a guide to detecting and delaying progress of chronic
TRANSCRIPT
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A GUIDE TO DETECTING AND DELAYING PROGRESS OF CHRONIC
KIDNEY DISEASERugmini Warrier, MD
Lincoln Nephrology and Hypertension
LEARNING OBJECTIVES
Describe screening tools, like GFR and ACR for early detection, diagnosis and monitoring of CKD
Define and classify CKD to guide treatment approaches
Recognize evidence-based management strategies that will help delay progression in at risk patients and improve outcomes
Referral criteria to nephrology
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WHAT IS CKD?
Group of disorders
Varying etiologies
Altered kidney (1) structure or (2) function
DEFINED BY:
National Kidney Foundation-Kidney Disease Outcome Quality Initiative : NKF-KDOQI 2002
Kidney Disease Improving Global Outcome: KDIGO 2009
1. Presence of Kidney damage (structure)
Imaging abnormalities: PKD, hydronephrosis
Lab abnormalities: Urinary sediment
Pathologic abnormalities: Kidney biopsy
Increased urinary albumin excretion
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2. Altered Kidney function
GFR: Glomerular filtration rate
Varies with age, gender, race, nutritional status
<60 ml/min/1.73 m2 is considered CKD
60 considered marker because...
Not one isolated GFR
Abnormal GFR lasting more than 3 months defines CKD
75% Labs report GFR along with creatinine
GFR
Sum of filtration rates of all nephrons together
True GFR measured by Iothalamate or Inulin
ESTIMATED GFR or eGFR from creatinine
Normal GFR: 130 ml/min/1.73 m2 for men and 120 ml/min/1.73 m2 for women
Decreases with age: 7.5 ml/min every decade of life
Normal GFR does not mean normal kidneys
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CREATININE
Derived from muscle metabolism
Released into blood at a constant rate
Freely filtered across glomerulus
Not metabolised by kidney
10% secretion by tubules
Affected by muscle mass
Variations can happen in production and secretion
GFR
GFR x Serum Creatinine=Urine volume x Urine creatinine
GFR= (Urine volume x Urine creatinine) / Serum creatinine
24 hour Urine creatinine clearance can be calculated
Usual daily creatinine excretion is 20-25 mg/kg
In practice we do creatinine and urea clearance in 24 hour urine volume
More cumbersome
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eGFR
Takes into account other variables that can affect creatinine generation
● Cockgroft-Gault Equation● MDRD Equation: Modification of Diet in Renal Diseases● CKD-EPI Equation● Cystatin C: low molecular weight protein, produced by all nucleated
cells, not affected by diet, filtered by glomerulus, not secreted
GFR Calculator | National Kidney Foundation
Average Measured GFR by Age in People Without CKD
Coresh J, et al. Am J Kidney Dis. 2003;41(1):1-12.
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GFR
Stable GFR does not mean stable disease. Can still have proteinuria
Normal GFR does not mean normal kidneys
GFR not accurate if not steady state, for example in hospitalized patients
Improvement of GFR does not mean improved kidneys in all cases. Could be loss of muscle mass, hyperfiltration…
GFR equations not very accurate in extremes of weight, transplant patients..
