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Biomedical subjects

Martin Karpinski

Publications and source records attributed to Martin Karpinski.

7 recordsLinked to original sources

Troponin I testing in dialysis patients presenting to the emergency room: does troponin I predict the 30-day outcome?

BACKGROUND: Troponins are often measured in acutely ill chronic dialysis patients admitted to the emergency room, irrespective of their clinical presentation. The significance of an elevated troponin level in this setting is unclear. METHODS: We identified all chronic dialysis patients presenting over 1 year to a tertiary care hospital emergency room who also had at least one cardiac troponin I (cTnI) level determination. We evaluated presenting complaints, risk factors for cardiac disease, cTnI levels, and major cardiac events (MCE; occurrence of cardiovascular death, myocardial infarction, de novo heart failure, or coronary revascularization) within 30 days by chart review in 149 patients (79 on hemodialysis, 70 on peritoneal dialysis). RESULTS: Chest pain was documented in only 29% of the patients. Twenty-two patients (15%) experienced an MCE. The incidence of an MCE was the same in patients with and without chest pain. A cTnI level >0.1 ng/l was a significant predictor of an MCE (odds ratio 15.2, 95% confidence interval CI 5.26, 43.6). The likelihood ratios for MCEs were 0.32 (CI 0.16, 0.63) for a cTnI level <0.1 ng/l, 0.72 (CI 0.09, 5.5) for cTnI concentrations 0.1-0.3 ng/l, 7.8 (CI 4.2, 15) for a cTnI level >0.3, and 11.7 (CI 4.4, 31) for a cTnI concentration >2.0 ng/l. CONCLUSION: In acutely ill chronic dialysis patients presenting to a hospital emergency room, an elevated cTnI level indicates an increased 30-day cardiac risk, regardless of their clinical presentation.

Aged↗

The impact of accepting living kidney donors with mild hypertension or proteinuria on transplantation rates.

BACKGROUND: As waiting times for kidney transplantation increase, individuals with hypertension or proteinuria may be considered as eligible living donors. We set out to determine how frequently donors are excluded because of hypertension or proteinuria and to what extent accepting such donors would increase transplantation rates. METHODS: Wait lists from 4 Canadian transplantation centers were examined for causes of living kidney donor exclusion. Donors with hypertension (clinic blood pressure >140/90 mm Hg or requiring antihypertensive medication) or proteinuria historically have been excluded at these centers. We define potentially acceptable hypertension as a clinic blood pressure less than 150/100 mm Hg or less than 140/90 mm Hg if administered a single antihypertensive medication and define acceptable proteinuria as protein of 0.15 to 0.3 g/d. RESULTS: Only 35% (124 of 352 patients) of wait-listed patients had a living donor evaluated (n = 180 potential donors). Primary reasons for donor exclusion were immunologic: a positive cross-match (32%; n = 59) or blood group type incompatibility (22%; n = 40). Hypertension or proteinuria were less common (17%; n = 31). Of 31 donors excluded for hypertension or proteinuria, only 13 had results in the acceptable range. Acceptance of these donors would have resulted in transplantation of 3% (12 of 352 patients) of the wait-list population. CONCLUSION: Accepting living donors with mild hypertension and proteinuria will lead to a slight increase in transplantation rates. Efforts to improve living donor awareness and overcome immunologic barriers to transplantation may have a greater impact.

Cross-Sectional Studies↗

Late recurrence of scleroderma renal crisis in a renal transplant recipient despite angiotensin II blockade.

Scleroderma renal crisis is the most severe renal manifestation of scleroderma and has been reported to recur rarely early after renal transplantation. Angiotensin II blockade is critical in preventing and treating scleroderma renal crisis, but some concern exists as to whether angiotensin II receptor blockers are clinically equivalent to angiotensin-converting enzyme inhibitors. The current case indicates that late recurrences of scleroderma renal crisis are possible in renal transplant recipients and that angiotensin-converting enzyme inhibitors, rather than angiotensin II receptor blockers, may be the superior drugs for such patients.

Adult↗

Proteomic-based detection of urine proteins associated with acute renal allograft rejection.

At present, the diagnosis of renal allograft rejection requires a renal biopsy. Clinical management of renal transplant patients would be improved by the development of non-invasive markers of rejection that can be measured frequently. This study sought to determine whether such candidate proteins can be detected in urine using mass spectrometry. Four patient groups were rigidly defined on the basis of allograft function, clinical course, and allograft biopsy result: acute clinical rejection group (n = 18), stable transplant group (n = 22), acute tubular necrosis group (n = 5), and recurrent (or de novo) glomerulopathy group (n = 5). Urines collected the day of the allograft biopsy were analyzed by mass spectrometry. As a normal control group, 28 urines from healthy individuals were analyzed the identical manner, as well as 5 urines from non-transplanted patients with lower urinary tract infection. Furthermore, sequential urine analysis was performed in patients in the acute clinical rejection and the stable transplant group. Three prominent peak clusters were found in 17 of 18 patients (94%) with acute rejection episodes, but only in 4 of 22 patients (18%) without clinical and histologic evidence for rejection and in 0 of 28 normal controls (P < 0.001). In addition, the presence or absence of these peak clusters correlated with the clinicopathologic course in most patients. Acute tubular necrosis, glomerulopathies, lower urinary tract infection, and cytomegalovirus viremia were not confounding variables. In conclusion, proteomic technology together with stringent definition of patient groups can detect urine proteins associated with acute renal allograft rejection. Identification of these proteins may prove useful as non-invasive diagnostic markers for rejection and the development of novel therapeutic agents.

