anaesthesia and renal transplant

Renal transplantation: 

Renal transplantation Dr.Nirav kotak Dr. S hradha Dr.Vadiraj Dr.Ashok

history: 

history Dr. Joseph Murray performed the first successful human kidney transplant in 1954 in Boston. The transplant was performed between identical twin brothers, with the healthy twin serving as a living donor. The recipient lived for eight years before succumbing to recurrent kidney disease . Although this and subsequent identical twin transplants did not address the problem of rejection, they did serve as a proof of concept. For his work in the field of organ transplantation, Murray was awarded the Nobel Prize in Medicine in 1990

: 

India started it’s kidney transplant program in 1970s. Indian parliament in 1994 passed the “transplantation of human organ act”(THO) The act provides the regulations for removal, storage and transplantation of human organs for therapeutic purposes . Prvention of commercial dealings in human organs The act also accept brain death.

PowerPoint Presentation: 

Kidneys are vital organs of the body Their main functions are : Removal of nitrogenouswaste Electrolyte and pH balance Calcium metabolism Erythropoetin production

Indications for renal transplantation: 

Indications for renal transplantation ESRD caused by- -DM(40%) - glomerular diseases -Hypertension - PCKD - tubulointerstitial diseases and -other familial and congenital diseases.

ESRD: 

ESRD End-stage renal disease (ESRD) is defined as irreversible decline in a person's own kidney function, which is severe enough to be fatal in the absence of dialysis or transplantation. ESRD is included under stage 5 of the National Kidney Foundation Kidney Disease Outcomes Quality Initiative classification of chronic kidney disease (CKD), where it refers to individuals with an estimated glomerular filtration rate less than 15 mL per minute per 1.73 m2 body surface area, or those requiring dialysis irrespective of glomerular filtration rate .

Stages of Chronic Renal Failure based on GFR: 

Stages of Chronic Renal Failure based on GFR STAGES GFR ml/min/1.73m2 of a body surface area STAGE-1 > 90 STAGE-2 60-89 STAGE-3 30-59 STAGE-4 15-29 STAGE-5 < 15

Pt. with ESRD can have two treatment options : 

Pt. with ESRD can have two treatment options DIALYSIS RENAL TRANSPLANT

PowerPoint Presentation: 

Treatment done 2-3 times a week. (2.5-5hr). Physical and financial dependancy . Emotional dependancy and depression. Children maintained with dialysis do not grow. Better quality of life. Better cost\ benifit ratio Possibly longer survival. In children promotes better growth and development. DIALYSIS RENAL TRANSPLANT

CONTRAINDICATIONS TO RENAL TRANSPLANTATION: 

CONTRAINDICATIONS TO RENAL TRANSPLANTATION ABO incompatibility. Cytotoxic antibodies against HLA antigens of donor. Recent or metastatic malignancy. Active infection. AIDS. Severe extrarenal disease (cardiac, pulmonary, hepatic). Active vasculitis or glomerulonephritis . Uncorrectable lower urinary tract disease. Noncompliance. Psychiatric illness including alcoholism and drug addiction. Age > 70 years. Persistent coagulation disorder. - Pregnant women. - Vesical or urethral abnormalities - Aortoiliac occlusive disease ( stenotic pathology) -Morbid obesity A bsolute Relative contraindications

Kidney Donor: 

Kidney Donor Living related. Living unrelated (emotionally motivated). Cadaveric (Brain-dead)

PowerPoint Presentation: 

Living related- first degree consanguinity-parents and children. Also include siblings, cousins, nephews, nieces and other blood relatives. Living unrelated- spouse, in-law, friends or altruist donor.

CRITERIA FOR LIVING DONOR SELECTION: 

CRITERIA FOR LIVING DONOR SELECTION Blood relative. Highly motivated. ABO blood group-compatible. HLA-identical or haploidentical with negative cross-match. Excellent medical condition with normal renal function.

