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CHRONIC KIDNEY DISEASE
Gülçin Kantarcı, MDYeditepe University Department of Internal MedicineDivision of Nephrology
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REFERENCE &SUGGESTED READING •Current Medical Diagnosis and Treatment,
Maxine A. Papadakis, Stephen J. McPhee, Eds. Michael W. Rabow, Associate Ed. http://accessmedicine.com Chapter 22. Kidney Disease
•http://www.uptodate.com .(Definition and staging of chronic kidney disease in adults, Screening for chronic kidney disease, Epidemiology of chronic kidney disease)
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AIMS & OBJECTIVESState • the definition,• pathophysiology, •clinical findings and •prevention methods of chronic kidney
disease.
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Chronic kidney 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-Stage Renal Disease(ESRD)Advanced CKD requiring renal replacement therapy (RRT) in order to maintain life.
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Major Causes of Chronic Kidney Disease Cause Examples Chronic tubulointerstitial nephropathies
Glomerulopathies (primary) Focal glomerulosclerosis Idiopathic crescentic glomerulonephritis IgA nephropathyMembranoproliferative glomerulonephritisMembranous nephropathy
Glomerulopathies associated with systemic disease DM,AmyloidosisHemolytic-uremic syndromePostinfectious glomerulonephritisSLEWegener's granulomatosis
Hereditary nephropathies Hereditary nephritis (Alport's syndrome)Medullary cystic diseaseNail-patella syndromePolycystic kidney disease
Hypertension Malignant glomerulosclerosisNephroangiosclerosis
Obstructive uropathy Benign prostatic hyperplasiaPosterior urethral valvesRetroperitoneal fibrosisUreteral obstruction (congenital, calculi, malignancies)Vesicoureteral reflux
Renal macrovascular disease Renal artery stenosis
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CKD Incidence CKD Prevalence
Prevalence is estimated to be 8—16% worldwide
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Pathophysiology of CKD
Loss of nephron mass
Structural and functional hypertrophy of the remaining nephrons
Restoration of
GFR
Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
Glomerular HyperperfusionHyperfiltrationHypertension
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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).
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GLOMERULAR ULTRAFILTRATION
Oncotic Pressure
HydraulicPressure
Hydraulic Pressure
Glomerular capillaries
Bowman’s capsule
• Rate of glomerular plasma flow• Total surface area+
Decreased GFR is expected when
• Glomerular hydraulic pressure is
• Tubule hydraulic pressure is • Plasma colloid pressure • Renal (glomerular) blood flow • Permeability is • Filtration surface area
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Loss of 50% of the total nephron mass
hyperfiltration withoutserious adverse consequences
Loss of > 50% of the total nephron mass
Over time: proteinuriaFocal and segmental glomerulosclerosis
CompensatoryAdaptive responses
Maladaptive responses
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Mechanisms of progressive renal scarring
•Glomerulosclerosis
•Tubulointerstital scarring
•Vascular sclerosis
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GLOMERULOSCLEROSIS
ß in renal functional mass
Glomerular HyperperfusionHyperfiltrationHypertension
• Endothelial &epithelial injury• Transudation of macromoleculesinto mesangium
Progressive mesangial expansion
GLOMERULOSCLEROSIS
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Tubulointerstitial Scarring
Injured tubular cells
Inflammatory mediatorsChemokinesCytokines
Growth factors
Inflammatory cells
Synthesis ECM
TUBULOINTERSTITIAL FIBROSIS
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Vascular Sclerosis•Afferent arteriolar hyalinosis
Glomerular sclerosis
•Postglomerular arterial hyalinosisInterstitial ischemia and fibrosisDamage to peritubular capillaries
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Factors Affecting The Progression of CKD
Non modifiable susceptibility factors• Age• Gender• Genetics• Race
Initiation factors• Glomerulonephritis• TIN• Hypertension• Diabetes• Dyslipidemia
Modifiable risk factors• ?
