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renal replacement therapy (hemodialysis (HEMODIAFILTRATION (benefits…
renal replacement therapy
Peritoneal Dialysis
The peritoneum serves as the dialysis membrane. Dialysate fluid is infused into the peritoneal cavity, then fluid and solutes from the peritoneal capillaries diffuse into the dialysate fluid, which is drained from the abdomen
Advantages
medical issues
Stable water balance (sustained ultrafiltration)
Good control of blood pressure
stable electrolytes (potasium)
No need to create a-v fistula
less anemia (low EPO dose)
Slower decline of residual renal function
beter control of heart failure and arrhytmias
social issues
PD is a home therapy
No need to travel (hospital visits every 4- 6 weeks)
Better opportunity to continue proffesion or learn at school
more liberal diet (fluid?, potassium)
better quality of life?
Why patients are less anemic on PD (use less EPO)?
no loss of blood with HD therapy
no loss of iron
better residual renal function
higher clearances of middle molecule toxins detrimental for erythropoesis?
Biocompatibility of PD (related to fluid incompatibility):
Metabolic complications (obesity, hyperglicemia, hyperlipidemia)
effect on host defence mechanisms in the peritoneal cavity
effect on structure and function of the peritoneal membrane
Factors responsible for PD fluid incompatibility:
low pH, glucose degradation products
high lactate concentration
high glucose concentration
high osmolarity
Complications of PD
infectious
peritonitis
exit site infection (Tenckhoff catheter)
Route of infection
Intraluminal (touch contamination, damage to the bag or tubing)
pericatheter (ESI, TI)
Through bowel wall, Systemc infection (TB), Gynecological
Clinical signs and symptoms
cloudy efluent, abdominal pain, fever, nausea, vomiting
overhydration, diarrhea, constipation, ileus paraliticus
Diagnosis of peritonitis
clinical sighs and symptoms
leukocyte count in dialysate( > 100/μl)
differential (> 50% neutrophiles)
Gram stain (important for G+, G-, or fungi)
dialysate culture
Noninfectious
Other diseases and its complications: e.g. DM, IHD, hypertension, infections, neoplasms
mechanical complications (hernias, fluid leaks)
catheter problems (malfunction)
deterioration of membrane function (effect of PD fluids on peritoneum)
psycho-social complications (burn-out syndrome)
fluid leak
Pericatheter
signs:
Accumulation of fluid (local edema)
Loss of ultrafiltration, weight gain
Fluid leak from the exit site
Early leak- less than 30 days after insertion
management:
conservative (low volume exchanges in supine positions) Usually successful
surgical
Late leak- more than 30 days after insertion
managemant:
conservative (usually unsuccesful)
surgical (new catheter insertion, revision of proximal cuff)
Pleural
Prevalence:
In less than 5% patients, only to right pleural space
Cause: Incompetence of the diaphragm
diagnosis:
Physical signs of fluid in right pleural space.
Exudate-like, high glucose concentration(>40mmol/l)
Technetium 99 labelled albumin scintigraphy
Management:
Plural tap if needed
Hemodialysis
Video-thoracoscopy and repair of the defect
Obliteration of plural space (oxytetracyclin, autologous blood, talc)
Return to PD therapy unlikely (small volumes, NPD)
Hernias
Common complication of PD!
carefully check for existing hernias before catheter insertion
related to increased intra-abdominal pressure
Localisation
umbilical, inguinal, In the place of catheter insertion
In linea alba, In postoperative wounds, Diaphragmatic
Treatment
Surgical (radical operation, mesh plug)
conservative (low volume exchanges in supine positions)
Genital edema
Cause: Fluid leak through patent processus vaginalis
signs: Massive edema of external genitalia
Treatment
conservative (low volume exchanges in supine positions) scrotum elevation)
Surgical repair
Problems related to peritoneal dialysis
low technique survival (peritonitis, low ultrafiltration)
malnutrition (loss of protein to dialysate)
changes in peritoneum (loss of ultrafiltration)
high peritonitis rate, hyperlipidemia, obesity
burn-out syndrome
hemodialysis
a process in which semipermeable membranes properties are employed for blood purification of substances dissolved in it, mainly small and medium particles
it is applied in treatment of patients with acute and chronic kidney failure, as well as intoxicated patients (e.g. drugs intoxication).