Matching between Recepient And Donor: 

Matching between Recepient And Donor A- Compatible ABO blood group B- Tissue typing C- Cross matching A- Compatible ABO blood group

Matching between Recepient And Donor: 

Matching between Recepient And Donor B-tissue typing Determined by 6 antigens located on cell surface encoded for by the HLA gen located on the short arm of chromosom 6. Class I antigens (HLA-A and HLA-B) . Class II antigen (HLA-DR) These 6 antigens are refered as major transplant antigens. The match between donor and recepient can range from 0 to six C- Cross matching A laboratory test that determines weather a potential transplant recepient has preformed antibodies against the HLA antigens of the potential donor. (Donor Lymphocytest + Recepient Serum)

PowerPoint Presentation: 

Effect of HLA-A, -B, -DR Mismatching on Kidney Graft Survival Degree of Donor Mismatch 1-Year Survival, % 5-Year Survival, % Cadaver donor (all) 89.2 61.3 0/6-HLA mismatch 91.3 68.2 3/6-HLA mismatch 90.1 60.8 6/6-HLA mismatch 85.2 55.3 Living related donor (all) 94.7 76.0 0/6-HLA mismatch 96.7 87.0 3/6-HLA mismatch 94.3 73.2 6/6-HLA mismatch 92.7 57.7 Living unrelated donor 95.3 77.4 Note: 0-mismatched related donor transplants are virtually all from HLA-identical siblings, while 3/6-mismatched transplants can be one haplotype mismatched (1-A, 1-B, and 1-DR antigen) from parent, child or sibling; 6/6-HLA-mismatched living related kidneys are derived from siblings or relatives outside of the nuclear family.

Effect Of HLA Matching On The Graft Outcome: 

Effect Of HLA Matching On The Graft Outcome T he better the HLA-match , better the long-term survival of the allograft . lesser degrees of matching also have good long-term survival of the allograft with the use of newer and more potent immunosuppressive drugs . Matching for DR antigens are more favorable than others . Living related donor has better survival than cadaver donor.

Living Donor transplantation : 

Living Donor transplantation Advantages -Better results -Lesser waiting time -Good early function -Less aggressive immunosuppression -Psychological gain Disadvantages -Anxiety also within family -Operative mortality - Long term morbidity -Risk of traumatic injury to the remaining kidney

Does Donation Of A kidney Pose A long-term Risk For The Donor?: 

Does Donation Of A kidney Pose A long-term Risk For The Donor ? Following nephrectomy , compensatory hypertrophy and increase in GFR occur in the remaining kidney. Slight risk of poteinuria and hypertension. Meta-analysis of data from donors followed for >20y confirmed safety of kidney donation.

C/I Living Kidney Donation: 

C /I Living Kidney Donation Renal parenchymal disease. Conditions that may predispose to renal disease History of stone disease History of frequent UTI Hypertension D.M. Conditions that increase the risks of anaesthesia and surgery. Recent malignancy.

CRITERIA FOR CADAVER DONOR SELECTION: 

CRITERIA FOR CADAVER DONOR SELECTION Age between 6to 50 years. Irreversible brain damage. No history of hypertension ,DM . Normal renal anatomy and renal function appropriate for age. No evidence of preexisting renal disease. No evidence of transmissible diseases. No malignancy other than primary brain tumor or treated superficial skin cancer. ABO blood group-compatible. Negative cross-match. Best HLA match possible, particularly at the DR and B loci.

CRITERIA FOR EXPANDED CRITERIA DONOR {ECD}: 

CRITERIA FOR EXPANDED CRITERIA DONOR {ECD} All donars greater than 60 yr. Donar older than 50 yr. with any two of the following criteria -hypertension. -cerebrovascular cause of death. - preretrival sr. creatinine levvel >1.5mg/dl. -with degree of glomerulosclerosis >15 % -prolonged cold ischemia >36hr. -non-heart beating donar .

