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CHRONIC K I DNEY D I SEASE. Gülçin Kantarcı, MD Yeditepe University Department of Internal Medicine Division of Nephrology. REFERENCE &SUGGESTED READING .

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chronic k i dney d i sease

CHRONIC KIDNEY DISEASE

Gülçin Kantarcı, MD

Yeditepe University

Department of InternalMedicine

Division of Nephrology

reference suggested reading
REFERENCE &SUGGESTED READING
  • CurrentMedicalDiagnosisandTreatment, Maxine A. Papadakis, Stephen J. McPhee, Eds. Michael W. Rabow, Associate Ed. http://accessmedicine.comChapter22. KidneyDisease
  • http://www.uptodate.com .(Definition andstaging of chronickidneydisease in adults, Screeningforchronickidneydisease, Epidemiology of chronickidneydisease)
aims objectives
AIMS & OBJECTIVES

State

  • the definition,
  • pathophysiology,
  • clinical findings and
  • prevention methods of chronic kidney disease.
slide4

Chronickidney disease (CKD)

Chronic kidney disease is defined based on the presence of either kidney damage or decreased kidney function for three or more months, irrespective of cause.

End-StageRenalDisease(ESRD)

AdvancedCKDrequiringrenalreplacementtherapy (RRT) in ordertomaintain life.

slide7

CKD Prevalence

CKD Incidence

Prevalence is estimated to be 8—16% worldwide

pathophysiology of ckd
Pathophysiology of CKD

Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR

Loss of

nephron

mass

Structural and functional

hypertrophy of the

remaining nephrons

Glomerular

Hyperperfusion

Hyperfiltration

Hypertension

Restoration

of

GFR

slide12

Chronic renal failure represents the end result of conditions that greatly reduce renal function by destroying renal nephrons and producing a marked decrease in the glomerular filtration rate (GFR).

glomerular ultrafiltration
GLOMERULAR ULTRAFILTRATION

Glomerular capillaries

Oncotic

Pressure

Hydraulic

Pressure

  • Rate of glomerular plasma flow
  • Total surface area

+

  • Decreased GFR is expectedwhen
  • Glomerularhydraulicpressure is 
  • Tubulehydraulicpressure is 
  • Plasmacolloidpressure 
  • Renal (glomerular) bloodflow 
  • Permeability is 
  • Filtrationsurfacearea 

HydraulicPressure

Bowman’s capsule

slide14

hyperfiltration without

serious adverse

consequences

Loss of 50% of

the total

nephron mass

Loss of > 50% of

the total

nephron mass

Over time: proteinuria

Focal and segmental

glomerulosclerosis

Compensatory

Adaptive responses

Maladaptive

responses

mechanisms of progressive renal scarring
Mechanisms of progressiverenalscarring
  • Glomerulosclerosis
  • Tubulointerstitalscarring
  • Vascularsclerosis
glomerulosclerosis
GLOMERULOSCLEROSIS

Glomerular

Hyperperfusion

Hyperfiltration

Hypertension

  • in renal

functional

mass

  • Endothelial &
  • epithelial injury
  • Transudation of
  • macromolecules
  • into mesangium

Progressive

mesangial expansion

GLOMERULOSCLEROSIS

tubulointerstitial scarring
Tubulointerstitial Scarring

Injuredtubular

cells

Inflammatorymediators

Chemokines

Cytokines

Growthfactors

Inflammatory

cells 

 SynthesisECM

TUBULOINTERSTITIAL FIBROSIS

vascular sclerosis
VascularSclerosis
  • Afferentarteriolarhyalinosis
    • Glomerularsclerosis
  • Postglomerulararterialhyalinosis
    • Interstitialischemiaandfibrosis
    • Damagetoperitubularcapillaries
factors affecting the progression of ckd
FactorsAffectingTheProgression of CKD
  • Nonmodifiablesusceptibilityfactors
  • Age
  • Gender
  • Genetics
  • Race
  • Initiationfactors
  • Glomerulonephritis
  • TIN
  • Hypertension
  • Diabetes
  • Dyslipidemia
  • Modifiable risk factors
  • ?
modulating factors of progressive renal scarring
Modulatingfactors of progressiverenalscarring
  • Genetic/Racial/ gender-related
  • Systemicandintraglomerularhypertension
  • Thedegree of proteinuria
  • Intrarenaldeposition of Ca, P, urate
  • Hyperlipidemia (LDL)
  • Use of NSAIDs(Pginhibitors)
  • High protein diet
  • Persistentmetabolicacidosis
  • Extent of tubulointerstitialdisease
screening for chronic kidney disease
Screening for chronic kidney disease

