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    Chronic Kidney Disease

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    Nadia Andriani Maizalius
    Chronic kidney disease is defined as a continued reduction in kidney function over 3 months as shown by a GFR below 60 or the presence of kidney damage. It affects 14% of the population and is most commonly caused by diabetes and hypertension. As kidney function declines, complications arise including anemia, bone disease, electrolyte imbalances, and metabolic acidosis. Treatment focuses on controlling blood pressure and proteinuria to slow disease progression, and managing complications through diet, medication, and addressing underlying diseases.

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    Chronic Kidney Disease

    Uploaded by

    Nadia Andriani Maizalius
    146 views11 pages
    Chronic kidney disease is defined as a continued reduction in kidney function over 3 months as shown by a GFR below 60 or the presence of kidney damage. It affects 14% of the population and is most commonly caused by diabetes and hypertension. As kidney function declines, complications arise including anemia, bone disease, electrolyte imbalances, and metabolic acidosis. Treatment focuses on controlling blood pressure and proteinuria to slow disease progression, and managing complications through diet, medication, and addressing underlying diseases.

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    Chronic Kidney Disease

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    Chronic kidney disease is defined as a continued reduction in kidney function over 3 months as shown by a GFR below 60 or the presence of kidney damage. It affects 14% of the population and is most commonly caused by diabetes and hypertension. As kidney function declines, complications arise including anemia, bone disease, electrolyte imbalances, and metabolic acidosis. Treatment focuses on controlling blood pressure and proteinuria to slow disease progression, and managing complications through diet, medication, and addressing underlying diseases.

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    © All Rights Reserved
    Download as DOC, PDF, TXT or read online from Scribd
    Download as doc, pdf, or txt
    146 views11 pages

    Chronic Kidney Disease

    Uploaded by

    Nadia Andriani Maizalius
    Chronic kidney disease is defined as a continued reduction in kidney function over 3 months as shown by a GFR below 60 or the presence of kidney damage. It affects 14% of the population and is most commonly caused by diabetes and hypertension. As kidney function declines, complications arise including anemia, bone disease, electrolyte imbalances, and metabolic acidosis. Treatment focuses on controlling blood pressure and proteinuria to slow disease progression, and managing complications through diet, medication, and addressing underlying diseases.

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    of 11

    CHRONIC KIDNEY DISEASE

    (Harrisons. 18th ed. 2010, KDOQI Guidelines, NEJM. 2010;362:56)

    Introduction

    Chronic kidney disease (CKD): continuing, irreversible reduction in


    nephron number leading to reduced GFR occurring over a period >
    3mo
    o eGFR < 60cc/min/1.73cm2 or presence of renal damage
    Kidney failure: eGFR < 15
    Complications of CKD doesnt usually manifest until eGFR < 30
    (stage 4)
    Uremia: literally urine in the blood. The accumulation of toxins that
    lead to a disturbance in homeostatic mechanisms regulated by the
    kidney
    o Occurs in CKD stage 5
    o Urea is not the toxin is a surrogate for the toxins
    Symptoms arent usually present until stage 3 or greater
    disease
    Population prevalence = 14%
    o 6% have CKD Stage 1-2
    o 8% have CKD Stage 3-4
    MDRD is the best way to estimate GFR (better than CockcroftGault)
    o All the calculations of GFR dont work at extremes of failure
    Diabetic nephropathy is the MCC of CKD followed by HTN
    The leading cause of death in CKD is coronary artery disease
    people do not die from renal failure w/ renal replacement
    therapy

    Classification

    Etiology of CKD

    Hypertension is MCC in age > 65


    Hypertensive nephropathy
    o Primary: subtle changes in the glomerulus that look like FSGS
    w/o nephrotic or nephritic features
    o Secondary: due to ischemia from atherosclerosis and systemic
    vascular disease

    Pathophysiology of CKD

    Incipient event
    o Something smokes the nephrons and gets the processes started
    o Most commonly, diabetes or immune complexes
    Propagating events
    o Glomerular hypertrophy/hyperfiltration:
    After a bunch of nephrons die, the remaining beef up their
    function. No one really knows how
    If you remove one kidney, the overall function by this
    mechanism will get you back to 80% of normal GFR
    o Renal progression:
    If the overall nephron number is reduced to < 20% we
    progress to ESRD
    The tubules start to die and become fibrotic

    Many mechanisms postulated. Likely related to cascade of


    events cumulating in severe, irreversible inflammation
    (lymphocytic infiltration)
    o The response to inflammation is to ultimately lay down collagen
    matrices fibrosis
    Sequelae of glomerular disruption
    o Glomerulosclerosis
    Loss of autoregulation: as the initial nephrons stop
    working, they no longer regulate the glomerular pressure
    Paradoxically, the response to this is increasing
    angiotensin II and aldosterone systemic
    hypertension and glomerular damage
    Both these hormones further destroy the glomerulus
    The overall result is that all the nephrons in the kidney
    start seeing systemic pressures hit the glomerulus they
    scar
    o Interstitial fibrosis/tubular atrophy
    As the glomerulus becomes more destroyed leaked
    protein sets off a downstream cascade of inflammation
    Ultimately leads to fibrosis and disruption of normal
    tubular cell function
    Complications of CKD these start to occur @ eGFR < 30
    o

