Embed Size (px)
DESCRIPTION
Citation preview
MANAGEMENT OF THE PATIENT WITH CHRONIC KIDNEY DISEASE
Medicine Housestaff Conference
2/13/2009
Margaret A Kiser MD PhD,
Outline Chronic Kidney Disease
Definitions Epidemiology
Screening for CKD Treating Complications of Advanced CKD
Hypertension Control of volume Alterations in bone metabolism Anemia Nutrition Hyperkalemia
Suggested K-DOQI action plan based on disease severity When to refer and why Slowing Progression of CKD Evidence supporting antihypertensive use Cardiovascular Risk Modification Getting the word out
What is Chronic Kidney Disease?
Defining CKD
Kidney damage for 3 months as defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifest by either: Pathological abnormalities; or Markers of kidney damage, including abnormalities in the
composition of the blood or urine, or abnormalities in imaging testing
Glomerular Filtration Rate (GFR) < 60 ml/min/1.73 m2 for 3 months, with or without structural kidney damage
Estimates of U.S. Chronic Kidney Estimates of U.S. Chronic Kidney Disease Population in 2000Disease Population in 2000
19,000,000
Chronic KidneyDisease
372,000
Dialysis80,000
Transplant
Stages of CKDStages of CKD
Proposed NKF-K/DOQI Guidelines. NKF Clinical Nephrology Meetings 2001; Orlando, Fla.
50 40 30 20 <15
GFR (mL/min/1.73 m2)
1
Kidney Damage
2
Mild GFR
3
Moderate GFR
4
Severe GFR
60708090
5
KidneyFailure
CKD Continuum
“CKD” ESRD
6
RRT
Prevalence of CKDPrevalence of CKD
11 Kidney damageKidney damage > 90> 90**** 10,25910,259 5.8 5.8
22 Mild GFR Mild GFR 60 – 8960 – 89**** 5,300 – 7,100 5,300 – 7,100 3 – 43 – 4
33 Moderate GFR Moderate GFR 30 – 5930 – 59****** 7,5537,553 3.3 3.3
44 Severe GFR Severe GFR 15 – 2915 – 29 363363 0.2 0.255 Kidney failureKidney failure < 15 or dialysis< 15 or dialysis 300300 0.1 0.1
12.4 – 12.4 – 13.413.4
GFR Prevalence in US Pop.* Stage Description (mL/min/1.73 m2) N (1,000s) %
*Population of 177 million adults age over 20
** with presence of proteinuria or hematuria +/- structural changes
*** do not need proteinuria or hematuria, just GFR <60
AGE AND RACEAGE AND RACE
Further, African Americans develop ESRD at a Further, African Americans develop ESRD at a younger age 55.8 vs 62.2 yoyounger age 55.8 vs 62.2 yo
Although only 12.6% of the US population, African Although only 12.6% of the US population, African Americans constitute 50% of the ESRD populationAmericans constitute 50% of the ESRD population
CaucasianCaucasian HispanicHispanic Native Native AmericanAmerican
African African AmericanAmerican
1151/1151/millionmillion
2243/2243/millionmillion
2669/2669/millionmillion
4863/4863/millionmillion
Point prevalence of ESRD
USRDS 2007 Annual Report AJKD 51, Suppl 1, Jan 2008
Familial InfluencesFamilial Influences
Inherited NephropathiesInherited Nephropathies Family history is a strong risk factor for diabetic Family history is a strong risk factor for diabetic
nephropathynephropathy In all ethnic groups studied to date diabetic In all ethnic groups studied to date diabetic
siblings of pts with ESRD 2/2 DM were at siblings of pts with ESRD 2/2 DM were at markedly increased risk of developing ESRD.markedly increased risk of developing ESRD.
