Approach to the patient
with chronic kidney
disease
Gülçin Kantarcı, M.D.
Nephrology Department
Learning objectives and training goals
of this lecture
• Define 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.
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)
chronic renal diseases (CKD)
• CKD is defined as abnormalities of kidney
structure or function, present for ≥3
months, with implications for health
Criteria for CKD
KDOQI Clinical Practice Guidelines for Chronic Kidney
Disease: Evaluation, Classification, and Stratification 2012
Staging of CKD
KDOQI Clinical Practice Guidelines for Chronic Kidney
Disease: Evaluation, Classification, and Stratification 2012

 GFR
 Serum creatinine  (muscle mass, dietary
meat intake, simetidin,
trimetoprim)
 Creatinine Clearance = Ucr x V
1440
P cr
 Cockcroft formula= 140-age
72 x P cr
 Estimated CrCl (MDRD Study)
x Body weight
(women x 0.85)
CKD-EPI
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 Symptoms
• In 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.
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

Renal excretory failure
› Uremia
› Hyperkalemia

Renal endocrine
failure
› Anemia
› Renal osteodystrophy

Renal metabolic
failure & acidosis
Fluid & electrolyte
disturbances
• Acid-Base disorders
• Cardiovascular complications
• Hematologic complications
• Neurologic complications
• Bone ,phosphate & calcium
abnormalities
• Endocrine disorders
•
• The most common
physical finding in CKD is
hypertension.
• It is often present in early
stages of CKD and tends
to worsen with CKD
progression as sodium
excretion is impaired.
• In later stages of CKD,
this sodium retention
may lead to typical
physical signs of volume
overload.

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
Uremic encephalopathy
 Inability to concentrate, drowsiness
 Insomnia, behavioral changes
 Neuromuscular irritability
› Hiccups, cramps, fasciculations
› Asterixis, chorea, stupor, seizures
Peripheral neuropathy
Restless Legs
 biosynthesis of 1,25-dihidroksikolekalsiferol
 Hypocalcemia
 Hyperphosphatemia
 Hyperparathyroidism
 Acidosis

•Renal
Osteodystrophy
•Osteomalacia
Secondary hyperparathyroidism
 Glucose intolerance
 Disturbances of insulin metabolism

› Hyperinsulinemia
› Peripheral insulin resitance
Pituitary, throid & adrenal are normal
 Libido and fertility 