physical processes
diffusion
movement of particles through the semipermeable membrane
diffusion rate depends on:
difference in concentration of substances dissolved at both sides of the membrane
molecular weight of the dissolved substances
semipermeable membrane resistance
convection/ultrafiltration
depends on: transit of dissolvent and dissolved substance particles through semipermeable membrane as a result of transmembrane pressure
difference between hydrostatic pressure (dissolved substances are passing from a solution with higher pressure to a solution with lower pressure)
difference between osmotic pressures (dissolved substances are passing from a solution with higher concentration to a solution with lower concentration)
dialysers
construction
High exchange surface
Low filling volume
High resistance for transmembrane pressure
membranes
natural – cuprophan
semi-synthetic – acetate, cellulose triacetate
synthetic: polysulfone, polyethersulfone, PMMA, polyamide, polyacrylonitryl, heparin grafted helixon, poliaryloeterosulfon (PAES)
features of the ideal membrane
high clearance for small and medium molecules
a correspondingly high ultrafiltration coefficient
high biocompatibility, non-toxic, low cost
minimal activation of the coagulation system
vascular access
natural fistula, i.e. made with use of patient’s own blood vessels.
fistula made of artificial material
temporal and permanent catheters
vascular prosthesis
vascular prosthesis should be placed only in case of no possibility of natural fistula.
aim of adequate dialysis (optimal dialysis) is:
maximal prolongation of patient’s life
morbidity reduction
achievement of high quality of life
dialysis dose
URR – Urea Removal Rate
Dialysis adequacy index - (Kt / V)
factors influencing Kt/V
In-vivo clearness K
calculation of Kt/V
R: BUN before dialysis / BUN after dialysis
t: effective time /hours/
UF: ultrafiltration volume /litres/
W: body weigh after dialysis /kg/
dry body mass - body weight after HD when the patients is not suffering from dehydration symptoms (muscle spasms, decrease in RR) and on the other hand is not overhydrated (oedema, high BP)
UF (ultrafiltration - volume of fluid removed from the patient during one HD treatment; the difference between body weight after the last HD and the one before current HD
most frequent causes of insufficient dialysis dose:
inadequate blood flow rate (discalibrated pump, to low prescribed blood flow rate, low BP)
vascular access dysfunction (recirculation)
reduced dialyser’s active surface (inadequate anticoagulation)
reduced dialysate flow rate
shorter effective session time
lack of patient’s compliance
typical mesures in case of lower Kt/V than recommended:
increase of blood flow rate
prolongation of dialysis session time
increased anticoagulation
assessment of A-V fistula (USG)
change of dialyser’s type
other available approaches to correct dialysis adequacy
dialysis session time prolongation
increased dialysis sessions frequency (quotidian dialysis / nocturnal dialysis)
Low flux dialysers - Kuf 3-10 ml/h/mm Hg
High flux dialysers - Kuf 30-60 ml/h/mm Hg
benefits from longer dializing
stability of hemodynamics of circulation resulting from slow ultrafiltration, less risk of ischemia of various organs
better pressure control
maintaining a dry body weight
improvement in the clearance of low molecules - improving the survival of patients
factors influencing Kt/V
in-vivo clearance K: blood composition, anticoagulation, ultrafiltration, type of dialysers
Effective session time t it is frequently reduced (alarms, bypasses, preliminary termination of dialysis session)
urea distribution volume V: age, gender, weight, height
HEMODIAFILTRATION
HDF is a blood purification therapy that combines two ways of transporting a transmembrane substance: diffusion and convection/UF
condition HF dialyser + high dialyser surface (1.5-2.1 m2)
QB >300ml/mim, ultra pure water
fluid balance is maintained by simultaneous administration directly to the patient's bloodstream, a sterile replacement fluid produced on-line. The fluid can be substituted in different constellations in relation to the dialyzer and thus to UF
CV + UF + substitution volume *CV >23L/1.73m2 BSA)
benefits
lower mortality (CV> 23L / 1.73m2 BSA)
maintaining the residual kidney function
better hemodynamic stability and fewer intradialytical blood pressure drops
better tolerance of dialysis (fewer episodes of nausea, cramps, headaches, weakness of sub-dialysis), particularly important in the group of elderly patients suffering from diabetes and cardiovascular disease,
reduction of left ventricular mass,
less demand for ESA,
better control of blood pressure,
reduction of inflammation and dialysis wasting,
better β2 - Microglobulin removal and lower risk of dialysis amyloidosis.