BRAINSTEM DEATH: 

BRAINSTEM DEATH A Clinical diagnosis of Brainstem death involves three steps: 1)Ascertain that certain preconditions have been met 2) Exclusion of reversible causes of non functioning Brainstem 3) Clinical test to establish that the comatose patient is apneic

BRAINSTEM DEATH: 

BRAINSTEM DEATH PRECONDITIONS 1. Patient must be comatose and on ventilator for atleast 6-24 hrs 2. Cause must be established and it must be a structural brain damage 3. Neurosurgical management and correction of any obvious metabolic disturbances should be done then only brain damage is considered irreversible Judgement should not be made on ct/ mri findings .

BRAINSTEM DEATH: 

BRAINSTEM DEATH CLINICAL TESTING: No pupillary response to light No corneal reflex No vestibulocochler reflex No motor response within the cranial nerve distribution No gag reflex or reflex response to bronchial stimulation by suction catheter.

BRAINSTEM DEATH: 

BRAINSTEM DEATH EXCLUSIONS - Drug intoxication Primary hypothermia Metabolic & endocrines disterbances

BRAINSTEM DEATH: 

BRAINSTEM DEATH APNEA Preoxygenate with 100% oxygen for 10 min. Disconnect ventilator for 8 min. no respiratory movements should occur Who does the test? Two or three physicians who are independant of trasplantation team, and at least one of the physicians is required to be a specialist in neurology, neurosurgery or anesthesiology. 2 examination are done in the interval of at least 6 hours

ORGAN DYSFUNTION IN CADAVER AND ITS MANAGMENT: 

ORGAN DYSFUNTION IN CADAVER AND ITS MANAGMENT HYPOVOLEMIA AUTONOMIC DYSFUNTION HORMONAL INSUFFICIENCY ACTIVATION OF INFLAMATORY MEDIATORS HYPOTHERMIA COAGULOPATHY

PowerPoint Presentation: 

Intraoperative Management (cadaver donor ): Maintaining PaO2 >100mm Hg with normocapnia Adequate intra vascular volume ( Ht >30 % CVP 6-10 mm of Hg HB-10gm%) Systolic B.P. >100mm Hg Low dose dopamine, Dobutamine , isoproterenol, or low dose epinephrine Urine output > 100ml/ hr Glucose <150-200mg/dl. Heparin should be administered before organ harvesting (INR<2 & platelet >50,000/mm3 acceptable) The kidneys are removed enblock with ureters

Evaluation In Potential Kidney Donor: 

Evaluation In Potential Kidney Donor History and clinical examination CBC Biochemical profile including both FBS and PLBS LFT. CxR PFT with chest medicine opinion Cardilogy work up and opinion (ECG,2-D ECHO stress test ) Urine –complete analysis IVP Aortography

Evaluation Of Kidney Function In Potential Kidney Donor: 

Evaluation Of Kidney Function In Potential Kidney Donor Serum creatinine . Creatinine clearance. Radionuclide glomerular filtration rate. Urine analysis. Urine Culture. GFR > 70 ml/min. Serum electrolytes. HIV,HBsAg ,CMV. Ruleout septic focus of infection-ENT,OPTHAL,SKIN and in females gynaecology .

ON THE DAY OF OPERATION : 

ON THE DAY OF OPERATION Papers to be checked. Consent for renal donation Consent for anaesthesia Registration from authorisation committee Permission for the hospital and team Affidavit of the donor

Conteaindication of Renal Transplantation in recipient : 

Conteaindication of Renal Transplantation in recipient Absolute : Severe vascular disease. Relative : Recent malignancy. Coronary artery disease. Active bacterial, fungal, or viral disease. HIV positivity. Social conditions. Others.

Preoperative preparation and evaluation of recepient: 

Preoperative preparation and evaluation of recepient History and clinical examination H/o dialysis-frequency, duration and access. H/o BT. Site and patency of AV fistula. Drug treatment.

