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ABSTRACT: Kidney allograft failure is most often caused by chronic allograft nephropathy, a process of interstitial fibrosis (GIF) and tubular atrophy (TA). We assessed the pathology of living donor (LD) grafts compared to deceased donor (DD). Included are 321 recipients (245 LD; 76 DD) with protocol biopsies the first 2 years of transplant. In LD, GIF was present in 7%, 31%, 61% and 71% of grafts at 0, 4, 12 and 24 months. TA progressed in parallel to GIF. Compared to LD, more DD grafts had GIF at time 0 (29%, p = 0.002); thereafter the incidence of GIF was similar. In LD, GIF was associated with lower glomerular filtration rate (GFR)(1 year) (no GIF, 62 +/- 16; GIF, 49 +/- 15 mL/min/m(2) iothalamate clearance, p = 0.001) and reduced graft survival (HR = 2.2, p = 0.009). GIF in LD related to acute rejection (HR = 2.6, p = 0.01), polyoma nephropathy (OR = 4.4, p = 0.02) and lower levels of GFR 3 weeks post-transplant (HR = 0.961; p = 0.03, multivariate). However, GIF also developed in 53% of recipients lacking these covariates. Thus, GIF/TA develops in the majority of LD grafts, it is often mild but is associated with reduced function and survival. GIF frequently develops in the absence of risk factors. Lower GFR post-transplant identify patients at highest risk of GIF.
American Journal of Transplantation 06/2005; 5(5):1130-6. · 6.39 Impact Factor
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Lourdes S Peña De La Vega,
Alvaro Torres,
Humberto E Bohorquez,
Julie K Heimbach,
James M Gloor,
Thomas R Schwab,
Sandra J Taler,
Scott L Nyberg,
Michael B Ishitani,
Mikel Prieto, Jorge A Velosa,
Timothy S Larson,
Mark D Stegall,
Fernando G Cosio,
Stephen C Textor,
Matthew D Griffin
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ABSTRACT: Donor age adversely affects deceased-donor kidney transplant outcomes, but its influence on living-donor transplantation is less well characterized.
Living-donor kidney transplants at a single center between 1998 and 2000 were reviewed. Data were abstracted for 52 transplants from donors aged > or =50 years and for a matched group of 104 transplants from donors aged <50 years. Survival indices were compared during the first three years' post-transplantation. Functional indices, including serial iothalamate clearances, were compared at 1, 12, and 24 months.
Predonation glomerular filtration rate (GFR) was lower among older donors (94 +/- 12 vs. 108 +/- 17 mL/min/SA) but post-transplant compensatory hypertrophy was similar (11.7 +/- 26.3% vs. 7.7 +/- 31.4%). Recipients of older-donor grafts were older (52.8 +/- 16.5 vs. 46.1 +/- 15.1 years) and more frequently unrelated to the donor (54% vs. 39%). Trends toward higher frequency of slow graft function, cytomegalovirus (CMV) infection, and polyomavirus nephropathy were observed for older-donor grafts. Three-year recipient, graft, and death-censored graft survivals were > or =90% for both groups. At 1, 12, and 24 months, serum creatinine was higher and GFR was lower among recipients of older- compared with younger-donor grafts. Other functional indices (urine total protein, serum potassium and uric acid, hemoglobin, and number of antihypertensives) were not different. Donor age correlated with graft GFR at 1, 12, and 24 months for the entire study cohort by linear regression.
Older donor age does not preclude excellent results from living-donor kidney transplantation but should be appreciated as being associated with relatively lower GFR.
Kidney International 10/2004; 66(4):1654-61. · 6.61 Impact Factor
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LOURDES S PE|[Ntilde]|A DE LA VEGA,
ALVARO TORRES,
HUMBERTO E BOHORQUEZ,
JULIE K HEIMBACH,
JAMES M GLOOR,
THOMAS R SCHWAB,
SANDRA J TALER,
SCOTT L NYBERG,
MICHAEL B ISHITANI,
MIKEL PRIETO, JORGE A VELOSA,
TIMOTHY S LARSON,
MARK D STEGALL,
FERNANDO G COSIO,
STEPHEN C TEXTOR,
MATTHEW D GRIFFIN
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ABSTRACT: Patient and graft outcomes from older living kidney donors are similar to those from younger donors despite lower GFR.Background Donor age adversely affects deceased-donor kidney transplant outcomes, but its influence on living-donor transplantation is less well characterized.