children on HDF are growing
problems and dangers connected with on-line HDF
equipment, staff
the need to use ultrapure water
the risk of endotoxin contamination
vascular access (high QB) resulting in selection of patients
costs
COMPLICATIONS
acute
hypotonia, muscular cramps, air embolism, haemolysis, decompensation syndrome, intradialytic hypertension, intradialytic hyperglycaemia, a-v fistula thrombosis, dialytic catheter infections, “First-use syndrome”—chest pain, back pain
chronic
impaired cellular and humoral immunity, viral hepatitis, anaemia, malnutrition, chronic inflammatory states, lipid disturbances, dialytic amyloidosis, dialytic encephalopathy, peripheral neuropathy, increased risk of cardio-vascular diseases
hemodialysis
peritoneal dialysis
kidney transplantation
preemptive kidney transplantation
Stages of chronic kidney disease
Kidney damage with normal or increased GFR ( >90)
Diagnosis, treatment, slowing progression
Kidney damage with mild decrease of GFR ( 60 - 89)
Estimating progression
3a & 3b Kidney damage with moderate decrease of GFR (30 - 59)
Evaluating and treating complications
Kidney damage with severe decrease of GFR (15 - 29)
Preparation for kidney replacement therapy
Kidney failure (<15 (or dialysis))
Replacement if uremia present
determination of RRT beginning time
a direct indication to begin RRT should be eGFR reduction below 10 ml/minute
appearing of clinical symptoms of uraemia (severe hyperphosphatemia, anaemia, acidosis, overhydration, vonitus, diarrhoea)
severe arterial hypertension resistant for treatment
hyperkalemia non reactive for pharmacological treatment
metabolic acidosis, Overload—hypervolemia, drugs intoxication- aspirin, methanol, lithium
home dialysis
costs
experience and support for patient and family
education of nephrological society
fear for injections, complications,
hospitalathome„sickhome”
Transplantation
optimal treatment for most patients with end-stage renal disease (ESRD).
benefits:
• improved quality of life
• improvements in patients survival
• reduced medical expense
causes of failure
lack if immunological assessment and compatibility
lack of immunosuppressive medicines
risk factors for patient survivial and graft survival
pretransplant factors
time spent on dialysis
HLA matching
donor source:live donor source is one of the strongest factors associated with good graft survival.
donor age:
is one of the strongest factors for poor long-term graft and recipient survivals.
higher susceptibility to ATN and AR
recipient sensitization:
three main sources of sensitization:
previous transplantation, blood transfusions, pregnancy
acute rejection
delayed graft function
renal function
recipient evaluation
education
surgical evaluation
immunologic evaluation
psychologic/social evaluation
medical evaluation
all patients:
cause of kidney failure, cancer risk, infections, cardiovascular risk, hepatobiliary status
patients with special comorbidities:
gastrointerstinal disorder, urologic problem, hyperparathyreoidism, obesity, advanced age, thrombofilia
cardiac and cardiovascular risk
low risk patients
Age < 50 years
Negative history of CVD and Diabetes
Limited CV risk factors Clinically asymptomatic
Proper ECG, ECHO and
Doppler of peripheral arteries (carolic, iliac)
{Kidney transplantation}
the most important cause of death for both dialysis and transplant patients
most common clinical manifestation of CV disease in those patients are:
IHD,LVH,CHF, cerebrovascular disease, peripheral vascular disease.
