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Biomedical subjects

M R Nampoory

Publications and source records attributed to M R Nampoory.

At least 19 recordsLinked to original sources
PubMed2007

Cerebral aspergillosis diagnosed by detection of Aspergillus flavus-specific DNA, galactomannan and (1-->3)-beta-D-glucan in clinical specimens.

A case of cerebral aspergillosis was diagnosed by the detection of Aspergillus flavus-specific DNA in brain biopsy and serum specimens. The diagnosis was also supported by detection of elevated levels of galactomannan and (1-->3)-beta-d-glucan in serum specimens. Despite the presence of dichotomously branched septate hyphae in brain biopsy, the culture remained negative. The inability to isolate the organism in culture suggested that combined therapy of AmBisome and caspofungin was fungicidal for the fungus in the brain abscess.

Amphotericin B↗
PubMed2000

Xanthomonas maltophilia infection in chronic peritoneal dialysis patients.

Xanthomonas maltophilia infection has only been occasionally reported in patients receiving chronic peritoneal dialysis. We describe four cases of Xanthomonas maltophilia infection associated with chronic peritoneal dialysis. Two patients presented with peritonitis and two with exit site infection. All patients were diabetics, who immediately prior to the study had not received antibiotic therapy. Failure to respond to multiple antibiotic therapy resulted in catheter removal in both patients with peritonitis. In those patients with only exit site infections, dialysis could be continued following antibiotic therapy and catheter replacement in one. Catheter loss in our patients was directly attributed to peritonitis with Xanthomonas maltophilia infection.

Adult↗
PubMed1999

Pediatric dialysis and renal transplantation in Kuwait over the past 11 years.

Data on end-stage renal disease (ESRD) patients and their renal replacement therapy (RRT) were collected retrospectively from the three dialysis centers, the pediatric urology unit, and the organ transplant center of Kuwait. The study period was from 1 January 1986 to 31 December 1996. A total of 61 children, 50 of whom were Kuwaiti nationals, required RRT for ESRD during those 11 years. This gave an average annual incidence rate of 18 per million Kuwaiti children. Glomerulonephritis was the most-frequent underlying disease and accounted for 44% of total cases, while pyelonephritis (including urinary tract anomalies and dysplastic kidneys) was responsible for 30%. Multisystem disease was responsible for ESRD in 7 patients (14%), 2 of whom had lupus nephritis, 2 vasculitis, 2 Henoch-Schönlein purpura, and 1 hemolytic uremic syndrome. Continuous ambulatory peritoneal dialysis and home intermittent peritoneal dialysis, using cycler machines, were not favored dialysis techniques by most parents, especially for those <6 years old. The actuarial survival on dialysis was 75%+/-7% at 12 months. Of the 8 patients who died, 7 were <6 years old. Thirty-eight patients received 46 kidney transplants, 13 of which were performed on a pre-emptive basis. The actuarial patient survivals at 12 months for those receiving first live and cadaveric kidney transplants were 90%+/-5% and 85%+/-2%, respectively, while those for grafts were 76%+/-8% and 66%+/-2%, respectively. This is the first nationwide long-term study of the incidence and etiology of pediatric ESRD in our area and the RRT in a country with adequate treatment facilities.

Adolescent↗
PubMed1997

Treatable intracranial hypertension in patients with lupus nephritis.

Idiopathic intracranial hypertension is a disorder of intracerebral pressure regulation and patients run the risk of permanent visual loss. Intracranial hypertension (IH) has been reported rarely in systemic lupus erythematosus (SLE). We reviewed the medical records of 127 patients with lupus nephritis (LN) who were followed up from 1987 to 1996 in our unit. There were six patients with IH which gave a disease prevalence of 4.7% in those with LN. All were females giving a disease prevalence of 5.2% for that sex, a high rate of occurrence of IH in patients with LN. Their age ranged from 22 to 34 y (27.8 +/- 3.6 y). Headache, vomiting and diplopia were the common presenting symptoms and had started 7.3 +/- 4.4 weeks prior to the diagnosis of IH. The cerebrospinal (CSF) opening pressure (413.3 +/- 77.0 mmH2O) was raised in all cases. Biochemical and cytological analyses of CSF were normal. The only abnormal radiological finding was partially empty sella in one patient on magnetic resonance imaging (MRI) (performed in three patients) or computed tomography (CT) (performed in all patients). All patients had serological evidences of active lupus disease at the time of diagnosis of IH. The renal histology was WHO type IV in four cases and III and V in one each indicating severe renal involvement. Laboratory evidences of procoagulant activity were found in the form of positive anticardiolipin antibody (aCL) in two patients, lupus anticoagulant (LA) in two and an otherwise unexplained isolated prolongation of activated partial thromboplastin time (APTT) in the other two. Clinically, one or more episodes of symptomatic venous or arterial thrombosis had occurred in all subjects. In addition to symptomatic measures, all subjects were treated with prednisolone, azathioprine, cyclophosphamide and plasmapheresis according to the protocol of our unit. One patient who did not receive plasmapheresis and cyclophosphamide had a relapse while all others recovered completely. None received anticoagulant therapy. Young females with serologically active lupus, severe forms of renal lesions, past history of venous or arterial thrombosis and laboratory evidences of procoagulant activity, appear to be at increased risk of IH. Thrombotic occlusion of the cerebral arteriolar or venous vascular bed eventually affecting the arachnoid villi and impeding CSF absorption is favoured compared to cerebral venous or sinus thrombosis as the pathogenic mechanism. Combined immunosuppression and plasmapheresis appeared to be beneficial in short and long term follow-up. We propose that patients with SLE and IH have definable risk and pathogenetic factors and are no more to be considered 'idiopathic'. The conditions calls for aggressive intervention which leads to an excellent outcome.