NKF recommends eGFR by CKD-EPI as more accurate
eGFR/ Creatinine ComparisonAge Sex Race SCr
mg/dleGFR ml/minper CKD-EPI
Weight in lbsHeight in Ft/in
eGFRAdj for BSA
25 M AA 1.6 68 2856’
97
49 F Hispanic 1.6 38 1805’4’’
41
67 M Asian 1.6 44 1555’8’’
46
92 F Caucasian 1.6 28 985’1’’
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Old Classification of CKD as Defined by Kidney Disease Outcomes Quality Initiative (KDOQI) Modified and Endorsed by KDIGO
Note: GFR is given in mL/min/1.732 m²National Kidney Foundation. KDOQI Clinical Practice Guidelines for Chronic Kidney Disease:
Evaluation, Classification, and Stratification. Am J Kidney Dis. 2002;39(suppl 1):S1-S266
Stage Description Classification by Severity
Classification by Treatment
1 Kidney damage with
normal or increased GFR
GFR ≥90
2 Kidney damage with
mild decrease in GFR
GFR of 60-89 T if kidney
transplant
3 Moderate decrease in GFR GFR of 30-59 recipient
4 Severe decrease in GFR GFR of 15-29 D if dialysis
5 Kidney failure GFR <15 D if dialysis
KDIGO, Kidney Disease: Increasing Global Outcomes
Assign GFR CategoryGFR Categories in CKD
Category GFR Terms Clinical Presentations
G1 ≥90 Normal or high Markers of kidney damage (nephrotic syndrome, nephritic syndrome, tubular syndromes, urinary tract symptoms, asymptomatic urinalysis abnormalities, asymptomatic radiologic abnormalities, hypertension due to kidney disease)G2 60-89 Mildly decreased*
G3a 45-59 Mildly to moderately decreased
· Mild to severe complications:o Anemiao Mineral and bone disorder
▪ Elevated parathyroid hormoneo Cardiovascular disease
▪ Hypertension▪ Lipid abnormalities
o Low serum albumin
G3b 30-44 Moderately to severely decreased
G4 15-29 Severely decreased
G5 <15 Kidney failure · Includes all of the above· Uremia
GFR = mL/min/1.73m2
*Relative to young adult levelIn the absence of evidence of kidney damage, neither GFR category G1 nor G2 fulfill the criteria for CKD.Refer to a nephrologist and prepare for kidney replacement therapy when GFR <30 mL/min/1.73m2.
Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. Kidney Int Suppls. 2013;3:1-
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ALBUMINURIA
Normal urine has small amounts of albumin <10 mg/day
Kidney disease can increase glomerular permeability
Spot ACR: Albumin/ Creatinine ratio: mg/gm
AER: Albumin excretion rate: 24 hour urine sample. Confirmation
First morning void is preferable
Nephrotic range proteinuria: >3.5 gm/day or UPCR > 3000 mg/g
• Normal AlbuminuriaAlbumin-to-creatinine ratio <30 mg/g creatinine
• Moderately Increased Albuminuria (Microalbuminuria)Albumin-to-creatinine ratio 30-299 mg/g creatinine24-hour urine albumin 30-300 mg/d
• Severely Increased Albuminuria (Macroalbuminuria)Albumin-to-creatinine ratio >300 mg albumin/g creatinine24-hour urine albumin >300 mg/d
• Proteinuria(+) urine dipstick at >30 mg/dl>200 mg protein/g creatinine
24-hour urine protein >300 mg/d
Definitions: Albuminuria and Proteinuria
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Assign Albuminuria Category
Albuminuria Categories in CKD
Category ACR (mg/g) TermsA1 <30 Normal to mildly increased
A2 30-299 Moderately increased*
A3 >300 Severely increased**
*Relative to young adult level. ACR 30-300 mg/g for >3 months indicates CKD.**Including nephrotic syndrome (albumin excretion ACR >2220 mg/g).
Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. Kidney Int Suppls. 2013;3:1-
CLINICAL EVALUATION OF A PATIENT WITH CKD
History
Physical Examination
Labs: RFP, Urine analysis, UPCR/ ACR
Special tests: Serology
Depending on CKD STAGE: PTH, Vit D, Phos
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●19
CKD or AKI from urinary obstructio• Voiding symptoms
Diabetics, older men,
anticholinergics, opiates
• Partial obstruction
Urine output variable
• Dx: Ultrasound
Kidney sizes normally 10-12 cm
< 10 cm implies CKD
• Rx: foley/nephrostomy tube
CKD Risk Factors
Modifiable
• Diabetes
• Hypertension
• History of AKI
• Frequent NSAID use
Non-Modifiable
• Family history of kidney disease, diabetes, or hypertension
• Age 60 or older (GFR declines normally with age)
• Race/U.S. ethnic minority status
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Classification of CKD Based on GFR and Albuminuria Categories: “Heat Map”
Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. Kidney Int Suppls.