Kidney International 09/2004; 66(4):1654-1661. · 6.61 Impact Factor
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Fernando C Fervenza,
Peter M Fitzpatrick,
Jim Mertz,
Stephen B Erickson,
Scott Liggett,
Sandy Popham,
Daniel N Wochos,
Arkady Synhavsky,
Steven Hippler,
Timothy S Larson,
Stephanie M Bagniewski, Jorge A Velosa
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ABSTRACT: Based on its success as a transplant immunosuppressor, there is intense interest in using rapamycin in the treatment of progressive glomerulopathies involving native kidneys. However, we call attention to the potential toxicity associated with the use of rapamycin in this setting.
We conducted a study to examine the efficacy and safety of rapamycin in patients with progressive chronic renal failure. Eleven patients with either focal segmental glomerulosclerosis, immunoglobulin A nephropathy, membranous nephropathy or membrano-proliferative glomerulonephritis and progressive renal failure (defined as an increase in >25% of baseline serum creatinine over the last year or loss of glomerular filtration rate > or =5 ml/min/year as determined by the Cockcroft-Gault formula), proteinuria > or =1.0 g/24 h and with a creatinine clearance of > or 20 ml/min/1.73 m(2) were entered into a 12 month study. Patients were treated with rapamycin, starting at 5 mg/day, orally, aiming for target blood levels of 7-10 ng/dl. All patients were on treatment with an angiotensin-converting enzyme inhibitor and/or an angiotensin receptor blocker, aiming to control blood pressure < or =145/90 mmHg.
Six patients developed acute renal failure, defined as an increase in serum creatinine > or =0.5 mg/dl (baseline: 3.2+/-0.9 mg/dl; peak: 5.6+/-1.6 mg/dl; P<0.01, paired t-test). In four patients, discontinuation of the drug resulted in improvement of renal function close to baseline levels. One patient required haemodialysis and had no subsequent recovery of renal function. In another patient, renal function recovered after discontinuation of the drug and then rapamycin was resumed at a lower dose when creatinine returned to baseline. This resulted in a second acute increase in serum creatinine that failed to return to baseline when the medication was discontinued. Four other patients had the following adverse events: skin rash, severe hypertriglyceridaemia, diarrhoea and hyperkalaemia. In none of the subjects were rapamycin levels >15 ng/dl.
Rapamycin can cause nephrotoxicity in some patients with chronic glomerulopathies. Whether the toxicity is solely related to rapamycin, due to the combination of proteinuria and rapamycin, or other unknown factor use is presently undetermined.
Nephrology Dialysis Transplantation 06/2004; 19(5):1288-92. · 3.40 Impact Factor
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ABSTRACT: Chronic allograft nephropathy (CAN) is characterized by progressive renal functional loss and histologic abnormalities of one or more tissue compartments. In this study, correlations between histologic abnormalities and graft function [glomerular filtration rate (GFR, measured by iothalamate clearance), serum creatinine (SCr) and urinary protein (UPr)] were investigated using biopsies from 49 patients with newly diagnosed CAN. Extent of tubulointerstitial fibrosis (%TIF), as assessed by a semi-quantitative score, correlated significantly with GFR, SCr and UPr. The close correlation between %TIF and GFR suggested that quantitative measurement of %TIF may predict functional consequences of CAN. Calculation of %TIF by computerized digital analysis was performed using four strategies: (a) quantitation of blue material in Masson's trichrome (MT)-stained sections, (b) quantitation of red material in Sirius Red-stained sections (SR-nonpolarized), (c) quantitation of birefringent material in Sirius Red stained-sections examined under polarized light (SR-polarized) and (d) quantification of brown material in sections stained by immunoperoxidase for alpha-smooth muscle actin. Only the SR-nonpolarized score correlated significantly with GFR at the time of biopsy-diagnosis of CAN. We conclude that digital analysis strategies demonstrate variable accuracy in quantifying %TIF. Validation of the SR-nonpolarized strategy against histologic scoring and GFR supports the application of this technique to longitudinal studies of CAN.