Particularly common in African Americans with an Particularly common in African Americans with an increased incidence rate of 4-25 fold greater increased incidence rate of 4-25 fold greater than Caucasiansthan Caucasians
AJKD 2008, 51 (1), 29-37
Etiology of Chronic Kidney DiseaseEtiology of Chronic Kidney Disease
Diabetes43%
HTN25%
GN12%
Other20%
DiabetesHTNGNOther
USRDS 2001
Identifying patients at risk:National Kidney Foundation Recommendations
(KDOQI)
Individuals at increased risk for CKD should be tested at the time of health evaluations to determine if they have CKD. This should include patients with:- DM HTN Autoimmune diseases Chronic systemic infections Recovery from acute renal failure Age > 60yrs Family history of kidney disease Exposure to drugs or procedures associated with an acute decline in
kidney function Kidney donors and transplant recipients
(AJKD, 39, 2002, pS214)
Relationship of Serum Creatinine to GFR
Estimation of GFR
GFR can be assessed by the renal clearance of a substance
Clearance of substance X (Cx) = UxVx/Sx
Recall GFR * Sx = UxVx
(amount filtered = amount excreted) Cx = UxV/Sx
Cx = GFR
Two important assumptions: Marker neither secreted or absorbed Steady state
Examples of markers: inulin, iothalamate, iohexol, serum creatinine, cystatin-C
Calculation of GFR
Methods of calculation Cockcroft-Gault formula MDRD formula/modified MDRD
The Cockcroft-Gault calculation
GFR ml/min/1.73m2 = (140-age) x Lean BW Kg
72 x S creatinine mg%
( x 0.85 for Females )
MDRD GFR Formula*170 x [SCr]-0.999 x [Age]-0.176 x
[0.762 if female] x [1.180 if black] x [Alb]+0.318
Modified MDRD Formula186.338 x [SCr]-1.154 x [Age]-0.203 x
[1.212 if black] x [0.742 if female]
MDRD GFR
*From Levey et al, 1999Ann Intern Med 130: 461-470
(A calculator may be found at www.hdcn.org)
84 F 22 M 66 M 66 F
• Wt (kg) 45.5 104.5 77.2 71.8
• Screat 1.2 1.2 1.2 1.2
• eGFR
26.9 142.7 66.1 52.3
(Calculated with Cockcroft-Gault)
Urine Protein / Creatinine Ratio
Based on the assumption that in the presence of stable GFR, urine creatinine and protein excretion constant
Ginsberg et al first demonstrated a strong correlation between single Urine P/C and 24 h urine in 46 ambulatory patients at a single center, r=0.97
Important caveats Lean body mass Timing of urine collection
Relationship of spot and 24 urine protein
Group A: Low creatinine excretion, slope=1.11Group B: Intermediate Cr excretion, slope=0.97Group C: High Cr excretion, slope = 0.77
Fig 1 Correlation between ln spot morning urine protein:creatinine ratio and log 24 hour urinary protein in 177 non-diabetic patients with chronic nephropathies and persistent clinical proteinuria
Physiologic Changes in ChronicPhysiologic Changes in ChronicKidney DiseaseKidney Disease
Increased single nephron GFRIncreased single nephron GFR Afferent arteriolar vasodilationAfferent arteriolar vasodilation Intraglomerular hypertensionIntraglomerular hypertension Loss of glomerular permselectivityLoss of glomerular permselectivity Inabilty to appropriately dilute or Inabilty to appropriately dilute or
concentrate the urine in the face of concentrate the urine in the face of volume challengevolume challenge
Anatomic and Histologic Features Due Anatomic and Histologic Features Due to to
Glomerular HypertensionGlomerular Hypertension
Glomerular hypertrophyGlomerular hypertrophy Focal segmental glomerulosclerosis with Focal segmental glomerulosclerosis with
hyalinosishyalinosis Interstitial fibrosisInterstitial fibrosis Vascular sclerosisVascular sclerosis Epithelial foot process fusion Epithelial foot process fusion
Pathogenesis of Secondary Pathogenesis of Secondary GlomerulosclerosisGlomerulosclerosis
Nephron Mass
Glomerular Volume andGlomerular Hypertension
Epithelial Cell Density andFoot Process Fusion
Glomerular Sclerosisand Hyalinosis
Primary Insult
Proteinuria
Hypertension in CKD
Recommendations for Anti-Recommendations for Anti-hypertensives in Patients with Chronic hypertensives in Patients with Chronic Kidney DiseaseKidney Disease
Treatment is indicated at any stage of the diseaseTreatment is indicated at any stage of the disease Use drugs that lower glomerular capillary pressure Use drugs that lower glomerular capillary pressure
(ACE inhibitors, ARB, verapamil and diltiazem) (ACE inhibitors, ARB, verapamil and diltiazem) Goal is to keep the blood pressure < 130/80 mmHg Goal is to keep the blood pressure < 130/80 mmHg
(< 120 SBP in DM)(< 120 SBP in DM)
Effects of Various Anti-hypertensives Effects of Various Anti-hypertensives on Glomerular Capillary Pressureon Glomerular Capillary Pressure
AfferentArteriole
Efferent Arteriole
DihydropyridinesNifedipineFelodipineAmlodipine
Vasodilate Pressure
ARBVerapamilDiltiazem
Vasodilate
Pressure
Vasoconstrict
ACE-I
Number of Medications to Achieve Goal Number of Medications to Achieve Goal BP in 5 Trials of DM/Renal DiseaseBP in 5 Trials of DM/Renal Disease
3.8
3.3
3.6
2.8
2.7
0 1 2 3 4
AASK (<92 mm Hg MAP)
HOT (<80 mm Hg DBP)
MDRD (<92 mm Hg MAP)
ABCD (< 75 mm Hg DBP)
UKPDS (<150/85 mm Hg)
Number of BP Meds
Bakris. J Clin Hypertens 1999;1:141.