    Volume overload (due to


    high Na)

    Hyperkalemia

    Low Calcium

    High Phosphate
    Low Vit D

    High PTH (secondary


    hyperPTH)

    Metabolic acidosis

    Bone disease

    ATII and aldosterone are ramped up increases tubular Na+


    absorption
    Dietary Na+ >> renal Na+ excretion
    Increased Na+ increased osmolality increased ADH
    release increased isotonic ECV hypervolemia + HTN
    HypoNa only occurs if H2O intake > renal H2O excretion
    In stage 5 due to GFR
    < stage 5 due to a combination of underlying disease (DM)
    and medications (ACE/ARB/Aldactone) that impair renal
    excretion from principal cell
    Precipitated by RBC infusion, hemorrhage, hemolysis, acidosis
    Decreased NH4 decreased urinary buffer and H+ excretion
    Retained organic anions anion-gap MA
    Due to combination of increased PO4 and decreased calcitriol
    production
    Due to decreased renal excretion
    Renal failure decreased expression of 25-OH 1-a-hydroxylase
    decreased conversion of calcidiol to calcitriol
    Due to combination of:
    o Hyperphosphatemia
    o Decreased 1,25-OH Vit D (calcitriol)
    o Hypocalcemia
    Parathyroid tissue becomes hyperplastic can be diffuse or
    localized
    Osteitis fibrosa cystica due to high PTH and high bone
    turnover
    Osteomalacia unmineralized bone matrix accumulates due
    to decreased Vit D, Aluminum accumulation and metabolic


    Low FGF-23

    acidosis
    Adynamic bone disease reduced bone volume and density
    due to excessive suppression of PTH and vitamin D
    supplementation
    A hormone that interacts with Vit D and PO4
    Tries to decrease PO4 by directly increasing renal excretion,
    increasing PTH and decreasing calcitriol (gut absorption)
    Turning out to be an independent risk factor for cardiac dz and
    indicator for PO4 Rx

    Pathophysiology of Uremia

    Uremia is the point where the kidney fails to do its job such that
    maintaining life is impossible without renal replacement therapy
    (transplant or dialysis) stage 5 CKD
    Creatinine and urea are used as surrogates of toxic build up from
    impaired renal excretion
    o Themselves are not toxic
    Uremia is the product of failure of 3 major renal functions +
    chronic systemic inflammatory damage in response:
    o Toxic metabolite excretion
    o Electrolyte, acid-base and water regulation
    o Hormonal regulation

    Caveats in CKD

    Hypovolemia
    o CKD = loss of ECV control. Sodium exchange is broken
    o Volume loss improper renal response + acute on chronic injury
    o You need to give this person back isotonic saline carefully to
    avoid dialysis

    Calculating GFR (eGFR)

    Just remember that creatinine is a good surrogate (see AKI), but


    doesnt start to rise until > 50% decline in GFR
    Modification of Diet in Renal Disease (MDRD) is the best
    o Takes into account gender and race
    Cockcroft-Gault was historically used, but is now outdated

    APPROACH TO CKD
    (Harrisons. 18th Ed. 2010, KDOQI Guidelines)

    Suspect CKD:
    o Presence of risk factors for CKD and conditions that cause CKD

    Age > 65
    African, SE Asian, Hispanic ancestry
    FHx of CKD
    Prior AKI
    Nephrolithiasis
    Proteinuria
    Structural abn of urinary tract (VER,
    recurrent pyelo)

    Think of the differential diagnosis


    o Break this into diabetes or not
    o NOT diabetes list is very similar to the AKI list, but with a couple
    variations
    o Any AKI cause can potentially progress to CKD if the initial insult
    leaves an injury lasting > 3mo

    Risk Factors for CKD

    Major Causes of CKD

    Diabetes
    HTN
    Autoimmune disease: SLE, vasculitis
    Infections: IE, HIV, hepatitis, schisto,
    malaria
    Drugs or toxins: NSAIDs, dye,
    antibiotics, etc.