American Journal of Transplantation 03/2004; 4(2):248-56. · 6.39 Impact Factor
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James M Gloor,
Steven R DeGoey,
Alvaro A Pineda,
S Breanndan Moore,
Mikel Prieto,
Scott L Nyberg,
Timothy S Larson,
Matthew D Griffin,
Stephen C Textor, Jorge A Velosa,
Thomas R Schwab,
Lynette A Fix,
Mark D Stegall
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ABSTRACT: Many patients who have an otherwise acceptable living-kidney donor do not undergo transplantation because of the presence of antibodies against the donor cells resulting in a positive crossmatch. In the current study, 14 patients with a positive cytotoxic crossmatch (titer </= 1 : 16) against their living donor underwent a regimen including pretransplant plasmapheresis, intravenous immunoglobulin, rituximab and splenectomy. Eleven of 14 grafts (79%) are functioning well 30-600 days after transplantation. Two grafts were lost to accelerated vasculopathy and one was lost to death with good function. No hyperacute or cellular rejections occurred. Antibody-mediated rejection occurred in six patients [two clinical (14%) and four subclinical (29%)] and was reversible with plasmapheresis and steroids. Our results suggest that selected crossmatch-positive patients can be transplanted successfully with living-donor kidney allografts, using a protocol of pretransplant plasmapheresis, intravenous immunoglobulin, rituximab and splenectomy. Longer follow-up will be needed, but the absence of anti-donor antibody and good early outcomes are encouraging.
American Journal of Transplantation 08/2003; 3(8):1017-23. · 6.39 Impact Factor
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Christopher K Buehrig,
Donna J Lager,
Mark D Stegall,
Michelle A Kreps,
Walter K Kremers,
James M Gloor,
Thomas R Schwab, Jorge A Velosa,
Mary E Fidler,
Timothy S Larson,
Matthew D Griffin
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ABSTRACT: Polyomavirus-associated nephropathy (PVAN) is an increasingly prevalent cause of allograft dysfunction.
In 18 histologically proven cases of PVAN managed by reduced immunosuppression, monitoring of serum creatinine, and repeated biopsy, graft outcomes were correlated with clinical and histologic indices. Six months postdiagnosis the status of each graft was classified as poor (N = 7) or satisfactory (N = 11). Poor transplant status was defined as graft loss, increased severity of PVAN on repeat biopsy, or serum creatinine>3.0 mg/dL. Diagnosis resulted from either surveillance allograft biopsies (N = 8) or biopsies performed for increased serum creatinine (nonsurveillance, N = 10).
The surveillance biopsy group was more likely than the nonsurveillance group to have satisfactory graft status at 6 months (eight of eight vs. three of ten, P = 0.004) and had significantly lower serum creatinine at diagnosis, 3, and 6 months. Histologic scoring for chronic interstitial and tubular injury was lower in diagnostic surveillance biopsies compared to nonsurveillance biopsies (P = 0.01). Satisfactory transplant status was also associated with reduced or absent virus on repeat biopsy (P = 0.01). Poor transplant status was associated with a higher frequency of recipientneg/donorpos cytomegalovirus (CMV) serology (71% vs. 9%, P = 0.01).
Surveillance allograft biopsy provides an important means for earlier detection of PVAN and permits timely alterations to immunosuppression. Early diagnosis is associated with a lesser degree of interstitial fibrosis at diagnosis and lower baseline and subsequent serum creatinine.
Kidney International 08/2003; 64(2):665-73. · 6.61 Impact Factor
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Christopher K Buehrig,
Donna J Lager,
Mark D Stegall,
Michelle A Kreps,
Walter K Kremers,
James M Gloor,
Thomas R Schwab, Jorge A Velosa,
Mary E Fidler,
Timothy S Larson,
Matthew D Griffin
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ABSTRACT: Influence of surveillance renal allograft biopsy on diagnosis and prognosis of polyomavirus-associated nephropathy.Background Polyomavirus-associated nephropathy (PVAN) is an increasingly prevalent cause of allograft dysfunction.
Kidney International 07/2003; 64(2):665-673. · 6.61 Impact Factor
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James M Gloor,
Donna J Lager,
S Breanndan Moore,
Alvaro A Pineda,
Mary E Fidler,
Timothy S Larson,
Joseph P Grande,
Thomas R Schwab,
Matthew D Griffin,
Mikel Prieto,
Scott L Nyberg, Jorge A Velosa,
Steven C Textor,
Jeffrey L Platt,
Mark D Stegall
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ABSTRACT: Given the scarcity of cadaveric organs, efforts are intensifying to increase the availability of living donors. The current study assessed the feasibility of using ABO-incompatible living-donor kidneys to expand the donor pool.