intermediate risk patients
negative history of CVD, CHF
Age > 50 years
Long dialysis treatment
Many CV risk factors (other than diabetes)
One of the above and
proper ECG, ECHO (EF>40%, no significant LVH, akinesis)
Doppler of peripheral arteries (carotic, iliac) - negative --> transplant
Doppler of peripheral arteries (carotic, iliac) - positive --> coronary angio
high risk patients
symptomatic CVD and/or
History of myocardial infarct
CHF
Long lasting diabetes
Age > 60 years
Arteriosclerosis in Dpppler of peripheral arteries (carotic, iliac)
ECHO (EF< 40%, LVH, akinesis)
{Coronary angiography}
CANCER RISK
malignancies with high recurrence rates after transplantation:
large renal cancers, bladder cancers, brest cancer,skin cancers (melanomas, nonmelanomas)
contra-indication for transplantation
active cancer, AIDS, active systemic infections (sepsis, tuberculosis) until recovery, and/or any condition with a life expectancy < 2 years
SURGICAL INTERVENTION BEFORE TRANSPLANTATION
Gallstones
Nephrectomy – recommended for patients with
• chronic renal parenchymal infections,
• infected stones, infected reflux,
• obstructive uropathy complicated by chronic infection,
• suspicious for cancer• large painful and/or infected polycystic kidney disease,
Urologic problems
IMMUNOGENIC WORK-UP OF THE RECIPIENT
ABO blood grouping and HLA typing
In cadaveric kidney transplantation, the donor should be ABO identical to recipient, and ABO compatibility should be discouraged.
In living donor kidney transplantation ABO identity or compatibility are equally acceptable.
Antibody screening to evaluate sensitization (PRA –panel reactive antibody)
Pre-transplant antibody cross-matching
evaluation and selection of donors
cadaveric heart-beating donors
The graft should be of good quality
Any comatose patient with irreversible cerebral damage who appears likely to progress to brain death prior to terminal circulatory failure must be considered as a potential donor, regardless of age.
Absolute contra-indication against organ donation are based on risk of disease (cancer, infection) transmission and include:
history of cancer (except those of extremely low risk of metastasis such as skin cancer).
HIV positive serology, hepatitis (HBV, HCV antibody positive, tuberculosis, severe untreated systemic sepsis.
Accepted eGFR > 70 ml/min (in some centres > 60 ml/min).
Factors reducing quality of graft:
high donor age, diabetes, proteinuria, vascular risk factors
marginal donors: age > 60 years
living kidney donors
favorable results
initial and maintenance immunosuppressive treatment
mandatory in renal transplantation in order to reduce the incidence of AR (acute rejection) episodes.
Maintenance immunosuppresion could lead to over-immnunosupression characterized by an increased incidence of
infections complication (mainly viral)
de novo malignancies which carry a great risk of morbidity and mortality
toxicity: nephrotoxicity, hyperlipidemia, malignancy, hypertension, gi-side effects, diabetes, infection, bm-suppression
Four major groups of immunosuppressants
Calcineurin-inhibitors (Cyclosporin A, Tacrolimus)
Proliferation-inhibitors (MMF, EC-MPA, azathioprine)
mTOR-inhibitors (Sirolimus, Everolimus)
Steroids
Anty IL-2 antibodies: daclizumab, basiliksimab Antylymphotic antibodies: ATG, OKT-3
complications
Surgical Complications Causing Early Graft Dysfunction:
bleeding at the graft site, graft thrombosis, renal artery stenosis, urine leaks, ureteral obstruction, lymphoceles, burst of the graft
Causes Of Acute Allograft Dysfunction (First 3 To 6 Months)
-acute rejection: cell-mediated, antibody-mediated (humaral)
-acute tubular necrosis: thrombotic microangiopathy,acute calcineurin inhibitor nephrotoxicity
-hemodynamic effects: volume depletion , low blood pressure
-recurrent glomerular disease
Clinical signs of kidney graft rejection:
Increase of serum creatinine
Decreased urinary output
Sonography (blood flow, ..)
Swelling of the graft
Cornerstone of targeted rejection therapy:
Fine needle biopsy (ultrasound guided)
Histology: Banff classification
ACUTE REJECTION
Acute cellular rejection (ACR) - T-lymphocyte attack on the allograft manifested most commonly by tubulitis and less frequently by inflammatory changes in the blood vessels („vascular rejection” –Banff class II and III).
antibody mediated (humoral)
Hyper-acute rejection caused by anti-donor HLA antibodies present in the serum of the recipient at the time of transplantation (negative cross-match should avoid this situation).
Acute anti-donor antibody mediated rejection – 37% of patients with steroid resistant acute rejection were found to have evidence of antibody mediated rejection.
Diagnosis
Histological evidence of tissue injury the deposition of complement break-down product C4d in peritubular capillaries
Serologic evidence of circulating antibodies to donor HLA or endothelial antigens.