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R Gohh

Publications and source records attributed to R Gohh.

10 recordsLinked to original sources
PubMed2005

Factors contributing to acute rejection in renal transplantation: the role of noncompliance.

Early episodes of acute rejection after renal transplantation reflect inadequate immunosuppression at a time of heightened immune challenge. Late acute rejection episodes, however, are less likely related to inadequacy of immunosuppression and may be due to patient noncompliance or overzealous weaning of immunosuppression. We evaluated 443 consecutive renal transplant recipients to determine the incidence and etiology of acute rejection. All episodes were confirmed by ultrasound-guided biopsy. The cause of each acute rejection was determined by chart review. Medication compliance was determined by history at the time of admission for biopsy. Over a follow-up period of 42 +/- 22 months, 87 patients (20%) suffered acute rejection. There was a trend toward fewer episodes of acute rejection with thymoglobulin induction and tacrolimus-based immunosuppression. Younger recipients had an increased risk of acute rejection (odds ratio 0.47, range 0.24-0.91, P = .027). Patient noncompliance with immunosuppression was associated with late acute rejection (P = .0002). Acute rejection increased the risk of allograft failure (P < .0001). Modifiable factors, including the choice of immunosuppression, reduce the risk of acute rejection. More importantly, the transplant recipient plays a substantial role in the maintenance of their allograft health through compliance with immunosuppressive drug therapy. Future strategies to improve compliance, including increased vigilance in high-risk patient groups, frequent medication review, and laboratory testing, should be encouraged.

Acute Disease↗
PubMed2005

Experience with sirolimus for calcineurin minimization/elimination in pancreas-after-kidney transplantation.

Pancreas after kidney (PAK) transplantation, associated with a persistent elevation in serum creatinine (defined as a >25% increase from baseline), was seen in 7 of 11 (64%) cases maintained on immunosuppressive therapy consisting of tacrolimus, mycophenolate mofetil, and prednisone. Patients were converted to sirolimus as a means of minimizing or eliminating exposure to tacrolimus, the presumed nephrotoxic agent. With the use of sirolimus-based immunosuppression, and with elimination or minimization of tacrolimus, renal function, as measured by serum creatinine, stabilized or improved in all cases.

Creatinine↗
PubMed2003

Oerskovia xanthineolytica endocarditis in a renal transplant patient: case report and review of the literature.

Oerskovia species were, until recently, only rarely associated with human disease. This gram-positive bacillus can be easily misidentified as a diphtheroid, a common contaminant in blood cultures. There have been 17 reports of invasive Oerskovia infection in immunocompromised hosts. We report a case of Oerskovia xanthineolytica endocarditis in a renal transplant patient and review the microbiologic and clinical characteristics of this potential pathogen.

Adult↗
PubMed2002

Donor-transmitted parvovirus infection in a kidney transplant recipient presenting as pancytopenia and allograft dysfunction.

Parvovirus B19 is a nonenveloped single-stranded DNA virus that commonly causes a benign childhood infection typically manifesting as a "slapped-cheek" rash. In immunodeficient hosts, this infection can cause persistent anemia and occasionally pancytopenia. Recently, direct renal involvement has been reported in renal transplant recipients leading to various forms of glomerulopathy and allograft dysfunction. Most cases are primary infections and are donor transmitted through the transplanted organ. Clinical and virological response to intravenous immunoglobulin (Ig) is usually excellent. We describe a case of donor-transmitted parvovirus infection in a 23-year-old male who received his first cadaver renal transplant. The patient had an uncomplicated postoperative course with immediate graft function. Eight weeks after transplantation, he presented with fever, polyarthralgia, pancytopenia, and allograft dysfunction. Serological studies revealed elevated IgM titers against parvovirus B19. A renal biopsy was performed, which showed no evidence of acute rejection but with moderate degree of tubular damage. Parvovirus B19 viral DNA was detected in the renal tissue via polymerase chain reaction (PCR). The patient received a 10-day course of intravenous Ig (400 mg/kg/day) with excellent response. His blood count normalized and the allograft improved to baseline function. The incidence of parvovirus infection in renal transplant patients is probably underestimated, because patients are not routinely screened for it and anemia and/or pancytopenia in these patients are often ascribed to immunosuppressive drugs. Because this infection is treatable, we conclude that parvovirus B19 infection should be actively considered in transplant patients presenting with pancytopenia and allograft dysfunction.