Acetazolamide↗
PubMed1996

Invasive fungal infections in renal transplant recipients.

In a retrospective analysis, 18 instances of invasive fungal infections were observed in 512 (3.5%) renal transplant recipients. These included candidiasis (8), aspergillosis (5), cryptococcosis (3) and zygomycosis (2). All patients with candidiasis had Candida isolated from blood and one or more additional sites. One of them had superadded fungaemia with Torulopsis glabrata. Pulmonary disease in four and subcutaneous infection in one were encountered in the five patients with aspergillosis. Central nervous system involvement in two and cutaneous lesion in one were the findings in patients with cryptococcosis. Zygomycosis involved the lung in one and the allograft itself in the other. Prolonged fever not responding to antibacterial drugs was the most common clinical presentation. Fungal infections occurred during the first 4 months in 10 (55.5%) and 12 to 108 months in eight (44.5%) patients. Infections with cytomegalovirus and hepatitis viruses were concommitantly present in 12 (66.7%) and eight (44.5%) patients respectively. Fourteen episodes of fungal infections (77.8%) occurred in live unrelated kidney recipients who formed only 48% of our total transplant population. Nine patients were treated with systemic and/or local amphotericin B and six with amBisome. Fluconazole was administered alone in three and in combination with amphotericin B in two. Fourteen patients died but mortality was only directly attributable to fungal infection in 11. We conclude that invasive fungal infections continue to be an important cause of morbidity and mortality in renal transplant recipients. A high index of suspicion. prompt diagnosis and early institution of specific antifungal therapy are needed.

Adult↗
PubMed1996

Erythropoietin deficiency and relative resistance cause anaemia in post-renal transplant recipients with normal renal function.

BACKGROUND: Following successful renal transplantation, blood erythropoietin (Epo) levels peak in two phases during the first 2-3 months, and blood haemoglobin/haematocrit (HB/Hct) levels are restored to normal in a period of 2-6 months. However, some transplant recipients continue to remain anaemic in spite of normal graft function and in the absence of recognizable causes. The role of endogenous Epo production in the causation of anaemia in such patients is poorly understood and has been investigated in this study. METHODS: Twenty-three post-renal transplant recipients with stable normal renal function were studied. Eleven of these patients had normal HB/Hct levels (group 1) and served as control for the rest 12 patients with anaemia (group 2). Patients included in group 2 had no readily recognizable cause for their anaemia. Other laboratory and clinical findings were similar in both groups. Patients with erythrocytosis were excluded. Serum Epo levels were measured in all patients. Five patients in group 2 were treated with recombinant human erythropoietin (rHuEpo) and their erythropoietic response was assessed. rHuEpo was discontinued when the target Hb/Hct levels (lowest normal range) were achieved and the patients were followed up for a further period of 9-12 months. RESULTS: Five patients in group 1 had normal expected serum Epo levels whereas the other six patients had inappropriately high serum Epo levels with respect to their Hb/Hct status suggestive of relative ¿EPO resistance'. Serum Epo levels in all patients except two in group 2 were low indicative of 'Epo deficiency'. The two exceptional patients in group 2 had higher serum Epo levels in the presence of anaemia suggestive of relative ¿Epo resistance'. All five patients treated with rHUEpo responded adequately by achieving normal Hb/Hct levels. Three of them were originally ¿Epo deficient' and they reached target Hb/Hct levels in a mean period of 4 weeks, requiring a mean cumulative rHuEpo dose of 428.3 units/kg. The other two patients with higher initial serum Epo levels, and considered to be ¿Epo resistant' required an average of 11 weeks of treatment and a mean cumulative rHuEpo dose of 1582.5 units/kg, indicating an increased Epo demand. On cessation of therapy the Hb/Hct levels fell in all five patients to pretreatment values in 6 months. CONCLUSIONS: There are important variations in the endogenous Epo production in renal transplant patients with normal renal function, the cause of which is not clear. Epo deficiency and relative Epo resistance play a causative role for anaemia in some post-renal transplant recipients with stable normal renal function. They respond adequately to rHuEpo administration.

Adult↗