Approach to CKD

Approach to Chronic Kidney Disease – Taylor Riggs

 

Background

  • Decreased kidney function or one or more markers of kidney damage for 3 or more months
  • GFR < 60; Staging helps risk-stratify pts likely to progress or develop complications of CKD
    • CKD IIIa: eGFR 45-60
    • CKD IIIb: eGFR 30-44
    • CKD IV: eGFR 15-30
    • CKD V: eGFR < 15

 

  • Markers of kidney damage
    • Albuminuria (albumin:creatinine > 300mg/g or urine protein:creatinine > 500mg/g)
    • Urine sediment: RBC cases, WBC casts, oval fat bodies or fatty casts, granular casts
    • Electrolytes or other abnormalities due to tubular disorders
    • Abnormalities on histology (glomerular, vascular or cystic disease, TIN)
    • Structural abnormalities: (cysts, hydronephrosis, scarring, masses, renal artery stenosis)
    • History of kidney transplant (rejection, drug toxicity 2/2 calcineurin inhibitors, BK virus nephropathy, recurrent disease leading to transplant)
  • Refer to AKI section for a detailed list of etiologies

 

When to refer to nephrology clinic

  • eGFR < 30
  • Persistent urine albumin/creatinine ratio > 300 mg/g
  • Urine protein/creatinine ratio greater than 500 mg/g
  • Rapid loss of kidney function (> 30% decline over 4 months)
  • Hematuria not 2/2 urologic condition or RBC casts
  • Inability to identify presumed cause of renal dysfunction
  • Difficult to manage complications (hyperkalemia, anemia, bone-mineral disease, HTN)
  • Confirmed or presumed hereditary kidney disease (PCKD suspected)

 

Albuminuria

  • Microalbuminuria: 30-300 mg/day
  • Macroalbuminuria: > 300 mg/day (UA typically only detects these pts)
    • In patients with albuminuria found on UA, confirm albuminuria with 2 repeat tests over 3-6 months. Early morning void sample is best. Ensure patient does not have UTI, fever, recent IV contrast, hematuria, or alkaline urine.
    • After confirmation, monitor annually.
    • For patients with CKD or DM but without albuminuria, monitor annually for development of albuminuria
  • Treatment: reducing proteinuria can slow the progression of renal disease
    • ACEi/ARBs: reduce intraglomerular pressure, thereby reducing proteinuria
    • Work over weeks to months. Not as rapid as anti-HTN effect.
    • Goal is to titrate ACEi/ARB to BP < 130/90
    • Most effective when used in conjunction with low Na diet (<2g/d) +/- diuretics
  • Can add other anti-hypertensives to achieve goal BP if ACEi/ARB alone not able to be tolerated due to side effects (e.g. hyperkalemia)

 

Metabolic acidosis

  • Goal bicarbonate: 23-30
  • Can calculate bicarbonate deficit (MDcalc has calculator) and use that to estimate dose
  • If bicarb < 22, consider starting:
    • Sodium bicarb 650 mg TID (8mEq bicarb per 650mg tablet). Can titrate up to 5850mg/day (70 mEq or 3 tabs TID)
    • Sodium citrate (bicitra): 1mL = 1 mEq
    • Baking soda: 1 teaspoon = 59 mEq HCO3 (often well-tolerated by patient compared to bicitra in terms of taste)

 

HTN in CKD

  • Goal BP < 130/80
  • CKD stage 1 or 2 without albuminuria or DM:
    • Usual first line BP medications (ACEi/ARB, CCB, or HCTZ)
  • CKD stage 3 or greater
    • ACEi or ARB is first line
    • Can add diuretics to ACEi/ARB for adjunctive therapy in CKD 4-5
    • HCTZ not effective with eGFR < 30
    • Low sodium diet effective in volume and BP control
  • Consider stopping ACEi/ARB if:
    • GFR declines >30% over 4 months and consider evaluation for renal artery stenosis with Duplex Doppler renal u/s vs CTA or MRA as initial screening
    • K > 5.5 despite efforts to decrease potassium (i.e. low K diet, optimizing dose of diuretics, adding K-binders)
    • If patient has an AKI on CKD, especially if pre-renal

 

