Download CKD talk[1].15.09 - Jacobi Medical Center

Chronic Kidney
Disease/Dialysis
Belinda Jim, MD
January 15, 2009
Definition

NKF’s (National Kidney Foundation’s) K/DOQI
(Kidney Disease Outcomes Quality Initiative) Work
Group criteria for CKD are:
 Kidney damage for >3months, 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 the imaging tests.
OR
 GFR < 60ml/min/1.73m2 for >3months
Causes of ESRD
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Regardless of acute or chronic, should calculate
renal function by eGFR
Used to evaluate extent of impairment, follow
course of disease and response to therapy
Dose adjustments
Equations to Estimate GFR

Gold Standard – inulin clearance, I-iothalmate, TcDTPA clearance. These tests are not uniform.
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Cockcroft-Gault equation (140-age) x wt/ 72 x SCr. (x 0.85 for women).
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MDRD (Modification of Diet in Renal Disease) –
Abbreviated version
 186 x SCr. To power of -0.203 (x 0.742 if female)
and (x1.210 if black).

24 hr. Urine for Cr.Cl –
 GFR = UCr.V/PCr x 0.70 (to convert to ml/min)
CKD Staging and Prevalence
CKD
Stage
GFR
(mL/min/1.73 m2)
Number of
Individuals
1
90 and evidence of kidney
damage
5.6 million
2
60-89 and evidence of kidney
damage
5.7 million
3
30-59
7.4 million
4
15-29
300,000
5
<15 or dialysis
431,284
Coresh et al , J Am Soc Nephrol, 2005; 16: 180-188
Data supplied by USRDS 2004 Annual Data Report.
Natural History of Renal Disease
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Initial injury may vary in pathogenesis
Kidney adapts by increasing filtration rate in remaining
normal nephronsadaptive hyperfiltration
Long-term damage, manifested by proteinuria and
progressive renal insufficiency
Gradual decline usually asymptomatic
No exact correlation between level of BUN and
symptoms
Uremic symptoms: anorexia, nausea, vomiting, fatigue,
hiccups, pruritis
General Management