A Hierarchy of AgentsA Hierarchy of Agents
ACE-IARB
-BlockersThiazide Diuretics
Vasodilators- Blockers
Central Agents
CCB’s
More PreferredMore Preferred
Less PreferredLess Preferred
Volume Management-Diuretics
% Filtered Na+
Site of Action Diuretic Excreted
Na+-K+-2Cl- carrier Furosemide in Loop of Henle Bumetanide 20 %
TorsemideEthacrynic acid
Na+-Cl- carrier Thiazides 3-5 % in the distal tubule Metolazone
Na+ channel in the Amiloride 1-2 % cortical collecting Triamterene duct Spironolactone (indirect)
Natriuretic Response to Furosemide at Different Levels of Renal Function
GFR 150 ml/min GFR 15 ml/min
1250 mEq 125 mEq
250 mEq 25 mEq
Diuretic Tolerance
Type I: Short-term Decrease in the response to a diuretic after the
first dose Teleologically-- appropriate response to
volume depletion
Type II: Long-term Hypertrophy of distal nephron segments
allowing greater sodium resorption
Algorithm for Diuretic Use
Renal Insufficiency CrCl < 50
•Loop Diuretic•Determine Effective Dose: 5-10X Usual Dose•Administer as Frequently as Necessary
Thiazide According to CrCl< 20ml/min 20-50 > 50ml/min
50-100mg/ 50-100mg/ 25-50mg/ day day day
ADD
Add Distal Diuretic DrugFrom Brater DG N Eng J Med 1998;339:387
Alterations in Bone and Mineral Metabolism
PTH
Pi Ca2+
Renal Mass
25(OH)D3 1,25(OH)2D3
1-alpha-hydroxylase1-alpha-hydroxylase
+
Acidosis
+
Hyperparathyroid Related Bone Disease
ImpairedAbsorption
Osteitis FibrosaCystica
Reduced Renal Mass
GFR
< 65
<40
<25
Increased PTH Secretion
Decreased 1,25-D
Hyperphosphatemia
Hypocalcemia
Calcium and Phosphorus Balance:National Kidney Foundation Recommendations
(KDOQI) In addition, it has become clear that CKD patients have a nutritional
deficiency of 25-OH Vitamin D which itself leads to an increase in PTH secretion
Levels of 25-OH D should be measured when PTH-Intact >70pg/ml and supplementation instituted if necessary, a level of <30ng/ml is abnormal and <15ng/ml, moderate to severe
Treatment <5ng/ml 50,000U Ergocalciferol/wk x12, then q mo x6 5-15ng/ml 50,000/wk x 4, then q mo x 6 16-30ng/ml 50,000/month x 6
Measure 25(OH)-D at 6months Maintenance 800-1200 IU qd
(AJKD, 39, 2002, pS214)
Calcium and Phosphorus BalanceKDOQI Recommendations
Stage 3 CKD, GFR 30-Stage 3 CKD, GFR 30-5959
Measure Ca, Phos and Measure Ca, Phos and PTH-I every 12 monthsPTH-I every 12 months
Target levelsTarget levels Calcium WNL for labCalcium WNL for lab Phos > 2.7- 4.6 mg/dLPhos > 2.7- 4.6 mg/dL Ca X Phos < 55Ca X Phos < 55 PTH-I 30-70 pg/mlPTH-I 30-70 pg/ml
Stage 4 CKD, GFR 15-29Stage 4 CKD, GFR 15-29 Measure Ca, Phos and Measure Ca, Phos and
PTH-I every 3 monthsPTH-I every 3 months Target levelsTarget levels
Ca preferably WNL for labCa preferably WNL for lab Phos > 2.7-</= 4.6mg/dLPhos > 2.7-</= 4.6mg/dL Ca X Phos < 55Ca X Phos < 55 PTH-I 70-110 pg/mlPTH-I 70-110 pg/ml
Calcium and Phosphorus BalanceKDOQI Recommendations
How are these goals achieved ? Control of dietary phosphorus intake to 0.8-1g/d May need initiation of “Phosphate binders” with meals When 25(OH)-D >30pg/ml and PTH-I > target, initiate