Anemia in CKD

  • Etiology: reduced EPO, chronic inflammation, uremic platelets/platelet dysfunction, loss of blood in dialysis circuit
  • Indications for iron supplementation in non-dialysis patients:
    • ALL patients with TSAT <20% and ferritin <100 ng/mL
    • Patients with Hb <13 and TSAT <30% and ferritin <500 ng/mL
    • Can consider oral iron supplementation unless severe anemia or iron deficiency
    • PO Iron dosing: New evidence shows that every other day oral iron leads to increased absorption and efficacy and decreased side effects
        • Ferrous sulfate 325mg (65mg elemental iron) every other day
        • Reassess iron levels in 1-3 mos; if not appropriately ↑, consider IV iron repletion
    • IV Fe dosing: 1000 mg IV, either via 1 dose or multiple doses depending on formulation
        • Ferric gluconate: max dose 250 mg over 1 hr, dosed weekly for 3-4 doses
        • Iron dextran: 1000 mg in a single dose, infused over one hour (less preferred due to higher risk of allergic reactions; requires test dose 5 min prior)
  • Dialysis patients:
    • IV Iron preferred method of repletion for HD patients with
        • TSAT < 20% and ferritin < 200
        • TSAT <30% and ferritin <500 AND with Hb < 10 OR are on EPO
    • Dosing: usually administered at HD sessions
        • 125 mg ferric gluconate at consecutive HD sessions x 8 doses
        • 100 mg iron sucrose at consecutive HD sessions x 10 doses
        • Ferumoxytol 510mg at the end of two HD sessions 1-4 weeks apart
  • Indications for EPO
    • Pts w/ Hb <10 who are not iron deficient or who’s anemia persists despite adequate iron repletion

 

Hyperkalemia (Goal K < 5.5)

  • Generally, only develops in patients who are oliguric or with other problems, such as high K diet or hypoaldosteronism (due to ACEi/ARB)
    • Low K diet (< 40-70 mEq/day or 1500-2700 mg/day)
    • Add loop diuretics if hypertensive or hypervolemic; Can use thiazide if GFR > 30
    • GI cation exchangers: work within hours
        • Patiromer (Veltassa): binds K in colon in exchange for calcium
        • Sodium zirconium cyclosilicate (Lokelma): binds K throughout intestine in exchange for sodium and H+
        • Need nephrology attending approval for Lokelma
    • Do not use Kayexelate as chronic therapy
    • Ensure acidosis is treated due to resulting extracellular K+ shift (see next section)
    • Consider discontinuing ACEi/ARB if K persistently > 5.5

 

Mineral bone disease in ESRD

  • Ca goal: < 9.5. Avoid supplementation in mild or asymptomatic hypocalcemia
  • Vit D25 goal: > 20. Replete as in normal population
  • Phos goal: < 5.5. Start phosphate binders (sevelamer or noncalcium-based binders typically preferred) with goal Phos 3.5-5.5
    • Sevelamer: use lowest dose effective to achieve Phos < 5.5
        • Phos 5.5-7.5: initial dose 800 TID with meals
        • Phos 7.5-9.0: initial dose 1200-1600 TID with meals
        • Phos > 9: initial dose 1600 TID
        • Can titrate dosing by 400 to 800 mg per meal at 2 week intervals
    • Restrict dietary phos to 900 mg/day
  • PTH goal: 2-9 x ULN, although exact goal unknown in assessing renal bone disease. Treatment involves calcimemetics, calcitriol, and synthetic vitamin D analogues.

 

Diabetes in CKD

  • A1c goal:
    • < 7% in patients with long lifespan, few comorbidities, and minimal hypoglycemia
    • < 8% in patients with multiple comorbidities and frequent/high risk for hypoglycemia
  • Treatment:
    • Metformin remains first-line but should be dose-reduced based on eGFR
        • eGFR > 45: Maximum daily dose of 2000mg/day (1000mg bid)
        • eGFR < 45: Reduce max daily dose to 1000mg/day (500mg bid)
        • eGFR < 30: Discontinue
    • SGLT-2 inhibitors for patients with eGFR > 30 reduces progression to ESRD and death from renal or cardiovascular causes

 

Dialysis initiation

  • Dialysis education is usually started once patients are in CKD IV with eGFR 15-30, so earlier referral to nephrology may be helpful in patients with eGFR 30-45 who you think may be heading towards eGFR <30
  • Late referral to a nephrologist (ie, less than three months before the start of dialysis therapy) is associated with higher mortality after the initiation of dialysis