Prognosis of CKD by GFRand Albuminuria Categories
Albuminuria categories
Description and range
A1 A2 A3
Normal to mildly
increased
Moderately
increased
Severely
increased
<30 mg/g
<3 mg/mmol
30‐299 mg/g
3‐29 mg/mmol
≥300 mg/g
≥30 mg/mmol
GFR
categor
ies
(mL/mi
n/1.73
m2)
Descrip
tion
and
range
G1 Normal or high ≥90
G2 Mildly decreased 60‐89
G3aMildly to moderately
decreased45‐59
G3bModerately to severely
decreased30‐44
G4 Severely decreased 15‐29
G5 Kidney failure <15
Green: low risk (if no other markers of kidney disease, no CKD); Yellow: moderately increased risk; Orange: high risk; Red, very high risk.
KDIGO 2012
Adjusted* Cardiovascular Mortality Risk by eGFR and albuminuria
*adjusted to the incidence rates of a 60 year-old, non-Hispanic white male
Astor et al. Am J Epidemiol 167:1226-1234 (2008)
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Reversible causes
• Decreased renal perfusion: Hypovolemia
Hypotension
NSAIDs, Diuretics
• Nephrotoxic drugs: Contrast, NSAIDs, Aminoglycosides, Bactrim, Vancomycin
• Urinary tract obstruction
Diabetes and hypertension are leading causes of kidney failure
Trends in (a) prevalent ESRD cases and (b) adjusted* prevalence of ESRD, per million, by primary cause of ESRD, in the U.S. population, 1980-2012.
Prevalent Cases Prevalence per million
*Point prevalence on December 31 of each year; Adjusted for age, sex, and race. The standard population was the U.S. population in 2011 ESRD patients
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HYPERTENSION CONTROL IN CKD
Present in 80-85% patients with CKD
Uncontrolled HTN increases proteinuria and CVS complications in CKD
Optimal BP uncertain
Target should be individualized
Volume expansion is a major contributor
Thiazides not used when GFR<30
HYPERTENSION CONTROL IN CKD
ACEI/ ARB: Proteinuric CKD. Diabetic or not
Non dihydropyridine CCB: Diltiazem and Verapamil has
antiproteinuric effect
Mineralocorticoid receptor antagonists: additive effect to
RAS inhibition
RAS inhibition effect less with high salt intake. Use salt restriction and diuretics
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HYPERTENSION CONTROL IN CKD
Type 1 Diabetes: ACEI
Type 2 Diabetes: ARB
Non Diabetic Proteinuria: ACEI or ARB
Non Proteinuric CKD(<500 mg/day): If edema, use diuretic. If not, any antihypertensive
NO ACEI/ ARB combination: More renal adverse effects, more hyperkalemia
Slowing CKD Progression: ACEi or ARB• Risk/benefit should be carefully assessed in the elderly and
medically fragile.
• Check labs 2 weeks after initiation.
If less than 25% SCr increase, continue and monitor.
If more than 25% SCr increase, stop ACEi and evaluate for RAS and volume contraction.
• Continue until contraindication arises, no absolute creatinine cutoff.
• Better proteinuria suppression with low Na diet and diuretics.
• Avoid volume depletion.1) Kunz R, et al. Ann Intern Med. 2008;148:30-48.2) Mann J, et al. ONTARGET study. Lancet. 2008;372:547-553.
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HYPERTENSION CONTROL IN CKD
Goal BP:
More intensive BP control slows down CKD progression in proteinuric patients, <130/80
SPRINT TRIAL: Excluded Proteinuric pts, Had CKD pts. No
difference in progression to ESRD. Actually there was increased risk of 30% decline in GFR
PKD trial: No difference in GFR decline between intensive BP
control(95-110) compared to less intensive(120-130)
Relationship Between Achieved BP and Decline in Kidney Function from Primary Renal Endpoint Trials
Update from Kalaitzidis R and Bakris GL In: Handbook of Chronic Kidney Disease. Daugirdas J (Ed.)
