Peritoneal dialysis involves exchanging dialysis fluid into the peritoneal cavity through a catheter to remove waste and excess fluid. There are different types of peritoneal dialysis including continuous ambulatory peritoneal dialysis (CAPD) and continuous cycling peritoneal dialysis (CCPD). A peritoneal equilibration test (PET) determines a patient's transporter status which guides the best dialysis regimen. High transporters have faster fluid and waste removal but poorer fluid status. New dialysis solutions aim to reduce glucose absorption and improve fluid management.
14. Principles of peritoneal dialysis
1)transcellular, water-only aquaporin; 2) intercellular gap lined by a dense glycocalyx
3) intercellular gap with a less dense glycocalyx that permits macromolecules to pass
19. Assessement of PD adequacy
PET (peritoneal equilibrium test)
determines quick or slow passage of toxins from
the blood into the dialysis fluid
‘high-fast transporters’ v.s. ‘low-slow
transporters’
helps to decide about the PD scheme (dwell
duration and intervals, CAPD vs. CCPD)
performed in hospital, takes 5 hours
involves doing a CAPD exchange using a 2.27%
G, samples of PD fluid and blood are taken at
set times
21. PET (peritoneal equilibration test)
Transporter Waste Water Best type of
removal removal PD
High Fast Poor Frequent
exchanges,
short dwells
– APD
Average OK OK CAPD or APD
Slow Slow Good CAPD, 5
exchanges
daily + 1
exchange at
night
36. Peritoneal Transport
Status + Mortality
Peritoneal transport status
is a highly significant risk
factor for both mortality and
death-censored technique
failure in incident PD patient
populations.
JASN January 2006
37. Peritoneal Transport
Status + Mortality
Peritoneal transport status
is a highly significant risk
factor for both mortality and
death-censored technique
failure in incident PD patient
populations.
This risk is independent of
demographic
characteristics, BMI,
comorbid clinical illnesses,
peritoneal small solute
clearances, and residual
renal function.
JASN January 2006
38. Peritoneal Transport
Status + Mortality
Peritoneal transport status
is a highly significant risk
factor for both mortality and
death-censored technique
failure in incident PD patient
populations.
This risk is independent of
demographic
characteristics, BMI,
comorbid clinical illnesses,
peritoneal small solute
clearances, and residual
renal function.
This association was not
found in APD patients.
JASN January 2006
40. Meta-Analysis: Peritoneal Membrane
Transport, Mortality, and Technique Failure
A higher rate of
peritoneal membrane
solute transport is
associated with increased
mortality in PD patients.
JASN September 2006
41. Meta-Analysis: Peritoneal Membrane
Transport, Mortality, and Technique Failure
A higher rate of
peritoneal membrane
solute transport is
associated with increased
mortality in PD patients.
Peritoneal solute
clearance does not
significantly influence
patient outcome within
usual PD dosing regimens
whereas clinical volume
status may.
JASN September 2006
42. PET (peritoneal equilibration test)
Transporter Waste Water Best type of
removal removal PD
High Fast Poor Frequent
exchanges,
short dwells
– APD
Average OK OK CAPD or APD
Slow Slow Good CAPD, 5
exchanges
daily + 1
exchange at
night
45. Ultrafiltration Failure in
PD
In UF failure, fluid removal is insufficient
This can lead to fluid overload
46. Ultrafiltration Failure in
PD
In UF failure, fluid removal is insufficient
This can lead to fluid overload
Excess of fluid and sodium can lead to
cardiovascular mortality
47.
48.
