Anatomy and Physiology of Urinary

System

WIDODO
BAGIAN ANESTESIOLOGI,
PERAWATAN INTENSIF, DAN
PENANGANAN NYERI
RSUP WAHIDIN
SUDIROHUSODO
MAKASSAR

Introduction
Organ system that produces, stores, and carries
urine
Humans produce about 1.5 liters of urine over 24
hours, although this amount may vary according to
the circumstances.
Increased fluid intake generally increases urine
production.
Increased perspiration and respiration may
decrease the amount of fluid excreted through the
kidneys.
Some medications interfere directly or indirectly
with urine production, such as diuretics.

Components of system
Kidneys
Ureters
Bladder
Urethra

Kidney Location and External

Anatomy

Functions of the Kidney:

Maintaining balance

Regulation of body fluid volume and

osmolality
Regulation of electrolyte balance
Regulation of acid-base balance
Excretion of waste products (urea, ammonia,
drugs, toxins)
Production and secretion of hormones
Regulation of blood pressure

The Kidney and the Nephron

A.

Renal Vein

B.

Renal Artery

C.

Ureter

D.

Medulla

E.

Renal Pelvis

F.

Cortex

1.

Ascending loop of Henle

2.

Descending loop of Henle

3.

Peritubular capillaries

4.

Proximal tubule

5.

Glomerulus

6.

Distal tubule

The Nephron
Functional unit of the kidney (1,000,000)
Responsible for urine formation:

Filtration
Secretion
Reabsorption

Components of the
nephron
Glomerulus
Afferent and Efferent
arterioles
Proximal Tubule
Loop of Henle
Distal Tubule
Collecting Duct

Overview of nephron function

From http://www.emc.maricopa.edu/faculty/farabee/BIOBK/BioBookEXCRET.html

Filtration

THE GLOMERULUS

Plasma is filtered through the glomerular

barrier
Components of plasma cross the three layers of the glomerular barrier
during filtration
Capillary endothelium
Basement membrane (net negative charge)
Epithelium of Bowmans Capsule (Podocytes filtration slits allow size
<60kD)
The ability of a molecule to cross the membrane depends on size, charge,
and shape
Glomerular filtrate therefore contains all molecules not contained by the
glomerular barrier - it is NOT URINE YET!

Glomerular Filtration Rate

(GFR)
Measure of functional capacity of the
kidney
Dependent on difference in pressures
between capillaries and Bowmans
space
Normal = 120 ml/min =7.2 L/h=180
L/day!! (99% of fluid filtered is reabs.)

The Response to a Reduction in the GFR

Reabsorption
and secretion

Reabsorption

Active Transport requires ATP

Na+, K+ ATP pumps

Passive Transport Na+ symporters (glucose, a.a.,

etc)
Na+ antiporters (H+)
Ion channels
Osmosis

Factors influencing
Reabsorption

Saturation: Transporters can get saturated

by high concentrations of a substance failure to resorb all of it results in its loss in
the urine (eg, renal threshold for glucose is
about 180mg/dl).
Rate of flow of the filtrate: affects the time
available for the transporters to reabsorb
molecules.

What is Reabsorbed Where?

Proximal tubule - reabsorbs 65 % of filtered Na+ as well as Cl-,
Ca2+, PO4, HCO3-. 75-90% of H20. Glucose, carbohydrates, amino
acids, and small proteins are also reabsorbed here.
Loop of Henle - reabsorbs 25% of filtered Na+.
Distal tubule - reabsorbs 8% of filtered Na+. Reabsorbs HCO3-.
Collecting duct - reabsorbs the remaining 2% of Na+ only if the
hormone aldosterone is present. H20 depending on hormone
ADH.

Secretion
Proximal tubule uric acid, bile salts,
metabolites,
some
drugs,
some
creatinine
Distal tubule Most active secretion
takes place here including organic
acids, K+, H+, drugs, TammHorsfall protein (main component
of hyaline casts).

