Kuliah CKD 2015

Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Chronic Kidney
Disease
A. A. Gede Budhitresna,MD,PhD,Int-CE,FINASIM
SCHOOL OF MEDICINE UNIVERSITY OF

WARMADEWA
2015
Chronic Kidney Disease

A 54 year old woman is evaluated for a Cr
of 1.3; 18 months ago it was 0.9. She has

a 5 year history of DM 2, dyslipidemia and
HTN well controlled with lisinopril, HCTZ,
and atenelol. She is also on glipizide and
simvastatin. Hemoglobin is normal. What
is the most appropriate for this patient?
24 hour collection for proteinuria
Kidney USG
Measurement of Urine micro albumin
SPEP
Measurement of HbA1C

In the United States, there is a rising incidence
and prevalence of Kidney Disease.

Nearly 350,000 of these are on dialysis.
Also, there is an increasing prevalence of earlier
stages of chronic kidney disease which
unfortunately is under-diagnosed and undertreated in the United States.
In 2000, the National Kidney Foundation
(NKF) Kidney Disease Outcomes Quality
Initiative (K/DOQI) Advisory Board approved
development of clinical practice guidelines to
define chronic kidney disease and to classify
stages in the progression of chronic kidney
disease.
CKD Risk Factors

Diabetes Mellitus Family history of
CKD
Hypertension
Kidney Stones
Cardiovascular
Disease
Infections like Hep
Obesity
C and HIV
Metabolic
Autoimmune
Syndrome
diseases
Age and Race
Nephrotoxics
Acute Kidney Injury
like NSAIDS
Malignancy
Diseases of the Kidney
Diabetes
Hypertension
Atherosclerosis
All global renal
Glomerular diseases
diseases affect
Toxins
glomerular filtration
Gentamicin
rate (GFR)
NSAIDS
Compound analgesics
Inherited diseases
Tubular disorders
K/DOQI (USA) Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Causes of End Stage Renal

Disease
USRDS Annual Data Report

CKD - Causes
Diabetic
Non Diabetic
Glomerular
Nephritic: PIGN, IgA, MPGN
Nephrotic:
FSGS,
Membranous,
Amyloidosis
Tubulointerstitial: Analgesic, Reflux, Ch. Obs
Vascular: Vasculitis, HTN, RAS
Cystic: ADPKD
CKD in transplantation
Increased Mortality in Patients With

Diabetes
and CKD: 2-Year Clinical Outcomes
100
No Events
ESRD, CKD Stage 5
Death
Patients (%)
80
60
61.6
67.6
84.0
40
6.1
2.9
20
0
15.7
+ DM,
- CKD
0.3
29.5
32.3
- DM,
+CKD
+ DM,
+ CKD
Medical Cohort
CKD identified as ICD-9-CM diagnosis code, includes CKD from diabetes, hypertension,
obstructive uropathy, and other diagnosis codes reported on USRDS ESRD registration forms.
DM = diabetes mellitus; ESRD = end-stage renal disease; ICD-9-CM = International Statistical
Classification of Diseases, 9th Revision, Clinical Modification.
Collins et al. Kidney Int. 2003;64(suppl 87):S24-S31.
2005
The Johns
University
Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate
of Elsevier
Inc. AllHopkins
Rights Reserved.
School of Medicine.

(CKD)
Involves progressive, irreversible
loss of kidney function
Defined as either presence of
Kidney damage
Pathological abnormalities
Glomerular filtration rate (GFR)

<60 ml/min for 3 months or longer
Gangguan Fungsi Ginjal

Klinis
Tanda, gejala, pemeriksaan fisik.
Laboratoris
Ureum , kreatitin , asam urat
Tes klirens kreatinin (TKK)

Kreatinin urin(mg/dL) x vol.urin(mL/24 jam
Kreatinin serum(mg/dL) x 1440
Rumus Cockrof-Gault
LFG
(140-umur) x BB (Kg)
72 x kreatinin serum (mg/dL
Wanita = 0,85 x priaCopyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Estimate of GFR
Measured GFR
Serum creatinine
Creatinine clearance
Formulae based on serum creatinine
Cockcroft and Gault
MDRD
Other
All based on measurements

of serum creatinine
Eg Cystatin C
Kriteria CKD
Kerusakan
ginjal > 3 bln,

struktural atau fungsional dengan
atau tanpa penurunan LFG
Kelainan patologi atau
Tanda kerusakan ginjal dalam darah
ataupun
urine
atau
pemeriksaan pencitraan
pada
LFG < 60mL/m/1,73m2, > 3bln