treatment with exogenous “Active Vitamin D” A few patients with very elevated PTH-I values may
benefit from Calcimimetics
(AJKD, 39, 2002, pS214)
Calcium and Phosphorus Balance:Limit Phosphorus intake to 0.8-1.0 g/d
High Phosphorus FoodsHigh Phosphorus Foods Dairy products (Cheese, ice cream, milk), Dairy products (Cheese, ice cream, milk),
nuts, peanut butter, biscuits, processed nuts, peanut butter, biscuits, processed meats-hotdogs, chocolate, dark sodas (Coke, meats-hotdogs, chocolate, dark sodas (Coke, Pepsi), beans Pepsi), beans
Lower Phosphorus ChoicesLower Phosphorus Choices Cream cheese, sour cream, Ginger ale/sprite, Cream cheese, sour cream, Ginger ale/sprite,
sherbet, non-dairy creamersherbet, non-dairy creamer
Use of Phosphate binders
Given with meals, timing essential Given with meals, timing essential Aluminum based medicines; (Basaljel, Amphogel)Aluminum based medicines; (Basaljel, Amphogel) Calcium BasedCalcium Based
Calcium Carbonate/Magnesium Carbonate (Magnebind)Calcium Carbonate/Magnesium Carbonate (Magnebind) Calcium Carbonate (Tums, Calcichew, Calcimix) Calcium Carbonate (Tums, Calcichew, Calcimix) Calcium Acetate (Phoslo)Calcium Acetate (Phoslo)
Use of Phosphate binders
The use of calcium based binders is now falling out of favor The use of calcium based binders is now falling out of favor because of the recognition of accelerated vascular calcification because of the recognition of accelerated vascular calcification proposed to be associated with them (Disputed by the proposed to be associated with them (Disputed by the manufacturers of same)manufacturers of same) Sevelamer hydrochloride (“Renagel”), cationic polymer, binds Sevelamer hydrochloride (“Renagel”), cationic polymer, binds
phosphate thru’ ion exchange, can promote/worsen metabolic acidosisphosphate thru’ ion exchange, can promote/worsen metabolic acidosis
New product Sevelamer carbonate (“Renvela”) does not lead to New product Sevelamer carbonate (“Renvela”) does not lead to acidosisacidosis
Lanthanum carbonate (“Fosrenol”), long term effects unknownLanthanum carbonate (“Fosrenol”), long term effects unknown
VERY EXPENSIVE (Sevelamer 800mg tab $1.93 each, dose varies 3-VERY EXPENSIVE (Sevelamer 800mg tab $1.93 each, dose varies 3-9 tabs a day, $173-521 each month, Fosrenol 1000mg tab $4.87 each, 9 tabs a day, $173-521 each month, Fosrenol 1000mg tab $4.87 each, dose 3 tabs daily, $438 each month)dose 3 tabs daily, $438 each month)
Vitamin D Sterols
Several Vitamin D sterols are now available to Several Vitamin D sterols are now available to replace naturally occurring 1,25 Vitamin - Dreplace naturally occurring 1,25 Vitamin - D3 3 , ,
levels of which fall with declining renal masslevels of which fall with declining renal mass
Rocaltrol (Calcitriol, oral)Rocaltrol (Calcitriol, oral) Doxercalciferol (Hectoral , DDoxercalciferol (Hectoral , D22 prohormone, available prohormone, available
in oral and parenteral forms)in oral and parenteral forms) Paracalcitol (Zemplar), oral and parenteral forms Paracalcitol (Zemplar), oral and parenteral forms
available available
KDOQI Recommendations for use of Vitamin D sterols