Countercurrent exchange

The structure and transport

properties of the loop of
Henle in the nephron create
the Countercurrent
multiplier effect.
A substance to be exchanged
moves across a permeable
barrier in the direction from
greater to lesser
concentration.
Image from http://en.wikipedia.org/wiki/Countercurrent_exchange

Loop of Henle
Goal= make isotonic filtrate
into hypertonic urine (dont
waste H20!!)
Counter-current multiplier:

Descending loop is permeable to

Na+, Cl-, H20
Ascending loop is impermeable to
H20- active NaCl transport
Creates concentration gradient in
interstitium
Urine actually leaves hypotonic
but CD takes adv in making
hypertonic

Hormones Produced by the

Kidney

Renin:
Released from juxtaglomerular apparatus when low blood
flow or low Na+. Renin leads to production of angiotensin II,
which in turn ultimately leads to retention of salt and water.

Erythropoietin:
Stimulates red blood cell development in bone marrow. Will
increase when blood oxygen low and anemia (low
hemoglobin).

Vitamin D3:
Enzyme converts Vit D to active form 1,25(OH)2VitD.
Involved in calcium homeostasis.

Renin, Angiotensin, Aldosterone:

Regulation of Salt/Water Balance

Aldosterone
Secreted by the adrenal glands in
response to angiotensin II or high
potassium
Acts in distal nephron to increase
resorption of Na+ and Cl- and the
secretion of K+ and H+
NaCl resorption causes passive
retention of H2O

Anti-Diuretic Hormone (ADH)

Osmoreceptors in the brain (hypothalamus)

sense Na+ concentration of blood.
High Na+ (blood is highly concentrated)
stimulates posterior pituitary to secrete ADH.
ADH upregulates water channels on the
collecting ducts of the nephrons in the kidneys.
This leads to increased water resorption and
decrease in Na concentration by dilution

Ureters
Slender tubes that convey urine from
the kidneys to the bladder
Ureters enter the base of the bladder
through the posterior wall

This closes their distal ends as bladder

pressure increases and prevents backflow
of urine into the ureters

Ureters

Ureters have a trilayered wall

Transitional epithelial mucosa
Smooth muscle muscularis
Fibrous connective tissue adventitia

Ureters actively propel urine to the

bladder via response to smooth muscle
stretch

Urinary Bladder
Smooth, collapsible, muscular sac that
temporarily stores urine
It lies retroperitoneally on the pelvic floor
posterior to the pubic symphysis

Males prostate gland surrounds the neck

inferiorly
Females anterior to the vagina and uterus

Trigone triangular area outlined by the

openings for the ureters and the urethra

Clinically important because infections tend

to persist in this
region
Chapter
25: Urinary System
29

Urinary Bladder

The bladder wall has three layers

Transitional epithelial mucosa
A thick muscular layer
A fibrous adventitia

The bladder is distensible and collapses

when empty
As urine accumulates, the bladder
expands without significant rise in
internal pressure
Chapter 25: Urinary System

30

Urinary Bladder

Chapter 25: Urinary System

3125.18a, b
Figure

Urethra

Muscular tube that:

Drains urine from the bladder
Conveys it out of the body

Urethra

Sphincters keep the urethra closed

when urine is not being passed
Internal urethral sphincter involuntary
sphincter at the bladder-urethra junction
External urethral sphincter voluntary
sphincter surrounding the urethra as it
passes through the urogenital diaphragm
Levator ani muscle voluntary urethral
sphincter

Urethra
The female urethra is tightly bound to the
anterior vaginal wall
Its external opening lies anterior to the
vaginal opening and posterior to the clitoris
The male urethra has three named regions

Prostatic urethra runs within the prostate gland

Membranous urethra runs through the
urogenital diaphragm
Spongy (penile) urethra passes through the
penis and opens via the external urethral orifice
Chapter 25: Urinary System

34

Urethra

Chapter 25: Urinary System

3525.18a. b
Figure

Micturition (Voiding or
Urination)

The act of emptying the bladder

Distension of bladder walls initiates spinal
reflexes that:
Stimulate contraction of the external urethral
sphincter
Inhibit the detrusor muscle and internal
sphincter (temporarily)
Voiding reflexes:
Stimulate the detrusor muscle to contract
Inhibit the internal and external sphincters

