1. DIALYSIS
Process where the solute composition of a
solution A is altered by exposing solution A
to a second solution(B) through a semi -
permeable membrane
SEMI-PERMEABLE MEMBRANE: sheet
perforated by holes or pores

5. Mechanisms of solute transport
Diffusion-random molecular motion
concentration gradient
molecular weight
membrane resistance
Ultrafiltration-water is pushed through
membrane
hydrostatic pressure
osmotic pressure

9. Sand is swept away

11. Access for Dialysis

12. Access for Dialysis

13. Vascular Access-synthetic

14. Access for Dialysis

15. Access for Dialysis

16. PERMCATH

17. Vascular Access-catheter

18. Vascular Access-catheter

20. Portable hemodialysis Wearable hemodialysis
Hemodialysis machine machine apparatus

21. Dialyzer-hollow fiber

23. Dialyzer

25. Dialyzers
Low- efficiency-surface area:0.8-2.1 m²,small pores
High- efficiency-bigger surface area, small or big pores
High- flux-big pores (pass middle molecules)

26. Dialyzers

27. Dialyzer membrane

28. The Dialyzer Membrane

29. The Dialyzer Membrane

31. Dialyzer clearance

32. Dialyzer clearance

35. Dialysis Adequacy: Urea Kinetics

36. Dialysis Adequacy

37. Dialysis Adequacy
Indices of urea removal
Kt/V
Reflects urea removal
Population studies suggest Kt/V should be >1.2
URR
Also reflects urea removal
Current goal is URR>65%

38. KT/V and mortality

39. Kt/V
K is the dialyzer blood urea
clearance (Liters per hour)
t is the dialysis session length [In a typical dialysis session:4 hs ]
(hours)
[Water content:~60% of dry body
weight: If BW=70 kg then water
V is the volume of distribution content is ( 0.6 X 70) 42 L ]
of urea ( Liters )

40. Dialysis Adequacy

41. Dialysis Adequacy

42. Dialysis Adequacy

43. Dialysis Adequacy

47. NO BREAK

48. Indications for Dialysis-acute
GI: nausea ; vomiting (morning) ; poor appetite Symptoms:
Mental status alteration; fatigued ; weakness
Signs : asterixis ; pericardial friction rub ; fluid overload
Lab : Hyperkalemia, Severe Metabolic Acidosis

49. Case 1
22 years old male, cocaine abuser, with a known obstructive uropathy presented
to hospital with severe sepsis secondary to pneumonia.
LAB: Hgb-9.6 g/dl ;WBC-25800 ;PLT-603000
Na-132meq/l; K-3.1meq/l; Cl-107; Glucose-90 ; BUN-130 mg/dl
Creatinine-4.7 ; Osm-330 ; pH-6.95; pO2-109; pCO2- 10 ;HCO3-2; L.A.-0.6
( Severe metabolic Acidosis with elevated Anion Gap )
Chest X ray: Middle lobe+lingular pneumonia.U.S. Bilat. moderate hydronephrosis
Follow-up: empiric Cephtriaxone and Vanco
Blood culture were positive for Staph. aureus and E.Coli
Admitted to ICU: despite IV Bicarbonate and 4 liters of crystalloids remained acidotic and
oliguric therefore a regular standard dialysis was prescribed.
2 ½ hours after starting dialysis became rapidly unresponsive and intubation was done
At completion of HD and over the subsequent 4 hs the neurologic status deteriorated

50. Case 1
Computerized Tomography (CT) head
showing diffuse cerebral
edema with effacement of basal cisterns and
generalized
loss of gray-white differentiation
LAB after dialysis: pH-7.36; HCO3-19 ;
Na-132 ; K-2 ; BUN-37
(URR- 71%)
AUTOPSY: Diffuse cerebral edema

51. Dialysis Disequilibrium Syndrome
Dialysis disequilibrium syndrome (DDS), a complication of haemodialysis,
is characterized by neurological symptoms including headache,
disorientation, nausea, seizures and coma. This syndrome is assumed
to result from brain swelling occurring as a consequence of a rapid
haemodialysis process.
PATHOGENESIS:
In uremic state there is a reduced expression of urea transporters and an
increased expression of AQP in brain cells – consequently
Acute urea removal occurs more slowly across BBB than from plasma
generating a “reverse osmotic gradient” promoting water movement
into brain.
AVOID DDS initiating dialysis “gently”: less efficient dialyzer, reduce session
length ,reduce blood flow rate , run blood and dialysate in the same direction
( less diffusion) , add osmols to dialysate