PowerPoint Presentation: 

CVS Hypertension Accelerated Atherosclerosis Hyperlipidemia Pericarditis Congestive Heart Failure Arrythmias Pulmonary Hyperventilation Interstitial edema Alveolar edema Pleural effusion CNS Peripheral Neuropathty Autonomic Neuropathty Myopathy Encephalopathy

Patients awaiting transplant have comorbidities : 

Patients awaiting transplant have comorbidities Antihypertensives Antidiabetics Antibiotic prophylaxis Immunosupressants Erytheropoetin . Anticoagulant/ antiplatlete

Preoperative preparation and evalvation of reciepient: 

Preoperative preparation and evalvation of reciepient INVESTIGATIONS ROUTINE -complete hitory and physical examination -CBC ,PCV. -blood chemistries -lipid profile -PT and PTT, BT -urine routine and c/s

PowerPoint Presentation: 

-blood group -hepatitis screen -VDRL and HIV - gynaec exam for females -x ray chest with reporting,PFT with chest med opinion. -x-ray abdomen and skeloton . -ECG,2-D ECHO , stress test followed by cardiology work up and opinion. -HLA typing and cytological abnormalities - CMV EBV TOXOPLASMA

PowerPoint Presentation: 

-Doppler USG of aorta and lower extremities - abd USG - Esophagogastrodeodenoscopy OPTIONAL - volding cystourethrogram -stress test and echo -coronary angiography -PSA -COLONOSCOPY AND BARIUM ENEMA -mammography - doppler USG of carotids. - psychiyatric evaluation. -rule out septic focus – ENT,OPTHAL,SKIN,DENTAL,and in females GYNAEC

RECIPIENT CAN BE KEPT IN GOOD HEALTH BY: 

RECIPIENT CAN BE KEPT IN GOOD HEALTH BY Crrection of fluid,water , acid overload and CHF. Rx of hyperkalemia by diet and drugs.Anaemia with erythropoetin . cardiovasccular effects Correction of renal osteodystrophy Modifying drugs and dosages. Rapid reversal of acute episodes of renal deterioration due to dehydration and infection. Dietary modifiation to reduce nitrogen load

BEFORE SHIFTING RECIPIENT TO OT: 

BEFORE SHIFTING RECIPIENT TO OT Papers to be checked Consent for renal transplant surgery. Permission from authorisation committee Consent for anaesthesia Permission for the hospital and the team Affidavit of the recipient Hemodialysis one day prior to surgery. Repeat Hb,PCV,renal function tests,Electrolytes , PT,INR after last preoperative dialysis, Preoperative weight .

PATHOPHYSIOLOGIC CONSEQUENCES OF CHRONIC RENAL FAILURE AND ANAESTHETIC MANAGEMENT IN DONOR AND RECIPIENT: 

PATHOPHYSIOLOGIC CONSEQUENCES OF CHRONIC RENAL FAILURE AND ANAESTHETIC MANAGEMENT IN DONOR AND RECIPIENT V adiraj

PowerPoint Presentation: 

PATHOPHYSIOLOGIC CONSEQUENCES OF CHRONIC RENAL FAILURE IMPORTANT FOR THE ANESTHESIOLOGIST Abnormality Mechanism of Abnormality/Clinical Presentation Anemia Decreased erythropoetin production, diminished erythrocyte survival ( normochromic , normocytic anemia), diminished erythrocyte production (fibrosis of the bone marrow) Platelet dysfunction Qualitative dysfunction (normal platelet count, decreased platelet factor III activity, abnormal platelet aggregation), bleeding diathesis Altered O 2 -carrying capacity Balanced between reduced O 2 -carrying capacity (anemia) and improved O 2 capacity (shift of oxyhemoglobin dissociation curve to the right) Cardiovascular abnormalities CHF (primary: uremic cardiomyopathy ; secondary: fluid overload), CAD (accelerated atherosclerosis), uremic pericarditis , cardiac tamponade , dysrhythmias ( hyperkalemia , hypocalcemia ) Arterial hypertension Left ventricular hypertrophy, hypertensive cardiomyopathy , hypertensive crises (malignant hypertension)

PowerPoint Presentation: 

