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Haemodialysis Related
Ascites
Prof. Mohamed Sobh
MD,FACP
Professor of Nephrology , Urology & Nephrology Center
Mansoura Univesity
• Nephrogenic ascites has been known by several
names such as nephrogenous ascites, hemodialysis
associated ascites, dialysis ascites, idiopathic
dialysis ascites(IDA),or ascites associated with
ESRD.
• Nephrogenic ascites is preferred, because the
onset of ascites may occur before the initiation of
dialysis and cases have been reported in patients
with failing kidney transplant.
• The term nephrogenic ascites was
coined to describe a syndrome
associated with refractory ascites
occurring in patients with end-
stage renal disease in whom
infectious, malignant, hepatic, and
cardiac causes have been excluded.
• Incidence of nephrogenic ascites seems
to decrease over time, because most cases
were reported more than 15 years ago.
• Technical improvements in HD, with
better control of fluid balance,as well as
progress in nutritional and psychologic
treatment of HD patients, and use of more
biocompatible membranse have been
pointed out as the main reasons for this
decreased incidence.
• Nephrogenic ascites is characterized
by a marked center-to-center
variability in incidence (0.7 to 20%),
a wide age range of onset ( 1 1 to 7 1
yr, mean 42 yr), and a male sex
(male:female = 2: 1 ), but no race
predilection (white:black = 1 : 1 ).
• Chronic ambulatory peritoneal dialysis
preceded hemodialysis in 69% of the
patients.
• Ascites accumulation can occur as early
as 18 months before or as late as 69
months after the initiation of hemodialysis.
• Approximately 70% of reported cases in
the past occurred in association with the
glomerulonephritides and hypertensive
renal disease.
Diagnosis And Clinical Course
• The diagnosis is made by exclusion,after ruling out
other causes such as infection, liver disease, and heart
failure.
• Most of the reported patients presented signs of
persistent fluid overload, cachexia, or low serum
albumin levels.
• The prognosis for nephrogenic ascites is very poor.
• The average survival ranges from 7 to 10.7 months, with
44% dying within 15 months of diagnosis.
• Patients suffering from IDA had a
characteristic clinical profile, most
showed a sustained fluid overload, with
disproportionate interdialysis body
weight increases and arterial
hypertension; hypoproteinemia and
malnutrition were frequent, and most of
the cases had antecedents of peritoneal
dialysis.
Recommended evaluationCriteria
History & physical examination
General chemistries including BUN,
creatinine,total protein& albumin
Paracentesis for complete blood cell
count with differential, total
albumin,amulase,culture,cytology,urea
,protrin & creatinine
Thyroid function tests, iron studies,
parathyroid hormone level,
peritoneoscopy with liver/peritoneal
biopsy, abdominal computed
tomography/magnetic resonance
imaging, portal venous presure
History/physical signs
Increasing abdominal girth
Anorexia & early satiety
Dialysis associated hypotension
Cachexia
Massive ascitis combined with minimal
edema.
Ascitic fluid characteristics
Straw colour
White blood cell count of 25 to 1,600/mm3
Serum-ascitis gradient˂ 9g/L (0.9g/dl)
-ve culture & cytologies
No evidence of:
Portal hypertension.
Cardiac/pericardial disease
Peritoneal infection or malignancy.
Pancreatic pseudocyst
Inferior vena cava obstruction
Budd chiari syndrome
Urinary extravasation
Diagnostic criteria
Possible pathogenetic processes of nephrogenic ascitis
Elevated hepatic venous hydrostatic pressure
Volume Overload
Increased peritoneal membrane permeability secondary to
Uremic toxins
Prior exposure to dialysis solutions
Renin-angiotensin activation
Circulating immune complexes
Hemosiderosis
Impaired lymphatic drainage
• Other possible contributing causes of
ascites in patients with ESRD include
hypoproteinemia, secondary
hyperparathynoidism-induced
serositis, congestive heart failure,
constrictive penicarditis,
pancreatitis,and liver cirrhosis with
portal hypertension .
