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Chronic Kidney Disease - Chronic Renal Insufficiency

Chronic Kidney Disease - Chronic Renal Insufficiency






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    Chronic Kidney Disease - Chronic Renal Insufficiency Chronic Kidney Disease - Chronic Renal Insufficiency Presentation Transcript

    • Chronic Kidney Disease Darrell Gray, II MD Internal Medicine Tenwek Hospital
    • 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
    • How do we apply GFR? . . . in Staging
    • 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
    • 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
    • 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
    • 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.
      • 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.
    • 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
    • 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
    • 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
    • Causes of Chronic Renal Failure
      • Glomerulonephritis
      • HTN
      • Diabetic nephropathy
      • Pulmonary-renal syndromes
      • Systemic diseases
      • Urinary tract pathology
      • Congenital
    • 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).
    • Hypertension / Renovascular Disease
      • Nephrosclerosis
      • Ischemic Renal Disease
        • Abdominal bruits.
        • Atherosclerotic disease elsewhere.
        • ARF on ACE inhibitors.
    • Pulmonary -Renal Syndromes
      • Goodpasture’s Syndrome (anti-basement membrane disease)
      • Wegener’s Granulomatosis and other ANCA (antineutrophil cytoplasmic antibody) associated diseases.
    • 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.
    • Urinary Tract Disease
      • Reflux Nephritis.
      • Ureteral or Urethral Obstruction.
      • Other causes of chronic or recurrent obstruction.
    • 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.
    • Therapy of Chronic Renal Failure
    • 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.
      • May need to use diuretics and fluid restrict for volume control.
      • Potassium restriction as needed.
      • Cholesterol treatment may be required.
    • One Suggested Approach
    • 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.
    • 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.
    • 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.
    • 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.
    • 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)