Pathophysiology Of CKD
Repeated injury to kidney
Gejala CKD
Nafsu makan hilang / kurang
Nausea vomiting
Gatal-gatal
Gangguan miksi, poli/oliguria,
nokturia, dll
Gejala-gejala anemia
Insomnia
Gelisah
Gangguan mental / kesadaran
coma
CKD - Manifestations
Abnormal Sodium-Water metabolism
Edema, Hypertension
Abnormal Acid-base abnormalities

Metabolic Acidosis due to uremia or RTA
Abnormal hematopoesis
Anemia of CKD
Cardiovascular Abnormalities
LVH, CAD, Diastolic Dysfunction
Abnormal Calcium-Phosphorus metabolism

Hyperphosphatemia, pruritus, arthralgia
Hyperparathyroidism
Renal Osteodystrophy
Manifestations of Chronic
Uremia

Clinical Manifestations
Uremia
Syndrome that incorporates
all signs and symptoms seen

in various systems
throughout the body

Urinary system
Polyuria
Results from inability of
kidneys to concentrate urine

Occurs most often at night
Specific gravity fixed around
1.010

Urinary system
Oliguria
Occurs as CKD worsens
Anuria
Urine output <40 ml per 24
hours

Metabolic disturbances
Waste product accumulation
As GFR , BUN and serum
creatinine levels
BUN
Not only by kidney failure but by protein
intake, fever, corticosteroids, and
catabolism
N/V, lethargy, fatigue, impaired thought
processes, and headaches occur

Electrolyte/acidbase imbalances
Potassium
Hyperkalemia
Most serious electrolyte disorder in
kidney disease
Fatal dysrhythmias

Sodium
May be normal or low
Because of impaired excretion,
sodium is retained
Water is retained
Edema
Hypertension
CHF

Calcium and phosphate alterations
Magnesium alterations
Metabolic acidosis
Results from
Inability of kidneys to excrete acid load
(primary ammonia)

Hematologic system
Anemia
Due to production of
erythropoietin
From of functioning renal
tubular cells
Bleeding tendencies
Defect in platelet function

Hematologic system
Infection
Changes in leukocyte
function
Altered immune response
and function
Diminished inflammatory
response

Cardiovascular system
Hypertension
Heart failure
Left ventricular hypertrophy
Peripheral edema
Dysrhythmias
Uremic pericarditis

Respiratory system
Kussmaul respiration-Why?
Dyspnea-Why?
Pulmonary edema-Why?
Uremic pleuritis-Why?
Pleural effusion
Predisposition to respiratory infections
Depressed cough reflex
Uremic lung

Gastrointestinal system
Every part of GI is affected
Due to excessive urea
Mucosal ulcerations
Stomatitis
Uremic fetor (urinous odor of the
breath)
GI bleeding
Anorexia
N/V

Neurologic system
Expected as renal failure progresses
Attributed to
Increased nitrogenous waste products

Electrolyte imbalances
Metabolic acidosis
Demyelination of nerve fibers
Altered mental ability

Seizures and Coma
Dialysis encephalopathy
Peripheral neuropathy

Neurologic system
Restless leg syndrome
Muscle twitching
Irritability
Decreased ability to concentrate

Musculoskeletal system
Renal osteodystrophy
Syndrome of skeletal changes
Result of alterations in calcium and
phosphate metabolism
Weaken bones, increase fracture risk
Two types associated with ESRD:

Osteomalacia
Osteitis fibrosa
Feedback Loops in SHPT

(Secondary hyperparathyroidism)
Decreased Vitamin D Receptors
and Ca-Sensing Receptors
PTH
PTH
Ca++
Bone Disease
Fractures
Serum P
Bone pain
Marrow fibrosis
Erythropoietin resistance
1,25D
Calcitriol
Systemic Toxicity
CVD
Hypertension
Inflammation
Calcification
Immunological
25D
Renal Failure
Ca = calcium; CVD = cardiovascular disease; P = phosphorus.
Courtesy of Kevin Martin, MB, BCh.
Copyright 2007, 2004, 2000, Mosby, Inc., an

of Elsevier
Inc.Hopkins
All Rights Reserved.
affiliate
2005 The
Johns
University
School of Medicine.
Renal Osteodystrophy

Integumentary system
Most noticeable change
Yellow-gray discoloration of the skin
Due to absorption/retention of urinary
pigments
Pruritus
Uremic frost
Dry, pale skin