• A role for CIC in altering penitoneal permeability
has been suggested by the decrease in ascites in
some patients after continuous ambulatory
penitoneal dialysis (CAPD), a dialytic modality
known to efficiently remove CIC .
• Hemosiderosis was reported in four patients with
nephrogenic ascites. Ascites decreased in response
to iv deferoxamine and recombinant human
erythropoietin therapy, suggesting a role for iron
deposition-induced alteration in peritoneal
permeability
• Ascitic fluid had characteristics of exudate (total proteins, 4.7 g/dL),
according to most previous reported cases of IDA
• Histological examination of peritoneal tissue showed chronic
inflammatory changes.
• IDA might be considered as a manifestation of uremic polyserositis ,
the peritoneal inflammatory changes could have a similar
pathogenesis to those occurring in pericardial or pleural seroses in
some HD patients, which cause the so-called dialysis-associated
pericarditis or pleuritis, respectively.
• However, the precise cause and pathogenesis of such dialysis-related
polyserositis remain uncertain.
• Normalization of renal function after the kidney graft, strengthens
the relationship between uremia and ascites.
DisadvantagesAdvantagesModality
Limited by hypovolemia &
hypotension
Decreases ascitisFluid & salt restriction with
intensified hemodialysis with
ultrafiltration and /or albumin
infusion
Not proven to reduce ascitisImproves nutritionHyperalimentation
Excessive protein lossReduces symptomsRepeated paracentesis
Fever, peritoneal catheterConserves protein. Reduces
ascitis.
Reinfusion of ultrafiltrated
Malfunctionavoids dialysis associated
hypotension
ascitis/Extracorporeal ascitis
Dialysis
Self limited early protein lossImproves nutrition. Reduces
ascitis. avoids dialysis
associated hypotension
CAPD
Shunt malfunction/infectionReduces ascitis. Improves
nutrition
Peritoneovenous shunt
Recurrence after graft failureResoution of ascitisKidney transplantation
Therapeutic options for nephrogenic ascitis
• Treatment of patients with ascites, which
includes paracentesis,fluid and sodium
restriction, aggressive intradialytic
ultrafiltration (UF), or additional isolated
UF ‘conventional treatment”, has been
successful in significantly decreasing ascites
in fewer than 50% of patients.
• Nonresponders often do poorly, developing
cachexia, malnutrition, and general
discomfort, with progressive deterioration
and death.
• A more aggressive approach to treatment,
which includes peritoneal instillation of steroids
,reinfusion of ultrafiltrated ascites ,bilateral
nephrectomy, peritoneal dialysis, renal
transplantation,and continuous reinfusion of
ascites directly into the venous system using a
peritoneovenous shunt (PVS).
• Renal transplantation is considered the most
effective. So far, all patients with IDA who have
received a functioning kidney graft have shown
a total resolution of ascites.
• Although the initial reports on
the use of a PVS for the
treatment of refractory ascites
in hemodialysis patients were
discouraging, subsequent
reports describe significant
relief of ascites after insertion
of a PVS.
• Complications of shunt placement, seen in over one-
half of the cases, include malfunction from occlusion or
migration of the venous end out of the superior vena
cava and infection.
• These complications require either minor revisions or
removal of the shunt.
• Shunts remained functional for up to 18 months in one
series (Denver) and for more than 3 yr in another
(LeVeen). Thus, shunt placement should be seriously
considered early in the treatment of such patients.
• CAPD is also effective in the treatment of ascites.
• The combination of routine daily exchanges and control of
fluid and salt intake allows control of the ascites.
• The patients subjectively feel better, with improved caloric
and protein intake and subsequent weight gain. Within 6
months of continued treatment, the amount of total
protein excretion in the dialysis effluent decreases from
26.5 to 50 to 7.8 to 9.44 g/day, with a subsequent rise in
the serum protein and albumin levels and the resolution of
ascites.
•Other treatments attempted
with only partial success that
are no longer recommended
Include the I.p.
administration of steroids
and bilateral nephrectomy .
• Although no prospective studies
have been performed comparing
various treatment modalities, on
the basis of current data,CAPD,
penitoneovenous shunt placement,
and renal
transplantation offer the best hope
for an improvement in the quality
of life and recovery.
