dialysis and transplant Flashcards
Goals of dialysis
remove toxins that are normally cleared by the kidney and to maintain euvolemia in the patient. Ideally, chronic dialysis will improve signs and symptoms of uremia
Indications for starting dialysis
Life threatening conditions (severe hyperkalemia, volume overload, uremic pericarditis). If patient doesn’t have appropriate dialysis access, use vascular catheter. Less severe symptoms (mild cognitive changes with uremia, etc) warrant dialysis initiation if appropriate access. Otherwise, weight the risks vs benefits of catheter infection. GFR alone is not sufficient
What is hemodialysis
Blood is rapidly moved through extracorporeal circuit, then removed by needle or catheter port into a tuble with semi-permeable membrane. A dialysate is outside the tube moving in counter current. Solutes in blood move into dialysate by diffusion (concentration gradient), then blood is returned to patient via separate needle/port. Fluids can also be removed by positive transmembrane pressure.
Methods for hemodialysis access
AV fistula, AV graft, lumen catheters
What is an AV fistula
Preferred access for dialysis: surgical anastomoses of artery to vein, usually in arm. Low infection rate but take 6weeks to 9 months to develop.
AV graft
synthetic grafts that are connected to the artery and vein. AVGs can be used more quickly and have a higher primary success rate than AV fistula. However, AVGs fail quicker than AVFs due to neointimal hyperplasia, require frequent interventions to maintain patency, and have a higher infection risk
Pros and cons to lumenal catheters
Catheters are most often placed in the internal jugular vein and can be used immediately for dialysis. Catheters have a much higher infection rate than AVFs or AVGs and also have a high rate of dysfunction.
Pros to convential hemodialysis
Rapid removal of small molecular solutes (ie urea), precise control of ultrafiltration
Cons to hemodialysis
Not continuous treatment, so large volume of fluid is removed in 4 hr period. Also, not effective at removing large solutes that are protein bound
Complications of dialysis
Muscle cramps, Hypotension, Headache, Chest pain, Air embolism (very rare), infection
Muscle cramps, Hypotension, Headache, Chest pain, Air embolism (very rare), infection
Muscle cramps, Hypotension, Headache, Chest pain, Air embolism (very rare), infection
What is peritoneal dialysis
continuous therapy done at home. Coiled catheter placed in peritoneal cavity, then high glucose fluid is instilled in peritoneal cavity. This fluid provides high oncotic pressure, so fluid moves from blood to peritoneal cavity, and solutes move with fluid by convection. The dialysate plus flitered fluid are then drained from cavity and new dialysate is added. 3-4 exchanges are done per day
Types of peritoneal dialysis
Continuous ambulatory peritoneal dialysis (CAPD) is a manual therapy. The patient does three to four manual exchanges of dialysate daily. Continuous cycling peritoneal dialysis (CCPD) is an automated therapy. A cycler machine instills and drains dialysate many times throughout the night and leaves a dwell of dialysate in the peritoneum in the morning.
Pros of peritoneal dialysis
lower cost, more freedom, fluid removal is gradual
Peritoneal dialysis complications
Infections (peritonitis and exit site infections), catheter dysfunction or problems draining, hernias due to increased abd pressure, metabolic problems such as hyperglycemia, scarring of peritoneal membrane
Prognosis on dialysis
bad
Prognosis with kidney transplant
Transplant improves long term patient survival compared to dialysis. Immediately following the surgery, however, relative risk of death is higher for transplant patients compared to dialysis due to surgical complications
Transplant procedure
Left kidney is preferred for donation due to longer length of the renal vein. • Renal vein and artery anastomosis to recipient external iliac vein and artery, commonly on the right due to accessibility of the right external iliac vein.Donor ureter anastomosed to recipient bladder.
Problems with deceased donor kidneys
- Warm ischemia: time from cardiac death to cold perfusion (max ~60 min)• Cold ischemia: time from cold perfusion to recipient anastomosis (max 24-36 hours)
- Warm ischemia: time from cardiac death to cold perfusion (max ~60 min)• Cold ischemia: time from cold perfusion to recipient anastomosis (max 24-36 hours)
Standard criteria donor
Donor brain death, organs remain perfused until cross-clamping (minimizing warm ischemia)
Donation after cardiac death
Organ recovery occurs after cardiopulmonary death. Increases warm ischemia time and risk of delayed function once transplanted. This is “controlled” in the US (ventilator and/or pressor support is withdrawn in the OR) and often uncontrolled in Europe (asystolic in the field after attempts at resuscitation).
