with chronic kidney disease Gülçin Kantarcı MD Nephrology Department Learning objectives and training goals of this lecture Define chronic kidney disease ID: 693524
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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
SYNDROMESlide11Slide12
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
Slide21Slide22
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 ???Slide29Slide30
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.Slide38Slide39
?????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.cfmSlide46Slide47
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?Slide52Slide53
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