49. UF failure occurs in 35% of long term PD
patients and is an important factor for transfer
to HD
50. UF failure occurs in 35% of long term PD
patients and is an important factor for transfer
to HD
51. UF failure occurs in 35% of long term PD
patients and is an important factor for transfer
to HD
UF failure is diagnosed from a 3.86% PET
52. UF failure occurs in 35% of long term PD
patients and is an important factor for transfer
to HD
UF failure is diagnosed from a 3.86% PET
53. UF failure occurs in 35% of long term PD
patients and is an important factor for transfer
to HD
UF failure is diagnosed from a 3.86% PET
Failure to achieve a UF of > 1.0L is associated
with increased mortality
54. UF failure occurs in 35% of long term PD
patients and is an important factor for transfer
to HD
UF failure is diagnosed from a 3.86% PET
Failure to achieve a UF of > 1.0L is associated
with increased mortality
55. UF failure occurs in 35% of long term PD
patients and is an important factor for transfer
to HD
UF failure is diagnosed from a 3.86% PET
Failure to achieve a UF of > 1.0L is associated
with increased mortality
Long term exposure to dialysis solutions is likely
to be the most important risk factor
56. Causes of UF failure
• Large vascular surface of peritoneum (due to neo-
angiogenesis, vasodilation), leading to high (fast)
transport including fast lost of osmotic (glucose)
pressure
• Decreased function of aquaporins
• High lymphatic absorption
57. Extraneal vs. 4.25%
Dextrose
600 *
*
Long Dwell Net UF (mL)
Icodextrin
500
400
300
4.25% Dextrose
200
100
0
Baseline Week 1 Week 2
*P < 0.005 vs 4.25% dextrose.
Finkelstein, et al. J Am Soc Nephrol 2005;16:546-554.
59. Icodextrin + fluid balance
Icodextrin vs 2.27%
dextrose in long
dwell.
Davies et al, JASN: 2003:14:2338
60. Icodextrin + fluid balance
Icodextrin vs 2.27%
dextrose in long
dwell.
Better preservation
of UF (+193 vs
-201)
Davies et al, JASN: 2003:14:2338
61. Icodextrin + fluid balance
Icodextrinvs 2.27%
dextrose in long
dwell.
Better preservation
of UF (+193 vs
-201)
Sustained reduction
in weight.
Davies et al, JASN: 2003:14:2338
62. Icodextrin + fluid balance
Icodextrin vs 2.27%
dextrose in long
dwell.
Better preservation
of UF (+193 vs
-201)
Sustained reduction
in weight.
Preservation of RRF
Davies et al, JASN: 2003:14:2338
66. Morphologic changes of peritoneum due to PD
After 3 years on PD, submesothelial fibrosis and neo-
angiogenesis (increase of vascular area of peritoneum)
67. Morphologic changes of peritoneum due to PD
COMPLICATION: Encapsulating peritoneal fibrosis
68. PERITONEAL FIBROSIS : SIMPLE SCLEROSIS AND
SCLEROSING PERITONITIS
Simple Sclerosis Sclerosing Peritonitis
Frequency very common very rare
poor biocompatibility
of peritoneal dialysis
due to osmotic agents, unknown, only risk factors
hyperosmolarity, low pH, peritoneal dialysis-dependent risk 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
69. Simple sclerosis Sclerosing Peritonitis
of macrophagic origin Giant
sclerotic tissue limited to visceral and cells
parietal peritoneum Fibroblasts and mesoblasts occur throughout
the thickness of sclerotic tissue in the sclerotic tissue, but are often more
frequent in deeper layers. In sclerosing
simple sclerosis does not exceed peritonitis unlike simple sclerosis, the muscle
40-50 µm layer is compressed. The thickness of the
sclerotic tissue is not uniform in a given patient
70. 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.
82. Development of new PD
solutions
New solutions
– Extraneal
– Gambrisol Trio
– Balance
– Physioneal
– BicaVera
– Nutrineal
83. Absorption of glucose from peritoneal
solutions
1. Solutions containing glucose (green) lead to significant glucose
absorbtion
2. Solutions based on another osmotic agent (blue, violet) do not
lead to glucose absorbtion, so decrease total daily glucose load).
1
2
84. Absorption of glucose from peritoneal
solutions
1. Solutions containing glucose (green) lead to significant glucose
absorbtion
2. Solutions based on another osmotic agent (blue, violet) do not
lead to glucose absorbtion, so decrease total daily glucose load).
Glucose absorbed = 159 g/day
1 2.5 L 2.5 L 2.5 L 2.5 L
Physioneal Physioneal Physioneal Physioneal
1.36% 1.36% 1.36% 3.86%
2
85. Absorption of glucose from peritoneal
solutions
1. Solutions containing glucose (green) lead to significant glucose
absorbtion
2. Solutions based on another osmotic agent (blue, violet) do not
lead to glucose absorbtion, so decrease total daily glucose load).
