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Approach   to   the   patient Approach   to   the   patient

Approach to the patient - PowerPoint Presentation

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Approach to the patient - PPT Presentation

with chronic kidney disease Gülçin Kantarcı MD Nephrology Department Learning objectives and training goals of this lecture Define chronic kidney disease ID: 693524

disease kidney gfr ckd kidney disease ckd gfr chronic renal min patients patient stage dialysis urinary diagnosis amp complications years weight history

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Slide1

Approach to the patient with chronic kidney disease

Gülçin Kantarcı, M.D.

Nephrology DepartmentSlide2

Learning objectives and training goals of this lectureDefine chronic kidney disease. Explain the pathophysiology of chronic kidney disease. Describe the clinical findings of chronic kidney disease. Take preventive measures against the development of chronic kidney disease.List the possible etiology of chronic kidney disease and make a differential diagnosis.Arrange the initial treatments and refer to a specialist.Slide3

REFERENCE &SUGGESTED READING Current Medical Diagnosis and Treatment, Maxine A. Papadakis, Stephen J. McPhee, Eds. Michael W. Rabow, Associate Ed. http://accessmedicine.comChapter 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)Slide4

chronic renal diseases (CKD) CKD is defined as abnormalities of kidney structure or function, present for ≥3 months, with implications for healthSlide5

Criteria for CKDKDOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification 2012Slide6

Staging of CKDKDOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification 2012Slide7

DIAGNOSIS OF CKD

GFR

Serum

creatinine

(

muscle

mass

,

dietary

meat

intake, simetidin, trimetoprim) Creatinine Clearance = Ucr x V P crCockcroft formula= 140-age 72 x P crEstimated CrCl (MDRD Study)

1440

x Body

weight

(

women

x 0.85)Slide8

GFR = 141 X min(Scr/κ,1)α X max(Scr/κ,1)-1.209 X 0.993Age X 1.018 [if female] X 1.159 (if black)The CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) equation was developed in an effort to create a formula more precise than the MDRD formula, especially when actual GFR is > 60 mL/min per 1.73 m2. Researchers pooled data from multiple studies to develop and validate this new equation. The CKD-EPI equation performed better than the MDRD (Modification of Diet in Renal Disease Study) equation, especially at higher GFR, with less bias and greater accuracy. CKD-EPISlide9

CKD SymptomsIn the early stages, CKD is asymptomatic. Symptoms develop slowly with the progressive decline in GFR, are nonspecific, and do not manifest until kidney disease is far advanced (GFR < 10–15 mL/min/1.73 m2).General symptoms of uremia may include fatigue and weakness; anorexia, nausea, vomiting, and a metallic taste in the mouth are also common. Patients or family members may report irritability, difficulty in concentrating, insomnia, restless legs, paresthesias, and twitching. Generalized pruritus without rash may occur.Slide10

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

SYNDROMESlide11
Slide12

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 drugsSlide13

Clinical Abnormalities in Uremia

Fluid & electrolyte disturbances

Acid-Base disorders

Cardiovascular complications

Hematologic complications

Neurologic complications

Bone ,phosphate & calcium

abnormalities

Endocrine disordersSlide14

Fluid & Electrolyte Disturbances in CRF

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

AcidosisSlide15

No change in arterial pH/ plasma HCO3 until GFR  30% of normalMetabolic acidosis in CRF is due to:

Decreased

nephron

mass

Leading

to

limited

NH4

production

and

HCO3 regenerationMETABOLIC ACIDOSIS IN CRFPlasma HCO3 (24mEq/L)  Decreased (14-18 mEq/L)pH and stable HCO3 levels maintained at the expense of buffering by bone (CaPO4-CaHCO3)Slide16

Cardiovascular complications in CRF

Hypertension

Salt and water retension

Hyperrenninemia

Pericarditis

Accelerated atherosclerosis

Coronary artery disease

Cerebrovascular disease

Peripheral vascular disease

Pulmonary edemaSlide17

Hematologic

complications

in CRF

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 infectionSlide18

Neurologic complications

Uremic encephalopathy

Inability to concentrate, drowsiness

Insomnia, behavioral changes

Neuromuscular irritability

Hiccups, cramps, fasciculations

Asterixis, chorea, stupor, seizures

Peripheral neuropathy

Restless LegsSlide19

Bone phosphate & calcium abnormalities in CRF

 biosynthesis of 1,25-dihidroksikolekalsiferol

Hypocalcemia

Hyperphosphatemia

Hyperparathyroidism

Acidosis

Renal

Osteodystrophy

OsteomalaciaSlide20

Endocrine

disorders

in CRF

Secondary hyperparathyroidism

Glucose intolerance

Disturbances of insulin metabolism

Hyperinsulinemia

Peripheral insulin resitance

Pituitary, throid & adrenal are normal

Libido and fertility

Slide21
Slide22

Essentials of Diagnosis• Decline in the GFR over months to years.• Persistent proteinuria or abnormal renal morphology may be present.• Hypertension in most cases.• Symptoms and signs of uremia when nearing end-stage disease.• Bilateral small or echogenic kidneys on ultrasound in advanced disease.Slide23