The authors performed 18 ABO-incompatible living-donor kidney transplants between May 1999 and April 2001. Ten patients received living-donor kidneys from A2 and eight patients received kidneys from non-A2 blood group donors. Immunosuppression consisted of Thymoglobulin antibody induction, tacrolimus, mycophenolate mofetil, and prednisone. Eight non-A2 and two A2 kidney recipients also received a pretransplant conditioning regimen of four plasmapheresis treatments followed by intravenous immunoglobulin and splenectomy at the time of transplantation. Antidonor blood group antibody titer was measured at baseline, pretransplant, at 1- to 3-month and 1-year follow-up, and at the time of diagnosis of antibody-mediated rejection.
No hyperacute rejection episodes occurred. One-year graft and patient survival rates in the 18 ABO-incompatible recipients were only slightly lower than those of 81 patients who received ABO-compatible kidney transplants during the same period (89% vs. 96% and 94% vs. 99%, respectively). Glomerular filtration rate and serum creatinine levels did not differ between the groups. Antibody-mediated rejection occurred in 28% of ABO-incompatible recipients, and was reversible with plasmapheresis, intravenous immunoglobulin, and increasing immunosuppression in all patients except one.
ABO-incompatible living donor kidney transplants can achieve an acceptable 1-year graft survival rate using an immunosuppressive regimen consisting of Thymoglobulin induction, tacrolimus, mycophenolate mofetil, and prednisone combined with pretransplant plasmapheresis, intravenous immunoglobulin, and splenectomy.
Transplantation 05/2003; 75(7):971-7. · 4.00 Impact Factor
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James M. Gloor,
Donna J. Lager,
S. Breanndan Moore,
Alvaro A. Pineda,
Mary E. Fidler,
Timothy S. Larson,
Joseph P. Grande,
Thomas R. Schwab,
Matthew D. Griffin,
Mikel Prieto,
Scott L. Nyberg, Jorge A. Velosa,
Steven C. Textor,
Jeffrey L. Platt,
Mark D. Stegall
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ABSTRACT: Background. Given the scarcity of cadaveric organs, efforts are intensifying to increase the availability of living donors. The current study assessed the feasibility of using ABO-incompatible living-donor kidneys to expand the donor pool.
Methods. The authors performed 18 ABO-incompatible living-donor kidney transplants between May 1999 and April 2001. Ten patients received living-donor kidneys from A2 and eight patients received kidneys from non-A2 blood group donors. Immunosuppression consisted of Thymoglobulin antibody induction, tacrolimus, mycophenolate mofetil, and prednisone. Eight non-A2 and two A2 kidney recipients also received a pretransplant conditioning regimen of four plasmapheresis treatments followed by intravenous immunoglobulin and splenectomy at the time of transplantation. Antidonor blood group antibody titer was measured at baseline, pretransplant, at 1- to 3-month and 1-year follow-up, and at the time of diagnosis of antibody-mediated rejection.
Results. No hyperacute rejection episodes occurred. One-year graft and patient survival rates in the 18 ABO-incompatible recipients were only slightly lower than those of 81 patients who received ABO-compatible kidney transplants during the same period (89% vs. 96% and 94% vs. 99%, respectively). Glomerular filtration rate and serum creatinine levels did not differ between the groups. Antibody-mediated rejection occurred in 28% of ABO-incompatible recipients, and was reversible with plasmapheresis, intravenous immunoglobulin, and increasing immunosuppression in all patients except one.
Conclusions. ABO-incompatible living donor kidney transplants can achieve an acceptable 1-year graft survival rate using an immunosuppressive regimen consisting of Thymoglobulin induction, tacrolimus, mycophenolate mofetil, and prednisone combined with pretransplant plasmapheresis, intravenous immunoglobulin, and splenectomy.
Living-donor kidney transplantation has several advantages over cadaveric kidney transplantation, including the possibility of transplantation without enduring a period of dialysis, better initial graft function, and increased long-term graft survival. The number of living-donor kidney transplantations performed in the United States increased from 2,095 in 1990 to 4,460 in 1999 (1). During the same period, the number of patients listed on the United Network for Organ Sharing waiting list increased 260%, whereas the number of cadaveric kidneys available annually increased only 9% (1). With approximately 46,000 people with end-stage renal disease currently on the United Network for Organ Sharing waiting list for cadaveric kidneys, waiting times of more than 3 years are common. Given this difficult situation, efforts are intensifying to increase the availability of living kidney donors. Protocols have been devised that permit transplantation in patients sensitized against human leukocyte antigens (HLA) using either plasmapheresis and intravenous immunoglobulin or high-dose intravenous immunoglobulin alone; these protocols have shown great promise (2-5).
