Nephrology - Chronic Kidney Disease

7/27/2019 Nephrology - Chronic Kidney Disease

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What you need to know about

CKD in the primary care setting

M3 renal session


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A 54-year-old woman with an 11-year history of type 2diabetes presents for care. She was first noted to haveproteinuria 4 years earlier; her serum creatinine level then

was 1.1 mg per deciliter (97 mol per liter). Her urinaryprotein excretion has progressively increased to 2.8 g per24 hours, and her serum creatinine level to 3.1 mg perdeciliter (274 mol per liter). The estimated glomerularfiltration rate (GFR) is 26 ml per minute per 1.73 m2 ofbody-surface area. Her blood pressure is 155/90 mm Hg,and the glycated hemoglobin level is 7.6 mg per deciliter.The medications she is currently taking include an oralhypoglycemic agent, an angiotensin-convertingenzyme (ACE)inhibitor, a statin, and a thiazide diuretic. How should hercase be managed?

Abboud and Henrich, Stage IV CKD, N Engl J Med 2010;362:56-65.


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Does a patient with proteinuria for >3months but GFR > 90 ml/min have CKD?

Stages of CKD

Stage Description GFR

(ml/min/1.73 m2)

1 kidney damage, nl/GFR 902 kidney damage, mild GFR 60-893 moderate GFR 30-594 severe GFR 15-295 kidney failure


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ScreeningThe Seventh Report of the Joint National Committee

on Prevention, Detection, Evaluation and Treatment of

High Blood Pressure (JNC 7) and the AmericanDiabetes Association recommend

testing adults with high blood

pressure or diabetes for chronic kidney disease

Is undirected screening recommended? NO


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Lab evaluation in CKD Estimate GFR

Check serum electrolytes Examine urine sediment and dipstick

Random microalbuminuria/proteinuriadetermination

Image kidneys


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Estimate creatinine clearanceHow best to estimate kidney function?

Timed 24 hour urine collections should beabandoned Fraught with inaccuracies/incomplete collections

limiting interpretation

serum creatinine is not accurate indicator of GFRmuscle mass

agediet

gender

race


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Important points Serum creatinine may remain normal despite

substantial kidney damage

Minor elevations in cr may signify significantreductions in GFR

Rate of GFR decline is highly variable among ptsand must be determined on an individual basis

CKD is an insidious problem,

often no overt symptoms


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Evaluation and Treatment of CKD Specific therapy for kidney dx

Assess medication dosages/toxicities Slowing progression of kidney dx

Complications of kidney dx

Manage comorbidities

Addressing cardiovascular risk and dx Behavioral modifications

Arranging RRT


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At what stage docomplications of CKDoccur?

At what stage do youimplement strategiesto slow progression?


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Question

Which of the following has been shown to retardprogression of renal disease?

A. Control of BP

B. Smoking cessation

C. Control of proteinuria with ACE

inhibitors/ARBsD. Glycemic control

E. Control of anemia

F. Correction of dyslipidemias


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Clinic Guidelinesfor patients with CKD

All CKD patients, approaching but not yet ondialysis, have several basic problems that should

be addressed at each clinic visit, relating to boththe attendant complications of CKD and thestrategies employed to delay progression of CKD.

Since their last clinic visit we assess each of these

components and the efficacy of their currenttherapy to reach recommended therapeutictargets.


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Issues in the CKD patient Strategies to retard

progression Optimizing HTN control

Reducing proteinuria Optimizing glycemic control Treating anemia Treating dyslipidemia

Managing CKDComplications HTN

Volume overload Anemia Secondary

hyperparathyroidism Acid base disturbances

(metabolic acidosis) Electrolyte disturbances

(hyperkalemia,hyponatremia).


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Threshold for Initiation of Treatmentand Target Values: JNC VII

Condition Initiation Target

SBP/ DBPmmHg

SBP/ DBPmmHg

Pre-Hypertension 120-139/80-89 Lifestyle Modif

Diastolic systolic HTN 140/90 160


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Impact of Mean Follow-up SBPon Risk of Renal Endpoint

180

Average Follow-up Seated Systolic Blood Pressure (mm Hg)

-1.1

-0.6

-0.1

0.4

0.9

1.4

ln(RelativeRiskofRenalE

ndpoint)

IDNT Study Group


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Number of Antihypertensive AgentsRequired to Reach Target BP

KDOQI clinical practice guidelines and clinical practice recommendations fordiabetes and CKD. Am J Kidney Dis 49 (Suppl 2): S1-S179, 2007.


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Hypertension Is blood pressure in target range according to JNC

VII guidelines? Systolic


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Proteinuria

Control of proteinuria is an important strategy todelay progression of CKD, reduce cardiovascular

risk and prevent further renal damage. Is the patients proteinuria


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Screen for proteinuria

Urine dipstick If positive, quantitate proteinuria

Spot (random) urine Prot:Cr ratio 200mg/gm

If negative in high risk patients (DM, HTN),

search for microalbuminuria

microalbumin: 25-200 mg/g creatinine


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Example

How much proteinuria would a patient have withthe following urinary findings on random specimen?

1 gram protein1 gram creatinine


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Proteinuria is a strong independentrisk factor for developing ESRD

2+

3+

(Iseki et al, KI 63 (2003), 1468-1474)


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Relative risk forkidney disease progression

Jafar et al, Ann Intern Med 139 (4), 2003, p244-252.