Abnormality Mechanism of Abnormality/Clinical Presentation Arterial hypertension Left ventricular hypertrophy, hypertensive cardiomyopathy , hypertensive crises (malignant hypertension) Peripheral neuropathy Muscle weakness ( peroneal nerve palsy with foot drop) Central nervous system dysfunction Behavioral changes, loss of memory, neuromuscular irritability, lethargy → coma (uremic encephalopathy), myoclonus , convulsions Electrolyte and fluid disturbances Hyperkalemia (cardiac dysrhythmias ), hypocalcemia ( osteodystrophic abnormalities, osteoporosis, pathologic bone fractures), hypermagnesemia (hypotension, potentiation of depolarizing muscle relaxants, coma), hypervolemia (CHF, pulmonary edema, pleural effusion, hypertension) Acid–base abnormalities Metabolic acidosis Gastrointestinal abnormalities Uremic gastroenteritis, nausea and vomiting, peptic ulcer disease, gastrointestinal bleeding Endocrine disturbances Secondary hyperparathyroidism, osteomalacia , renal osteodystrophy (bone pain, fractures) Dialysis-related problems Dialysis dementia, dysequilibrium syndrome after acute dialysis (cerebral edema), hypovolemia (hypotension after anesthetic induction following recent dialysis), peritonitis (peritoneal dialysis), systemic anticoagulation (after dialysis)

VOLUME STATUS IN RECIPIENT : 

VOLUME STATUS IN RECIPIENT Importance for allograft survival Volume expansion – caution in cardiac disease Loop diuretics Mannitol Albumin Ca. channel blockers ? Dopamine / Dopexamine

Preoperative Dialysis: 

Preoperative Dialysis goals – optimise fluids/electrolytes BUN < than 100 mg/dl Facilitate blood transfusion ideal – day before surgery 8 hour dialysis  b.w . by 1.5 kg  pl.vol.by 0.7 L Peritoneal dialysis May continue till surgery Post-op: assess ventilatory status

Preoperative transfusions: 

Preoperative transfusions not if HCT > 25% trigger  if CAD present stored blood – danger of hyperkalaemia no evidence in favour of leucocyte depleted blood

Choice of Anaesthesia: 

Choice of Anaesthesia G.A. Better haemodynamic control, no sympathetic blockade Safe in coagulopathy Maintains control over airway,provides amnesia,analgesia,hypnosis ,immobility(optimal surgical conditions ) REGIONAL Pts with autonomic neuropathy are at risk of hypotension induced by sympathetic blockade Prolonged bleeding time Risk of arrythmias if epinephrine is added to local anaesthetic Catheter site infection Poor patient psycholgical status Long anticapated duration of surgery

Preoperative preparation: 

Preoperative preparation Premedication IV glycopyrrolate IV midazolam IV fentanyl IV ranitidine

POSITIONING / CARE OF A.V.FISTULA : 

POSITIONING / CARE OF A.V.FISTULA Padding of extremities Limb with AV fistula Padding No NIBP / DAP monitoring No venipuncture No I.V. cannulae

ANAESTHESIA TECHNIQUE: 

ANAESTHESIA TECHNIQUE General anaesthesia with rapid sequence induction using endotrachaeal intubation and maintaining the patient on controlled ventillation with muscle relaxant

Anaesthetic Management : 

Anaesthetic Management Induction Agents : thiopentone / propofol Barbiturates Increased sensitivity Increased free drug fraction Unaltered total drug elimination Decrease the rate of administration rather than decreasing drug dosage Propofol No alteration in terminal half life or clearance. No effect on plasma protein binding.

Anaesthetic Management : 

Anaesthetic Management Induction Agents Cont’d…. Ketamine Elimination of metabolites is reduced. it causes sympathetic stimulation so best avoided Etomidate Significant decrease in plasma protein binding. No studies on disposition in CRF. Suppression of steroidgenesis is short lived .