Acute Disease↗

Leukocyte reduction of red blood cell transfusions does not decrease allosensitization rates in potential kidney transplant candidates.

A significant proportion of potential kidney transplant candidates continue to periodically require blood transfusions that carry a risk of allosensitization. Leukocyte reduction (leukoreduction) of blood products has been proved to reduce transfusion-associated allosensitization in patients with hematologic malignancies; however, the effect in potential kidney transplant candidates is unknown. A total of 112 kidney transplant candidates who received red blood cell transfusions while on the transplant waiting list were identified retrospectively. Sixty received a transfusion before leukoreduction (non-LR), and 52 received a transfusion after the local implementation of universal leukoreduction of blood products (LR). There was no difference in transfusion-associated allosensitization rates in patients who received a transfusion during the two eras (non-LR 27% [16 of 60] versus LR 33% [17/52]; NS). Likewise, no difference was observed in subgroups identified as being at high risk of allosensitization (previous pregnancy, transplant, or five or more previous transfusions) or at low risk (no previous allogeneic exposures) (high risk: non-LR 52% versus LR 55%; low risk: non-LR 10% versus LR 8%). Multivariate analysis revealed previous pregnancy to be the only significant risk factor associated with transfusion-associated allosensitization (relative risk, 8.2; 95% confidence interval, 2.4 to 24.0; P = 0.0001). Leukoreduction, in particular, was not associated with any protective effect. In summary, leukoreduction of red blood cell transfusions does not confer any protection against transfusion-associated allosensitization for potential kidney transplant candidates. Physicians who care for patients with ESRD must continue to practice careful transfusion avoidance while alternative strategies to minimize transfusion associated allosensitization are sought.

Adult↗

Heightened peripheral blood lymphocyte CD69 expression is neither sensitive nor specific as a noninvasive diagnostic test for renal allograft rejection.

It has been reported that acute allograft rejection is associated with heightened expression of the peripheral blood lymphocyte (PBL) early activation marker CD69 and that this may serve as a potential biomarker of rejection. This study sought to determine whether PBL CD69 expression correlates with both acute clinical and subclinical renal allograft rejection as well as clinically inapparent cytomegalovirus (CMV) infection. Flow cytometric determination of PBL CD69 expression was performed at the time of clinical and protocol biopsies (n = 131) in 45 renal transplant recipients. Nineteen patients also underwent weekly monitoring of PBL CD69 expression for the initial 15 wk after transplantation. Simultaneous screening for CMV viremia was performed with a semiquantitative PCR assay. No differences were seen in either CD4+ or CD8+ lymphocyte CD69 expression between the biopsy diagnoses. CMV viremia however, independent of rejection, was associated with greater CD69 expression on CD8+ lymphocytes (17.8 +/- 10.4% versus 9.6 +/- 4.8%; P < 0.0001) but not CD4+ lymphocytes. No individuals experienced clinical CMV disease. Weekly monitoring of PBL CD69 expression did not change coincident with the diagnosis of rejection; however, CMV viremia coincided with a substantial rise in the proportion of CD8+69+ lymphocytes in a number of individuals. Thus, PBL CD69 expression is neither sensitive nor specific for the noninvasive diagnosis of renal allograft rejection. Furthermore, clinically inapparent CMV viremia is associated with heightened expression of this activation marker on CD8+ lymphocytes. This latter finding suggests that clinically inapparent CMV viremia may be a potential confounder for biomarkers of rejection that examine peripheral blood lymphocytes.

Antigens, CD↗

Flow cytometric crossmatching in primary renal transplant recipients with a negative anti-human globulin enhanced cytotoxicity crossmatch.

Flow cytometric crossmatching (FCXM) and panel reactive antibody (PRA) screening techniques are more sensitive than anti-human globulin enhanced cytotoxicity (AHG-CDC) techniques at detecting anti-HLA antibodies. The clinical significance of a positive FCXM in primary renal transplant recipients with a negative AHG-CDC crossmatch is unclear. We performed retrospective FCXM and flow cytometric panel reactive antibody (FlowPRA) determinations in primary renal transplant recipients with a negative T cell AHG-CDC crossmatch and a negative B cell CDC crossmatch pretransplant. Eighteen (13%) of 143 patients exhibited a positive retrospective T cell FCXM. Of these patients, six (33%) experienced early graft loss with explant histology, demonstrating antibody-mediated rejection in five of six cases. The 12 patients with positive T cell FCXM who maintained their grafts experienced more adverse events posttransplant, including more early, steroid-resistant, and recurrent rejection. Furthermore, in a subgroup of patients undergoing protocol biopsies, those with a positive T cell FCXM exhibited more subclinical rejection. Anti-HLA antibodies were detected by FlowPRA in all 18 patients with a positive T cell FCXM, whereas AHG-CDC PRA detected antibodies in only 8 of 18 patients. Therefore, flow cytometric techniques identify sensitized primary renal transplant recipients undetected by AHG-CDC techniques. In those patients, a positive T cell FCXM is associated with an increased risk of early graft loss due to antibody-mediated rejection and may represent a relative contraindication to transplantation. Moreover, those patients are also at increased risk of severe and recurrent rejection, which may carry implications for long-term graft outcomes.

Adult↗