patients who are at risk for developing CKD should be screened with both

  • a urine test for proteinuria and
  • a blood test for creatinine to estimate glomerular filtration rate (GFR).
  • Risk factorsfor CKD
  • History of diabetes, cardiovascular disease, hypertension, hyperlipidemia, obesity, metabolic syndrome, smoking, human immunodeficiency virus (HIV) or hepatitis C virus infection, and malignancy
  • Family history of kidney disease
  • Treatment with potentially nephrotoxic drugs
diagnosis of ckd
DIAGNOSIS OF CKD
  • Careful history taking and physical examination
  • Assessment of renal function by estimation of the glomerular filtration rate (GFR)
  • Careful examination of the urine
  • Radiographic imaging of the kidneys
  • Serologic testing and tissue diagnosis with renal biopsy if noninvasive evaluation is not sufficient for diagnosis
assessment of renal function
Assessment of renalfunction

GFR = [UCr x V]/SCr

60 kg woman:

SCr = 1.2 mg/dL (106 micromol/L)

UCr= 100 mg/dL (8800 micromol/L)

V = 1.2 L/day

  • CrCl = [100 x 1.2]/1.2 = 100 L/day
  • This value has to be multiplied by 1000 to convert into mL and then divided by 1440 (the number of minutes in a day) to convert into units of mL/min.
  • CrCl = [100 x 1000]/1440 = 70 mL/min
estimation equations
Estimationequations
  • Cockcroft-Gault
  • MDRD
  • CKD-EPI
  • Cockcroft-Gault equation

(140 - age) x lean body weight [kg]

  • CCr (mL/min) = ———————————————

Cr [mg/dL] x 72

Forwoman X0.85

slide30

KDOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification 2012

slide31

Classification:

KDOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification 2012

clinical abnormalities in ckd
ClinicalAbnormalities in CKD
  • Fluid & electrolytedisturbances
  • Acid-Base disorders
  • Cardiovascularcomplications
  • Hematologiccomplications
  • Neurologiccomplications
  • Bone ,phosphate & calcium

abnormalities

  • Endocrinedisorders
fluid electrolyte disturbances in ckd
Fluid & ElectrolyteDisturbances in CKD
  • Early findings: poliuria- nocturia
  • Expansionof ECF
  • Hyponatremia
    • Dilutional
    • ImpairedNaconservation
  • Hyperkalemiaonlywhen
    • GFR<10ml/min
    • Oliguria /anuriadevelops
    • Potassiumsparingdiureticsused
    • ACEI and Beta blockers
    • Acidosis
slide34

Peritubularincrease in hydraulicpressure

  • Atrialnatriureticpeptides
  • Osmoticdiuresis
  • Salt wastingforms of CRF

Fex of

Na

INCREASED

Fractional excretion of solutes per nephron 

Solute diuresis (obligatory water loss)

  • Urineosmolality is decreased
  • Isosthenuriawhen GFR <25ml/min
  • Polyuria
  • Nocturia

Fex of

Water

INCREASED

hydrogen and bicarbonate transport
HYDROGEN AND BICARBONATE TRANSPORT

Ph =7.35-7.45

(H+ concentration)

Acidsconsumebuffers

HCO3

Daily acidproduction:

1mmol H/kg bw

HCO3 is regenerated in the kidney

Reabsorbed from the ultrafiltrate

maintaining plasma HCO3 concentrations

H+ excreted in the urine combines with NH3  NH4 +

metabolic acidosis in ckd
METABOLIC ACIDOSIS IN CKD

No change in arterialpH/ plasma HCO3 until

GFR < 30% of normal

Plasma HCO3 (24mEq/L)  Decreased (14-18 mEq/L)