Nondiabetes
MDRD. N Engl J Med. 1993AIPRI. N Engl J Med. 1996 REIN. Lancet. 1997AASK. JAMA. 2002Hou FF, et al. N Engl J Med. 2006Parsa A et.al. NEJM 2013
Diabetes Captopril Trial. N Engl J Med. 1993 Hannadouche T, et al. BMJ. 1994 Bakris G, et al. Kidney Int. 1996 Bakris G, et al. Hypertension. 1997 IDNT. NEJM. 2001RENAAL. NEJM. 2001 ABCD. Diabetes Care (Suppl). 2000
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Managing Hyperglycemia
• Hyperglycemia is a fundamental cause of vascular complications, including CKD.
• Poor glycemic control has been associated with albuminuria in type 2 diabetes.
• Risk of hypoglycemia increases as kidney function becomes impaired.
• Declining kidney function may necessitate changes to diabetes medications and renally cleared drugs.
• Target HbA1c ~7.0%.
Can be extended above 7.0% with comorbidities or limited life expectancy, and risk of hypoglycemia.
NKF KDOQI. Diabetes and CKD: 2012 Update.Am J Kidney Dis 2012;60:850-856
Managing Hyperglycemia
SGLT 2: expressed in proximal tubules and mediates glucose reabsorption. SGLT 2 inhibitors: promote glucose excretion
Trials using Empagliflozin(JARDIANCE) and Canagliflozin(INVOKANA): secondary outcomes of incident/ worsening nephropathy was reduced in the drug group compared to placebo
Issues include: Urosepsis, Hypotension (osmotic diuresis, volume
contraction), AKI (especially in pts using diuretics or ACEI)
METFORMIN: Contraindicated if GFR<30ml/min/1.73 m2
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Lipid Disorders in CKD
A 32% reduction in LDL→17% reduction in primary outcome (nonfatal MI, coronary death, nonhemorrhagic stroke, arterial revascularization).
No reduction in CKD progression, overall or CAD mortality, other individual CAD end-points. Baigent C, et al. Study of Heart and Renal
Protection (SHARP) Lancet 2011;11:60739-
LIPID DISORDERS IN CKDCommonest is hypertriglyceridemia due to decreased clearance, also accelerated by secondary hyperparathyroidism
More risk in Diabetics and Nephrotic syndrome
Primary prevention in Non HD CKD pts controversial
CKD considered CAD equivalent
Treat with statins if CKD AND CAD
Fibrates need dose adjustment
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10-Year Coronary Risk Based on Age and Other Patient Characteristics
CABG, coronary artery bypass grafting; CHD, coronary heart disease; CKD, chronic kidney disease; CVA, cerebrovascular accident; DM, diabetes mellitus; MI, myocardial infarction; PTCA, percutaneous transluminal
i l t TIA t i t i h i tt k
1) Kidney Disease: Improving Global Outcomes (KDIGO) Lipid Work Group. Kidney Int Suppl. 2013;3:259-305.2) Hemmelgarn BR et al Overview of the alberta
Future 10-year coronary risk based on patient characteristics. Unadjusted rates from 1,268,029 participants.1,2
OTHER FACTORS FOR CKD PROGRESSION
Avoid NSAIDs
Avoid hypotension
Smoking cessation
Low sodium diet
Dose adjustment of renally excreted meds
Weight loss in obese patients
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Complications of Kidney Failure Start in Stage 3 and Progress
Kidney Failure
Malnutrition
Bone DiseaseBrittle bones and fractures Anemia/blood loss
Decrease production of red blood cells
Fluid OverloadWater Overload
Acid Base ImbalanceAcidic BloodElectrolyte Abnormalities
HypertensionCardiac DiseaseVascular Disease
Anemia in CKD• Due to decrease in Erythropoietin production
• Individualize erythropoiesis stimulating agents (ESA) therapy –Start ESA if Hb <10 g/dl, and maintain Hb <11.5 g/dl. Ensure adequate Fe stores.