Thank You

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Haemodialysis related ascites prof. mohamed sobh

  • 1. Haemodialysis Related Ascites Prof. Mohamed Sobh MD,FACP Professor of Nephrology , Urology & Nephrology Center Mansoura Univesity
  • 2. • Nephrogenic ascites has been known by several names such as nephrogenous ascites, hemodialysis associated ascites, dialysis ascites, idiopathic dialysis ascites(IDA),or ascites associated with ESRD. • Nephrogenic ascites is preferred, because the onset of ascites may occur before the initiation of dialysis and cases have been reported in patients with failing kidney transplant.
  • 3. • The term nephrogenic ascites was coined to describe a syndrome associated with refractory ascites occurring in patients with end- stage renal disease in whom infectious, malignant, hepatic, and cardiac causes have been excluded.
  • 4. • Incidence of nephrogenic ascites seems to decrease over time, because most cases were reported more than 15 years ago. • Technical improvements in HD, with better control of fluid balance,as well as progress in nutritional and psychologic treatment of HD patients, and use of more biocompatible membranse have been pointed out as the main reasons for this decreased incidence.
  • 5. • Nephrogenic ascites is characterized by a marked center-to-center variability in incidence (0.7 to 20%), a wide age range of onset ( 1 1 to 7 1 yr, mean 42 yr), and a male sex (male:female = 2: 1 ), but no race predilection (white:black = 1 : 1 ).
  • 6. • Chronic ambulatory peritoneal dialysis preceded hemodialysis in 69% of the patients. • Ascites accumulation can occur as early as 18 months before or as late as 69 months after the initiation of hemodialysis. • Approximately 70% of reported cases in the past occurred in association with the glomerulonephritides and hypertensive renal disease.
  • 7. Diagnosis And Clinical Course • The diagnosis is made by exclusion,after ruling out other causes such as infection, liver disease, and heart failure. • Most of the reported patients presented signs of persistent fluid overload, cachexia, or low serum albumin levels. • The prognosis for nephrogenic ascites is very poor. • The average survival ranges from 7 to 10.7 months, with 44% dying within 15 months of diagnosis.
  • 8. • Patients suffering from IDA had a characteristic clinical profile, most showed a sustained fluid overload, with disproportionate interdialysis body weight increases and arterial hypertension; hypoproteinemia and malnutrition were frequent, and most of the cases had antecedents of peritoneal dialysis.
  • 9. Recommended evaluationCriteria History & physical examination General chemistries including BUN, creatinine,total protein& albumin Paracentesis for complete blood cell count with differential, total albumin,amulase,culture,cytology,urea ,protrin & creatinine Thyroid function tests, iron studies, parathyroid hormone level, peritoneoscopy with liver/peritoneal biopsy, abdominal computed tomography/magnetic resonance imaging, portal venous presure History/physical signs Increasing abdominal girth Anorexia & early satiety Dialysis associated hypotension Cachexia Massive ascitis combined with minimal edema. Ascitic fluid characteristics Straw colour White blood cell count of 25 to 1,600/mm3 Serum-ascitis gradient˂ 9g/L (0.9g/dl) -ve culture & cytologies No evidence of: Portal hypertension. Cardiac/pericardial disease Peritoneal infection or malignancy. Pancreatic pseudocyst Inferior vena cava obstruction Budd chiari syndrome Urinary extravasation Diagnostic criteria
  • 10. Possible pathogenetic processes of nephrogenic ascitis Elevated hepatic venous hydrostatic pressure Volume Overload Increased peritoneal membrane permeability secondary to Uremic toxins Prior exposure to dialysis solutions Renin-angiotensin activation Circulating immune complexes Hemosiderosis Impaired lymphatic drainage
  • 11. • Other possible contributing causes of ascites in patients with ESRD include hypoproteinemia, secondary hyperparathynoidism-induced serositis, congestive heart failure, constrictive penicarditis, pancreatitis,and liver cirrhosis with portal hypertension .
