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Management of AKIER, Hospital and office

MICHELLE SHIELDS, RN, MSN, CRNPPCNP 2017

< 15 Stage 5

15–29 Stage 4

30–59 Stage 3

60–89 Stage 2

> 90 Stage 1

The Prevalence of CKD in the General Population

5.9M

5.3M

0.3M

0.4M

7.6M

Levey et al. Ann Intern Med. 2003;139:137-147.

< 15 Stage 5

15–29 Stage 4

30–59 Stage 3

60–89 Stage 2

> 90 Stage 1

26 Million CKD Patients

5.9M

5.3M

0.3M

0.4M

7.6M

Coresh et al: JAMA Nov 7, 07; 298(17):2038-2047.

X

CKD Incidence

1 in 9 Adults

3 times that of cancer

600 times that of AIDS

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< 15 Stage 5

15–29 Stage 4

30–59 Stage 3

60–89 Stage 2

> 90 Stage 1

26 Million CKD PatientsX

CKD Incidence

15% of Adults

96% of stage 1-2 are not aware

48% of CKD stage 4 are not aware

X30

Centers for Disease Control and Prevention. Chronic Kidney Disease Surveillance System—United States.2017 website. http://www.cdc.gov/ckd

Kidney Failure Is a Rapidly Growing Problem

0

100

200

300

400

500

600

700

1984 1986 1988 1990 1992 1994 1996 1998 2000 2002 2004 2006 2008 2010

Num

ber

of P

atients

(in th

ousands)

372,407

661,330

172,667

98,953

Incidence

Prevalence

Adapted from: US Renal Data System 2000 Annual Data Report.

Year

Centers for Disease Control and Prevention. Chronic Kidney Disease Surveillance System—United States. 2017website. http://www.cdc.gov/ckd

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Centers for Disease Control and Prevention. Chronic Kidney Disease Surveillance System—United States. 2017website. http://www.cdc.gov/ckd

Centers for Disease Control and Prevention. Chronic Kidney Disease Surveillance System—United States. 2017website. http://www.cdc.gov/ckd

Centers for Disease Control and Prevention. Chronic Kidney Disease Surveillance System—United States. 2017website. http://www.cdc.gov/ckd

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Centers for Disease Control and Prevention. Chronic Kidney Disease Surveillance System—United States.website. http://www.cdc.gov/ckd

Cardiovascular Disease (CVD) MortalityGeneral Population versus ESRD Patients

Foley RN, Parfrey PS, Sarnak MJ. Am J Kidney Dis. 1998;32(suppl):S112-S119.

GP=General PopulationESRD=End-Stage Renal Disease

Annual CVD mortality (%)

Age (years)

0.001

0.01

0.1

1

10

100

25-34 35-44 45-54 55-64 65-74 75-84 >85

GP maleGP femaleGP blackGP white

Dialysis maleDialysis femaleDialysis blackDialysis white

Expected Remaining Lifetimes (Years)

0

5

10

15

20

25

30

35

Age

Years

50-54

General population End-stage renal disease

60-64

20.4

4.4

28.6

6.0

US Renal Data System (USRDS) 2006 Annual Data Report: Atlas of End-Stage Renal Disease in the United States, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, 2006.

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Medicare costs are 2.7 times greater for CKD patients than for non-CKD patients

$6,060

$16,476

$62,676

$0

$10,000

$20,000

$30,000

$40,000

$50,000

$60,000

$70,000

Non-CKD CKD Dialysis

Hunsicker LG. J Am Soc Nephrol . 2004;15:1363-1374

Based on data from USRDS 2002; costs based on diagnostic codes obtained from billing data; patients> 67 years of age

An

nu

al M

edic

are

Co

st P

er P

atie

nt

($)

2016 Annual Data Report, Vol 2, ESRD, Ch 1 14

Data Source: Reference Table D1. Abbreviation: ESRD, end‐stage renal disease.

.

Figure 1.2  Trends in the annual number of ESRD incident cases (in thousands) by modality, in the U.S. population, 1996‐2014

Ishani A et al. J Am Soc Nephrol 2009

N= 233.803

Acute kidney injury increases risk of ESRD among elderly

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Acute Kidney Injury (AKI)

AKA: Acute renal failure, renal insufficiency Definition: Abrupt reversible decline in glomerular filtration rate (GFR) Demonstrated by increased metabolic waste products, ie blood

urea nitrogen (BUN) and creatinine

Definition of AKI

a sudden, sustained, and usuallyreversible decrease in the glomerularfiltration rate (GFR) occurring over aperiod of hours to days.