  • Metabolicacidosis in CKD is dueto:
  • Decreasednephronmass
  • Leadingtolimited NH4 productionand HCO3 regeneration

pHandstable HCO3 levelsmaintained at

theexpense of bufferingby bone (CaPO4-CaHCO3)

cardiovascular complications in ckd
Cardiovascularcomplications in CKD
  • Hypertension
    • Salt and water retension
    • Hyperrenninemia
  • Pericarditis
  • Accelerated atherosclerosis
    • Coronary artery disease
    • Cerebrovascular disease
    • Peripheral vascular disease
  • Pulmonary edema
hematologic complications in ckd
Hematologiccomplications in CKD
  • Normochromicnormocyticanemia
    •  biosynthesis of erythropoetin
    • Bone-marrowdepressiveeffect of uremictoxins
    • Hemolysis
    • GI loss of blood
  • Abnormalhemostasis
    •  bleeding time
    • Abnormalplateletaggregation &adhesiveness
    •  activity of plateletfactor 3
  • Enhancedsusceptibilitytoinfection
slide40

INCIDANCE OF ANEMIA IN CKD

  • CrCl >50ml/dk %25
  • CrCl 35-49ml/dk %44
  • CrCl 25-34ml/dk %51
  • CrCl < 25ml/dk %87
slide41

ERITROPOESIS

CD 34

Eritron

Apoptosis

Pronormoblast,

eritroblast

Matur cells

BFU-E

CFU-E

Stem cell

EPO

EPO

GM-CSF,IL3,IGF-1

neurologic complications
Neurologic complications

Uremicencephalopathy

  • Inabilitytoconcentrate, drowsiness
  • Insomnia, behavioralchanges
  • Neuromuscularirritability
    • Hiccups, cramps, fasciculations
    • Asterixis, chorea, stupor, seizures

Peripheralneuropathy

RestlessLegs

bone phosphate calcium abnormalities in ckd
Bone phosphate & calciumabnormalities in CKD
  •  biosynthesis of 1,25-dihidroksikolekalsiferol
  • Hypocalcemia
  • Hyperphosphatemia
  • Hyperparathyroidism
  • Acidosis
  • Renal
  • Osteodystrophy
  • Osteomalacia
tubular phosphate transport
TUBULAR PHOSPHATE TRANSPORT
  • Under physiologicconditions 80-90% is reabsorbed
  • Parathyroidhormoneaugmentsphosphateexcretion

Transient  in

Plasma P

Transient  in

Plasma Ca

Dietary P 

(CaPO4 deposition in bone)

X

PTH secretion 

P excretion

P balance

restored

InCKD PTH is persistentlyelevated

alterations in vitamin d metabolism
Alterations in Vitamin D metabolism

1,25(OH2)

kolekalsiferol

in thekidney

Vit D

synthesized

in the skin

25(OH)kolekalsiferol

in the liver

X

Synthesis of activeVit D is reduced in CKD

Contributestohypocalcemiaandhyperparathroidism

endocrine disorders in ckd
Endocrinedisorders in CKD
  • Secondaryhyperparathyroidism
  • Glucoseintolerance
  • Disturbances of insulinmetabolism
    • Hyperinsulinemia
    • Peripheralinsulinresitance
  • Pituitary, throid & adrenal are normal
  • Libido andfertility
slide47

GFR  35-50% of normal  symptom-free

BUN and Cr. levels Normal

renal functions maintained

*endocrine

*excretory

*regulatory

GFR  20-35% of normal  azotemia

still asymptomatic

GFR  < 20% of normal  overt renal failure

UREMIC SYNDROME

esrd uremic syndrome
ESRDUremicSyndrome
  • Renalexcretoryfailure
    • Uremia
    • Hyperkalemia
  • Renalendocrinefailure
    • Anemia
    • Renalosteodystrophy
  • Renalmetabolicfailure & acidosis
uremic toxins
UREMIC ‘TOXINS’

Productsof protein and amino acidmetabolism:

