Chronic Kidney Disease

dr. Tjatur Winarsanto SpPD

Chronic Kidney Disease

Definition
Chronic, irreversible loss of
kidney function attributable
to loss of functional
nephron mass
pathophysiologic processes
for more than 3 months.

definisi
Kronis kerugian, tidak
dapat diubah fungsi ginjal
disebabkan hilangnya
massa nefron fungsional proses pathophysiologic
untuk lebih dari 3 bulan.

Pathophysiology of CKD
Final Common Pathway is loss of nephron mass

Diabetes
Hypertension
Chronic GN
Cystic Disease
Tubulointerstitial disease

Structural/ Functional
Loss of
Nephron Mass Hypertrophy of remnant nephrons

Sclerosis
of remnant
nephrons

Mediated by vasoactive
molecules, cytokines
and growth factors,
renin angiotensin axis

Estimation of GFR
Modification of Diet in Renal
Disease (MDRD) Formula
Estimated GFR = 1.86 (Serum
Creat) -1.154 X (age) -0.203
Multiply by 0.742 for women
Multiply by 1.21 for African
Americans

Cockroft Gault Formula

(140 age) X Body Weight (Kg)
72 X Serum Creatinine (mg/dL)
Multiply by 0.85 for women

Modifikasi Diet di Penyakit Ginjal

(MDRD) Formula
Perkiraan GFR = 1,86 (Serum
Creat) -1,154 X (umur) -0,203
Kalikan dengan 0,742 untuk wanita
Kalikan dengan 1,21 untuk Afrika
Amerika
Cockroft Gault Formula
(140 - umur) X Badan Berat (Kg)
72 X serum kreatinin (mg / dL)
Kalikan dengan 0,85 untuk wanita?

Staging of Chronic Kidney Disease

Stage

Description

GFR (ml/min/1.73 m2)

At increased risk

90 (with CKD risk factors)

Kidney damage with normal or

increased GFR

90

Mildly decreased GFR

60-89

Moderately decreased GFR

30-59

Severely decreased GFR

15-29

Renal Failure

<15 (or dialysis)

Who is at Risk for CKD?

Family history of
heritable renal disease
Diabetes
Hypertension
Auto-immune disease
Old age
Prior episode of ARF
Current evidence of
renal damage, even
with normal or
increased GFR

Riwayat keluarga dari

penyakit ginjal diwariskan
diabetes
hipertensi
Auto-imun penyakit
tua
Sebelum episode GGA
Sekarang bukti kerusakan
ginjal, bahkan dengan GFR
normal atau meningkat

Etiology and Epidemiology

6% of the US
population has CKD
(Stage 1 and 2)
Additional 4-5% have
Stage 3 and 4 CKD
Diabetic nephropathy
Hypertension chronic
ischemic nephropathy
Very high CV disease
burden

6% dari penduduk AS
telah CKD (Tahap 1 dan
2)
4-5% tambahan memiliki
Tahap 3 dan 4 CKD
diabetes nefropati
Hipertensi - nefropati
iskemik kronis
Sangat tinggi CV beban
penyakit

Monitoring of CKD
Serial measurements of
Creatinine
GFR

Albumin
Albumin-creatinine ratio
in the 1st morning
sample
Electrolytes including
HCO3, Ca, Phos; alkaline
phosphatase, iron
studies, intact PTH
Renal sonogram
Renal biopsy

Serial pengukuran
kreatinin
GFR
albumin
Albumin-kreatinin rasio
dalam sampel pagi 1
Elektrolit termasuk
HCO3, Ca, phos,
fosfatase alkali, studi
besi, PTH utuh
sonogram ginjal
biopsi ginjal

Symptoms of CKD
Stage 1 and 2
Asymptomatic,
hypertension

Stage 3 and 4
Anemia loss of energy
Decreasing appetite; poor
nutrition
Abnormalities in Calcium,
Phosphorus metabolism
Sodium, water, potassium
and acid base abnormalities

Stage 5
All of the above
accentuated; eventually
overt uremia

Tahap 1 dan 2
Tanpa gejala, hipertensi
Tahap 3 dan 4
Anemia - kehilangan energi
Penurunan nafsu makan;
gizi buruk
Kelainan pada Kalsium,
Fosfor metabolisme
Natrium, air, kalium dan
asam basa kelainan
tahap 5
Semua hal di atas ditekankan; uremia akhirnya
terbuka