    DIABETES

    Type 1 or Type 2 DM
    PRE-RENAL
    Decreased EABV
    o Hypovolemia, 3rd spacing
    o Cardiac impairment
    o Systemic vasodilation

    HRS

    Anaphylaxis
    o Sepsis (has independent toxicity)
    Renal vasoconstriction
    o NSAIDS
    o ACE-I
    o Contrast
    o Hypercalcemia
    Large/medium vessel disease
    o HTN
    o Bilat stenosis + ACE-I
    o Atheroemboli
    o Thombosis (APLA, AFib, IE)
    o Vasculitis
    o Compression (abdominal HTN)
    RENAL
    Glomerular
    o Glomerulonephritis

    IgA nephropathy

    Anti-GBM, immune complex, pauci-immune


    o Nephrotic syndrome lesions (non-inflammatory)
    o Alports syndrome
    Tubular
    o ATN: ischemia, toxins, contrast
    o Obstructive nephropathy:

    Cancer

    Myeloma

    Nephrolithiasis

    o Fabrys disease
    Interstitial (can start as AIN)
    o Allergic: beta-lactams, sulfa drugs, NSAIDs, PPIs
    o Infection: pyelo (xanthogranulomatous infection), legionella, TB
    o Infiltrative: sarcoid, lymphoma/leukemia
    o Autoimmune: Sjogrens, TINU, IgG4, SLE
    Small-vessel disease
    o Cholesterol emboli
    o Thrombic microangiopathy

    TTP/DIC

    Pre-eclampsia

    APLA

    Scleroderma

    HTN
    Cystic diseases
    o Polycystic kidney disease
    o Tuberous sclerosis
    o Von Hippel Lindau
    Transplant kidneys
    o Rejection
    o Drug toxicity
    o Recurrence of disease

    Do a good history based on your DDx. Always think about the


    MCC:
    o DM
    o HTN
    o Glomerular disease
    o Interstitial (allergies, drugs)
    o Cystic kidney disease

    Do a good physical exam. Dont forget to look for comorbidities:


    o Diabetes
    o CHF
    o COPD
    o HTN changes

    Dont forget to look for indications for dialysis


    Order the basics for ALL patients with new CKD:

    CBC, electrolytes
    Serum creatinine, BUN & measure GFR w/ MDRD

    Urine dip

    HbA1C, fasting BGL, lipid profile

    Urine microscopy looking for RBC/WBC/crystals


    Urine protein or albumin (if DM)/Urine Creatinine ratio
    o Multiply x 8.8 to get 24hr estimation
    SPEP/UPEP
    HIV/HBsAg/anti-HCV
    Renal U/S

    If eGFR < 30 think about CKD sequeale:

    PTH, Ca/PO4/Mg, Vitamin D

    Practically, you will have most of this when you 1st see the
    patient
    o Using the above DDx, start narrowing down the list based on if
    the urine has isolated protein, blood or both
    Based on H + P and initial work-up, do more if needed

    MANAGEMENT
    (NEJM. 2010;362:56)
    Therapy

    GFR < 30
    Rapidly declining
    kidney function
    GN
    Remove
    exacerbators
    Diet
    Weight
    Exercise

    Evidence
    BASICS
    Referral to Nephrologist Arch Int
    Med 2002;162:20026

    Comments

    Drugs (NSAIDs)
    Low Na+, PO4, K+ (if
    oliguric), protein
    BMI < 25
    Abdo circ < 102 (men);
    < 88 (women)
    > 30min/d modintensity > 4x/wk

    Treat underlying
    disease
    Hypertension

    SLOW DISEASE PROGRESSION


    Target: BP < 130/80
    General:

    Na+ < 2g/d


    1st line:

    ACE/ARB
    2nd:

    Beta-blockers

    CCB (only if on
    ACE/ARB)
    Additional:

    Lasix

    Metalazone

    Check Cr, lytes in 1


    week
    Be careful when K
    > 5.4 prior to
    initiation
    Stop if Cr 30%
    Initial in GFR
    expected
    Consider co-

    morbidities in
    selection (DM, CAD)

    Proteinuria

    Glycemic control
    PTH

    Cardiovascular

    Anemia

    Metabolic Acidosis

    Etacrynic acid in
    pts with sulfa allergy
    Independent RF for
    disease progression

    Target: < 500mg/d


    General:

    < 1g/kg/d
    protein diet
    1st line:

    ACE/ARB
    Target: HbA1C 7.0

    Also reduces CV
    risk/death

    No evidence

    CKD SEQUELAE
    Target:

    Stage 3: < 70

    Stage 4: < 110

    Stage 5: < 300


    General: low PO4 diet
    1st line: PO4 binders

    PO4, Ca:
    CaCO4

    PO4 + Ca:
    Sevelamer

    PO4: AlOH
    (short)
    2nd line:

    Calcitriol
    3rd line:

    Cinacalcet
    Target:

    LDL < 2.6


    General: low fat diet,
    exercise, wt loss
    1st line:

    Just LDL: Lipitor

    HDL and LDL:


    Crestor
    Target:

    HgB 100-120
    g/L

    TSat > 20%


    General:

    Iron
    supplementatio
    n
    1st line:

    EPO
    (darbapoeitin,
    erythropoietin)
    Target:

    HCO3 > 22
    1st line:

    Start NaHCO3 if
    HCO3 < 22

    ACE + ARB
    controversial
    See Diabetic
    Nephropathy
    High PTH
    independently
    increases CV
    mortality

    Only need dose


    adjust for fibrates
    Consider co-morbid
    for targets

    Increased mortality,
    CV events w/ Hgb >
    120

    Watch Na+ load in


    patients with CHF

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