> 30 definitions used in published studies

KDIGO Classification of AKI

Stage Serum creatinine Urine output

1 1.5-1.9× baselineOR>0.3 mg/dL

<0.5 ml/kg/hr for 6-12 hrs

2 2-2.9× baseline<0.5 ml/kg/hr > 12 hrs

3 3 times baselineORincrease in Cr to ≥4.0 mg/dLOR Initiation of RRT

<0.3 ml/kg/hr > 24 hrsORAnuria > 12 hrs

KDIGO( Kidney Disease: Improving Global Outcomes)Clinical Practice Guideline for AKI. Kidney Int 2012

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Initial Evaluation of AKI

Evaluate for reversible causes: hypotension, volume depletion, obstruction

Evaluate for complications of AKI: hyperkalemia, acidosis, volume overload, hypocalcemia, hyperphosphatemia, anemia

Determine differential diagnosis of AKI: Prerenal, intrinsic damage, post renal etiology.

The kidney functions properly in patients with prerenal azotemia. True volume depletion can be treated with normal saline. Decreased effective arterial blood volume can be present in

CHF, Cirrhosis or nephrotic syndrome. Treatment should focus on the underlying disease.

Prerenal azotemia is the most common cause of acute kidney injury in the outpatient setting Look for patients with decreased PO, diarrhea, vomiting,

tachycardia, orthostasis…. Order: UA, Uosm, Una, Ucr, BMP, Uurea (if on diuretics)

Prerenal Azotemia

ATN - Acute Tubular Necrosis Usually occurs after an ischemic event or exposure to

nephrotoxic agents. Look for muddy brown casts and FeNa>2%

AIN - Acute Interstitial Nephritis Classic presentation is fever, rash, eosinophilia and Cr

bump 7-10 days after drug exposure. Urine may show leukocytes, leukocyte casts and

erythrocytes, cultures will be negative.

CIN - Contrast Induced Nephropathy Increased Cr of 0.5mg/dl or 25% 48hrs after contrast

administration.

Others – Glomerular Disease, Pigmented Nephropathy, Thrombotic Microangiopathy

Intrinsic Kidney Diseases

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Obstruction anywhere in the urinary tract Bladder outlet obstruction can be seen with bladder scan and

relieved with catheterization

Ureteral obstruction and hydronephrosis may be seen on ultrasound and noncontrast CT

Order: Order: UA, Uosm, Una, Ucr, BMP, Uurea (if on diuretics)

Patients often have a history of pelvic tumors, irradiation, congential abnormalities, kidney stones, genitourinary, procedures or surgeries, and prostatic enlargement.

Post renal Disease

Hou SH, Bushinsky DA, Wish JB. Am J Med 1983; 74: 243-8.Nash K, Hafeez A, Hou S. Am J Kidney Dis. 2002; 39: 930-6.

Kaufman J, Dhakal M, Patel B, Et al. Am J Kidney Dis 1991; 17: 191-8.

Etiology of AKI

0

10

20

30

40

50

60

70

80

Prerenal Intrarenal Obstruct Idiopath

Outpatient

Inpatient

ATN is the cause in more than 90%.

Sepsis is the leading cause of ATN

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Management of AKIImmediate Therapy

Volume status: Volume depletion:

Any patient with clinical history of volume loss, ie vomiting, hypotension, tachycardia or oliguria should be trialed on IVF.

Initial therapy crystalloid. Target fluid replacement to MAP, urine output or improved cardiac output if

invasive monitor is used. Bolus then maintenance fluid if tolerated. Closely monitor for signs of volume

overload.

Volume overload: From excessive correction of volume depletion or primary LV dysfunction, ie

Cardiorenal syndrome. Diuretics initial therapy, loop preferred as greater naturetic effect than thiazides.

Initial dose 40-80smg IV furosemide, if not responsive double the dose, add metolazone. If ineffective, acute dialytic therapy.

Management of AKIImmediate Therapy

Hyperkalemia Common and potentially life-threatening complication of AKI Stablize, translocate, Increase excretion If not responsive to medical therapy, dialyze

Acidosis: Both excretion of acid and regeneration of bicarbonate is impaired with decreased GFR. Other factors may increase acidosis including sepsis, trauma and multi organ failure with elevated lactic acidosis. Mild: oral bicarbonate replacement, Moderate: IVF with bicarbonate, Severe/refractory: dialysis.

