ul><ul><li>Membranoproliferative Glomerulonephritis Type I and II (MPGN I and II). </li></ul>
  14. 14. Hypertension / Renovascular Disease <ul><li>Nephrosclerosis </li></ul><ul><li>Ischemic Renal Disease </li></ul><ul><ul><li>Abdominal bruits. </li></ul></ul><ul><ul><li>Atherosclerotic disease elsewhere. </li></ul></ul><ul><ul><li>ARF on ACE inhibitors. </li></ul></ul>
  15. 15. Pulmonary -Renal Syndromes <ul><li>Goodpasture’s Syndrome (anti-basement membrane disease) </li></ul><ul><li>Wegener’s Granulomatosis and other ANCA (antineutrophil cytoplasmic antibody) associated diseases. </li></ul>
  16. 16. Secondary to Systemic Diseases <ul><li>Systemic Lupus Erythematosis (SLE). </li></ul><ul><li>Other collagen vascular diseases. </li></ul><ul><li>Microscopic polyarteritis (vasculitis). </li></ul><ul><li>Thrombotic Microangiopathies (HUS, TTP, PSS, malignant HTN). </li></ul><ul><li>Multiple Myeloma (MM). </li></ul><ul><li>Amyloidosis </li></ul><ul><li>Henoch-Schonlien Purpura (HSP). </li></ul><ul><li>Aids Nephropathy. </li></ul>
  17. 17. Urinary Tract Disease <ul><li>Reflux Nephritis. </li></ul><ul><li>Ureteral or Urethral Obstruction. </li></ul><ul><li>Other causes of chronic or recurrent obstruction. </li></ul>
  18. 18. Congenital <ul><li>Adult Polycystic Kidney Disease (APKD). </li></ul><ul><ul><li>Most common inherited form of renal disease. </li></ul></ul><ul><ul><li>Characterized by numerous cysts in both kidneys. </li></ul></ul><ul><ul><li>Cysts can also be present in liver, pancreas, ovaries. </li></ul></ul><ul><ul><li>Other findings can include mitral valve prolapse, cerebral aneurysms, diverticular disease. </li></ul></ul><ul><li>Alport’s Syndrome. </li></ul>
  19. 19. Therapy of Chronic Renal Failure
  20. 20. Diet Therapy <ul><li>Low sodium diet for blood pressure and volume control. </li></ul><ul><li>Maintain adequate nutrition. </li></ul><ul><li>No proof that low protein (< 0.8 g ptn / kg / day) slows progression although it may help in management of acidosis. </li></ul>
  21. 21. <ul><li>May need to use diuretics and fluid restrict for volume control. </li></ul><ul><li>Potassium restriction as needed. </li></ul><ul><li>Cholesterol treatment may be required. </li></ul>
  22. 22. One Suggested Approach
  23. 23. Phosphate Control <ul><li>Dietary phosphate should be restricted. </li></ul><ul><li>Phosphate binders must be given with meals. </li></ul><ul><li>Calcium carbonate usually first choice, but as disease progresses may need to switch to calcium acetate or non calcium containing binders such as sevelamer or lanthanum carbonate. </li></ul><ul><li>Aluminum hydroxide binders should be avoided if possible. </li></ul><ul><ul><li>Use with citrate solutions has resulted in aluminum toxicity and death. </li></ul></ul>
  24. 24. PTH Control <ul><li>Use of vitamin D analogs often needed to reduce iPTH levels (calcitriol, paracalcitol or doxercalciferol). </li></ul><ul><li>In addition, calcimimetic such as cinacalcet may also be needed to lower iPTH. </li></ul><ul><li>Issues currently revolve around iPTH/Ca/PO4 and cardiac risk. </li></ul>
  25. 25. Hypertension <ul><li>Good control of blood pressure can slow progression of renal failure. </li></ul><ul><li>Evidence that early use of ace inhibitors in Type I diabetics with nephropathy slows the progression of renal disease. </li></ul><ul><li>Evidence to suggest this also applies to Type II diabetics. </li></ul><ul><li>Evidence for ARBs as first line in Type II diabetics. </li></ul><ul><li>Often used interchangeably or in combination. </li></ul>
  26. 26. What Does Good Care do? <ul><li>Diabetic renal disease progression can be decreased from 12 ml/min/year to 4 ml/min/year. </li></ul><ul><li>Non diabetic renal disease progression can be slowed from 4-6 ml/min/year down to 2 ml/min/year. </li></ul><ul><li>These results are in established chronic disease with no active primary process. </li></ul>
  27. 27. Summary of recommendations <ul><li>Aggressive BP control (<130/80) </li></ul><ul><ul><li>– ACEI or ARB preferred </li></ul></ul><ul><li>Excellent control of DM (HgBA1C<7%) </li></ul><ul><li>Avoid renal insults (nephrotoxins, etc) </li></ul><ul><li>Cardiovascular disease prevention (lipids, etc) </li></ul><ul><li>Monitor for anemia </li></ul><ul><li>Minimize bone disease </li></ul><ul><li>Appropriate nutritional counseling </li></ul><ul><li>Smoking cessation (for everybody, not just renal patients) </li></ul><ul><li>Early referral to nephrologist (Cr>1.7) </li></ul>

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