Integumentary system
Dry, brittle hair
Thin nails
Petechiae
Ecchymoses

Reproductive system
Infertility
Experienced by both sexes
Decreased libido
Low sperm counts
Sexual dysfunction
CKD - Management
Diagnostic work up to decide underlying
etiology
Treatment of Hypertension and Dyslipidemia
Treatment of Anemia
Treatment of Hyperphosphatemia
Avoidance of Dehydration & Nephrotoxic
agents
Proper Dosing of Drugs
Preparation for Renal Replacement Therapy
CKD - Evaluation
Serum electrolytes
Urine spot protein analysis (24 hour no
longer recommended).
ANA, C3, C4
Kidney Ultrasound
Urine sediment analysis
Biopsy
Evidence of glomerular disease without
diabetes
Sudden onset of nephrotic syndrome or
glomerular hematuria
CKD - Management
etiology
Treatment of Anemia
agents
CKD - Hypertension
Anti-Hypertensive Agents
Single
most important measure could be

adequate BP control
Target BP <130/80 with minimal proteinuria and
BP<125/75 with significant proteinuria (>1g).
ACEIs and ARBs have been demonstrated to
slow both diabetic and non-diabetic renal disease
in both experimental and human studies.
Decrease the sodium intake to 2.5 g /day
Usually requires more than 2 medications.
Diuretics enhance the antihypertensive and
antiproteinuric effects of other agents..
Recommendations for BP and

RAS Management in CKD
Patient
Group
Goal BP
(mm Hg)
First Line
Adjunctive
+ Diabetes
<130/80
ACE-I or ARB Diuretics then CCB or BB
Diabetes
+ Proteinuria
<130/80
ACE-I or ARB Diuretics then CCB or BB
Diabetes
Proteinuria
<130/80
No specific preference:
Diuretics then ACE-I, ARB, CCB, or BB
EXPECT TO NEED TO USE 3+ AGENTS TO ACHIEVE GOALS

Recommendations largely consistent across JNC 7, ADA, and K/DOQI
BP = blood pressure; RAS = renin angiotensin system; CCB = calcium channel blocker;
BB = -blocker; JNC 7 = The Seventh Report of the Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure.
ADA. Diabetes Care. 2005;28(suppl 1); Chobanian et al. JAMA. 2003;289:2560-2572; Kidney Disease Outcomes
Quality Initiatives (K/DOQI). Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.
Relationship Between Achieved

BP
and
GFR
MAP = Mean Arterial Pressure*
r = 0.69
P<0.05
Untreated
Hypertension
130/80
140/90
*MAP = [SBP + (2 DBP)]/3 mm Hg.

Summary of 9 studies used in figure.
Parving et al. 1989; Viberti et al. 1993; Klahr et al. 1993; Hebert et al. 1994; Lebovitz et al. 1994;
Moschio et al. 1996; Bakris et al. 1996; Bakris et al. 1997; GISEN Group. 1997.
Bakris et al. Am J Kidney Dis. 2000;36:646-661.
2005 The Johns Hopkins University School of Medicine.

Collaborative Care
Drug therapy
Hypertension (contd)
Antihypertensive drugs
Diuretics
-Adrenergic blockers
Calcium channel blockers
Angiotensin-converting enzyme (ACE)
inhibitors
Angiotensin receptor blocker (ARB)
CKD - Dyslipidemia
Dyslipidemia
and
Cardiovascular
morbidity
Several studies like the 4D study showed no
benefit of statins in dialysis patients.
However, post hoc analysis of this data
does suggest that the management of
dyslipidemia in CKD 2 4 improves cardiac
mortality and morbidity.
Dyslipidemia
is
frequently
seen
in
glomerular
disease
with
proteinuria
(nephrotic syndrome) and its control
reduces atherosclerosis related morbidity
and mortality.
CKD - Management
etiology
Treatment of Anemia
agents
CKD - Anemia
Decreased quality
of life with anemia.

Diagnosis of
exclusion.
Mostly apparent in
the stage 4 and 5 of
CKD.
Due to decrease in
EPO production in
the kidney.

Collaborative Care
Drug therapy
Anemia
Erythropoietin
Epoetin alfa (Epogen, Procrit)

Administered IV or subcutaneously
Increased hemoglobin and hematocrit in
2 to 3 weeks
Side effect: Hypertension

Collaborative Care
Drug therapy
Anemia (contd)
Iron supplements
If plasma ferritin <100 ng/ml
Side effect: Gastric irritation,
constipation
May make stool dark in color

Collaborative Care
Drug therapy
Anemia (contd)
Folic acid supplements
Needed for RBC formation
Removed by dialysis
Avoid blood transfusions
CKD - Management
etiology
Treatment of Anemia
agents
CKD - Hyperphosphatemia
Control of Hyperphosphatemia
Due to decreased excretion in urine.
Control of hyperphosphatemia by dietary measures
slow progression in experimental models of CKD.