Appropriate iron supplementation is needed for ESA to be effective.
• ESA usually not required for CKD related anemia until stage 4/5.
• Diagnostic workup of anemia is particularly important if severity of anemia is disproportionate to CKD staging.
• Important to avoid transfusion in transplant candidates.
If transfused use leukocyte filter to reduce HLA sensitization.
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CKD-Mineral Bone Disorder (MBD) Testing
CKD StageCalcium,
PhosphorusPTH
25(OH)D
Stage 3 Every 6-12 monthsOnce then based on
CKD progression
Once, then based on level and treatments
Stage 4 Every 3-6 months Every 6-12 months
Stage 5 Every 1-3 months Every 3-6 months
Use CKD progression, presence or absence of abnormalities, treatment response, and side effects to guide testing frequency.
CKD-MBD: Chronic Kidney Disease – Mineral and Bone
CKD-MBD
• Treat with D3 as indicated to achieve normal serum levels.
• 2000 IU D3 po qd is cheaper and better absorbed than 50,000 IU of D2 monthly dose.
• Limit phosphorus in diet, with emphasis on decreasing packaged products - Refer to renal RD.
• May need phosphate binders.
• DEXA doesn’t predict fracture risk in CKD 3-5.
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Metabolic acidosisTendency to retain hydrogen ions when GFR falls. Often becomes
apparent at GFR <25-30 ml/min/1.73m2.
More severe with higher protein intake.
May contribute to bone disease, protein catabolism, decreased myocardial contractility, malaise, hypotension and progression of CKD.
Sodium bicarbonate causes less volume overload than sodium chloride (reason unknown)
3 times more risk of GFR decline if HCO3 less than 25 compared to HCO3 >25 in AASK trial
Fruits and Vegetables diet
Metabolic Acidosis.
• Correction of metabolic acidosis may slow CKD progression and improve patients functional status.1,2
eGFR 15-30 ml/min/1.73m2
Bicarbonate 16-20 mmol/L; treated with sodium bicarbonate for 2 years.2
1) Mahajan, et al. Kidney Int. 2010;78:303-309.2) de Brito-Ashurst I et al J Am Soc Nephrol 2009;20:2075-
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Metabolic Acidosis• Maintain serum bicarbonate > 22 mmol/L.
Start with 0.5-1 mEq/kg per day.Sodium bicarbonate tablets:• 325mg, 625 mg tablets; 1 g = 12 mEq.
Sodium citrate solution: • 1 mEq/ml.• Avoid if on aluminum phosphate binders.
Baking soda:• 54 mmol/level tsp(54mEq).
Chronic Management of Hyperkalemia• Loop or thiazide diuretics.• Laxatives:
As effective as cation exchange resins in sorbitol.
Those that induce secretory diarrhea may be more effective (e.g. bisacodyl).
• Cation exchange resins:
Sodium polystyrene sulfonate (KAYEXALATE)
Mechanism: Bound Na+ exchanged for K+ in colonic/ rectal lumen. Likely: Accompanying sorbitol induces diarrhea.
• Patiromer: a non-absorbed, cation exchange polymer that contains a calcium-sorbitol counterion, increases fecal potassium excretion through binding of potassium in the lumen of the gastrointestinal tract
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Risk Factors for Infection in People with CKD
• Advanced age
• High burden of coexisting illnesses (e.g., diabetes)
• Hypoalbuminuria
• Immunosuppressive therapy
• Nephrotic syndrome
• Uremia
• Anemia and malnutrition
• High prevalence of functional disabilitiesKidney Disease: Improving Global Outcomes
(KDIGO) CKD Work Group. Kidney Int Suppls. 2013;3:1-150.
Vaccination in CKD• Annual influenza vaccine for all adults with CKD, unless
contraindicated.