In compliant patients with stable renal function, Initiate “Active Vitamin D” (1,25-OH D3) supplements
when: 25-(OH)D > 30pg/ml, PTH-I >target, Ca < 9.5, Phos > 4.6
Calcitriol 0.25-1.0 mcg po qd (Rocaltrol) Doxercalciferol 2.5-10 mcg po tiw (Hectoral) Paracalcitol 1-4 mcg po qd (Zemplar)
Check Ca and Phos q month x 3months then q 3 months and check PTH-I q 3 months
Monitor closely because of the significant risk of developing hypercalcemia
(AJKD, 39, 2002, pS214)
The CalcimemeticsThe Calcimemetics
CalciumSensing Receptor(CaR)
Cinacalcet (Sensitizes CaR to Ca2+)
Nucleus
VDR
Vitamin D
Serum Calcium
PTH
Inhibitory
StimulatoryCellularProliferation
The parathyroid cell
Treatment of Secondary Treatment of Secondary HyperparathyroidismHyperparathyroidism
Calcimimetic agentsCalcimimetic agents Rapid onset (hours)Rapid onset (hours) Inhibit PTH secretionInhibit PTH secretion Inhibit PTH synthesisInhibit PTH synthesis Inhibit parathyroid Inhibit parathyroid
cellular proliferationcellular proliferation Decrease serum Decrease serum
calciumcalcium
Vitamin D SterolsVitamin D Sterols Act on genomic Act on genomic
receptorreceptor Slow onset (days to Slow onset (days to
weeks)weeks) Inhibit PTH synthesisInhibit PTH synthesis Increase serum Increase serum
calciumcalcium
Phosphorus
Ca2+
1,25(OH)2D3
(Use Cautiously)
New Paradigm in Treatment of Secondary Hyperparathyroidism
Non-calciumBased Binders
Cinacalcet
PTH
Complications of Long Term Calcium and Phosphorus imbalance
Tertiary hyperparathyroidismTertiary hyperparathyroidism Renal osteodystrophyRenal osteodystrophy
DemineralizationDemineralization Bone painBone pain FracturesFractures
Systemic toxicitySystemic toxicity Cutaneous - CalciphylaxisCutaneous - Calciphylaxis Cardiovascular, accelerated vascular calcificationCardiovascular, accelerated vascular calcification NervousNervous
ParathyroidectomyParathyroidectomy
IndicationIndication Bio-Intact PTH > 800 pg/mL refractory to Bio-Intact PTH > 800 pg/mL refractory to
medical therapymedical therapy Severe hypercalcemiaSevere hypercalcemia Progressive high turnover bone diseaseProgressive high turnover bone disease
ComplicationsComplications May result in excessive low PTH levelsMay result in excessive low PTH levels Symptomatic hypocalcemiaSymptomatic hypocalcemia Risk for injury to recurrent laryngeal nerveRisk for injury to recurrent laryngeal nerve
Anemia of Chronic Kidney DiseaseAnemia of Chronic Kidney Disease
Develops when the GFR decreases to < 30-35 ml/min Develops when the GFR decreases to < 30-35 ml/min decreasing production of erythropoietin 2/2 reduced renal decreasing production of erythropoietin 2/2 reduced renal
massmass Uremic inhibition of bone marrowUremic inhibition of bone marrow Decreased RBC life-spanDecreased RBC life-span PTH induced marrow fibrosisPTH induced marrow fibrosis Iron deficiencyIron deficiency Aluminum related bone diseaseAluminum related bone disease
Normochromic, normocyticNormochromic, normocytic
Why Treat Anemia?
Levin et al. Levin et al. Am J Kidney DisAm J Kidney Dis. 1996;27:347-354.. 1996;27:347-354.
