The document provides an overview of the anatomy and physiology of the urinary system. It discusses the key components including the kidneys, ureters, bladder, and urethra. It describes the functions of the kidneys in maintaining fluid balance, regulating electrolytes, and filtering waste. It also explains urine production through glomerular filtration, reabsorption, and secretion in the nephron. Hormonal regulation of the urinary system by renin, aldosterone, and ADH is also summarized.

1. Anatomy and Physiology of Urinary System
WIDODO
BAGIAN ANESTESIOLOGI,
PERAWATAN INTENSIF, DAN
PENANGANAN NYERI
RSUP WAHIDIN SUDIROHUSODO
MAKASSAR

2. 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.

3. –Kidneys
–Ureters
–Bladder
–Urethra
Components of system

4. Kidney Location and External Anatomy

5. 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

6. 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 Kidney and the Nephron

7. The Nephron
 Functional unit of the kidney (1,000,000)
 Responsible for urine formation:
– Filtration
– Secretion
– Reabsorption

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

9. From http://www.emc.maricopa.edu/faculty/farabee/BIOBK/BioBookEXCRET.html
Overview of nephron function

10. Filtration

11. THE GLOMERULUS

12. •Components of plasma cross the three layers of the glomerular barrier
during filtration
•Capillary endothelium
•Basement membrane (net negative charge)
•Epithelium of Bowman’s 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!
Plasma is filtered through the glomerular
barrier

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

14. The Response to a Reduction in the GFR

15. Reabsorption
and secretion

16. Reabsorption
 Active Transport –requires ATP
– Na+, K+ ATP pumps
 Passive Transport-
– Na+ symporters (glucose, a.a., etc)
– Na+ antiporters (H+)
– Ion channels
– Osmosis

17. 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.

18. 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.

20. 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, Tamm-Horsfall protein
(main component of hyaline casts).

21. 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

22. Loop of Henle
– Goal= make isotonic filtrate into
hypertonic urine (don’t 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

23. 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.

24. Renin, Angiotensin, Aldosterone:
Regulation of Salt/Water Balance

25. 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

26. 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

27. 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

28. 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

29. Chapter 25: Urinary System 29
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

30. Chapter 25: Urinary System 30
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

31. Chapter 25: Urinary System 31
Urinary Bladder
Figure 25.18a, b

32. Urethra
 Muscular tube that:
– Drains urine from the bladder
– Conveys it out of the body

33. 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

34. Chapter 25: Urinary System 34
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

35. Chapter 25: Urinary System 35
Urethra
Figure 25.18a. b

36. 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

37. 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

38. ACUTE KIDNEY INJURY
WIDODO
RSUP WAHIDIN sUDIROHUSODO
MAKASSAR

39. Pendahuluan
Salah satu kondisi yang paling sering terjadi pada
kasus-kasus trauma dan penyakit kritis.
Gagal ginjal akut (ARF)
Sistem scoring keparahan penyakit seperti
APACHE III dan SOFA, memberi bobot yg cukup besar terhadap disfungsi
ginjal

40. Pendahuluan
Disfungsi
Ginjal
• Berat
• Memerlukan RRT
• Ringan  Perubahan kecil nilai
kreatinin atau produksi urin
Mempengaruhi morbiditas dan
mortalitas pasien
ARF paling sering terjadi
ICU dan sering
merupakan bagian dari
disfungsi organ lainnya

41. 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

42. DEFINISI
Belum ada konsensus terhadap berapa besar disfungsi
ginjal yg dsb AKI.
Acute Kidney Injury
klasifikasi Risk, Injuri, Failure, Loss and End Stage
Kidney RIFLE
ADQI

43. 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

44. Gambar 1. Skema klasifikasi AKI berdasarkan kriteria RIFLE
(dikutip : Belomo A, Ronco C,Kellum JA,et al.ARCritical care 2004,8:R204-R212 )

45. DEFINISI
Pasien Masuk RS
Asumsi GFR awal
normal
Tidak ada data awal
fungsi ginjal
Gunakan Nilai
Kreatinin Serum
Usul ADQI
Rumus MDRD untuk perhitungan GFR
Modification of Diet in Renal Disease
75-100 ml/menit per
1,73m2
Rumusan MDRD ini hanya dipakai untuk memperkirakan kreatinin serum
baseline
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 )

46. Tabel 1. Perkiraan kreatinin serum baseline
Age (years)
Black males
(mg/dl [μmol/l])
Other males
(mg/dl [μmol/l])
Black females
(mg/dl [μmol/l])
Other females
(mg/dl [μmol/l])
20–24 1.5 (133) 1.3 (115) 1.2 (106) 1.0 (88)
25–29 1.5 (133) 1.2 (106) 1.1 (97) 1.0 (88)
30–39 1.4 (124) 1.2 (106) 1.1 (97) 0.9 (80)
40–54 1.3 (115) 1.1 (97) 1.0 (88) 0.9 (80)
55–65 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)

47. 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

48. DEFINISI
AKIN Mengusulkan penyempurnaan kriteria RIFLE
Penelitian Terbaru  Perubahan Kecil Kreatinin Serum Berhubungan
dengan ↑ mortalitas
< 48 jam Termasuk AKI
Kreatinin ≥ 26,2umol/l
Memerlukan RRT
Termasuk AKI Stadium I
AKI Stadium III