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Modulating factors of progressive renal scarring
•Genetic/Racial/ gender-related•Systemic and intraglomerular hypertension•The degree of proteinuria• Intrarenal deposition of Ca, P, urate•Hyperlipidemia (LDL)•Use of NSAIDs(Pg inhibitors)•High protein diet•Persistent metabolic acidosis•Extent of tubulointerstitial disease
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Screening for chronic kidney diseasepatients 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 factors for 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
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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
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Assessment of renal functionGFR = [UCr x V]/SCr60 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
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Estimation equations • Cockcroft-Gault • MDRD • CKD-EPI
• Cockcroft-Gault equation
(140 - age) x lean body weight [kg]• CCr (mL/min) = ——————————————— Cr [mg/dL] x 72For woman X0.85
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Finding CommentPrior in serum Cr CKDSmall kidneys in U/S CKDNormal/ kidneys AKI
Exceptions:PCKDDiabetic NephropathyMultiple Myeloma
Anemia/Hyperhosphatemia/ Hypocalcemia
CKD
Oliguria/ daily in Cr/BUN AKI
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KDOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification 2012
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Classification:
KDOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification 2012
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Clinical Abnormalities in CKD
•Fluid & electrolyte disturbances•Acid-Base disorders•Cardiovascular complications•Hematologic complications•Neurologic complications•Bone ,phosphate & calcium abnormalities•Endocrine disorders
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Fluid & Electrolyte Disturbances in CKD
▫Early findings: poliuria- nocturia▫Expansion of ECF▫Hyponatremia
Dilutional Impaired Na conservation
▫Hyperkalemia only when GFR<10ml/min Oliguria /anuria develops Potassium sparing diuretics used ACEI and Beta blockers Acidosis
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• Peritubular increase in hydraulic pressure• Atrial natriuretic peptides• Osmotic diuresis• Salt wasting forms of CRF
• Urine osmolality is decreased• Isosthenuria when GFR <25ml/min
PolyuriaNocturia
Fex of Na
INCREASED
Fex of Water
INCREASED
Fractional excretion of solutes per nephron
Solute diuresis (obligatory water loss)
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HYDROGEN AND BICARBONATE TRANSPORT
Ph =7.35-7.45(H+ concentration)
Daily acid production:1mmol H/kg bw
Acids consume buffersHCO3
HCO3 is regenerated in the kidneyReabsorbed from the ultrafiltrate
maintaining plasma HCO3 concentrations
H+ excreted in the urine combines with NH3 NH4 +
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No change in arterial pH/ plasma HCO3 until GFR < 30% of normal
Metabolic acidosis in CKD is due to:• Decreased nephron mass• Leading to limited NH4 production and HCO3 regeneration
METABOLIC ACIDOSIS IN CKD
Plasma HCO3 (24mEq/L) Decreased (14-18 mEq/L)
pH and stable HCO3 levels maintained at the expense of buffering by bone (CaPO4-CaHCO3)
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Cardiovascular complications in CKD
•Hypertension▫Salt and water retension▫Hyperrenninemia
•Pericarditis•Accelerated atherosclerosis
▫Coronary artery disease▫Cerebrovascular disease▫Peripheral vascular disease
•Pulmonary edema
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13 March 2014
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Hematologic complications in CKD
•Normochromic normocytic anemia▫ biosynthesis of erythropoetin▫Bone-marrow depressive effect of uremic
toxins▫ Hemolysis▫ GI loss of blood
•Abnormal hemostasis▫ bleeding time▫Abnormal platelet aggregation
&adhesiveness▫ activity of platelet factor 3
•Enhanced susceptibility to infection
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INCIDANCE OF ANEMIA IN CKD• CrCl >50ml/dk %25
• CrCl 35-49ml/dk %44
• CrCl 25-34ml/dk %51
• CrCl < 25ml/dk %87
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BFU-E CFU-E
Pronormoblast, eritroblast
Stem cell
Matur cells
EPO
GM-CSF,IL3,IGF-1
ERITROPOESISCD 34 Eritron
Apoptosis
EPO
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Neurologic complications
Uremic encephalopathy• Inability to concentrate, drowsiness• Insomnia, behavioral changes•Neuromuscular irritability
▫Hiccups, cramps, fasciculations▫Asterixis, chorea, stupor, seizures
Peripheral neuropathyRestless Legs
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Bone phosphate & calcium abnormalities in CKD
• biosynthesis of 1,25-dihidroksikolekalsiferol
•Hypocalcemia•Hyperphosphatemia•Hyperparathyroidism•Acidosis
• RenalOsteodystrophy• Osteomalacia
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TUBULAR PHOSPHATE TRANSPORT• Under physiologic conditions 80-90% is
reabsorbed• Parathyroid hormone augments
phosphate excretion
Dietary P Transient inPlasma P