52. Dialysis Disequilibrium Syndrome
Dialysis disequilibrium syndrome (DDS), a complication of haemodialysis,
is characterized by neurological symptoms including headache,
disorientation, nausea, seizures and coma. This syndrome is assumed
to result from brain swelling occurring as a consequence of a rapid
haemodialysis process.
PATHOGENESIS:
In uremic state there is a reduced expression of urea transporters and an
increased expression of AQP in brain cells – consequently
Acute urea removal occurs more slowly across BBB than from plasma
generating a “reverse osmotic gradient” promoting water movement
into brain.
AVOID DDS initiating dialysis “gently”: less efficient dialyzer, reduce session
length ,reduce blood flow rate , run blood and dialysate in the same direction
( less diffusion) , add osmols to dialysate

54. ‫הגיע הזמן לנוח... אבל קודם לחדר‬
‫…‬
‫דיאליזה‬

55. Dialysis Adequacy

56. Dialysis Adequacy

57. Dialysis Adequacy

58. Dialysis Adequacy

59. Dialysis Adequacy

60. Dialysis Adequacy

62. Dialysis Adequacy

63. Dialysis Adequacy

64. Dialysis Adequacy

65. Access Recirculation

68. Peritoneal Dialysis

70. Peritoneal Dialysis
Tenckhof catheter

73. Principles of peritoneal dialysis

74. Principles of peritoneal dialysis
Continuous Ambulatory
Peritoneal Dialysis-CAPD

75. Principles of peritoneal dialysis
Continuous Cycling Peritoneal Dialysis or
Automated Peritoneal Dialysis ( APD )
Cycler
Nightly Intermittent Peritoneal Dialysis

77. Peritoneal Equilibration Test

87. PERITONEAL FIBROSIS : SIMPLE SCLEROSIS AND
SCLEROSING PERITONITIS
Simple Sclerosis Sclerosing Peritonitis
Frequency very common very rare
poor biocompatibility
of peritoneal dialysis unknown, only risk factors
due to osmotic agents, peritoneal dialysis-dependent risk
hyperosmolarity, low pH, factors:
buffer duration of dialysis
poor biocompatibility
acetate buffer
Etiology disinfectants
catheter
in-line bacterial filters
particles of plastics
plasticizers
peritonitis
peritoneal dialysis-independent risk
factors:
beta-blockers
tumors
genetic predisposition
Reproducibility yes with dialysis no with dialysis
in animal models no without dialysis yes without dialysis
Clinical severe
absent
manifestations high mortality

88. Simple sclerosis Sclerosing Peritonitis
of macrophagic origin Giant cells
sclerotic tissue limited to visceral and Fibroblasts and mesoblasts occur throughout the
parietal peritoneum sclerotic tissue, but are often more frequent in
deeper layers. In sclerosing peritonitis unlike simple
the thickness of sclerotic tissue in sclerosis, the muscle layer is compressed. The
simple sclerosis does not exceed thickness of the sclerotic tissue is not uniform in a
given patient but normally reaches very high values
40-50 µm between 1,000 and 4,000 µm

89. In sclerosing peritonitis, unlike simple sclerosis, a dramatic
progression of the sclerosis occurs. This is combined with aspects
not found in simple sclerosis, such as inflammatory infiltrates,
calcifications and typical vascular alterations.
The peritoneal surface is reduced to a rough thickened membrane
similar to the sole of a shoe .In extreme cases of sclerosing
encapsulating peritonitis, the sclerotic process completely fixes
groups of intestinal loops, almost completely preventing their
movement.
Often the sclerosis is not homogeneous, but one area of the
abdomen may be more affected than others, forming a mass. This
situation has been described with the term "abdominal cocoon“.
The cocoon may be perfectly palpable, like a tumor; the sclerotic
tissue of the cocoon usually contains loops of the small intestine
and sacs of ascites, and often calcifications.

91. Encapsulating sclerosing peritonitis