Glucose absorbed = 159 g/day
1 2.5 L 2.5 L 2.5 L 2.5 L
Physioneal Physioneal Physioneal Physioneal
1.36% 1.36% 1.36% 3.86%
Glucose absorbed = 50 g/day
2.5 L 2.5 L
2 Physioneal 2.5 L Physioneal 2.5 L
1.36% Nutrineal 1.36% Extraneal
96. Perspectives - New dialysis solutions
protect peritoneal membrane
Physioneal1
↓ GDPs and AGEs Extraneal2
↓ Lactate • Isosmolar to plasma
Physiologic pH and pCO2 • No glucose exposure
↑ Membrane and immune cell • ↓ GDPs and AGEs
function • ↑ Membrane and immune cell
function
Nutrineal2
No glucose exposure
No GDPs or AGEs
↑ Membrane and immune cell
function
Hinweis der Redaktion
another way to clean the blood- while leaving it in the body\n- put water in peritoneal membrane- has 2 m\n- the waste products will come out through the dialysis\n(dont have to take the blood out of the body)\n- peritoneal cavity = reservoir of dialysis solution\n- need to put catheter in body\n- dialysis will go out with waste products\n
\n
diff kinds of catheters\n\n
when finish dialysis- disconnect, and put catheter in bandage on abdomen/ underwear...\n\n\n
venous clamp-\nhow make out fluid? cant put clamp on venous side of splanchnic circulation- so how take out water?\n- how take the excessive water from the blood\n= osmotic force: needs to be concentrated- put osmotic substance in the water that you are putting into the peritoneum so that it will pull out the water form the blood\n- glucose is the osmotic substance used\n\n
\n
water out in, close: 7-12, then take it out.....\n- can do it alone at home- ambulatory- doesnt need to come in\n- all the time there is fluid - occurs throughout the whole day\n
small machine nowadays- that only have to do it at night\nNIPD: nightly intermittent peritoneal dialysis\n- more small cycles are done- continuous small cycle dialysis\n\n
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3 kinds of pores in peritoneum\n- aquaporin (1)\n- small pores- btw the cells\n glycocalyx- lets molecules to pass through small pore (medium molecules)\n- bigger pore- bigger molecules can pass through\n\nso a lot of materials can be cleared- many sizes\n\n\n\n-the protein can pass through- so peritoneal dialysis- lose protein: hypoalbuminemic\n\n
\n
\n- height and weight differs\n\n\n
- peritoneum moves- some molecules go in and out\n\n\n
distribution in pop of how the peritoneum transports the fluids\n- most ppl: peritoneum is average transporter\n- some high transporters\n- some low transporter\n
we need to know if the peritoneum is an active or lazy one- wich determines how the dialysis will work\n- PET: in oreder to assess the peritoneum quality\n- help determine the PD scheme- how long the dialysis needs to be in the stomach (if high transporter- doesnt need to be in for very long)\n
osmotic power lost quickly if high transporter- so, blood will be more osmotic than the fluid, and then it will be absorption of water, rather than clearance of the blood\n- need to change the dialysis on time- or high transporter pt will gain weight\n\n- depend on how transporters work in individual pt\n
\n
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after 4 hours- need to change\n\n- if glucose more concentrated - take more time to lose\n\n\n
but glucose not so kind to the body\npolyglucose molecules- not as small as glucose- cant pass- so there is osmosis at all times- so can stay in the abdomen for a long time- wont lose its osmosis\n\n\nIcodextrin is a starch-derived high molecular weight (MW) glucose polymer that is structurally similar to glycogen.1 It consists of oligosaccharide polymers of D-glucopyranose linked by >90% &#x3B1;1-4 and <10% &#x3B1;1-6 glucosidic bonds. \nIcodextrin differs from glycogen in that it has a lower percentage of alpha1-6 linkages, and is thus not as highly branched.2,3 The number of linked glucose molecules ranges anywhere from 4 to >300 with a number-average MW between 5,000 and 6,500 Daltons. The weight-average MW of icodextrin, the most common and accurate way of reporting average MW for large polymers, is between 13,000 and 19,000 Daltons.1,2 \nAs a high molecular weight glucose polymer, icodextrin does not readily diffuse across the peritoneal membrane. Rather, it is slowly removed from the peritoneal cavity via lymphatic absorption. As a result, icodextrin is able to maintain osmotic forces and sustain ultrafiltration over longer dwell periods compared with conventional dextrose-based peritoneal dialysis solutions.\n\n\n