Transient inPlasma Ca
(CaPO4 deposition in bone)
PTH secretion P excretion P balancerestored
In CKD PTH is persistently elevated
X
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Alterations in Vitamin D metabolism
Vit Dsynthesized in the skin
25(OH)kolekalsiferolin the liver
1,25(OH2)kolekalsiferolin the kidney
Synthesis of active Vit D is reduced in CKD
Contributes to hypocalcemia and hyperparathroidism
X
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Endocrine disorders in CKD
•Secondary hyperparathyroidism•Glucose intolerance•Disturbances of insulin metabolism
▫Hyperinsulinemia▫Peripheral insulin resitance
•Pituitary, throid & adrenal are normal•Libido and fertility
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GFR 35-50% of normal symptom-freeBUN and Cr. levels
Normalrenal functions
maintained*endocrine*excretory*regulatory
GFR 20-35% of normal azotemia still asymptomatic
GFR < 20% of normal overt renal failure
UREMIC SYNDROME
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ESRDUremic Syndrome•Renal excretory failure
▫Uremia▫Hyperkalemia
•Renal endocrine failure▫Anemia▫Renal osteodystrophy
•Renal metabolic failure & acidosis
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UREMIC ‘TOXINS’
Products of protein and amino acid metabolism:
▫Urea (80% of total (excreted nitrogen)▫Guanidino compounds
Guanidine Creatinine Creatin
▫Urates and Hippurates▫End - products of nucleic acid metabolism▫End - products of aliphatic amine metabolism▫End – products of aromatic amino acid
metabolism▫Other nitrogenous substances
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UREMIC TOXINS
•Advanced glycation end-products•Parathyroid hormone• Inhibitors of somatomedin and insulin
action•β–melanocyte–stimulating hormone•Glucagon•Luteinizing hormone•Prolactin
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•Uremic toxins cause:
▫Anorexia▫Malaise▫Pigmentation▫Vomiting▫Pruritus▫Headache▫Platelet dysfunction (Guanidinosuccinic acid)
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Pigmentation: a diffuse brown pigmentation is typical of longstanding renal failure; it may be caused by retention of β–melanocyte–stimulating hormone.
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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.
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Objectives in the Management of CKD
•To Calculate the functional reserve•To Correct the reversible factors that may
lower the functional reserve•Treat underlying disease where possible•To stop or slow down the progression•To prevent and treat the uremic
complications Increase quality of life and life expectation
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Management of CKD•Dietary management
▫Protein restriction (0.6g-0.8 g/kg/day)▫Salt restriction (3-4g/day)▫Potassium restriction▫Phosphorus restriction▫Magnesium restriction
•Management of hypertension•Management of anemia (erythropoetin)•Management of renal bone disease•Avoiding nephrotoxic medication,
hypovolemia•Preperation for renal replacement
therapy
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Management of hyperphosphatemia
•Phosphorus restriction in the diet•Oral P binding agents
▫CaCO2▫Ca acetate▫AlOH▫Sucralfate▫Iron containing agents▫Lantanium▫Sevelamer HCL
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Management of Hypertension•Salt restriction•ACE inhibitors
▫Especially in diabetic nephropathy, in all CKD patients except: renal artery stenosis
▫Monitor for possible in serum Cr and K•Diuretics•Calcium channel blockers•Beta blockers•Alpha blockers•Central acting agents
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Management of Anemia•Erythropoetin administration (sc/iv)•Replacement when necessary of
▫Iron▫Folic acid▫B12
•Blood transfusion
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Management of Renal Bone Disease•Normalization of serum Ca and P
▫Oral P binding agents▫Prefer Ca containing ones▫Except when serum Ca x P > 55
(extraskeletal calcifications)•Follow up serum PTH levels
▫Start calcitriol/1aOH D when PTH > 2-3xN
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Vascular Calcification in a ESRD patient
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Smooth tissue calcification
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Avoiding Nephrotoxic Medication
•Nonsteroidal antiinflammatory drugs
•Vancomycin
•Aminoglycosides
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Preparation for Renal Replacement Therapy•Patient education for RRT options
• Inform about Transplantation
•Vascular access if HD anticipated
•PD catheter replacement if CAPD planned
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END STAGE RENAL FAILURE
HEMODIALYSIS
TRANSPLANTATIONPERITONEAL DIALYSIS
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Hollow fiber dialyzer
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‘Acute’ on ‘Chronic’ concept•Acute Impairment of renal function due to an additional problem over underlying CKD:▫Acute hypovolemia▫Nefrotoxic drug use▫Infection▫Obstruction▫Heart Failure▫Accelerated hypertension