49. DEFINISI
Tabel 2: Perbandingan Definisi dan Skema Klasifikasi AKI berdasarkan RIFLE dan AKIN
Risk
Injury
Failure
Peningkatan Cr serum≥1,5x baseline atau penurunan GFR≥25%
Peningkatan Cr serum≥ 2 x baseline atau penurunan GFR≥50%
Peningkatan Cr serum≥ 3 x baseline atau penurunan GFR≥ 75%
atau Cr ≥ 354umol/L dengan peningkatan akut sekurangnya 44umol/L
<0,5 mL/kg/h ≥ 6 jam
<0,5 mL/kg/h ≥12jam
<0,5 mL/kg/h ≥24jam
atau anuria ≥ 12 jam.
AKIN
Kriteria
Kriteria kreatinin serum Kriteria Urin Output
Stage 1
Stage 2
Stage 3
Peningkatan Cr serum ≥ 26,2umol/L atau ≥150-199%(1,5-1,9kali)baseline
Peningkatan Cr serum 200-299%(>2-2,9 kali) baseline
Peningkatan Cr serum ≥354umol/L dengan peningkatan sekurangnya 44umol/L atau
dimulainya RRT
<0,5 mL/kg/h ≥ 6 jam
<0,5 mL/kg/h ≥12jam
<0,5 mL/kg/h ≥24jam
atau anuria ≥ 12 jam
RIFLE Kriteria Kreatinin Serum Kriteria urin output

50. 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
DEFINISI
Perbandingan Kriteria AKIN & RIFLE
penelitian multisenter terhadap 120.123 pasien sakit kritis oleh Bangshaw dkk
AKIN tdk lbh sensitif dari pd RIFLE dlm mendiagnosis AKI dlm 24 jam pertama di ICU
penelitian secara kohor pd 471 pasien yd dirawat di ICU selama 1 thn oleh Barrantes dkk

51. EPIDEMIOLOGI
AKI berat & perlu
RRT
5% di ICU
ARF 20 tahun terakhir
ARF yang
memerlukan RRT
20 tahun terakhir
61  288 per 100.000 populasi
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

52. 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.

53. Tabel 3. Penyebab AKI
Pre Renal Volume
responsive Intrinsik Post renal
Hipovolemia
- Muntah dan diare
- Perdarahan
Berkurangnya volume
sirkulasi efektif
- Gagal jantung
- Septic shock
- Sirosis
Obat
- ACE inhibitors
Glomerular
- Glomerulonefritis
Glomerular endothelium
- Vaskulitis
- HUS
- Hipertensi maligne
Tubular
- ATN
- Rhabdomyolisis
- Myeloma
Intersisial
- Nefritis intersisial
Obstruksi
- Batu ginjal
- Fibrosis retroperitoneal
- Hypertrophy prostat
- Carcinoma
- Striktur uretra
- Neoplasma bladder
- Neoplasma pelvis
- Neoplasma retroperitoneal
ETIOLOGI

54. OUTCOME
Mortalitas 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.

55. 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.

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

57. 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.

58. PENATALAKSANAAN
Renal Replacment Therapy (RRT)
Berdaarkan mekanisme utama removal solute  difusi dan konveksi
Removal solute yang Predominan pada masing-masing jenis RRT
1. Intermittent haemodialysisi ( IHD) – difusi
2. Continous venovenous haemofiltration (CVVH) – konveksi
3. Continous venovenous haemodialysis ( VVHD) – difusi
4. Continous venovenous haemodiafiltration (VVHDF) – difusi
dan konveksi

59. PENATALAKSANAAN
Renal Replacment Therapy (RRT)
Inisiasi:1. Oliguria (UO < 200 ml/12 jam
2. 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

60. PENATALAKSANAAN
Renal Replacment Therapy (RRT)
Penggunaan kriteria konvensional untuk memulai RRT Grade D
RRT seharusnya dimulai sebelum terjadi komplikasi Grade E
Laju perubahan urea dan kreatinin lebih bermakna
daripada nilai absolutnya
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.

61. PENATALAKSANAAN
Renal Replacment Therapy (RRT)
Pilihan Metode RRT
IHD CRRT SLED
Mekanism
removal cairan
Ultrafiltrasi Ultrafiltrasi Ultrafiltrasi
Mekanisme removal
solute
Difusi Difusi dan atau
konveksi
Difusi
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

62. PENATALAKSANAAN
Renal Replacment Therapy (RRT)
Keuntungan dan pertimbangan khusus
IHD CRRT SLED
Removal cairan yang cepat √
Bersihan solute cepat √
Hiperkalemia berat √
Hempdinamik tak stabil √ √
Kontrol cairan lebih baik √ √
-High nutritional Support
-Removal solute MMW
√
√
?

63. Chronic Kidney Disease

64.  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 “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.
Chronic Kidney Disease

65. 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)

66. Causes of End Stage Renal Disease
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
All
W
hite
Black
Asian
Am
erIndian
%
Other
Interstit N
Cystic KD
GN
BP
Diabetes
USRDS Annual Data Report

67. 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.

68.  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.
Chronic Kidney Disease

69. 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

70. 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

71. CKD - Causes

72. CAUSES OF DEATH IN ESRD
39%
5%26%
11%
15%
4%
Cardiac
Cerebrovascular
Other known
Unknown
Infection
Malignancy
U.S. Renal Data System: USRDS 2002

73.  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 - Manifestations

74. 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

75. CKD - Evaluation

76.  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 - Evaluation

77. 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..

78. 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.

79. 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.

80. 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.

81. 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

82. 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.

83. 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

84. 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

85. 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.

86. 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

87. 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.

88. 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