Adult↗
PubMed1997

Correlation of clinical outcomes after tacrolimus conversion for resistant kidney rejection or cyclosporine toxicity with pathologic staging by the Banff criteria.

BACKGROUND: Refractory rejection and cyclosporine (CsA)-induced nephropathy remain important causes of renal allograft loss. Previous studies demonstrated that 70-85% of the episodes of refractory acute rejection (AR) occurring in renal allograft recipients on a CsA-based immunosuppressive regimen could be salvaged by conversion to tacrolimus. No data are available regarding the correlation between allograft histology at the time of conversion and the response to tacrolimus. We examined the response to tacrolimus conversion in relation to preconversion biopsies stratified by the Banff criteria. METHODS: Since May 1992, we have converted 22 patients from CsA to tacrolimus as part of a rescue protocol. We report on 18 patients in whom 6-month follow-up was available after conversion for biopsy-proven AR (n=13) or CsA toxicity (n=5). Sixteen patients were recipients of renal allografts, including three second transplants, and two were recipients of kidney-pancreas transplants. All patients with AR were treated with one or more courses of methylprednisolone and OKT3 before conversion. Renal allograft biopsies were interpreted by a transplant pathologist blinded to the clinical history, and graded according to the Banff criteria. Responses to tacrolimus were scored as improved (creatinine returned to within 150% of baseline), stabilized (creatinine rise arrested), or failed (returned to dialysis). RESULTS; Mean follow-up was 17.3+/-8 months. Fourteen of 18 patients (78%) showed improvement or stabilization in renal function as assessed by creatinine at 6 months or 1 year (when available). Of the 13 patients with histological AR, nine (69%) improved, including five of six with borderline AR, two of three with grade I AR, and two of four with grade II AR. Of the four other patients with AR, two stabilized and two failed. Three of five patients with severe clinical rejection requiring dialysis (range 2-16 weeks) recovered renal function after conversion. Of five patients with CsA toxicity, two (40%) improved. Seven of eight patients who were converted to tacrolimus less than 90 days after transplantation improved, compared with only 4 of 10 who were converted more than 90 days after transplantation. No grafts were lost in patients with a creatinine <3.0 mg/dl at the time of conversion versus two of seven grafts lost when the creatinine was 3.1-5.0 mg/dl and two of eight grafts lost when the creatinine was >5.0 mg/dl. CONCLUSION: The majority of steroid and antilymphocyte antibody (OKT3 or ATGAM) unresponsive rejections in patients on CsA-based immunosuppression will improve or stabilize after conversion to tacrolimus. There was no correlation with allograft histology stratified by the Banff criteria and the response to tacrolimus. Although there was a trend toward a poorer response with more severe histological rejection, higher serum creatinine at the time of conversion, and longer time from transplantation to conversion, favorable responses were noted in all groups. This indicates that a trial of conversion is warranted, irrespective of the histological severity of injury.

Antilymphocyte Serum↗
PubMed1996

Acute renal failure and the MELAS syndrome, a mitochondrial encephalomyopathy.

Melas (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes) is one of a group of heterogeneous yet clinically distinct syndromes ascribed to a defect in mitochondrial function. Here, the case of a patient diagnosed with the MELAS syndrome who subsequently developed acute renal failure is reported. Although no clear renal insult was evident at the time, the clinical picture was consistent with the diagnosis of acute tubular necrosis. The patient's renal function subsequently returned to baseline. This article reviews the literature concerning renal involvement in the mitochondrial encephalomyopathies, including MELAS, and proposes a mechanism by which patients suffering from mitochondrial disorders may be more susceptible to renal hypoxic injury and acute renal failure.

Acidosis, Lactic↗