  • Urea (80% of total (excretednitrogen)
  • Guanidinocompounds
    • Guanidine
    • Creatinine
    • Creatin
  • UratesandHippurates
  • End - products of nucleicacidmetabolism
  • End - products of aliphatic amine metabolism
  • End – products of aromatic amino acidmetabolism
  • Othernitrogenoussubstances
uremic toxins1
UREMIC TOXINS
  • Advancedglycationend-products
  • Parathyroidhormone
  • Inhibitors of somatomedinandinsulinaction
  • β–melanocyte–stimulating hormone
  • Glucagon
  • Luteinizinghormone
  • Prolactin
slide51

Uremictoxinscause:

    • Anorexia
    • Malaise
    • Pigmentation
    • Vomiting
    • Pruritus
    • Headache
    • Plateletdysfunction(Guanidinosuccinicacid)
slide52

Pigmentation: a diffuse brown pigmentation is

typical of longstanding renal failure; it may be

caused by retention of β–melanocyte–stimulating hormone.

slide53

Nodular prurigo: extensive nodular prurigo associated with

severe pruritus (note the scratch marks) in a man with advanced

renal failure shortly before the initiation of renal replacement therapy.

objectives in the management of ckd
Objectives in theManagement of CKD
  • ToCalculatethefunctionalreserve
  • ToCorrectthereversiblefactorsthatmaylowerthefunctionalreserve
  • Treatunderlyingdiseasewherepossible
  • To stop orslowdowntheprogression
  • Topreventandtreattheuremiccomplications

 Increasequality of life and life expectation

slide56

Management of CKD

  • Dietarymanagement
    • Protein restriction (0.6g-0.8 g/kg/day)
    • Salt restriction (3-4g/day)
    • Potassiumrestriction
    • Phosphorusrestriction
    • Magnesiumrestriction
  • Management of hypertension
  • Management of anemia (erythropoetin)
  • Management of renal bone disease
  • Avoidingnephrotoxicmedication, hypovolemia
  • Preperationforrenalreplacementtherapy
management of hyperphosphatemia
Management of hyperphosphatemia
  • Phosphorusrestrictionin thediet
  • Oral P bindingagents
    • CaCO2
    • Caacetate
    • AlOH
    • Sucralfate
    • Ironcontainingagents
    • Lantanium
    • Sevelamer HCL
management of hypertension
Management of Hypertension
  • Salt restriction
  • ACE inhibitors
    • Especially in diabeticnephropathy, in all CKD patientsexcept: renalarterystenosis
    • Monitorforpossible in serum Crand K
  • Diuretics
  • Calciumchannelblockers
  • Beta blockers
  • Alphablockers
  • Centralactingagents
management of anemia
Management of Anemia
  • Erythropoetinadministration (sc/iv)
  • Replacementwhennecessary of
    • Iron
    • Folicacid
    • B12
  • Blood transfusion
management of renal bone disease
Management of Renal Bone Disease
  • Normalization of serum Caand P
    • Oral P bindingagents
    • PreferCacontainingones
    • Exceptwhen serum Ca x P > 55 (extraskeletalcalcifications)
  • Followup serum PTH levels
    • Start calcitriol/1aOH D whenPTH > 2-3xN
avoiding nephrotoxic medication
AvoidingNephrotoxicMedication
  • Nonsteroidal antiinflammatory drugs
  • Vancomycin
  • Aminoglycosides
preparation for renal replacement therapy
PreparationforRenalReplacementTherapy
  • Patienteducationfor RRT options
  • InformaboutTransplantation
  • Vascularaccessif HD anticipated
  • PD catheterreplacementif CAPD planned
slide66

HEMODIALYSIS

END STAGE RENAL

FAILURE

TRANSPLANTATION

PERITONEAL DIALYSIS

acute on chronic concept
‘Acute’ on ‘Chronic’ concept
  • AcuteImpairment of renalfunctiondueto an additional problem overunderlyingCKD:
    • Acutehypovolemia
    • Nefrotoxicdruguse
    • Infection
    • Obstruction
    • HeartFailure
    • Acceleratedhypertension