Chemical Composition of
Urine
Urine is 95% water and 5% solutes
Nitrogenous wastes include urea, uric acid,
and creatinine
Other normal solutes include:

Sodium, potassium, phosphate, and sulfate ions

Calcium, magnesium, and bicarbonate ions

Abnormally high concentrations of any

urinary constituents may indicate pathology

ACUTE KIDNEY INJURY

WIDODO
RSUP WAHIDIN
sUDIROHUSODO
MAKASSAR

Pendahuluan
Gagal ginjal akut
(ARF)
Salah satu kondisi yang paling sering terjadi
pada kasus-kasus trauma dan penyakit kritis.

Sistem scoring keparahan penyakit seperti

APACHE III dan SOFA, memberi bobot yg cukup besar terhadap disfungsi
ginjal

Pendahuluan
Disfungsi
Ginjal

ARF paling sering

terjadi ICU dan sering
merupakan bagian
dari disfungsi organ
lainnya

Berat
Memerlukan RRT
Ringan Perubahan kecil nilai
kreatinin atau produksi urin

Mempengaruhi morbiditas
dan mortalitas pasien

Pendahuluan
Jaringan Kolaborasi berbagai kelompok :
ADQI= the Acute Dialysis Quality Initiative
ASN = American Society of Nephrology
NKF = the National Kidney Foundation
dan European Society of Intensive Care Medicine

AKIN

the Acute Kidney Injury Network

AKI

DEFINISI
Acute Kidney Injury
Belum ada konsensus terhadap berapa besar disfungsi
ginjal yg dsb AKI.

ADQI
klasifikasi Risk, Injuri, Failure, Loss and End Stage
Kidney RIFLE

DEFINISI
mendefenisikan 3 tingkatan
keparahan
Risk ( kelas R )
Injuri ( Kelas I )
Failure ( Kelas
F)
Loss dan End
Stage Kidney
Disease

Risiko disfungsi ginjal

Sdh terjadi injuri pd ginjal

Gagal ginjal

kelas outcome

Kelas
Tingkatan

Gambar 1. Skema klasifikasi AKI berdasarkan kriteria RIFLE

(dikutip : Belomo A, Ronco C,Kellum JA,et al.ARCritical care 2004,8:R204-R212 )

DEFINISI
Pasien Masuk RS
Tidak ada data awal
fungsi ginjal

Usul
ADQI

Asumsi GFR
awal normal

Gunakan Nilai
Kreatinin Serum

75-100 ml/menit per

1,73m2

Rumus MDRD untuk perhitungan GFR

Modification of Diet in Renal Disease
GFR perkiraan 75(ml/min per 1.73 m2)

= 186 x (Scr) - 1.54 x (umur) - 0.0203

x (0.742 Perempuan )x(1.210 Kulit hitam )

Rumusan MDRD ini hanya dipakai untuk memperkirakan kreatinin serum

baseline

Age (years)

Black males
(mg/dl [mol/l])

Other males
(mg/dl [mol/l])

Black females
(mg/dl [mol/l])

Other females
(mg/dl [mol/l])

2024

1.5 (133)

1.3 (115)

1.2 (106)

1.0 (88)

2529

1.5 (133)

1.2 (106)

1.1 (97)

1.0 (88)

3039

1.4 (124)

1.2 (106)

1.1 (97)

0.9 (80)

4054

1.3 (115)

1.1 (97)

1.0 (88)

0.9 (80)

5565

1.3 (115)

1.1 (97)

1.0 (88)

0.8 (71)

>65

1.2 (106)

1.0 (88)

0.9 (80)

0.8 (71)

Tabel 1. Perkiraan kreatinin serum

baseline

DEFINISI

AQDI

AKIN

Berkurangnya fungsi ginjal

secara mendadak (dlm
48
jam) yg didefenisikan sebagai
peningkatan kreatinin serum
lebih dari atau sama dengan
0,3mg/dl (26,4 umol/l),atau
peningkatan
persentase
kreatinin serum lebih dari atau
sama dengan 50% (1,5 kali
base line) atau berkurangnya
urin output (oligurio kurang
dari 0,5 ml/kg per jam selama
lebih dari 6 jam

