Chronic Kidney Disease - Chronic Renal Insufficiency
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Chronic Kidney Disease - Chronic Renal Insufficiency

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Chronic Kidney Disease - Chronic Renal Insufficiency Presentation Transcript

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