Hypocalcemia: due to hyperphosphatemia, reduced 25D, elevated PTH. Calcium is protein bound, correct for hypoalbuminemia. If asymptomatic, initiate phosphate binders, vitamin D therapy. If symptomatic, IV calcium.

Management of AKI:

Nutrition: adjust TPN/protein intake Medication dosing: adjustment for eGFR to avoid under or over

dosing, timing for dialytic therapy, reassess dosing for renal recovery or dialysis modality)

Procedural considerations (prefer non-contrast CT, appropriate to delay contrast exposure, prophylaxis)

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Nephrotoxic Drug Exposure

Minimizing nephrotoxin Avoid Aminoglycosides, Amphotericin,

Bactrim, Vancomycin, NSAIDs, IV contrast, Fleet’s enemas

Renal dose medications – especially antibiotics and monitor level

Cautious use (metformin, long acting oral hypoglycemic agents, insulin, gemfibrozil and statins, neurotin, colchicine/allopurinol, morphine/codeine, lmwh)

Management of AKIIndications for dialysis

Fluid overload refractory to diuretics Hyperkalemia Metabolic acidosis; pH < 7.1 refractory to IV bicarbonate Signs of uremia such as pericarditis, neuropathy, or bleeding

disorders due to qualitative platelet dysfunction.

Case Study #1Evaluation of AKI in the ER.

89 y.o. female with history of DM, HTN, CHF recently with malaise, fever/chills, body aches, nausea and vomiting. Presents to ER for evaluation.

Home medications, ASA 81mg qd, lisinopril 10mg qd, spironolactone 25mg qd, HCTZ 25mg qd, lantus 24u qhs, Vit D 1000iu qd, naprosynprn body aches.

Physical exam: BP lying 102/64, HR 68, sitting 100/64, HR 72, standing 82/58, HR 110. Normocephalic, no JVD, lungs clear, cardiac exam with RRR, ii/vi murmur, abdomen softly distended, + 2 edema

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Case study #1

Labs: Sodium 148, K 5.4, Chloride 112, Co2 21, BUN 45, creatinine 1.2 UA benign. CXR no acute process A&P? D/Dx: 1. Viral illness 2. AKI?

Creatinine 1.2

Age/race/sex 32 AA male 54 AA female 68 w male 89 w femaleCreatinine 1.2 1.2 1.2 1.2GFR 90 ml/min 60 ml/min 64 ml/min 45 ml/min

Date 8/1/17 2/1/17 8/4/16 2/4/16Creatinine 1.2 mg/dL 0.7 mg/dL 0.8 mg/dL 0.7 mg/dLGFR 45 ml/min 83ml/min 71 ml/min 83ml/min

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Case Study #1Evaluation of AKI in the ER.

89 y.o. female with history of DM, HTN, CHF recently with malaise, fever/chills, body aches, nausea and vomiting. Presents to ER for evaluation.

Home medications, ASA 81mg qd, lisinopril 10mg qd, spironolactone 25mg qd, HCTZ 25mg qd, lantus 24u qhs, Vit D 1000iu qd, naprosynprn body aches.

Physical exam: BP lying 102/64, HR 68, sitting 100/64, HR 72, standing 82/58, HR 110. Normocephalic, no JVD, lungs clear, cardiac exam with RRR, ii/vi murmur, abdomen softly distended, + 2 edema

Differential Diagnosis

Prerenal: Dehydrated on diuretics, hypotensive, tachycardic, lisinopril

Intrinsic: Naprosyn, hypotension could lead to ATN Post renal: No clear urinary symptoms/abnormalities on exam

Treatment Plan

NSS at 125ml/hr Stop lisinopril, HCTZ, spironolactone, Naprosyn. If BP stabilizes, Discharge home with follow up/labs in 2-3 days with

PCP. Teach patient, sick day rule of holding lisinopril/HCTZ and

spironolactone if not taking in adequate fluids.

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Case Study #2 ER evaluation of AKI

69 yo AA male presents to the emergency room with dysuria. Noted hesitancy starting 3-6 months ago, difficulty initiating his urine stream, now decreased urine output over the last few days and flank pain.