Hyperphosphatemia leads to pruritus, calcification
in synovial membranes, blood vessels and even
cardiac valves.
Therapy
includes
Phosphorus
restriction
to
800mg/day and use of phosphrous binders with
food.
Calcium Carbonate (TUMS), Ca-acetate (PHOSLO)
Lanthanum
Renagel
CKD Bone and Mineral disease
Hyperparathyroidism:
High phosphorus and low Vitamin D
causing low calcium.

Monitor Intact PTH levels and keep
between 100 and 500.
Maintain Phosphorus and Calcium
within normal ranges.
Vitamin D analog paricalcitol.
Calcimimetic agents like cinacalcet.

Collaborative Care
Drug therapy
Renal osteodystrophy
Phosphate intake restricted to
<1000 mg/day
Phosphate binders
Calcium carbonate (Tums)

Bind phosphate in bowel and excreted
Sevelamer hydrochloride (Renagel)
Lowers cholesterol and LDLs

Collaborative Care
Drug therapy
Renal osteodystrophy (contd)
Phosphate binders (contd)
Should be administered with each meal
Side effect: Constipation
Supplementing vitamin D
Calcitriol (Rocaltrol)
Serum phosphate level must be lowered before
administering calcium or vitamin D
CKD - Management
etiology
Treatment of Anemia
agents
CKD - Nephrotoxics
Avoidance of Dehydration/Nephrotoxic Agents
Drugs such as Aminoglycosides, NSAIDs
Avoiding exposure to Radio contrast agents.
In presence of dehydration, even in absence of
renovascular disease, ACEIs or ARBs can

aggravate renal dysfunction
Dehydration is frequent in tubulo-interstitial
disorders
where
urinary
concentration
is
impaired.
Proper Dosing of Drugs eg. Allopurinol
0

Collaborative Care
Drug therapy
Hyperkalemia
IV insulin and glucose
IV 10% calcium gluconate
Raises threshold for excitation
Sodium bicarbonate
Shift potassium into cells
Correct acidosis

Collaborative Care
Drug therapy
Hyperkalemia (contd)
Sodium polystyrene sulfonate
(Kayexalate)
Cation-exchange resin
Resin in bowel exchanges potassium for
sodium
Evacuates potassium-rich stool from body
Educate patient that diarrhea may occur due
to laxative in preparation

Collaborative Care
Nutritional therapy
Protein restriction
0.6 to 0.8 g/kg body weight/day
Water restriction
Intake depends on daily urine output

Collaborative Care
Nutritional therapy
Sodium restriction
Diets vary from 2 to 4 g depending on
degree of edema and hypertension

Sodium and salt should not be equated
Patient should be instructed to avoid
high-sodium foods
Salt substitutes should not be used because
they contain potassium chloride

Collaborative Care
Nutritional therapy
Potassium restriction
2 to 4 g
High-potassium foods should be
avoided
Oranges
Bananas
Tomatoes
Green vegetables

Collaborative Care
Phosphate restriction
1000 mg/day
Foods high in phosphate
Dairy products
Most foods high in phosphate are also
high in calcium
CKD - Management
etiology
Treatment of Anemia
agents
CKD Medication Dosing

Uremia affects GI absorption; eg Iron.
Impaired plasma protein binding of drugs; eg
Dilantin.
Increased volume of distribution;
Excretion of many drugs depends upon the
kidney;
Some drugs used in normal dose will lead to
nephrotoxic effects eg. Allopurinol

Other drugs when used in normal dose will lead to
other toxic effects eg. Vancomycin.
Dose Reduction or Interval Extension

CKD - Management
etiology
Treatment of Anemia
agents
CKD - RRT
Preparation
for
Replacement Therapy
Renal
Education for Options of Dialysis & Renal
Transplantation for Renal Replacement

Hemodialysis Vs Peritoneal Dialysis
Avoidance of Veni-puncture & insertion of
catheters in peripheral veins once GFR <
60mls.
Timely placement of vascular access or
PD catheter.
CKD - RRT
Indications (Absolute):
Uncontrolled hyperkalemia and acidosis

Uncontrollable hypervolemia (pulmonary edema)
Pericarditis
AMS and somnolence (advanced encephalopathy)
Bleeding diathesis
Indications (Relative):
Nausea, vomiting and poor nutrition