• Polyvalent pneumococcal vaccine when eGFR <30 ml/min/1.73m2 and at high risk of pneumococcal infection (e.g., nephrotic syndrome, diabetes, receiving immunosuppression), unless contraindicated. Offer revaccination within 5 years.
• Hepatitis B immunization when GFR <30 ml/min/1.73m2. Confirm response with appropriate serological testing.
• Use of a live vaccine should consider the patient’s immune status (e.g., immunosuppression).
Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. Kidney Int Suppls. 2013;3:1-150.
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Key Points on Medications in CKD • CKD patients at high risk for drug-related adverse events.
• Several classes of drugs renally eliminated.
• Consider kidney function and current eGFR (not just SCr) when prescribing meds.
• Minimize pill burden as much as possible.
• Remind CKD patients to avoid NSAIDs.
• No Dual RAAS blockade.
• Any med with >30% renal clearance probably needs dose adjustment for CKD.
• No bisphosphonates for eGFR <30 mL/min/1.73m2.
• Avoid GAD for eGFR <30 mL/min/1.73m2.
Common Medications Requiring DoseReduction in CKD
• Allopurinol
• Gabapentin
o CKD 4- Max dose 300mg qd
o CKD 5- Max dose 300mg qod
• Reglan
o Reduce 50% for eGFR< 40
o Can cause irreversible EPS with chronic use
• Narcotics
o Methadone and fentanyl best for ESRD patients
• Lowest risk of toxic metabolites
• Renally cleared beta blockers
o Atenolol, bisoprolol, nadolol
• Digoxin
• Some Statins & Fibrates
o Lovastatin, pravastatin, simvastatin. Fluvastatin, rosuvastatin
• Antimicrobials
o Antifungals, aminoglycosides, Bactrim, Macrobid
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Education and Counseling• Ethical, psychological, and social care (e.g., social bereavement, depression,
anxiety).
• Dietary counseling and education on other lifestyle modifications (e.g., exercise, smoking cessation).
• Involve the patient, family and children if possible.
• Offer literature in both traditional and interactive formats.
• Use educational materials written in the patient’s language.
• Assess the need for low-level reading materials.
• Use internet resources and smartphone apps as appropriate.
• Use visual aids such as handouts, drawings, CDs, and DVDs.
• Involve other health care professionals in educating patients/families.
• Be consistent in the information provided.
Mental Health Counseling• Psychiatric illnesses like depression are associated with many
chronic diseases.
• Depression is linked to early CKD, progressive CKD, kidney failure, hospitalization and increased mortality. 1-4
• Patients with GFR <60 mL/min/1.73m2 should undergo regular assessment for impairment of functioning and well-being.5
1) Palmer S, et al. Am J Kidney Dis. 2013;62:493-505. 2) Hedayati S, et al. Am J Kidney Dis. 2009;54(3):424-32. 3) Kimmel P, et al. Kidney Int. 2000;57:2093-2098.4) Tsai Y, et al. Am J Kidney Dis. 2012;60:54-61.
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Kidneydamage and
normal or ↑ GFR
Kidneydamage and
mild ↓
GFR
Severe↓ GFR
Kidneyfailure
Moderate ↓ GFR
Stage 1 Stage 2 Stage 3 Stage 4 Stage 5
NephrologistPrimary Care Practitioner
The Patient (always) and other subspecialists (as needed)
GFR 90 60 30 15
Who Should be Involved in the Patient Safety Approach to CKD?
Patient safety
Consult?
Impact of Primary Care CKD Detection with a Patient Safety Approach
Fink et al. Am J Kidney Dis. 2009,53:681-
Ideal Patient Time-Course
FollowingCKD detection
Improved diagnosis creates opportunity for strategic preservation of kidney function.