Medications: ASA, levocetirizine, multivitamin PE: no acute findings other than left CVA tenderness and slightly

fullness over palpation of the bladder. Labs: BUN 26, creatinine 1.4, GFR 64 ml/min.

Differential diagnosis

Prerenal: normotensive Intrinsic: no new medications/UA bland Post renal: s/sx of bladder tenderness, CVA tenderness

On levocetirizine which causes urine retention

Case Study #2

Unable to obtain Renal imaging Admit for observation

Need renal imaging

Evaluate urine C&S, Initiate antibiotics if needed

Insert foley catheter, observe for improvement in renal function and possibility of post-obstructive diuresis.

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Case Study #3 Hospital Evaluation of AKI

41 yo obese female with history of DM type 2 for 10 years, HTN, one previous episode of AKI 2 years ago during hospitalization for pneumonia presents with worsening shortness of breath. She had seen PCP 5 days ago with complaints of cough, productive of yellow secretions, fevers, started on trimethoprim sulfa DS bid. Initial BP 72/58, HR 118, RR 32, SpO2 81% on room air

Initial Therpy? NSS wide, ABG, CXR

CXR

ABG: pH 7.18, Co2 68, O2 68, HCO3 18 Intubate Vitals: BP 82/68, HR 110, RR 12/12. start norepinephrine gtt Change IV include bicarbonate:

Sterile water with 3 amps sodium bicarbonate

¼ NSS with 2 amps of sodium bicarbonate

½ NSS with 1 amp of sodium bicarbonate

Labs

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Laboratory Evaluation

CBC/diff, CMP, lactic acid, UA, Urine and blood cultures Results:

Sodium: 154 Potassium: 5.4 Chloride: 113 Co2: 18 BUN: 112 Creatinine: 5.2 BUN/creat ratio =21 (> 20 prerenal) Lactic Acid 4.8 CPK 18,324

Evaluation of AKI

Prerenal: hypotensive, hypovolemic, sepsis Intrinsic: Rhabdomylosis, interstitial nephritis

UA: wbc 100, -leukocytes, -nitrate, WBC casts, Culture negative

Post renal: Obstruction Renal ultrasound with PVR:

R kidney 9.8cm, L kidney 8.9cm, increased cortical echogenicity, no bladder wall thickening, PVR 33cc.

-5 liters positive fluid balance/24 hours. CXR with pulmonary edema-IV furosemide initiated,

40mg IV, oliguric:80mg IV, oliguric,IV gtt at 10mg/hr initiated, nonoliguric,

CXR remains with pulmonary edema, by day 4, unable to wean from vent, initiate dialysis.

Day Day 1 Day 2 Day 3 Day 4BUN 112 106 102 108Creatinine 5.4 5.1 6.4 7.2Urine Output 468cc/24 hr 696cc/24 hr 1876 cc/24 hr 1272cc/24 hr

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-5 liters positive fluid balance/24 hours. CXR with pulmonary edema-IV furosemide initiated, 40mg IV, oliguric, 80mg IV, oliguric, IV gtt at 10mg/hr initiated, nonoliguric, CXR remains with pulmonary edema, by day 4, unable to wean from vent,

initiate dialysis.

Day Day 1 Day 2 Day 3 Day 4BUN 112 106 102 108Creatinine 5.4 5.1 6.4 7.2Urine Output 468cc/24 hr 696cc/24 hr 1876 cc/24 hr 1272cc/24 hr

Case #4, Evaluation of AKI in the Hospital

A 72 year old male with DM, HTN, hx of CAD with LAD stent placed in 2011, presents to the ER with left sided chest pain

Creatinine 2.2 (GFR 29 ml/min) baseline Creat 1.5 (GFR 39 ml/min) Plan for cardiac cath

Contrast induced nephropathy CIN - Contrast Induced Nephropathy

At risk: Existing CKD

289 patients with eGFR 30-59%, post exposure 4.2% developed AKI (Nijssen, 2017)

124 patients with creatinine >3, eGFR <30, 31% developed AKI (Rihal, 2002) type and amount of contrast; less if <125ml of low osmolar contrast Diabetic nephropathy; 250 pts with DN/creat >1.5, 33% AKI (Rudnick,

1995) Reduced renal perfusion: heart failure, hypotension, ACE, NSAID

Increased Cr of 0.5mg/dl or 25% 48hrs after contrast administration. Most patients are nonoliguic Urine studies benign vs muddy/granular casts associated with ATN Creatinine starts to decline 3-7days

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Prevention of CIN hold NSAIDs, metformin and diuretics for 24-48hrs. No evidence of holding

ACE beneficial Acetylcysteine — 1200 mg orally twice daily the day before and the day of

the procedure. Fluid administration — For all at-risk patients undergoing procedures involving

intra-arterial contrast administration, if there are no contraindications to volume expansion, we administer intravenous isotonic saline prior to and continued for several hours after contrast administration. No benefit to bicarbonate containing fluids over NSS.