Some patients who have otherwise suitable living donors do not receive the kidney because of ABO blood group incompatibility. Early attempts to perform ABO-incompatible kidney transplantations led to hyperacute rejection because of the presence of anti-blood group antibodies in the recipient (6,7). In the late 1980s and early 1990s, successful ABO-incompatible kidney transplantations were reported, but the procedure did not gain widespread acceptance (8-13). Most studies used donors of the A2 subgroup, thought to be less immunogenic than the non-A2 blood group because of qualitative and quantitative differences in antigen (14,15). In Japan, the transplantation of non-A2 ABO-incompatible living-donor kidneys has been practiced on a limited basis for several years, and the 8-year graft survival rate is 73% (16). The immunosuppressive regimen used consisted of cyclosporine A, azathioprine, corticosteroids, antilymphocyte globulin, deoxyspergualin, and local irradiation in addition to splenectomy and plasmapheresis.
The overall purpose of this study was to explore the feasibility of performing ABO-incompatible kidney transplantation using both A2 and non-A2 living donors using a conventional immunosuppressive regimen of Thymoglobulin induction, tacrolimus, mycophenolate mofetil, and corticosteroids. In addition, the authors sought to determine the importance of several factors in the outcome of ABO-incompatible kidney transplants, including donor blood type (A2 vs. non-A2); baseline anti-donor antibody titer; and pretransplant conditioning with plasmapheresis, intravenous immunoglobulin, and splenectomy. The patients constituting this report were chosen to provide 1-year outcome data.
Transplantation 04/2003; 75(7):971-977. · 4.00 Impact Factor
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James M Gloor,
Ari J Cohen,
Donna J Lager,
Joseph P Grande,
Mary E Fidler, Jorge A Velosa,
Timothy S Larson,
Thomas R Schwab,
Matthew D Griffin,
Mikel Prieto,
Scott L Nyberg,
Sylvester Sterioff,
Walter K Kremers,
Mark D Stegall
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ABSTRACT: Subclinical rejection, defined as histologic acute rejection in the absence of graft dysfunction, has been suggested as a cause of chronic allograft rejection. In cyclosporine-treated patients, the incidence of subclinical rejection 3 months after transplant is reported to be approximately 30%. The intent of our study was to determine the incidence of subclinical rejection in tacrolimus-treated renal allograft recipients.
We prospectively studied the incidence of subclinical rejection on surveillance biopsies performed 3 months after transplantation in 114 patients transplanted between September 1, 1998 and November 30, 2000. All patients received tacrolimus, mycophenolate mofetil, and prednisone, and 56% received antibody induction.
Subclinical rejection was detected in 2.6% of patients (3/114, 95% confidence interval 0.5-7.5%). Borderline changes were detected in 11% (12/114). Subclinical rejections were treated with bolus methylprednisolone.
The incidence of subclinical rejection early after kidney transplantation is extremely low in tacrolimus-treated patients in whom early rejections are aggressively treated, suggesting that surveillance biopsies may not be necessary with this regimen.
Transplantation 07/2002; 73(12):1965-8. · 4.00 Impact Factor
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ABSTRACT: Early renal functional adaptation was examined in 81 haploidentical donor and recipient pairs, as well as long-term stability of glomerular filtration rate (GFR) in 78 recipients. GFR was determined pre- and 1 month postnephrectomy in donors and 1 month post-transplant and yearly thereafter in recipients. Compensatory increase in filtration (CIF) of transplanted and native kidneys was calculated using donor pretransplant GFR: [CIF= (GFR at 1 month/donor prenephrectomy GFR) x 100]. Annual rates of change in GFR were estimated using within-patient linear regression analysis (slopes). Recipients without rejection (n = 62) and their donors had similar early GFR and CIF. Those with acute rejection (n = 19) had significantly lower GFR and CIF than their donors (61 +/- 16 mL/min/1.73 m2 and 57 +/- 14% vs. 75 +/- 11 and 69 +/- 9; p = 0.01 and p < 0.001). Recipients without cyclosporine (n = 52) had 1 month GFR and CIF of 70 +/- 14 and 67 +/- 14 vs. 72 +/- 11 and 69 +/- 11 for their donors. Those with cyclosporine (n = 29) had 1 month GFR and CIF of 64 +/- 14 and 62 +/- 16 vs. 69 +/- 12 and 67 +/- 11 for their donors (p = 0.15 and 0.16). Comparison of median (25th, 75th) rates of change of GFR with and without acute rejection or cyclosporine did not demonstrate significant effects of either on stability of allograft function, although there was a trend towards greater loss of GFR in cyclosporine-treated patients [-1.1 (-2.5, 0.8) vs. 0.0 (-1.8, 1.2) mL/min/1.73 m2/year, p = 0.47]. We conclude that, in the absence of rejection, the transplanted kidney maintains the same capacity for functional adaptation as its native partner. Therapy with cyclosporine does not significantly inhibit early physiological adaptation of renal transplants.