Anaesthetic Management : 

Anaesthetic Management Muscle Relaxants: Atracurium Suxamethonium to be avoided if K raised Drug Renal Excretion Elimination half life Suxamethonium <10% 2m----2m Atracurium 10% 0.3hr---0.4hr Cisatracurium 16% Mivacurium <10% 2m----2m Vecuronium 15-20% 0.9-1.3 hr ---1.4-1.6hr Pancuronium 35-50% 2.2hr--- 4.3 hr Rocuronium 9% 1.2hr--- 1.6hr Rapacuronium 30 %

Anaesthetic Management : 

Anaesthetic Management Maintenance: Oxygen + Nitrous oxide + Isoflurane + Atracurium Inhalational agents- ISOFLURANE AND DESFLURANE ARE INHALATIONAL AGENTS OF CHOICE Isoflurane – no arrythmia Desflurane --- no EFFECT ON RFTS, NO effect of sodalimme , fluoride < 1 Sevoflurane – sevo + nitrous oxide in esrd is associated with higher post operative level of BUN,Creatinine ~13.4 hrs ---- > 40 m mole fluoride Halothane, enflurane ------- Arrythmias

Anaesthetic Management : 

Anaesthetic Management Intra-operative Problems Hypertension Hypotension Arrhythmias Intraoperative fluid administration Electrolyte imbalance Renal protection(CVP, dopamine infusion minimum warm ischemia and cold ischemia time)

The Surgical Procedure: 

The Surgical Procedure Left kidney is preferred because of long left renal vein Left Transplanted kidney is placed in the R quadrant of the abdomen in an extraperitoneal position. This approach places pelvis and ureter anteriorly and facillitates reconstuction Oblique or curvilinear incision in right lower quadrant parallel to the inguinal ligament and 2 cm above it Arterial anastomosis or venous anastomosis is done depending on final position kidney and choice of surgeon Arterial anastomosis is done first when renal artery is anatomosed to internal iliac artery Venous anastomosis is done first when renal artery is anatomosed to external iliac artery

Anaesthetic management of kidney recipient: 

Anaesthetic management of kidney recipient Once the transplant anastomoses completed the early onset of urine output is paramount The early onset of urine output indicates the graft survival ( Dawidson et.al) Measures to stimulate urine production and to improve kidney viability Intravascular volume : the CVP 10mm Hg to 15mm Hg. Aggressive Intraoperative volume expansion is warranted. Maintaining mean P.A. pressure over 20mm Hg shown to reduce occurance of post operative tubular necrosis

Preservation of harvested organ: 

Preservation of harvested organ Warm ischemia time : starts when donor vessels clamped and interrupted by cold perfusion . Cold ischemia time : the kidneys are preserved at 4 °c. ideally cold ischemic time is <24hrs. Short and long term survival of graft depends on cold ischemic time Rewarm time – removal of kidney from cold storage or prefusion to the completion of renal arterial anastomosis Rewarm time can be minimized by cooling the kidney during surgery.

Preservative solution : 

Preservative solution Euro-Collins solution Potassium 115meq Sodium 10meq Chloride 15meq Bicarbonate 10meq Dihydrogen phosphate 15meq Monohydrogen phosphate 85meq Measured osmolality 375meq pH(4°c) 7.25 Belzer’s (U.W) solution K+ lactobionate 100mmol KH2PO4 25mmol Mgso4 5mmol Adenosine 5mmol Glutathione 3mmol Raffinose 30mmol Allopurinol 1mmol Tosulin 100units Penicillin 40units Dexamethasone 8mg Hydroxyethyl starch 50gm Osmolality 320-330mosmol pH(4°c) 7.4

Anaesthetic Management : 

Anaesthetic Management Reversal Inj Neostigmine titrated dose with Glycopyrrolate Extubation / ventillatory support as per situation Auscultate lungs for sub- clinical pulmonary edema Patient shifted to AKD

Factors Influencing The Longivity Of Renal Allograft: 

Factors Influencing The Longivity Of Renal Allograft Age HLA matching Delayed graft function Ischemia time. Number of acute rejection episodes. Native kidney disease. Ethnicity. Others

PowerPoint Presentation: 

What Are The Major Causes Of Long-Term Allograft Failure ? What Are The Most Common causes Of Death AfterKidney Transplantation? Chronic rejection Death with funtioning geaft . Cardiovascular disease. Infection.

