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Biomedical subjects

H Mahanty

Publications and source records attributed to H Mahanty.

4 recordsLinked to original sources
PubMed2004

Polyomavirus-associated nephropathy in simultaneous kidney-pancreas transplant recipients: a single-center experience.

BACKGROUND: With the introduction of more potent immunosuppressive agents, rejection rates have decreased markedly in simultaneous pancreas-kidney transplant (SPK) recipients. However, with more intense immunosuppression, opportunistic infections such as polyoma virus have been more frequent. The purpose of this article is to outline the clinical course of SPK patients who developed documented polyoma infection in the transplanted kidney. METHODS: A retrospective review of 146 consecutive SPK recipients from 1996 to 2002 was performed. Induction and maintenance immunosuppression, surgical complications, rejection episodes, and opportunistic infections were reviewed. Patients who developed biopsy-proven polyoma virus infection in the renal allograft were identified. RESULTS: Nine patients (6%) were identified who developed polyoma. All had received induction therapy with either OKT3 (5 mg/d for 10.5 days) or thymoglobulin (5.7 mg/kg). Patients without polyoma had received similar induction. Maintenance immunosuppression included Prograf/MMF in six patients, CsA/MMF in two, and CsA/azathioprine in one. Time to diagnosis was an average of 359.3 days (range 136 to 836) after transplantation. Two patients had undergone treatment for kidney rejection prior to the diagnosis of polyoma. Immunosuppression was decreased in all patients when polyoma was identified, and more recently Cidofovir has been administered. Despite these interventions, five of the nine lost kidney function (creatinine > 5.0 or resumption of dialysis). However, none of the nine developed pancreatic abnormalities as demonstrated by normal blood glucose and amylase and no requirement for exogenous insulin. Two patients underwent LRRT more than 1 year after polyoma diagnosis; both have normal kidney function (Cr < 1.5 mg/dL) at 4 years of follow-up. Polyoma virus was the leading cause of renal loss in this cohort of patients. CONCLUSIONS: Polyoma is a serious concern for SPK transplant recipients. The pancreas, however, is spared from clinical evidence of infection, and no rejection was noted when immunosuppression was decreased. These graft losses appear to be a penalty of more potent immunosuppression, and a better treatment strategy is needed to prevent renal graft loss when polyoma is diagnosed. Retransplantation can be considered based on our limited experience.

Humans↗
PubMed1996

Enterocyte functional adaptation following intestinal resection.

Following massive small bowel resection, the remaining intestine undergoes compensatory adaptation to maintain absorptive capacity. The purpose of this study was to determine the relative importance of mucosal hyperplasia and functional adaptation by individual enterocytes in this process. Distal ileum was harvested from rats 2 weeks following 70% small bowel resection or transection with reanastomosis. Transport parameters were determined in Ussing chambers. Short-circuit current (Isc) responses to additions of 3-0-methylglucose were measured to assess Na+/glucose cotransporter kinetics. Microvillus absorptive surface areas were calculated with computer-assisted morphometric modeling. These surface area values were used to normalize transport parameters. Ileal absorptive surface area was 70% greater in resection tissues than in transection tissues (P < 0.05). Na+ and Cl- fluxes were generally lower in the resection group. Na+/glucose cotransporter delta Isc max (an index of cotransporter quantity) for resection and transection tissues were 0.3 +/- 0.1 and 1.8 +/- 0.3, respectively (P < 0.05). Km (an index of cotransporter affinity for substrate) did not differ significantly. Following intestinal resection, ileal surface area increases; however, transport parameters, when normalized to absorptive surface area values, diminish. During early postresection adaptation, expansion of ileal absorptive surface area due to hyperplasia seems to play a greater role than upregulation of enterocyte Na+, Cl- , and glucose absorption.

Adaptation, Physiological↗
PubMed1996

Endotoxin inhibitor prevents sepsis-induced alterations in intestinal ion transport.

BACKGROUND: The intestine is a target of septic insult. The aims of this study were to characterize sepsis-induced alterations in intestinal ion transport and to determine the role endotoxin plays in mediating these changes. METHODS: Rats underwent cecal manipulation alone (control), cecal ligation and puncture (CLP), or CLP plus intraperitoneal injection of 0.2 mg of a recently synthesized endotoxin inhibitor. At 24 hours, distal ileum was harvested, and transport parameters were determined. RESULTS: Cecal ligation and puncture produced a significant increase in short-circuit current (Isc) that was attributable to the induction of chloride secretion. There were no alterations in transepithelial resistance or fluxes of mannitol and sodium. The sepsis-induced increase in Isc was prevented by administration of the endotoxin inhibitor. CONCLUSIONS: In this model of sepsis, the primary alteration in ileal ion transport is an induction of electrogenic chloride secretion. Endotoxin inhibition may represent a strategy for prophylaxis against the intestinal effects of sepsis.

Animals↗