DEFINISI
AKIN

Mengusulkan penyempurnaan kriteria

RIFLE

Penelitian Terbaru Perubahan Kecil Kreatinin Serum Berhubungan

dengan mortalitas

< 48 jam
Kreatinin
26,2umol/l

Memerlukan
RRT

Termasuk AKI
Termasuk AKI Stadium I
AKI Stadium III

DEFINISI
<0,5 mL/kg/h 6
Peningkatan Cr serum1,5x baseline atau penurunan GFR25% jam
Risk

Peningkatan Cr serum 2 x baseline atau penurunan GFR50%

Injury

Peningkatan Cr serum 3 x baseline atau penurunan GFR

75%

Failure

atau Cr 354umol/L dengan peningkatan akut sekurangnya

44umol/L

AKIN
Kriteria kreatinin serum
Kriteria
Peningkatan Cr serum 26,2umol/L atau 150-199%(1,5Stage 1 1,9kali)baseline
Stage 2

Peningkatan Cr serum 200-299%(>2-2,9 kali) baseline

Stage 3

Peningkatan Cr serum 354umol/L dengan peningkatan sekurangnya

44umol/L atau dimulainya RRT

<0,5 mL/kg/h
12jam
<0,5 mL/kg/h
24jam
atau anuria 12
jam.
Kriteria Urin Output
<0,5 mL/kg/h 6 jam
<0,5 mL/kg/h 12jam
<0,5 mL/kg/h 24jam
atau anuria 12 jam

Tabel 2: Perbandingan Definisi dan Skema Klasifikasi AKI berdasarkan RIFLE dan AKIN

DEFINISI

Perbandingan Kriteria AKIN &

RIFLE
AKIN tdk lbh sensitif dari pd RIFLE dlm mendiagnosis AKI dlm 24 jam
pertama di ICU
penelitian multisenter terhadap 120.123 pasien sakit kritis oleh Bangshaw dkk

pasien yg memenuhi defenisi AKI memiliki 3 kali kecenderungan mati

selama perawatan di RS. Mereka secara bermagna memerlukan dialisis dan
lama perawatan lbh lama dibandingkan pasien tanpa AKI
penelitian secara kohor pd 471 pasien yd dirawat di ICU selama 1 thn oleh Barrantes dkk

EPIDEMIOLOGI
AKI
berat
perlu RRT
ARF
20
terakhir

&

tahun

5% di ICU
61 288 per 100.000 populasi

ARF
yang
memerlukan RRT
20 tahun terakhir

4 27 per 100.000 populasi

AKI di USA
periode penelitian
15 tahun

4 kali lipat dari 610 menjadi

2880 pasien

AKI di Australia

18%

AKI di AS

12,4% masuk kategori RIFLE Risk, 26,7%

RIFLE Injury dan 28,1% RIFLE Failure

ETIOLOGI
Bersifat fungsional dan secara definisi tidak
disertai perubahan histopatologi.
Jika sdh terjadi kerusakan pada struktur
nefron sprti: glomerulus,tubulus,pembuluh
darah dan interstisial.

Terjadi pd obstruksi traktus urinarius.