Estimation equations

Cockcroft-Gault

MDRD

CKD-EPI

Cockcroft-Gault equation

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

CCr (mL/min) = ———————————————

Cr [mg/dL] x 72Slide24

TREATMENTSlowing ProgressionTreatment of the underlying cause of CKD is vital. Control of diabetes should be aggressive in early CKD; risk of hypoglycemia increases in advanced CKD, and glycemic targets may need to be relaxed to avoid this dangerous complication. Blood pressure control is vital to slow progression of all forms of CKD; agents that block the renin-angiotensin-aldosterone system are particularly important in proteinuric disease

Current guidelines suggest a blood pressure goal of 130/80 mm Hg for patients with CKD; a goal of 125/75 mm Hg is recommended for patients with proteinuria.Slide25

Dietary ManagementEvery patient with CKD should be evaluated by a renal nutritionist. Specific recommendations should be made concerning protein, salt, water, potassium, and phosphorus intake to help manage CKD progression and complications.Protein restriction to 0.6–0.8 g/kg/d may retard CKD progression Salt and water restriction. A goal of 2 g/d of sodium is reasonable for most patients. A daily intake of 2 L of fluid maintains water balance.Potassium restriction. Restriction is needed once the GFR has fallen below 10–20 mL/min/1.73 m2, or earlier if the patient is hyperkalemic. Patients should receive detailed lists describing potassium content of foods and should limit their intake to < 50–60 mEq/d (2 g).Phosphorus restriction. The phosphorus level should be kept in the ‘normal’ range (<4.5 mg/dL) predialysis,Slide26

Medication ManagementMany drugs are excreted by the kidney; dosages should be adjusted for GFR. Insulin doses may need to be adjusted. Magnesium-containing medications, such as laxatives or antacids, should be avoided as should phosphorus-containing medicines, particularly cathartics. Morphine metabolites are active and can accrue in advanced CKD; Drugs with potential nephrotoxicity (NSAIDs, intravenous contrast) should be avoidedThe anemia of CKD is primarily due to decreased erythropoietin production, which often becomes clinically significant during stage 3 CKD. Many patients are iron deficient as well due to impaired GI iron absorption.Slide27

END STAGE RENAL FAILUREHEMODIALYSISTRANSPLANTATION

PERITONEAL DIALYSIS

Treatment of End-Stage Renal Disease

When GFR declines to 5–10 mL/min/1.73 m2 (with or without overt uremic symptoms), renal replacement therapy (hemodialysis, peritoneal dialysis, or kidney

transplantation) is required to sustain life. Slide28

Kidney transplant sourcesLiving Related UnrelatedDeceasedXenotransplant ???Slide29
Slide30

Vascular access for HDSlide31

Native AV FistulaSlide32

Vascular access for HDSlide33

Principle of hemodialysis

cellophane sausage casings, a cooling system from an old Ford, parts from a crashed German fighter plane, and washing machine tubs. Slide34

Principle of PDSlide35

When to Refer• Patient education is important in understanding which mode of therapy is most suitable, as is timely preparation for treatment; therefore, referral to a nephrologist should take place in late stage 3 CKD, or when the GFR is declining rapidly. Such referral has been shown to improve mortality• A patient with other forms of CKD such as those with significant proteinuria (> 1 g/d) or polycystic kidney disease should be referred to a nephrologist at earlier stages.Slide36

Prognosis in ESRDCompared with kidney transplant recipients and age-matched controls, mortality is higher for patients undergoing dialysis. There is likely little difference in survival for well-matched peritoneal versus hemodialysis patients.Survival rates on dialysis depend on the underlying disease process. Five-year Kaplan-Meier survival rates vary from 36% for patients with diabetes to 53% for patients with glomerulonephritis. Slide37

Prognosis in ESRDOverall 5-year survival is currently estimated at 39%. Patients undergoing dialysis have an average life-expectancy of 3–5 years, but survival for as long as 25 years may be achieved depending on comorbidities. The most common cause of death is cardiac disease (50%). Other causes include infection, cerebrovascular disease, and malignancy.Slide38
Slide39

?????Slide40

Case 135 years old maleNocturia since 2006He had a history of pyelonephritis with kidney stonesSince then he had no hospital admissionSlide41

PHYSICAL EXAMINATIONBP: 186/100mmHg P: 90/min/R Weight 72 kg, Height 175 cm Temperature: 36.4 0C

Raised JVP

Dyspneic

with crackles over the lung basesSlide42

Laboratory testsHb: 10.6g/dl Htc:31.9% Na: 137mEq/LSerum BUN: 78mg/dl ;Kr: 3.6mg/dLUrine specific gravity: 1012Ca  8.3mg/dL     Pi 4.6 mg/dL            Albumin 3.6 g/dL

              

Fe 16  

ug

/

dL

     (59 - 158 )          

TIBC 205 

ug

/

dL

     (228 - 428)    Slide43

What is your likely Diagnosis ?Slide44

140-age)x Wt 72 x pCr For Female= x0.85Estimated CrCl (Cockcroft-Gault formula)