●Outpatients ─ 3 mL/kg over one hour preprocedure and 1 to 1.5 mL/kg/hour during and for four to six hours postprocedure, with administration of at least 6 mL/kg postprocedure.

●Inpatients ─ 1 mL/kg/hour for 6 to 12 hours preprocedure, intraprocedure, and for 6 to 12 hours postprocedure.

Uptodate, 2017; AKI

Evaluation of AKI in the office

Acute, Subacute or Chronic Kidney Disease (CKD)? AKI develops in hours to days after insult. KDIGO stages 1-3 as

outlined earlier. Subacute defines a presentation that develops more slowly than

AKI, but results in elevated creatinine in less than three months. CKD is defined as an elevation in creatinine over more than three

months. NKF stages 1-5D as evidenced by reduced GFR/presence of kidney damage, ie albuminuria, abnormal findings on renal imaging present for more than three months.

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Evaluation of AKI in the office

Evaluation begins with careful history and physical exam Evaluation of lab results including duration of elevated creatinine,

assessment of GFR Careful examination of the urine with qualitative analysis (UA) and

microscopic exam Radiographic imaging Serologic testing and tissue diagnosis with kidney biopsy if indicated.

Evaluation of AKI in the office

If lab values not available for comparison Recent onset of symptoms or signs, ie sudden onset of anasarca or

discolored urine

Marked oliguria (urine output < 500cc/24 hr) or anuria (urine output < 100cc/24 hr)

Daily progressive increase in creatinine if serial labs drawn

Imaging showing small kidneys and increased echogenicity of renal parenchyma more likely CKD, normal sized kidneys with normal echogenicity less likely CKD but does NOT exclude.

Radiographic evidence of renal osteodystrophy.

Hou SH, Bushinsky DA, Wish JB. Am J Med 1983; 74: 243-8.Nash K, Hafeez A, Hou S. Am J Kidney Dis. 2002; 39: 930-6.

Kaufman J, Dhakal M, Patel B, Et al. Am J Kidney Dis 1991; 17: 191-8.

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Evalutation of Etiology: Office

Prerenal: Causes:

Overdiuresis, decreased oral intake, diarrhea, unreplensished insensible losses

decompensated heart failure/cardiorenal syndrome,

decompensated liver failure/hepatorenal syndrome,

NSAID causing afferent arteriole vasoconstriction, efferent vasoconstriction by renin-angiotensin system blockade, ACE-I, ARB

Evaluation of Etiology: office

Intrinsic: Renovascular: Atheroembolic disease, renal infarction, renal artery

aneurysm microangiopathy (hemolytic anemia/thrombocytopenic purpura TTP/hemolytic uremic syndrome HUS) scleroderma, malignant hypertension

Glomerular disease: Nephritic variable proteinuria, dysmorphic RBC, RBC casts

Nephrotic >3gm, active/inactive urine sediment

Interstitial: drug induced interstitial nephritis (WBC casts), cast nephropothy (multiple myloma) tumor lysis syndrome, acute urate nephropathy

Evaluation of etiology: office

Postrenal: Without history of CKD, reduced GFR suggests bilateral obstruction or

unilateral with known solitary kidney.

Stone, prostate or metastic obstruction most likely causes

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Clinical manifestations

Signs/symptoms related to reduced kidney function: edema, hypertension, decreased urine output. Weakness, fatigue, decreased appetite, dysguesia, mental status changes, seizures.

Symptoms often mild, severe symptoms as CKD progresses. Systemic symptoms such as fever, arthralgias and/or pulmonary

lesions suggestive of systemic disease such as vasculitis Livedo reticularis and splinter hemorrhages suggest atheroembolic

disease. Unilateral flank pain suggest obstruction, renal infarction or infection.