ETIOLOGI
Pre Renal Volume
responsive

Intrinsik

Post renal

Hipovolemia

Glomerular

Obstruksi

-Muntah dan diare

-Glomerulonefritis

-Batu ginjal

-Perdarahan

Glomerular endothelium

-Fibrosis retroperitoneal

Berkurangnya

volume -Vaskulitis

-Hypertrophy prostat

sirkulasi efektif

-HUS

-Carcinoma

-Gagal jantung

-Hipertensi maligne

-Striktur uretra

-Septic shock

Tubular

-Neoplasma bladder

-Sirosis

-ATN

-Neoplasma pelvis

Obat

- Rhabdomyolisis

-Neoplasma retroperitoneal

- ACE inhibitors

- Myeloma
Intersisial
- Nefritis intersisial

Tabel 3. Penyebab AKI

OUTCOME
19 83%.
Kematian di
RS dgn RIFLE

Klas R 8,8%,
Klas I 11,4%,
Klas F 26,3%
Pasien tanpa AKI 5,5%

Lama Perawatan
ICU dan RS

Pasien dengan AKI memiliki lama perawatan di

ICU dan rumah sakit yang lebih lama jika
dibandingkan dengan pasien tanpa AKI

Morbiditas
End Stage

Biaya yang mahal

Menurunnya kualitas kesehatan seseorang,
Mortalitas yang lebih besar dari populasi
secara umum ( 28,1%)
Pemulihan fungsi ginjal menjadi salah satu
outcome Yang penting untuk dievaluasi

PENATALAKSANAAN
Konsensus Mengenai Terapi AKI Yang Efektif
Belum ada karena:
1. Penyebab AKI yang multifaktorial
2. Bervariasinya definisi AKI.
3. Penilaian penurunanGFR yang tergantung pada
perubahan kreatinin serum.
4. Tingginya angka mortalitas AKI
5. Tidak ada konsensus kapan dan jenis dialisis apa
yang tepat untuk penderita AKI.

PENATALAKSANAAN
Penelitian pd Hewan agent yg terbukti
efektif utk AKI
Penelitian secara
Loop diuretik
klinis tidak ada yg
Low-dose dopamin
terbukti efektif
ANP
Hormon tyroid
IGF-1

PENATALAKSANAAN
Renal Replacment Therapy (RRT)
Pengganti ginjal ( Renal Replacement)
Pendukung fungsi ginjal/organ lainnya (Renal/multi-organ
support
Berdasarkan mekanisme pengeluaran cairan/solud dan
Intermitten atau Kontinyu
Semua RRT kecuali PD dicapai dengan Ultrafiltrasi
Gradient tekanan akan mendorong cairan
melewati membran semipermiabel.
Laju UF dipegaruhi oleh:
gradien tekanan trensmembran,
permeabiltas air membran, dan
luas permukaan membran.

PENATALAKSANAAN
Renal Replacment Therapy (RRT)
Berdaarkan mekanisme utama removal solute difusi dan
konveksi
Removal solute yang Predominan pada masing-masing jenis RRT
1.
2.
3.
4.

Intermittent haemodialysisi ( IHD) difusi

Continous venovenous haemofiltration (CVVH)
konveksi
Continous venovenous haemodialysis ( VVHD) difusi
Continous venovenous haemodiafiltration (VVHDF)
difusi dan konveksi

PENATALAKSANAAN
Renal Replacment Therapy (RRT)
(UO < 200 ml/12 jam
Inisiasi:1.2. Oliguria
Anuria ( UO : 0-50 ml/12jam)
3. Urea > 35 mmol/l
4. Creatinin > 400 umol/l
5. K > 6,5 mmol/L atau peningkatan yang cepat
6. Udem pulmo yang refrakter dengan diuretik
7. Asidosis metabolik yang tak terkompensasi ( pH<7,1)
8. Na < 110 dan > 160 mmol/l
9. Temperatur > 40C
10. Komplikasi uremia : ( ensefalopati,miopati, neuropati dan perikarditis)
11. Overdosis obat/ toksin yang dialyzable

Jika ada satu kriteria, RRT harus dipertimbangkan. Jika ada dua kriteria
secara bersamaan, RRT sangat dianjurkan

Tabel 4.Indikasi modern (R.Bellomo ) untuk memulai RRT pada AKI

PENATALAKSANAAN
Renal Replacment Therapy (RRT)
Grade D
Grade E
Grade C
Tetapi pada kebanyakan kasus, RRT dimulai sebelum urea
mencapai 20-30 mmol/L).
RRT harus dimulai berdasarkan balans cairan, jumlah
urin, kadar kalium ataupun derajat asidosis tergantung
kondidi klinis pasien.