Slide45

http://www.kidney.org/professionals/kdoqi/gfr_calculator.cfmSlide46
Slide47

Stage 4 CKDSlide48

What else do you need to know?Slide49

URINARY USGRK 85 mm, 5x7 mm mid pole kidney stoneLK 88 mm, 7x6 mm apical pole kidney stoneGII Renal Parenchimal Dis.Proteinuria: 354 mg/daySlide50

Renal bx. ?Urinary CT?Urinary Ca? Stone analysis?Slide51

How would you manage this patient?Slide52
Slide53

Treatment StrategiesAnemia EPO, Parenterally forms of ironHyperphosphatemia Phosphate bindersHT Do not use ACEIs+ARBs

Do not

use

contrast

agents

Do not

use

NSAIDsSlide54

Case 248 years old femaleLeft flank pain, vomiting, fever

History

of PCKD (

diagnosed

in 1999)

Her

mother

died

because

of

intracranial

hemorage

(AVM? and AVA?)Slide55

PHYSICAL EXAMINATIONBP: 100/60mmHg P: 118/min/R Weight 59 kg, 38.2 0CDyspne(+), tachipne (+)

turgor

,

Pale

face

,

Looks

weak

and

unwell

fullness of neck veins (+)Slide56

Laboratory testsWBC: 12.860/mm3Hb: 12.2g/dl Htc:37.3% Na: 137mEq/LBUN: 156mg/dl ;Kr: 10.3mg/dL

ABG

analysis

PH 7.26

HCO3

12.8

BE-12

Urine

specific

gravity

: 1010

S.Na

133mEq/l S.K 6.7mEq/l

Ca  8.3mg/dL     Pi 6.8 mg/dLCRP 184                         Slide57

What is your likely Diagnosis ?Slide58

What else do you need to know?Slide59

URINARY USGRK 186 mm with multiple cystis and stones, LK 167 mm with multiple cystis and stonesR ureter and pelvis dilatatedSlide60

Culture of the urine ?Culture of blood?Urine analysis ?Urinary CT ?( Contrast agent)Slide61

How would you manage this patient?

?Slide62

Case 328 years old maledyspnea, vomiting, bad feutorHistory of urinary tract infections before age 12. His brother on dialysis

because

of VUR

nephropathySlide63

PHYSICAL EXAMINATIONBP: 110/70mmHg P: 88/min/R Weight 72 kg, 36.5 0CDyspne(-), tachipne (-)

turgor

n,

fale

face

,Slide64

Laboratory testsHb: 9.6g/dl Htc:31% MCV 79 Na: 135mEq/L, K 3.5mEq/LCa  7.6mg/dL     Pi 9.6 mg/dL            

Albumin

 3.6 g/

dL

 ; CRP 30             

Fe 27 

ug

/

dL

     (59 - 158 )          

TIBC 308 

ug

/

dL

     (228 - 428)    

Serum BUN: 168mg/dl ;Kr: 12.3mg/dLUrine specific gravity: 1010, Urinary sediment: 8-10 leucocytes, 2-3 waxy casts in every field of microscopic areasSlide65

What else do you need to know?Slide66

US Solitery enlarged left kidney and proximal segments of ureterSlide67

Urinary bt( Without contrast)Slide68

PTH 354 pg/mlUric acid 8.9 mg/dlCulture of urine : (-)What is your likely diagnosis ?Slide69

Nephropathy of VURSlide70

What else do you need to

confirme

your diagnosis?Slide71

Voiding cystouretrographySlide72

How would you manage

this patient ?Slide73

END STAGE RENAL FAILURE

HEMODIALYSIS

PERITONEAL

DIALYSIS

TRANSPLANTATIONSlide74

Anemia EPO, Parenterally forms of ironHyperphosphatemia Phosphate bindersHT Do not use ACEIs+ARBsDo not use contrast agentsDo not use

NSAIDs

Nephrectomy

or

Defflux

inj

.

Befor

renal

transplantationSlide75

Case 457 years old femaleDispnea and vomiting History of NIDDM (

diagnosed

in 1985)

Her

father

died

because

of CAD

Her

mother

had

the

history of dialysis & died because of sepsisSlide76

PHYSICAL EXAMINATIONBP: 190/60mmHg P: 92/min/R Weight 72 kg, BMI 30edeama (+++/+++) turgor n, pale

face

,

Dyspneic

and

orthopneic

with

crackles

over

the lung bases, tachipne (+) Slide77

LABORATORY FINDINGSHb:8.7 Htc: 25% WBC:7200BUN:58mg/dL Cr:3.2mg/dL K:6.7mEq/L Na:135mEq/L S.alb 3.1 g/dl

Urinalysis

= D 1010

35-40 WBCSlide78

Diagnosis ?Slide79

Chronic Kidney Failure(Due to diabetic nepropathy)

Stage

5Slide80

How would you manage this patient ?Slide81

END STAGE RENAL FAILURE

HEMODIALYSIS

PERITONEAL

DIALYSIS

TRANSPLANTATION