Kidney Transplantation – A+ Graded Nursing
Exam | End Term Paper with Complete Solution
What are some considerations for a differential of low urine output in a transplant patient? -
✔✔-Acute/chronic issues with the donor (anything that could cause AKI/CKD in a donor would
fit here)
-Cold/warm ischemia times
-Surgical difficulties (anastamoses, thrombosis, lymph fluid accumulation, ureteral necrosis)
-Recipient volume status, infection, or CV problems
-Acute rejection (consider HLA matching, preoperative measures like inductive therapy,
proper antirejection med dosing)
-Nephrotoxicity of immunosuppressant drugs
What is delayed graft function? - ✔✔A diagnosis of exclusion in the event that a transplanted
kidney doesn't begin making sufficient quantities of urine post-transplant. Once all other
differentials have been considered, this is the diagnosis given.
What is the principle of immunosuppression in transplantation? - ✔✔Use of drugs that
suppress the immune system balances survival of the allograft versus survival of the whole
person.
When do most adverse immunologic events occur in kidney transplantation? - ✔✔Within the
first year (thus, immunosuppressant drugs are typically reduced after this time.
What is induction therapy? - ✔✔Administration of a lymphocyte depleting medication (e.g.
an antibody)
What is the time course for: hyperacute rejection? accelerated acute rejection? acute
rejection? chronic rejection? - ✔✔minutes to hours; 1-4 days; days to months; years
Mechanism of hyperacute rejection - ✔✔Preformed antibodies to blood group glycoproteins;
no cellular immune response is activated
, Mechanism of accelerated acute rejection - ✔✔Endothelial cell rupture and hemorrhage
mediated by activated T cells; preventable with induction therapy
Mechanism of acute rejection - ✔✔T-cell attack against the endothelium (arteritis) or tubules
(tubulitis); also get mononuclear infiltrates (acute rejection is a form of interstitial nephritis)
Mechanism of chronic rejection - ✔✔Obliterative vascular lesions, interstitial fibrosis, tubular
atrophy, glomerulosclerosis; initial insult appears to be proliferation of vascular smooth
muscle with massive thickening of the elastic lamina; this results in ischemic and fibrotic
changes in the kidney
What are the most common infections seen in kidney transplant? - ✔✔Mostly opportunistic
infections (CMV, pneumocystis, aspergillis, etc), reactivation of pre-existing infections (e.g.
mycobacteria), or chronic progressive infections (HBV, HCV, polyoma virus, HPV)
What malignancies are most commonly increased in transplant? - ✔✔Skin and cervical cancer
most common; can also see an increase in lymphoma (particularly in patients who received
induction therapy)
What are some of the major damaging effects (both reversible and irreversible) of
cyclosporine on the kidney? - ✔✔Reversible: tubulopathy (in the PCT) --> isometric vacuoles,
giant mitochondria, single cell necrosis, microcalcifications
Irreversible: vasculopathy (afferent arteriole) --> endothelial cell damage, smooth muscle
damage, arteriolar occlusion, vessel obliteration --> glomerular obsolescence, localized
ischemia, tubular atrophy, striped interstitial fibrosis
What percent of transplant patients will have hypertension at one year post-transplant? What
percent will die of CV disease? - ✔✔75% (exacerbated by calcineurin inhibitors); 40%
What percent of patients get de novo diabetes after transplant? What factors contribute to
this? - ✔✔20%; contributing factors include steroids, calcineurin inhibitors (diabetogenic),
resumption of normal kidney gluconeogenesis, improved appetite and weight gain,
elimination of dietary restrictions
Exam | End Term Paper with Complete Solution
What are some considerations for a differential of low urine output in a transplant patient? -
✔✔-Acute/chronic issues with the donor (anything that could cause AKI/CKD in a donor would
fit here)
-Cold/warm ischemia times
-Surgical difficulties (anastamoses, thrombosis, lymph fluid accumulation, ureteral necrosis)
-Recipient volume status, infection, or CV problems
-Acute rejection (consider HLA matching, preoperative measures like inductive therapy,
proper antirejection med dosing)
-Nephrotoxicity of immunosuppressant drugs
What is delayed graft function? - ✔✔A diagnosis of exclusion in the event that a transplanted
kidney doesn't begin making sufficient quantities of urine post-transplant. Once all other
differentials have been considered, this is the diagnosis given.
What is the principle of immunosuppression in transplantation? - ✔✔Use of drugs that
suppress the immune system balances survival of the allograft versus survival of the whole
person.
When do most adverse immunologic events occur in kidney transplantation? - ✔✔Within the
first year (thus, immunosuppressant drugs are typically reduced after this time.
What is induction therapy? - ✔✔Administration of a lymphocyte depleting medication (e.g.
an antibody)
What is the time course for: hyperacute rejection? accelerated acute rejection? acute
rejection? chronic rejection? - ✔✔minutes to hours; 1-4 days; days to months; years
Mechanism of hyperacute rejection - ✔✔Preformed antibodies to blood group glycoproteins;
no cellular immune response is activated
, Mechanism of accelerated acute rejection - ✔✔Endothelial cell rupture and hemorrhage
mediated by activated T cells; preventable with induction therapy
Mechanism of acute rejection - ✔✔T-cell attack against the endothelium (arteritis) or tubules
(tubulitis); also get mononuclear infiltrates (acute rejection is a form of interstitial nephritis)
Mechanism of chronic rejection - ✔✔Obliterative vascular lesions, interstitial fibrosis, tubular
atrophy, glomerulosclerosis; initial insult appears to be proliferation of vascular smooth
muscle with massive thickening of the elastic lamina; this results in ischemic and fibrotic
changes in the kidney
What are the most common infections seen in kidney transplant? - ✔✔Mostly opportunistic
infections (CMV, pneumocystis, aspergillis, etc), reactivation of pre-existing infections (e.g.
mycobacteria), or chronic progressive infections (HBV, HCV, polyoma virus, HPV)
What malignancies are most commonly increased in transplant? - ✔✔Skin and cervical cancer
most common; can also see an increase in lymphoma (particularly in patients who received
induction therapy)
What are some of the major damaging effects (both reversible and irreversible) of
cyclosporine on the kidney? - ✔✔Reversible: tubulopathy (in the PCT) --> isometric vacuoles,
giant mitochondria, single cell necrosis, microcalcifications
Irreversible: vasculopathy (afferent arteriole) --> endothelial cell damage, smooth muscle
damage, arteriolar occlusion, vessel obliteration --> glomerular obsolescence, localized
ischemia, tubular atrophy, striped interstitial fibrosis
What percent of transplant patients will have hypertension at one year post-transplant? What
percent will die of CV disease? - ✔✔75% (exacerbated by calcineurin inhibitors); 40%
What percent of patients get de novo diabetes after transplant? What factors contribute to
this? - ✔✔20%; contributing factors include steroids, calcineurin inhibitors (diabetogenic),
resumption of normal kidney gluconeogenesis, improved appetite and weight gain,
elimination of dietary restrictions