PENATALAKSANAAN

Renal Replacment Therapy (RRT)

Pilihan Metode RRT

Mekanism

IHD

CRRT

SLED

Ultrafiltrasi

Ultrafiltrasi

Ultrafiltrasi

removal cairan
Mekanisme

removal Difusi

solute

Difusi

dan

atau Difusi

konveksi

Blood Flow rate

200 ml/menit

< 200 ml/menit

200 ml/menit

Dialysate flow rate

500 ml/menit

17-34 ml/menit

300 ml/menit

Durasi

3-4 jam

24 jam/ hari

6-12 jam/hari

PENATALAKSANAAN

Renal Replacment Therapy (RRT)

Keuntungan dan pertimbangan khusus
IHD
Removal cairan yang cepat

Bersihan solute cepat

Hiperkalemia berat

CRRT

SLED

Hempdinamik tak stabil

Kontrol cairan lebih baik

-High nutritional Support

-Removal solute MMW

Chronic Kidney Disease

Chronic Kidney Disease

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 underdiagnosed and under-treated 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.

Stages of Chronic Kidney Disease

Stage 1

Kidney damage with

normal or GFR

GFR 90 ml/min/1.73
m2

Stage 2

Kidney damage with

mild GFR

GFR 60-89

Stage 3

Moderate GFR

GFR 30-59

Stage 4

Severe GFR

GFR 15-29

Stage 5

Kidney failure

GFR <15 (or dialysis)

Causes of End Stage Renal Disease

USRDS Annual Data Report

Chronic Kidney Disease

Many terms are used to describe states of

reduced glomerular filtration (GFR) not requiring
renal replacement therapy;

Chronic Renal Insufficiency

Chronic Renal Failure
Renal Insufficiency
Pre dialysis renal disease
Pre uremia
Renal dysfunction

They are imprecise & poorly defined.

Chronic Kidney Disease

Measurement of GFR
Gold standard is Inulin Iothalamate.
Creatinine Clearance calculated by timed (24h) urine
collection along with serum collection for Creatinine.
Overestimate GFR when CKD is severe due to an
increase in tubular secretion of creatinine.
This factor can be corrected by cimetidine.

Estimation of GFR
More than 10 formulae for estimation of GFR.
MDRD most widely accepted now.

CKD Risk Factors

Diabetes Mellitus
Hypertension
Cardiovascular Disease
Obesity
Metabolic Syndrome
Age and Race
Acute Kidney Injury
Malignancy

Family history of CKD

Kidney Stones
Infections like Hep C
and HIV
Autoimmune
diseases
Nephrotoxics like
NSAIDS

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

CKD - Causes

CAUSES OF DEATH IN ESRD

U.S. Renal Data System: USRDS 2002

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

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

CKD - Evaluation

Serum electrolytes
Urine spot protein analysis (24 hour no longer
recommended).
ANA, C3, C4
SPEP, UPEP
Kidney Ultrasound
Urine sediment analysis
Biopsy
Evidence of glomerular disease without diabetes
Sudden onset of nephrotic syndrome or glomerular
hematuria

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..

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 - 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.

CKD - Anemia

Erythropoietin
Epoetin alfa :Procrit , Epogen
Darbepoietin Alpha: ARANESP

Target Hg levels between 11g and 12g but

not exceeding 13g.
Greater than 13g showed increased
mortality as per the CHOIR study.
Sufficient Iron should be administered to
correct iron stores.

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.

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

CKD Medication Dosing

Proper Dosing of Drugs

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 - RRT

Preparation for Renal Replacement Therapy

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

CKD - RRT

Transplantation:
Preemptive transplant
carries both patient and
graft survival
advantage.
Graft survival better
with living donor
kidneys.
Immunosuppresion is
almost always a must.

CKD - RRT

Transplantation:
Diseases like FSGS may reccur early in the
transplanted kidney.
Increased risk for infection, bone loss,
cardiovascular disease.
Contraindications:
Malignancy (recent or metastatic)
Current infection
Severe extra renal disease
Active use of illicit drugs