Initial evaluationMild injury: (<0.5 mg/dL above baseline creatinine)

Evaluate volume status, discontinue diuretics

repeat in 1-2 weeks, add UA, microalbumin/protein to creatinine ratio

evaluate for offending agents/etiology. Ie, NSAIDS, ACE-I, ARB, diuretics, PPI, hypotension, obstruction.

Initial Evaluation:Moderate injury (>0.5mg/dL)

Obtain UA, microscopy, renal US with PVR, microalbumin/creatinine ratio

Evaluate for Glomeruleronephritis, interstitial nephritis, ATN If no clear etiology, elevated creatinine, anemia, hypercalcemia,

SPEP, UPEP with immunofixation r/o myeloma Continued elevation of creatinine, no clear etiology, nephrology

evaluation, consider renal biopsy

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Case Study #5 68 yo male who presents to office with right knee pain after

completing yard work at home. Not worse in mornings, Increased pain with ambulation/stairs.

No clear effusion, edema or muscle abnormality on exam. Prescribed naproxyn 500mg twice daily. He returns with fatigue and weakness 2 weeks later. Labs:

Sodium 143 Co2 21

Potassium 5.6 BUN 31

Chloride 110 Creatinine 1.9

Labs: present, last office visit

Date 8/25/17 3/1/17BUN 31 23Creatinine 1.9 0.9GFR 32 ml/min 54 ml/mi

Medications: ASA, lisinopril, metoprolol, metformin, omeprazole, HCTZ

PE: Wt up 3 pounds, BP 110/70, HR 54Normocephalic, dry mucous membranes, no JVD, lungs clear to auscultation, S1, S2 reg, abdomen soft, trace edema.

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Differential Diagnosis

Prerenal: volume depleted with low BP on diuretic decreased cardiac output with bradycardia Naprosyn High risk for AKI given Diabetes, NSAIDS, ACE-I, diuretic

Intrinsic: NSAIDS Post renal: No s/sx urinary tract obstruction

Discontinue Naprosyn, HCTZ, ACE-I Repeat labs 2 weeks, consider restarting ACE-I. If no improvement, consider d/c omeprazole

Case study #6

87 year old presents to office for q 6 month appointment. Usual state of health, no change in medications, no illness, no

hospitalizations Medications: Lantus, glipizide, omeprazole, Lasix 20 qod, ASA 81,

metoprolol, levothyroxine Labs:

Sodium 148 Co2 18 Phos 5.2 Potassium 3.8 BUN 87 Ca 10.8

Chloride 108 Creatinine 2.6 GFR 16ml/min UA: sp grav 1.020, clear, no WBC, no Blood, no RBC, no Leuk, no nitrite, no bacteria, no

protein

cbc: wbc 4.5, rbc 2.1, hgb 8.4, hct 25

AKI evaluation

Prerenal: On diuretics

BUN/Creatinine ratio > 20

Intrinsic: On omeprazole, no new medications, UA bland

Post renal: Renal ultrasound without hydro, increased cortical echogenicity. R kidney 9.2cm, L kidney 10.3, no calculi

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Date 8/23/17 8/3/17 7/21/17 3/1/17 3/1/16BUN 48 56 87 23 25Creat 2.4 2.0 2.6 1.3 0.9GFR 17 22 16 37 57

Treatment Plan

Hold omeprazole, consider H2 Blocker Continue diuretics SPEP/UPEP with immunofixation Urine microscopy Refer to Nephrology

When to refer to Nephrology?

eGFR < 60 ml/min/1.73 m Multiple Risk Factors Heavy or Increasing proteinuria Uncontrolled hypertension Rapid progression or Acute Renal Failure

Target decline in GFR < 4 ml/min/1.73 m per year1

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Goals of Management in CKD Early identification and management of co-

morbid conditions. Early recognition of kidney disease Early referral to nephrology Early management of complications of CKD Empower patients through education to make

informed decisions in regards to their disease process, ability to impact disease progression and dialysis modality choice

Patient Education in CKD Education begins in primary care Continues through referral to Nephrology CKD Stage 1-3: CKD, risk factor reduction, co-

morbid disease management, CKD progression CKD Stage 4-5: Complications of CKD,

Signs/symptom management, Transplant, Dialysis Options Education, Fistula First/Vein preservation

RD, RN, NP, PA-C, MD and all staff empower patient to make a difference in the progression of their CKD.