P P = 0.0062= 0.0062
==1g/dL 1g/dL decrease decrease
in Hgbin Hgb
6%6%increaseincreasein risk of in risk of
LVH LVH
175-Patient CKD Study175-Patient CKD Study
Anemia-Treatment Guidelines
Goal Hgb 11-12Goal Hgb 11-12 Recombinant erythropoeitinRecombinant erythropoeitin
Epogen/Procrit 50-150 U/kg/wk SQEpogen/Procrit 50-150 U/kg/wk SQ Darbopoetin alfa (ARANESP) Start 0.45mcg/kg SQ once every 2 Darbopoetin alfa (ARANESP) Start 0.45mcg/kg SQ once every 2
weeks, usually dosed every three to four weeks when patient is weeks, usually dosed every three to four weeks when patient is stable in the therapeutic rangestable in the therapeutic range
Recent concerns re increased risk of cardiovascular events Recent concerns re increased risk of cardiovascular events associated with an elevated Hgb in association with use of high associated with an elevated Hgb in association with use of high doses of these productsdoses of these products
IronIron Goal Ferritin >200, TSAT >20%Goal Ferritin >200, TSAT >20% Oral agentsOral agents
Chromagen: 33% ironChromagen: 33% iron Ferrous sulfate: 20% ironFerrous sulfate: 20% iron Niferex (Polysaccharide with Vit C): 150mg elemental ironNiferex (Polysaccharide with Vit C): 150mg elemental iron Ferrous fumurate: 33% ironFerrous fumurate: 33% iron Ferrous gluconate (Fergon): 12% ironFerrous gluconate (Fergon): 12% iron
Oral agents do not work well, primarily b/o ill tolerated GI side Oral agents do not work well, primarily b/o ill tolerated GI side effectseffects
Nutrition
Balancing the impact of decreased protein intake on the rate of progression of renal disease, against hypoalbuminemia and malnutrition
Can we restrict protein intake sufficiently, without leading to malnutrition, especially important in patients with eGFR < 25 ml/min
Serum Albumin at the Start of Dialysis in the U.S. ESRD Population
Obrador et al. J Am Soc Nephrol 1999; 10; p. 1795
15%
22%
30%
23%
10%
0%
5%
10%
15%
20%
25%
30%
35%
<2.5 2.6 - 3.0 3.1 - 3.5 3.6 - 4.0 4.1+
Serum Albumin (g/dL)
Mean 3.2 +/- 0.7Median 3.3
Serum Albumin Concentration (gm/dl) Odds Ratio of Death
Lowrie, Seminars in Dialysis. Vol 10, No 2 (Mar-Apr) 1997, p. 116
1994 Data
< 2.5 2.5-3.0 3.0-3.5 3.5-4.0 4.0-4.5 >4.50.5
0.7
1.0
1.5
2.02.53.0
4.05.06.0
8.010.012.014.0
Albumin (gm/dl)
Od
ds
Ra
tio
of
De
ath
Albuminunadj.
Case Mixadj.
Case Mix+ Lab adj.
Reference
are not different fromBars without symbols
= p < .05 = p < .01
Reference
0
Hyperkalemia
A common reason for initiation of RRT
The kidney is the only route for excretion of dietary intake, thus there is limited excretion as GFR falls, potentially leading to increased serum levels
Many patients with CKD also have a tendency to retain potassium because of stimulation of the Renin/Angio/Aldo system
Diabetics may have a type IV RTA (hyporeninemic hyperaldosteronism)
Use of ACE-I can exacerbate hyperkalemia
Hyperkalemia
TreatmentTreatment
Restriction of intakeRestriction of intake DiureticsDiuretics Kayexelate, long term use can lead to colonic mucosal Kayexelate, long term use can lead to colonic mucosal
defectsdefects
HyperkalemiaHigh Potassium foods
Fruits Vegetables Other foods
Apricot Artichoke Bran/bran products
Avocado Asparagus Coffee, Tea
Banana Beans Chocolate
Cantaloupe, Honeydew Brussel sprouts Coconut, Granola
Dates,Figs, dried fruits Lentils, legumes Molasses
Mango,Papaya Limas, Peas, Okra Milk, Ice cream
Orange, Nectarine Parsnips, Rutabaga Nuts/seeds
Peaches, Prunes Potatoes Snuff/chewing tobacco
Raisins, Persimmons Tomatoes Salt subs/Lite salt
Juices of these Winter squash
fruits Salt free veg. juice
HyperkalemiaLow Potassium foods
Fruits Vegetables StarchesApples/applesauce Broccoli Rice
Blackberries Beans, green/wax Noodles
Blueberries/Cranberries Beets/carrots/corn Bread/bread products
Cherries/grapes/gooseberries Cabbage/cauliflower Cereals
Fruit cocktail Cucumber, lettuce Cakes, cookies
Pears, canned/pineapple Eggplant/onions Pies (not chocolate or
Plums/raspberries/Strawberries Summer squash high K fruit)
Mandarin oranges/Tangerines Mushrooms, raw
Rhubarb, Watermelon Parsley, radish, turnip
Juices of these fruits Greens (collards, kale
turnip, mustard)
Peas, green
Cardiovascular Risk
Individuals with CKD are at increased risk for CVD, they Individuals with CKD are at increased risk for CVD, they should be considered in the “highest risk group for should be considered in the “highest risk group for evaluation and management” according to NKF evaluation and management” according to NKF recommendations.recommendations.