Renal Allograft Rejection: 

Renal Allograft Rejection 1- Hyperacute . 2- Acute. 3- Chronic.

Hyperacute Rejection: 

Hyperacute Rejection Is mediated by preformed antibodies that recognize HLA antigens in donor organ. Usually these are formed as a consequence of blood transfusion, pregnancy, prior organ transplantation, autoimmune diseases. Fibrinoid necrosis lead to immediate graft loss. Delayed form may occur several days following transplantation. Plasmapheresis and pulse steroid may be used.

Acute Renal Allograft Rejection: 

Acute Renal Allograft Rejection IS mediated by activated T-lymphocytes. Activations of T-cells occure after recognition of graft antigen either directly or after being processed and presented by APC. This usually occur during the first 6 mon. It manifest as increase in s. creatinine with or without oliguria.

IMMUNOSUPPRESSIVE TREATMENT: 

IMMUNOSUPPRESSIVE TREATMENT Prior to the advent of immunosuppression, kidney transplantation was limited to HLA-identical siblings and was not applicable to the vast majority of patients with end-stage renal disease . In 1963, the introduction of azathioprine and steroid combination therapy produced encouraging results and became the mainstay of immunosuppression . The introduction of cyclosporine in 1983 was one of the most pivotal events in the history of organ transplantation, as it significantly improved the outcomes of all solid organ transplants by reducing the risk of rejection . Further innovations, including anti–T-cell antibodies (both monoclonal and polyclonal preparations), as well as other maintenance immunosuppressants ( eg , tacrolimus , mycophenolate , sirolimus ), have made a significant impact on both patient and graft survival . Currently, one-year patient and graft survival rates exceed 90% in most transplant centers .

Principles underlying current immunosuppressive treatment: 

Principles underlying current immunosuppressive treatment 1- The benefits of a successful transplant outweight the risks of chronic immunosuppression. 2- Immunosuppressive therapy is required indefinitely. 3- Multidrug regimens are generally employed. 4- Large doses of immunosuppressant drugs are used in the early transplant period.

Immunosuppression. : 

I mmunosuppression . Two phases- Induction phase- Large, tapering doses of corticosteroids(methylprednisolone) Large doses of calcineurin inhibitors(cyclosporine, tacrolimus ) Polyclonalantibodies ( antithymocyte globulin), monoclonal antibody( basiliximab , daclizumab or muromonab-CD3) Maintenance phase- Less intense than induction phase. Use for life of allograft. It involves triple-drug combination calcineurin inhibitors. Antiprolifrative agents(azathioprine, mycophenolic acid or sirolimus ) Corticosteroids.

Some commonly used combinations of maintenance Immunosuppressive drugs: 

Some commonly used combinations of maintenance Immunosuppressive drugs 1- Prednisolon e + Azathiaprine 2- Prednisolone + cyclosporine (or tacrolimus ) 3- Prednisolone + cyclosporine + Azathioprine 4- MMF (cell cept ) may replace Azathioprine . 5- Sirolimus ( Rapaimmune ) may replace Azathioprine or cyclosprine 6- TRIPLE THERAPY(KEM ) 1) Cyclosporin ,7mg/kg,BD,2days prior 2) AZT , 2mg/kg,OD,1day prior. 3) Methyl Prednisolone I/O 1gm IV 2nd & 3rd day 500mg OD

Common drug interactions: 

Common drug interactions Cyclosporine enhances the effect of neuromuscular blocked . Requirement of nondepolarizing muscle relaxants are reduced.

Risks associated with chronic Immunosuppression: 

Risks associated with chronic Immunosuppression Malignancy Infection Side effects of different drugs (steroids, CsA , tacrolimus , MMF, …..)

Transplannt pt.coming for nontransplant Sx.: 

Transplannt pt.coming for nontransplant Sx . Native kidney disease Immunosuppression, bone marrow suppression DM HTN atherosclerosis

. THANK YOU: 

. THANK YOU