Treatment of reversible causes
Decreased renal perfusion
 Administration of nephrotoxic drugs
 Urinary tract obstruction
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Prevention or slow the progression
Treatment of complications
Identification and adequate preparation of renal
replacement therapy (RRT)
Factors Affecting Progression of
CKD
Non-Modifiable Risk Factors:
 Age – incidence climbs after 65
 Gender – more common in males with a
faster rate of decline.
 Race – incidence higher in AA and
Hispanics.
 Genetics – diabetic and non-diabetic
nephropathies cluster in families.
Modifiable Risk Factors
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Proteinuria – aim for <500mg/24hr.
Hypertension – aim for <130/80 or MAP <90
with ACE I/ARB.
Glycemic control – Evidence is conflicting in
progression of CKD.
Dyslipidemia – elevated levels associated with
more rapid decline – esp in DN.
Obesity - linked to faster rate of progression in
CKD.
Hyperuricemia – May cause renal injury and HTN
through stimulation of renin-angiotensin system.
Treatment of Complications
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Volume overload
Hyperkalemia
Metabolic acidosis
Hyperphosphatemia
Anemia
Hyperparathyroidism
Bone disease
Uremic symptoms
Volume Overload
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Sodium and intravascular volume balance usually
maintained until GFR falls below 10 to 15
ml/min
Mild to moderate CKD less able to respond to
rapid infusions of sodium, prone to overload
Respond to combination of dietary sodium
restriction and diuretic therapy
Hyperkalemia
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Problem with
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Aldosterone
Distal flow in kidney (eGFR<10 -15ml/min).
Patient is either:
 Oliguric.
 Has high K diet.
 Has increased tissue breakdown.
 Has Hypoaldosteronism (eg. ACE Inhibitors,
type IV RTA).
Treatment consists of low K diet (2gm/day),
diuretics and kayexalate.
Ion transport in collecting tubule cell
Metabolic Acidosis
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Increasing tendency to retain H+
Decreased HCO3-, usually between 12-20meq/L
Bone buffering of excess H+ ions associated with
release of Ca2+ and Phos from bone
Uremic acidosis increase skeletal muscle breakdown
and diminish albumin synthesis loss of lean muscle
mass and fatigue
Sodium bicarbonate or sodium citrate to keep HCO3
above 22meq/L
Secondary Hyperparathyroidism
Treatment of Secondary Hyperparathyroidism
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Phosphate binders:
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Ca based:
 CaCO3
 Ca acetate
 Non absorbable agent:
 Sevelamer Hydrochloride (Renagel)
 Sevelamer Carbonate (Renvela)
 Lanthanum carbonate (Fosrenol)
 Aluminum binders.
Vitamin D analogs:
 Calcitriol (Rocaltrol)
 Paricalcitol (Zemplar)
 Doxercalciferol (Hectoral)
Calcimimetic: Cinacalcet (Sensipar)
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Low Phos diet (<800 mg/day)
Renal Osteodystrophy
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Types of Bone Disease
Osteitis fibrosa
 Osteomalacia
 Adynamic bone disease
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Target PTH
Stage 3 (GFR 30-59): 35-70 pg/mL
 Stage 4 (GFR 15 to 29): 70-110 pg/mL
 Stage 5 (GFR less than 15): 150-300 pg/mL
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Metastatic Calcification
Hypertension
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Mostly volume mediated
Start with ACEI/ARB and diuretic
Thiazides become ineffective when GFR falls
below 20
Goal is less than 130/80, but even lower systolic
with urine prot/creat >1
Anemia in CKD
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The primary cause of anemia in patients
with CKD is insufficient production of
erythropoietin (EPO) by the diseased
kidneys.
Other causes include:
 Iron deficiency.
 Secondary hyperparathyroidism.
 Decreased RBC lifespan.
 Folate deficiency.
K/DOQI Guidelines for Anemia in CKD
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Target Hgb between 11-12 g/dL
Anemia work-up when
 Hgb <11g/dL (Hct is <33 percent) in premenopausal females and pre-pubertal patients.
 Hgb <12g/dL (Hct is <37 percent) in adult
males and post-menopausal females.
Use of erythropoietic agents
(Epo,Procrit,Aranesp)
Dyslipidemia
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Primary finding in CKD is hypertriglyceridemia
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Goal of LDL in CKD in similar to CHD – LDL
<100, but there is not much evidence whether this
is beneficial.
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One large study in CKD Stage V showed a
negative association with very low cholesterol
levels
Preparation for Renal Replacement Therapy
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Refer to nephrology when GFR < 60
Early education of CKD
Choice of renal replacement therapy
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In-center hemodialysis
Peritoneal dialysis
Home hemodialysis
Access placement
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Referral to vascular surgery of AVF placement if patient
choses HD and advising patient to save non-dominant arm
from venopuctures and heplocks.
What is Dialysis?
Initiation of Emergent Dialysis
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Uremic syndrome
Refractory volume overload
Uncontrollable hyperkalemia
Severe metabolic acidosis
Steady worsening of renal function, with
BUN exceeding 70-100 mg/dL or creatinine
clearance of less than 15-20 ml/min/1.73 m2
Diffusion
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Transport process by which a solute passively diffuses
down its concentration gradient from one fluid
compartment into the other
Dialysis Membrane
Contents of Dialysate Solution
Ultrafiltration (UF)
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Fluid removal occurs via hydrostatic pressure
gradient across membrane generated by dialysis
machine
Peritoneal Dialysis (PD)
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Uses peritoneal
membrane to transport
solutes and water across
two compartments
One compartment is
blood in the peritoneal
capillaries, second
compartment is dialysate
solution in peritoneal
cavity
Continuous Renal Replacement
Therapies (CRRTs)
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Slower rate of solute or fluid removal per unit
of time
Slower blood flow rate for the hemodynamically
unstable patient
Better tolerated than conventional therapy
Complications
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Hypotension
Infection
Catheter Dysfunction
Hypotension
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Common Causes
Fluctuations in UF rate
High UF rate
Target dry weight set too low
Dialysis solution too warm
Food ingestion
Autonomic neuropathy
Antihypertensive medications
Hypotension-Cardiac
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Diastolic dysfunction due to LVH, ischemic
heart disease
Failure to increase cardiac rate
Inability to increase cardiac output for other
reasons
Hypotension
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Less common reasons
Pericardial tamponade
 Myocardial infarction
 Arrhythmia
 Occult hemorrhage
 Dialyzer reaction
 Hemolysis
 Air embolism
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Dialysis Catheter Infections
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Localized exit site infection
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Tunnel Infection
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Erythema and/or crust, no purulent discharge, treat with
antibiotics for up to 2 weeks
Purulent exudate present, and pain/warmth along the tunnel,
removal of catheter with antibiotic administration for 3
weeks
Systemic Infection
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Fever, leukocytosis, may have no overt signs of catheter
infection
Microbiology
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Staph species (40-81%)
Enterococci, gram neg organisms, fungal
organisms
Empiric treatment with Vancomycin and
Gentamicin
Treat with Nafcillin if MSSA!
Complications of Catheter Infection
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Endocarditis
Osteomyelitis
Thrombophlebitis
Spinal epidural abscess
Catheter Dysfunction
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Early
less than 5 days
 Due to malposition or to intracatheter thrombosis
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Fibrin sleeves and mural thrombi
Treatment
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Catheter exchange
TPA
Catheter Dysfunction
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Late (more than 5 days)
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More likely due to intracatheter thrombosis than
malposition
Treatment
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TPA
Catheter exchange
Vascular Access
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Permanent catheter
AV graft
AV fistula
Permanent Catheter
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Cuffed venous catheters an alternative form of
long-term access
High rate of complications
Thrombosis
 Infection
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Inadequate blood flow
AV Graft
Advantages
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AV connection made using a tube graft from
synthetic material
Maturation requires 2-3 weeks for adhesion of
subcutaneous tunnel and graft
Disadvantages
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Higher rates of infection
Higher rates of thrombosis
Shorter lifespan
AV fistula
Advantages
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Subcutaneous anastomosis of artery to adjacent vein
Safest longest lasting permanent access
Excellent patency
Lower morbidity
Lower complication
Disadvantages
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Long maturation time
Failure to mature in some patients
May not be feasible in patients with vascular disease