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.
TREATMENT
Slowing Progression
• Treatment 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-angiotensinaldosterone 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.
Dietary Management
• Every 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,
Medication Management
• Many 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 avoided
• The 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.
Treatment of End-Stage Renal Disease
HEMODIALYSIS
END STAGE RENAL
FAILURE
PERITONEAL
DIALYSIS
TRANSPLANTATION
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.
Kidney transplant sources
• Living
Related
Unrelated
Deceased
Vascular access for HD
Native AV Fistula
Vascular access for HD
Principle of hemodialysis
cellophane sausage casings, a cooling
system from an old Ford, parts from
a crashed German fighter plane, and
washing machine tubs.
Principle of PD
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.
Prognosis in ESRD
• Compared 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. Overall
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.
Case 1
• 35 years old male
• Nocturia since 2006
• He had a history of pyelonephritis with kidney
stones
• Since then he had no hospital admission
PHYSICAL EXAMINATION
• BP: 186/100mmHg P: 90/min/R
• Weight 72 kg, Height 175 cm
Temperature: 36.4 0C
Raised JVP
Dyspneic with crackles over the lung bases
Laboratory tests
•
•
•
•
Hb: 10.6g/dl Htc:31.9% Na: 137mEq/L
Serum BUN: 78mg/dl ;Kr: 3.6mg/dL
Urine specific gravity: 1012
Ca 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)
Estimated
formula)
CrCl (Cockcroft-Gault
140-age)x Wt
72 x pCr
For Female= x0.85
http://www.kidney.org/professionals/kdoqi/gfr_calculator.cfm
Stage 4 CKD
URINARY USG
• RK 85 mm, 5x7 mm mid pole kidney stone
• LK 88 mm, 7x6 mm apical pole kidney stone
• GII Renal Parenchimal Dis.
Proteinuria: 354 mg/day
•
•
•
•
Renal bx. ?
Urinary CT?
Urinary Ca?
Stone analysis?
How would you manage
this patient?
Treatment Strategies
•
•
•
•
•
Anemia EPO, Parenterally forms of iron
Hyperphosphatemia Phosphate binders
HT Do not use ACEIs+ARBs
Do not use contrast agents
Do not use NSAIDs
Case 2
•
•
•
•
48 years old female
Left flank pain, vomiting, fever
History of PCKD ( diagnosed in 1999)
Her mother died because of intracranial
hemorage (AVM? and AVA?)
PHYSICAL EXAMINATION
•
•
•
•
•
•
BP: 100/60mmHg P: 118/min/R
Weight 59 kg, 38.2 0C
Dyspne(+), tachipne (+)
turgor , Pale face,
Looks weak and unwell
fullness of neck veins (+)
Laboratory tests
• WBC: 12.860/mm3
• Hb: 12.2g/dl Htc:37.3% Na: 137mEq/L
• BUN: 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/dL
• CRP 184
URINARY USG
• RK 186 mm with multiple cystis and stones,
• LK 167 mm with multiple cystis and stones
• R ureter and pelvis dilatated
•
•
•
•
Culture of the urine ?
Culture of blood?
Urine analysis ?
Urinary CT ?( Contrast agent)
How would you manage
this patient?
Case 3
•
•
•
•
28 years old male
dyspnea, vomiting, bad feutor
History of urinary tract infections before age 12.
His brother on dialysis because of VUR
nephropathy
PHYSICAL EXAMINATION
• BP: 110/70mmHg P: 88/min/R
• Weight 72 kg, 36.5 0C
• Dyspne(-), tachipne (-)
• turgor n, fale face,
Laboratory tests
• Hb: 9.6g/dl Htc:31% MCV 79
• Na: 135mEq/L, K 3.5mEq/L
Ca 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/dL
• Urine specific gravity: 1010,
• Urinary sediment: 8-10 leucocytes, 2-3 waxy casts in
every field of microscopic areas
US
• Solitery enlarged left kidney and proximal
segments of ureter
Urinary bt( Without contrast)
• PTH 354 pg/ml
• Uric acid 8.9 mg/dl
• Culture of urine : (-)
What is your likely diagnosis ?
Voiding cystouretrography
END STAGE RENAL
FAILURE
•
•
•
•
•
•
Anemia EPO, Parenterally forms of iron
Hyperphosphatemia Phosphate binders
HT Do not use ACEIs+ARBs
Do not use contrast agents
Do not use NSAIDs
Nephrectomy or Defflux inj. Befor renal
transplantation
Case 4
•
•
•
•
•
57 years old female
Dispnea and vomiting
History of NIDDM ( diagnosed in 1985)
Her father died because of CAD
Her mother had the history of dialysis & died
because of sepsis
PHYSICAL EXAMINATION
•
•
•
•
•
BP: 190/60mmHg P: 92/min/R
Weight 72 kg, BMI 30
edeama (+++/+++)
turgor n, pale face,
Dyspneic and orthopneic with crackles over the
lung bases, tachipne (+)
LABORATORY FINDINGS
• Hb:8.7 Htc: 25% WBC:7200
• BUN:58mg/dL Cr:3.2mg/dL K:6.7mEq/L
Na:135mEq/L
• S.alb 3.1 g/dl
• Urinalysis = D 1010
35-40 WBC
Chronic Kidney Failure
(Due to diabetic nepropathy)
Stage 5
END STAGE RENAL
FAILURE