American Journal of Transplantation 03/2002; 2(3):252-9. · 6.39 Impact Factor
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ABSTRACT: Background. Already there is evidence that simultaneous pancreas and kidney (SPK), or pancreas after kidney (PAK) transplantation, in patients with type 1 diabetes mellitus and end-stage kidney disease prevents worsening of diabetic polyneuropathy, but neuropathic improvement is delayed and incomplete.
Methods. In 85 patients with type 1 diabetes mellitus who underwent SPK or PAK transplantations, we performed sequential neuromuscular evaluations before, every 3 months after, and yearly after transplantation, quantitating muscle weakness separately from overall severity of polyneuropathy.
Results. We found that, on average, the weakness subscore of the Neuropathy Impairment Score of the lower limbs [NIS(LL)-W] was significantly worse at 3, 6, 9, and 12 months (by about 5 points) than at baseline. By contrast, for these times after transplantation, a composite score of nerve conduction abnormalities, an independent measure of severity of polyneuropathy, was not significantly worse and, in fact, was significantly improved. In multivariate analysis, length of hospital stay correlated with the increased weakness.
Conclusions. We conclude that: (1) increased neuromuscular impairment after transplantation is mainly due to muscle weakness and not to worsening polyneuropathy; (2) in multivariate analysis, duration of hospitalization after transplantation was significantly associated with this increased weakness; (3) increased weakness is probably due to development of myopathy, which may be related to graft rejection, immunosuppression, sepsis, and intercurrent infections; (4) in future transplantation trials, weakness should be evaluated separately from neuropathic status, and the lowest efficacious dosages of immunotherapy should be used; and (5) essentially all diabetic patients reported that SPK or PAK transplantation was worthwhile because it freed them from diabetic lifestyle concerns.
Transplantation 10/2001; 72(8):1403-1408. · 4.00 Impact Factor
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ABSTRACT: We studied early renal function in 241 consecutive patients who received cadaveric renal transplants at two different transplantation centers (group 1, n = 90; group 2, n = 151). Univariate and multivariate analyses of data from group 1 showed a significant correlation between seven donor variables and early renal function after cadaveric renal transplantation. A scoring system was developed from these seven donor variables (cause of death, 0–6 points; history of hypertension, 0–6; final creatinine clearance before procurement, 0–6; age, 0–6; history of diabetes mellitus, 0–3; cold ischemia time, 0–3; and severity of renal artery plaque, 0–3). Data from group 2 were used to validate the donor scoring system and stratify cadaver kidneys on the basis of score: grade A, 0–5 points; grade B, 6–10; grade C, 11–15; and grade D, 16–32. A significant decline in early renal function was observed with increasing donor score and grade of cadaver kidney. In conclusion, a donor scoring system based on information available at the time of procurement can be used to estimate early graft function after cadaveric renal transplantation and may assist in the allocation of marginal organs.
American Journal of Transplantation 06/2001; 1(2):162 - 170. · 6.39 Impact Factor
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ABSTRACT: Blood pressure determinants in living–related renal allograft donors and recipients. We studied 99 living related allograft donors with follow–up information of at least 10 years and the 50 recipients who had successful outcomes. Recipients were younger and had significantly lower blood pressures at follow–up than their donors. Borderline and definite hypertension were present in 22.2% and 4.0% of donors prior to donation, in 14.4% and 21.1% of donors at follow–up, and in 2.0% and 18.0% of the 50 recipients at follow–up. Age, relative weight, and mean arterial pressure (MAP) prior to donation were the key variables in predicting the follow–up ranked MAP of the donors. CPAH prior to donation was inversely correlated with the age of the donors and, indirectly, with the follow–up MAP. Donor CPAH prior to donation was significantly correlated with the renal allograft function of the recipients but not with the recipient ranked MAP at follow–up. No correlation of the ranked MAP or blood pressure outcome categories between donors and recipients was found. We conclude that donation of one kidney can accelerate the development of hypertension in those donors with predisposition to develop hypertension. In addition, the predisposition of the donors to develop hypertension and their age, within the range observed in the study, does not significantly influence the long–term blood pressure status of the recipient.