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Indications for referral to Nephrology
• eGFR <30 ml/min/1.73m2• ACR >300mg/g• Hematuria not due to urological conditions• Urinary sediment abnormalities• Inability to identify a cause for CKD• Serum K >5.5 mEq/L• Resistant hypertension (4 or more agents)
Indications for referral to Nephrology
• Recurrent or extensive nephrolithiasis• Hereditary kidney disease• Atypical progression of CKD: rapid drop of >25 %
decline of GFR or >5ml/min/1.73m2 drop in GFR/year
• Difficult to manage complications like anemia, hyperphosphatemia or volume overload
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Observational Studies of Early vs. Late Nephrology Consultation
Chan M, et al. Am J Med. 2007;120:1063-1070.http://download.journals.elsevierhealth.com/pdfs/journals/0002-9343/PIIS000293430700664X.pdfKDIGO CKD Work Group Kidney Int Suppls 2013;3:1
Additional Online Resources for CKD Learning• National Kidney Foundation: www.kidney.org
• United States Renal Data Service: www.usrds.org
• CDC’s CKD Surveillance Project: http://nccd.cdc.gov/ckd
• National Kidney Disease Education Program (NKDEP): http://nkdep.nih.gov
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Case Question 1
Which of the following patients have CKD?
1. 50 year old male with Type 2 diabetes, eGFR 32ml/min/1.73 m2 and ACR<30mg/g
2. 50 year old male with Type 2 diabetes, eGFR 50 ml/min/1.73 m2 and ACR 1500mg/g
3. 30 year old male Type 1 diabetes, eGFR 120 ml/min/1.73 m2 and ACR 500mg/g
4. 30 year old female, no diabetes, creatinine 1.0, eGFR 120ml/min/1.73 m2, urine analysis showing 3+protein and red cell casts
5. 30 year old female s/p renal transplant, creatinine 0.86. All of the above
Case Question 2
A 55 year-old Caucasian-American man, with a history of type 2 diabetes (15 years), hypertension (3 years) dyslipidemia (5 years) and cardiovascular disease (myocardial infarction 3 years ago). He was recently diagnosed with CKD. His most recent labs reveal an eGFR of 45 ml/min/1.73m2 and an ACR of 38 mg/g. Which of the following should be avoided?A. ACE and ARB in combination
B. Daily low-dose aspirin
C. NSAIDs
D. Statins
E. A and C
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Case Question 3
Which of these patients should be treated with ARB?( if no allergy)
1. 50 year old male with Type 2 diabetes, eGFR 32ml/min/1.73 m2 and ACR<30mg/g, BP 156/94mmHg
2. 50 year old male with Type 2 diabetes, eGFR 50 ml/min/1.73 m2 and ACR 1500mg/g, BP 156/94mm Hg
3. 30 year old male Type 1 diabetes, eGFR 120 ml/min/1.73 m2 and ACR 500mg/g, BP 156/94mmHg
4. 50 year old male, non diabetic, BP 156/94mm Hg, hypertensive nephrosclerosis, creatinine 1.5, ACR <30 mg/g
5. All of the above6. All except 4
Case Question 4
All of the following adult patients should be referred for nephrology consultation, EXCEPT?
A. Initial visit: eGFR 26 & 3 months later: eGFR 28 (mL/min/1.73m2)
B. Initial visit: eGFR 55, & 3 months later: eGFR 43 confirmed with repeat eGFR 45 (mL/min/1.73m2)
C. Initial visit: ACR 450 & 3 months later: ACR 355 (mg/g) on both dates the eGFR >60 mL/min/1.73m2
D. Initial visit: eGFR >60 & 3 months later: eGFR >60 (mL/min/1.73m2) with personal history of Autosomal Dominant Polycystic Kidney Disease
E. Initial visit: eGFR 42 & 3 months later: eGFR 44 (mL/min/1.73m2) on both dates the ACR <30 mg/g
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TAKE HOME POINTS
Assess GFR and proteinuria as tools to detect CKD
Identify factors to prevent progression
PCP to co manage complications of CKD
Referral to Nephrology when appropriate
References
Dr Michael Choi, NKF president
Dr Les Spry, MD. Lincoln Nephrology
NKF educational resources
Online: uptodate.com
Various Journals