Metabolic acidosis
Lethargy and Malaise
Worsening kidney function <10 ml or <15 ml in
diabetics
Nursing Management
Nursing Implementation
Health promotion
Identify individuals at risk for CKD
History of renal disease

Hypertension
Diabetes mellitus
Repeated urinary tract infection
Regular checkups and changes in
urinary appearance, frequency and

volume should be reported
CKD - Summary
In creasing prevalence of CKD in the
population.
Early detection and prevention of
progression.
Early involvement of nephrologists in the
care (when GFR<30).
Treatment
of
Manifestations
and
complications.
Renal Replacement Therapy
Timely referral for Access
Timely Transplant Work up.
Stages in Progression of Chronic

Kidney Disease and Therapeutic
Strategies
Complications
Complications
Normal
Screening
for CKD
risk factors
Increased
Increased
risk
CKD risk
reduction;
Screening for
CKD
Damage
Damage
Diagnosis
& treatment;
Treat
comorbid
conditions;
Slow
progression
GFR
GFR
Kidney
Kidney
failure
failure
Estimate
Replacement
progression;
by dialysis
Treat
& transplant
complications;
Prepare for
replacement
CKD
death
death
The Story of Mr. George Lopez

45 yr HM with Diabetes for 10 yrs,
reasonably well controlled
PMH:
Hypertension for 7 yrs..well
controlled
BMI of 30
Dyslipidemia
Fam Hx: Diabetes;

Soc Hx: Sedentary; non smoker;
Comedian
Exam
139/85 Mild Obesity, rest fairly
normal
Labs
BUN 28, Creatinine 1.8, Urine
protein (dipstick) 2+
MDRD GFR for Mr Lopez

Diabetic, Hypertension, Metabolic
Syndrome X
Stage 3 CKD
GFR = 44 ml/min/1.73 m2

A 70 yr old woman comes for F/U of recently diagnosed
CKD and HTN. She is asymptomatic. Her only

medications is Lisinopril which has been titrated to its
maximum dose in the last 3 months. She is compliant
and uses salt restriction. BP is 160/90. exam is normal
except for trace pedal edema. Cr is 1.3, K is 5 and
Urine Prot is 2.1 gm. Which of the following is the most
appropriate treatment for this patient?
Chlorthalidone
Losartan
Metoprolol
Minoxidil
Amlodipine
In
God
we
trust,everything
else
should
be
based
on
evidence (Claude Organ)
Copy right: agbudhitresna@yahoo.com

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Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

SCHOOL OF MEDICINE UNIVERSITY OF

Chronic Kidney Disease

of 1.3; 18 months ago it was 0.9. She has

Chronic Kidney Disease

and prevalence of Kidney Disease.

CKD Risk Factors

Diseases of the Kidney

Causes of End Stage Renal

USRDS Annual Data Report

Increased Mortality in Patients With

Chronic Kidney Disease

Glomerular filtration rate (GFR)

Gangguan Fungsi Ginjal

Tes klirens kreatinin (TKK)

All based on measurements

ginjal > 3 bln,

LFG < 60mL/m/1,73m2, > 3bln

Abnormal Acid-base abnormalities

Abnormal Calcium-Phosphorus metabolism

Chronic Kidney Disease

Syndrome that incorporates

all signs and symptoms seen

Chronic Kidney Disease

kidneys to concentrate urine

Chronic Kidney Disease

Occurs as CKD worsens

Urine output <40 ml per 24

Chronic Kidney Disease

Chronic Kidney Disease

Chronic Kidney Disease

Chronic Kidney Disease

Chronic Kidney Disease

From of functioning renal

Chronic Kidney Disease

Chronic Kidney Disease

Chronic Kidney Disease

Chronic Kidney Disease

Uremic fetor (urinous odor of the

Chronic Kidney Disease

Increased nitrogenous waste products

Altered mental ability

Chronic Kidney Disease

Chronic Kidney Disease

Weaken bones, increase fracture risk

Two types associated with ESRD:

Feedback Loops in SHPT

Copyright 2007, 2004, 2000, Mosby, Inc., an

Chronic Kidney Disease

Chronic Kidney Disease

Chronic Kidney Disease

Evidence of glomerular disease without

most important measure could be

Recommendations for BP and

ACE-I or ARB Diuretics then CCB or BB

ACE-I or ARB Diuretics then CCB or BB

EXPECT TO NEED TO USE 3+ AGENTS TO ACHIEVE GOALS

Relationship Between Achieved

*MAP = [SBP + (2 DBP)]/3 mm Hg.

Chronic Kidney Disease

of life with anemia.

Chronic Kidney Disease

Epoetin alfa (Epogen, Procrit)