Common Causes and Presentation

Cause

Clinical Presentation

Diabetic kidney
disease

History of diabetes, proteinuria and retinopathy

Hypertension

Elevated BP, normal UA, family history

Non diabetic
Nephritic or nephrotic presentations
glomerular disease
Cystic kidney
disease

Urinary symptoms, abnormal sediment, radiologic findings

Tubulointerstitial
disease

UTI, reflux, chronic med use, drugs, imaging abnormalities,

urine concentrating defects

Clinical Features of Diabetic CKD

Clinical Features of Non-Diabetic

CKD

Pathophysiology of Uremia
Azotemia refers to the
retention of nitrogenous
waste products. Uremia
advanced stages of azotemia
with end organ dysfunction
Accumulation of products of
protein metabolism
Urea anorexia, malaise,
vomiting and headaches

Loss of other renal functions

Erythropoietin deficiency
anemia
Metabolic bone disease;
endocrine abnormalities
Fluid, electrolyte and acid
base disorders

Azotemia - mengacu pada retensi

produk limbah nitrogen. Uremia stadium lanjut azotemia dengan
disfungsi organ akhir
Akumulasi produk dari
metabolisme protein
Urea - anoreksia, malaise, muntah
dan sakit kepala
Kehilangan fungsi ginjal lainnya
Erythropoietin kekurangan anemia
Tulang metabolik penyakit;
kelainan endokrin
Cairan, elektrolit dan asam basa
gangguan

Symptoms of Uremia
Organ System

Symptoms

Signs

General

Fatigue, weakness

Sallow-appearing, chronically ill

Skin

Pruritus, easy bruisability

Pallor, ecchymoses,
excoriations, edema, xerosis

ENT

Metallic taste in mouth, epistaxis

Urinous breath / fetor

Eye

Pale conjunctiva

Pulmonary

Shortness of breath

Rales, pleural effusion

Cardiovascular

Dyspnea on exertion, retrosternal pain on

inspiration (pericarditis)

Hypertension, cardiomegaly,
friction rub

Gastrointestinal

Anorexia, nausea, vomiting, hiccups

Genitourinary

Nocturia, impotence

Neuromuscular

Restless legs, numbness and cramps in legs

Neurologic

Generalized irritability and inability to

concentrate, decreased libido

Isosthenuria

Stupor, asterixis, myoclonus,

peripheral neuropathy

Mineral Metabolism
Calciphylaxis
Calcemic uremic arteriopathy
Extraosseous/metastatic calcification of soft
tissues and blood vessels
Devastating complication
Treatment: controversial
Sodium thiosulfate
Parathyroidectomy
calciphylaxis
Calcemic uremik arteriopathy
Extraosseous / metastatik kalsifikasi jaringan lunak
dan pembuluh darah
menghancurkan komplikasi
Pengobatan: kontroversial
natrium tiosulfat
Parathyroidectomy

Cardiovascular Abnormalities

Leading cause of morbidity and

mortality in patients with CKD at
all stages
Ischemic CAD
Hypertension and LVH
Congestive heart failure
Uremic
Penyebab utama morbiditas dan
mortalitas pada pasien dengan
CKD pada semua tahap
iskemik CAD
Hipertensi dan LVH
Gagal jantung kongestif
uremic perikarditis pericarditis

Hematological Abnormalities

Anemia

Coagulopathy

Chronic blood loss, hemolysis,

marrow suppression by uremic
factors, and reduced renal production
of EPO
Normocytic, normochromic
Rx: Iron and Epo as needed
Mainly platelet dysfunction
decreased activity of platelet factor
III, abnormal platelet aggregation and
adhesiveness and impaired thrombin
consumption
Increased propensity to bleed post
surgical, GI Tract, pericardial sac,
intracranial
Increased thrombotic tendency
nephrotic syndrome

anemia
Darah kronis kerugian, hemolisis,
penekanan sumsum oleh faktor
uremik, dan produksi ginjal
berkurang EPO
Normositik, normokromik
Rx: Besi dan Epo sesuai kebutuhan
koagulopati
Terutama trombosit disfungsi aktivitas penurunan III faktor
platelet, agregasi platelet
abnormal dan kelengketan dan
konsumsi trombin gangguan
Peningkatan kecenderungan untuk
berdarah - posting bedah, GI Tract,
pericardial sac, intrakranial
Peningkatan trombotik
kecenderungan - sindrom nefrotik