Remember, there are an estimated 7.5 million people in Remember, there are an estimated 7.5 million people in the US with stage 3 CKD and 363,000 at Stage 4 CKD the US with stage 3 CKD and 363,000 at Stage 4 CKD but only 372,00 on dialysis with only a further 80,000 but only 372,00 on dialysis with only a further 80,000 having received a kidney transplant. having received a kidney transplant.
If we consider the patients at Stages 3 and 4, they have If we consider the patients at Stages 3 and 4, they have a higher risk of death than progressing to need for a higher risk of death than progressing to need for dialysis !!!!dialysis !!!!
When to Refer to Nephrology:When to Refer to Nephrology:General IndicationsGeneral Indications
Serum Creatinine >/= 1.7 mg/dl (M) and >/= Serum Creatinine >/= 1.7 mg/dl (M) and >/= 1.4 (F)1.4 (F)
Poorly controlled HTNPoorly controlled HTN Diabetes mellitus with atypical renal Diabetes mellitus with atypical renal
manifestationsmanifestations Proteinuria or nephrotic syndrome without Proteinuria or nephrotic syndrome without
retinopathyretinopathy Renal insufficiency without proteinuria or retinopathyRenal insufficiency without proteinuria or retinopathy Sudden onset of nephrotic syndrome or rapidly Sudden onset of nephrotic syndrome or rapidly
changing serum creatininechanging serum creatinine Systemic disease associated with renal Systemic disease associated with renal
involvementinvolvement Heavy proteinuriaHeavy proteinuria Urine-sediment abnormalitiesUrine-sediment abnormalities PriorPrior to onset of uremic symptoms to onset of uremic symptoms
Goals of Early ReferralGoals of Early Referral
Patient education, soon Medicare Patient education, soon Medicare reimbursement for CKD education reimbursement for CKD education Choice of modality: HD vs PD vs TransplantChoice of modality: HD vs PD vs Transplant Planning of vascular access if HD is the Planning of vascular access if HD is the
chosen intervention and catheter placement chosen intervention and catheter placement if PDif PD
Planning of timing of transplantation work-Planning of timing of transplantation work-upup
Institution of interventions to slow progression Institution of interventions to slow progression of renal diseaseof renal disease
Avoidance of acute exacerbation of function
Volume depletion IV Radiographic contrast Gadolinium Aminoglycosides and amphoterecin NSAIDS/COX II inhibitors (Tordal) ACE-I/ARB in certain populations CyA / Tacrolimus in the transplant population Obstructive uropathy
Stage 1: GFR > 90
Stage 2: GFR 60-89
Stage 3: GFR 30-59
Stage 4: GFR 15-29
Stage 5: GFR < 15
K-DOQI Action Plan for the Management of CKD
Clinical evaluationSlowing ProgressionCVD Risk Reduction
ReplacementTherapy
Symptom control &preparation for replacement therapy
Slowing ProgressionCVD Risk ReductionTreat Complication
In Summary: Important Early Conservative Therapies
ACE Inhibitor, Angiotensin II Receptor Antagonist, and Beta Blocker ACE Inhibitor, Angiotensin II Receptor Antagonist, and Beta Blocker Therapy, to control HTNTherapy, to control HTN
Adequate volume control with diureticsAdequate volume control with diuretics Early Treatment of hyperphosphatemia with Phosphate binders Early Treatment of hyperphosphatemia with Phosphate binders Early Treatment with Active Vitamin D Early Treatment with Active Vitamin D Early Treatment with Erythropoietin/Darbepoetin (PROCRIT/ARANESP)Early Treatment with Erythropoietin/Darbepoetin (PROCRIT/ARANESP) Early Treatment with Iron ProductsEarly Treatment with Iron Products Aggressive control of glucose levels in DiabeticsAggressive control of glucose levels in Diabetics
THE END