\n
polyglucose- doesnt lose its osmotic force!\n
can cause peritoneal membrane abnormalities\n- glucose degradation products are bad all the time\n
\n
right: accum of glycose end-products (stained brown) after long term peritoneal dialysis \n(diabetics- proliferation of vessels in the eye- retinopathy- glucose can cause proliferation of the vessels- tx of diabetic nephropathy= laser)\n-hypoxia: VEGF\n- when put glucose: make hyperglycemic environment int he abdomen: some pts that are prone to diabetes, become diabetic due to this dialysis\n- EVGF in peritoneum- more blood vessels are formed (similarly to the retina)\n- peritoneum can then transform from average transporter to high transporter- bc absorb faster bc have more vessels\n
right: with time- more VEGF staining\n
\n
during time- start dialysis\n- ppl transform form average transporter to high transporters\n
high transporters- greater mortality\n
high transporters- greater mortality\n
high transporters- greater mortality\n
\n77% higher RR for mortality HI vs LA\n
\n77% higher RR for mortality HI vs LA\n
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less water pulled out from pt\n
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Figure 3. Changes in (a) total body water and (b) extracellular fluid determined from bioelectrical impedance. At each time point, values represent mean &#xB1; SEM change from baseline for patients randomized to icodextrin ( ) or 2.27% glucose ( ). Between-group differences, P < 0.04, P < 0.008. Longitudinal differences from baseline, * P < 0.002, ** P < 0.001. \n
Figure 3. Changes in (a) total body water and (b) extracellular fluid determined from bioelectrical impedance. At each time point, values represent mean &#xB1; SEM change from baseline for patients randomized to icodextrin ( ) or 2.27% glucose ( ). Between-group differences, P < 0.04, P < 0.008. Longitudinal differences from baseline, * P < 0.002, ** P < 0.001. \n
Figure 3. Changes in (a) total body water and (b) extracellular fluid determined from bioelectrical impedance. At each time point, values represent mean &#xB1; SEM change from baseline for patients randomized to icodextrin ( ) or 2.27% glucose ( ). Between-group differences, P < 0.04, P < 0.008. Longitudinal differences from baseline, * P < 0.002, ** P < 0.001. \n
Figure 3. Changes in (a) total body water and (b) extracellular fluid determined from bioelectrical impedance. At each time point, values represent mean &#xB1; SEM change from baseline for patients randomized to icodextrin ( ) or 2.27% glucose ( ). Between-group differences, P < 0.04, P < 0.008. Longitudinal differences from baseline, * P < 0.002, ** P < 0.001. \n
- after 5 yrs dialysis: peritoneum is MUCH THICKER\n- peritoneum can also become fibrotic- more collagen, more VEGF\n
\n
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more vessels and more fibrosis in the peritoneum\n
rare complication: \n- strangulate/encapsulate the small bowels- obstruction of the intestine\n(after 7/8 yrs)- switch ppl over to hemodialysis: not more than 7 yrs- bc of danger of complications\n
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right: calcification fo peritoneum- intestine- \n\nstrangulation of the bowels \n
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very difficult surgery\n
rare- but can happen\n\nLAST SLIDE\n
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Category: Peritoneal Membrane Preservation \nThis slide shows the beneficial effects of the newer PD solutions containing alternate buffers and osmotic agents.\nAll three solutions reduce levels of GDPs and AGEs. With Physioneal, it is because glucose is sterilized at a very low pH. With Extraneal and Nutrineal, it is because there is no glucose in either solution.\nAdditional benefits of Physioneal : Physiologic pH and pCO2, reduced lactate levels.\nAdditional benefit of Extraneal: Same osmolarity as plasma.\nAs a result of its unique properties, each solution has been shown to improve membrane and peritoneal immune cell function.\n