Other Abnormalities

Neuromuscular

Gastrointestinal

Endocrine

Dermatologic

Central, peripheral and autonomic neuropathy

Peripheral Sensory/Motor Neuropathy
Stage 4 for more than 6 months
Restless leg syndrome

Uremic fetor
Gastritis, peptic disease, mucosal ulcerations,
AVMs

Glucose metabolism
Estrogen levels amenorrhea, frequent abortions
Male: oligospermia, germinal cell dysplasia,
delayed sexual maturation
Pallor, ecchymoses, hematomas, calciphylaxis,
pruritus, uremic frost

neuromuskular
Tengah neuropati, perifer dan otonom
Peripheral Sensory / Motor Neuropati
Tahap 4 selama lebih dari 6 bulan
Restless leg syndrome
gastrointestinal
uremic bau mulut
Gastritis, penyakit lambung, ulserasi
mukosa, AVMs
kelenjar endokrin
glukosa metabolisme
Tingkat estrogen - amenore, aborsi sering
Pria: oligospermia, displasia sel germinal,
kematangan seksual tertunda
Dermatologic
Pucat, ekimosis, hematoma,
calciphylaxis, pruritus es, uremik

Therapeutics in CKD
Non Pharmacologic
Risk Factor Modification

Pharmacologic
Treatment of complications

Therapeutics in CKD
Non Pharmacologic
Risk Factor Modification

Pharmacologic
Treatment of complications

Therapeutics in CKD
Non Pharmacologic
Risk Factor Modification

Pharmacologic
Treatment of complications

Sodium and water

ImbalanceKetidakseimbanga
n

Glomerulotubular feedback is disrupted

sodium retention, contributes to
hypertension; hyponatremia is unusual.
Higher than usual doses for diuretics. In
situations with volume depletion can be
severe, because of inadequate sodium
retention.
Treatment: Salt restriction; high
doses of diuretics
Umpan balik Glomerulotubular
terganggu - retensi natrium,
memberikan kontribusi untuk
hipertensi; hiponatremia tidak biasa.
Lebih tinggi dari dosis biasa untuk
diuretik. Dalam situasi dengan
penurunan volume - mungkin parah,
karena retensi natrium memadai.
Pengobatan: pembatasan garam; dosis
tinggi diuretik

Potassium Imbalance
Potassium
GI excretion is augmented
Constipation, dietary
intake, protein catabolism,
hemolysis, hemorrhage,
transfusion of stored blood,
metabolic acidosis,
Drugs: ACE inhibitors,
ARBs, B blockers, K sparing
diuretics and NSAIDs
Hyporeninemic
hypoaldosteronism:
Diabetes, sickle cell disease

Acid Base Imbalance

Damaged kidneys are unable
to excrete the 1 mEq/kg/d of
acid generated by metabolism
of dietary proteins.

NH3 production is limited

because of loss of nephron mass
Decreased filtration of titrable
acids sulfates, phosphates
Decreased proximal tubular
bicarb reabsorption, decreased
positive H ion secretion

Arterial pH: 7.33 - 7.37; serum

HCO3 rarely below 15
buffering offered by bone
calcium carbonate and
phosphate
Should be maintained over 21
Treatment: Sodium
bicarbonate, calcium
carbonate, sodium citrate

Bone Disease

Treatment of Secondary
Hyperparathyroidism
Phosphorus control in
diet
Phosphate binders
Calcium acetate (Phoslo),
calcium carbonate
(TUMS), sevelamer
(Renagel) , lanthanum
(Fosrenol)

Oral Vitamin D
Calcimemetic agent:
Cinacalcet (Sensipar)

Fosfor kontrol dalam diet

fosfat binder
Kalsium asetat (Phoslo),
kalsium karbonat (Tums),
sevelamer (Renagel),
lantanum (FOSRENOL)
Oral Vitamin D
Calcimemetic agent:
cinacalcet (Sensipar)