  • 12. • A role for CIC in altering penitoneal permeability has been suggested by the decrease in ascites in some patients after continuous ambulatory penitoneal dialysis (CAPD), a dialytic modality known to efficiently remove CIC . • Hemosiderosis was reported in four patients with nephrogenic ascites. Ascites decreased in response to iv deferoxamine and recombinant human erythropoietin therapy, suggesting a role for iron deposition-induced alteration in peritoneal permeability
  • 13. • Ascitic fluid had characteristics of exudate (total proteins, 4.7 g/dL), according to most previous reported cases of IDA • Histological examination of peritoneal tissue showed chronic inflammatory changes. • IDA might be considered as a manifestation of uremic polyserositis , the peritoneal inflammatory changes could have a similar pathogenesis to those occurring in pericardial or pleural seroses in some HD patients, which cause the so-called dialysis-associated pericarditis or pleuritis, respectively. • However, the precise cause and pathogenesis of such dialysis-related polyserositis remain uncertain. • Normalization of renal function after the kidney graft, strengthens the relationship between uremia and ascites.
  • 14. DisadvantagesAdvantagesModality Limited by hypovolemia & hypotension Decreases ascitisFluid & salt restriction with intensified hemodialysis with ultrafiltration and /or albumin infusion Not proven to reduce ascitisImproves nutritionHyperalimentation Excessive protein lossReduces symptomsRepeated paracentesis Fever, peritoneal catheterConserves protein. Reduces ascitis. Reinfusion of ultrafiltrated Malfunctionavoids dialysis associated hypotension ascitis/Extracorporeal ascitis Dialysis Self limited early protein lossImproves nutrition. Reduces ascitis. avoids dialysis associated hypotension CAPD Shunt malfunction/infectionReduces ascitis. Improves nutrition Peritoneovenous shunt Recurrence after graft failureResoution of ascitisKidney transplantation Therapeutic options for nephrogenic ascitis
  • 15. • Treatment of patients with ascites, which includes paracentesis,fluid and sodium restriction, aggressive intradialytic ultrafiltration (UF), or additional isolated UF ‘conventional treatment”, has been successful in significantly decreasing ascites in fewer than 50% of patients. • Nonresponders often do poorly, developing cachexia, malnutrition, and general discomfort, with progressive deterioration and death.
  • 16. • A more aggressive approach to treatment, which includes peritoneal instillation of steroids ,reinfusion of ultrafiltrated ascites ,bilateral nephrectomy, peritoneal dialysis, renal transplantation,and continuous reinfusion of ascites directly into the venous system using a peritoneovenous shunt (PVS). • Renal transplantation is considered the most effective. So far, all patients with IDA who have received a functioning kidney graft have shown a total resolution of ascites.
  • 17.
  • 18. • Although the initial reports on the use of a PVS for the treatment of refractory ascites in hemodialysis patients were discouraging, subsequent reports describe significant relief of ascites after insertion of a PVS.
  • 19.
  • 20. • Complications of shunt placement, seen in over one- half of the cases, include malfunction from occlusion or migration of the venous end out of the superior vena cava and infection. • These complications require either minor revisions or removal of the shunt. • Shunts remained functional for up to 18 months in one series (Denver) and for more than 3 yr in another (LeVeen). Thus, shunt placement should be seriously considered early in the treatment of such patients.
  • 21. • CAPD is also effective in the treatment of ascites. • The combination of routine daily exchanges and control of fluid and salt intake allows control of the ascites. • The patients subjectively feel better, with improved caloric and protein intake and subsequent weight gain. Within 6 months of continued treatment, the amount of total protein excretion in the dialysis effluent decreases from 26.5 to 50 to 7.8 to 9.44 g/day, with a subsequent rise in the serum protein and albumin levels and the resolution of ascites.
  • 22. •Other treatments attempted with only partial success that are no longer recommended Include the I.p. administration of steroids and bilateral nephrectomy .
  • 23. • Although no prospective studies have been performed comparing various treatment modalities, on the basis of current data,CAPD, penitoneovenous shunt placement, and renal transplantation offer the best hope for an improvement in the quality of life and recovery.