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Benefits of ACE-I or ARBs Diabetic renal diseases

Nondiabetic renal diseases

Pharmacologic inhibition of RAAS slows progressionof renal failure in chronic proteinuric nephropathies

ACE inhibitors

Angiotensin Receptor Blockers

Role of spironolactone in resistant HTN and proteinuria

When are the effects of ACE -I to decreaseproteinuria apparent?

2-3 mths after initiation of therapy


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Question

What is an acceptable increase in serum creatinine in apatient with more advanced kidney disease (GFR < 60ml/min) after starting treatment with an ACE inhibitor

or ARB?

A. 10%

B. 20%

C. 30%D. 40%

E. 50%

From Managing CKD: Key Therapeutic Issues, CJASN, January 2008, vol 3, suppl 1.

Palmer, Angiotensin converting enzyme inhibitors and angiotensin receptro blockers: what to do if theserum creatinine and/or serum potassium concentration rises, NDT 2003, 18, pp1973-5


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Question

Which of the following is not a side effect of adrug that is used to interfere with the Renin-Angiotensin-Aldosterone system?

A. Gynecomastia

B. Cough

C. Angioedema

D. Peripheral edema

E. Hyperkalemia


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Which is better at reducingproteinuria?

ACE inhibitor at supramaximal dose

ARB at supramaximal dose

ACE inhibitor + ARB ACE inhibitor + spironolactone


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Issues in the CKD patient Strategies to retard

progression Optimizing HTN control

Reducing proteinuria Optimizing glycemic control Treating anemia Treating dyslipidemia

Managing CKDComplications HTN

Volume overload Anemia Secondary

hyperparathyroidism Acid base disturbances

(metabolic acidosis) Electrolyte disturbances

(hyperkalemia,hyponatremia).


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Stage GFR Metabolic consequences

1 90

2 60-89 Hyperparathyroidism

3 30-59 Impaired Ca absorption

MalnutritionLVH developsOnset of anemia

4 15-29 Hyperphosphatemia developsMetabolic acidosisTendency to hyperkalemia

5


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Anemia(Target Hgb 11-12)

Have any signs or symptoms of anemiadeveloped?

Have there been any blood losses (occultGI bleeding) or other causes of anemia?

Have hemoglobins been stable?

Is the patient on synthetic erythropoietin(Procrit or Aranesp)?

Are the iron stores adequate (ferritin 100

ng/mL, TSAT 20%)?


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Effects of anemia in CKD Cardiovascular

LVH regression

Decrease mortality

Quality of life

Cognitive function

Physical function/exercise performance

Quality of sleep Predictive risk factor for morbidity/mortality

???correction slows progression of renal dx


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Metabolic Bone Disease

Have recent calcium, phosphorus, alkalinephosphatase, and PTH been assessed and havechanges occurred since the last visit?

Have bone pain or pathologic fracturesdeveloped?

Is patient on phosphorus binders?

Is the patient compliant with a low phosphorusdiet? Has patient seen a dietician?


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Control of Hyperphosphatemia,

Hyperparathyroidism and Hypocalcemia

1) DIET: reduce dietary P intake

2) BINDERS: prevent gut absorption of P with binders

1) Calcium based if Ca1) Phoslo (calcium acetate)2) Tums (calcium carbonate)

2) Non-calcium, non-aluminum based if normal serum Ca1) Sevelamer (Renagel)2) Lanthanum (Fosrenol )

3) Prevent severe secondary hyperparathyroidismand attendanteffluxes of P and Ca from bone1) Rx elevated PTH with Vitamin D/Vitamin D analogues


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Hyperphosphatemia:

associated mortality risk (ESRD)

Block et al, 1998


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Metabolic acidosisIncreases bone resorption and stimulates

bone turnoverIncreases protein degradationAssociated with muscle wasting and

weakness

Aim for serum HCO3 is > 22 mmol/L

Use supplementsbaking soda (50 meq/tsp)sodium bicarbonate tabs (650 mg tab = 8.5 meq)

Recommended dose: 0.5-1.0 meq/kg/d


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Managing co-morbidities

After you have reviewed these problems, you willneed to assess other concurrent problems andtheir impact on the management of chronic kidney

disease (i.e. diabetes mellitus, CHF, angina,cardiovascular disease, hyperlipidemia, peripheralvascular disease, emotional problems, etc.)


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Risk Factors for CVD Classical Risk Factors Hypertension

DM Poor metabolic control

Lipid abnormalities

Male sex

Smoking Family history

CKD


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Dyslipidemia

Prevalence of hyperlipidemia is increased in CKD GFR < 50-60, prevalence of lipid abnormalities is 30%

Some observational studies in diabetic andnondiabetic nephropathy link hyperlipidemia toprogression of renal disease

NKF CV task force: every patient with ckdshould be screened for hyperlipidemia Diet, exercise, drugs NCEP ATP III guidelines


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30-20-10 rule

30 refer to Nephrologist

20 place access

10 initiate dialysis


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Early identification & comprehensivetreatment plan for pts with CKD

Timely introduction of therapies to slowprogression of CKD

Management of common complications of CKD Anemia Renal osteodystrophy Metabolic acidosis

Identification and management of the

comorbidities DM Hypertension

Smooth transitions to RRT

Nephrology - Chronic Kidney Disease

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