Extended criteria donor
Donor > 60 years old, or Donor age 50-59 with at least two of either 1) history of hypertension, 2) death by stroke, or 3) elevated terminal creatinine. Associated with 70% increased risk of graft failure within 2 years vs. SCD. For this reason, ECD kidneys are generally reserved for patients with especially high mortality while on dialysis (older patients and patients with diabetes)
Donor > 60 years old, or Donor age 50-59 with at least two of either 1) history of hypertension, 2) death by stroke, or 3) elevated terminal creatinine. Associated with 70% increased risk of graft failure within 2 years vs. SCD. For this reason, ECD kidneys are generally reserved for patients with especially high mortality while on dialysis (older patients and patients with diabetes)
How many HLA matches are taken into account with kidney transplant
6- Two copies each of HLA-A, HLA-B and HLA-DR. (A and B are class 1 MHC/HLA antigens and DR is class II MHC/HLAantigen). Matching at these 6 loci is the most important for successful long term transplant. The degree of HLA matching does NOT impact the risk of acute rejection though.
Why is HLA matching important
•Unless donor/recipient are HLA identical, recipient T cells will recognize foreign donor HLA antigens as “non-self” and mount a response (rejection).
Treatment of transplant rejection
If T cell mediated, IV steroids, anti-thymocyte globulin. If antibody/B cell mediated, plasmapheresis or IVIG/rituximab to inhibit antibody production
Immunosuppresion regimen for transplant
triple therapy: Calcineurin inhibitor + proliferation inhibitor + prednison
calcineurin inhibitors examples and side effects
cyclosporin and tacrolimus. Nephrotoxicity (vasoconstriction of afferent arteriole, then interstitial fibrosis and sclerosis, gingival hyperplasia, neurotoxicity
Proliferation inhibitor examples
1) Mycophenolate Mofetil (MMF, cellcept, myfortic, MPA)- inhibit purine synthesis. 2) mTOR Inhibitors (sirolimus, everolimus)
cancer and transplant
Increased risk of cancer after transplant due to immunosuppression
Pre-renal causes of AKI in transplant
• Volume depletion from post-operative fluid shifts, blood loss, etc. • Thrombosis of the transplanted renal artery or vein (surgical emergency)• Calcineurin inhibitor effects on the afferent arteriole
Post-renal causes of AKI in transplant
- Transplant ureter obstruction due to fluid collection: requires surgical drainage o Lymphocele o Hematoma • Urine leak: due to break down of transplant ureter to bladder anastomosis. Creatinine rises due to absorption through peritoneal membrane (Cr concentration is much higher in urine vs. serum). Requires ureteral stenting and often surgical repair.
- Transplant ureter obstruction due to fluid collection: requires surgical drainage o Lymphocele o Hematoma • Urine leak: due to break down of transplant ureter to bladder anastomosis. Creatinine rises due to absorption through peritoneal membrane (Cr concentration is much higher in urine vs. serum). Requires ureteral stenting and often surgical repair.
Renal causes of AKI in transplant
Delayed graft function, acute rejection, recurrent primary kidney disease, infection (UTI, polyoma virus)
Which primary renal diseases are likely to re-occur in a transplant
Primary focal segmental glomerulosclerosis, myeloproliferative glomerulonephropathy II (100% recurrance), atypical HUS (100% recurrence). Membranous nephropathy IgA nephropathy, SLE, diabetic nephropathy tend to recur though are often not clinically significant
Imaging/labs for suspect AKI
a. Ultrasound to evaluate for post-renal obstruction/fluid collections. b. Calcineurin inhibitor drug level to evaluate for potential toxicity. c. Urinalysis for infection, proteinuria. d. Serum for bacterial/viral (BK) culture or PCR, antibodies against donor HLA antigens
