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Biomedical subjects

T Manis

Publications and source records attributed to T Manis.

At least 19 recordsLinked to original sources
PubMed2001

Symptomatic atrial arrhythmias in hemodialysis patients.

BACKGROUND/AIMS: Cardiac arrhythmias are frequent in hemodialysis patients and can interrupt treatment. However, the frequency and risk factors have remained unclear because previous reports of arrhythmias in dialysis patients have usually been continuous-monitoring studies that looked at all cardiac ectopy regardless of its seriousness. METHODS: We reviewed retrospectively only symptomatic atrial arrhythmias in a population of 106 maintenance hemodialysis patients over three years, in order to estimate their actual frequency and any risk factors. RESULTS: Ten patients, seven men and three women, required treatment for atrial arrhythmias (9.4%): four for supraventricular tachycardia, three for atrial flutter, and three for atrial fibrillation. Their mean age was 53.7 +/- 6.1 years; five of them were < or = 40 years. Seven arrhythmias were new, three were recurrences. All but one occurred between 3 and 4 hours of hemodialysis, and dialysis had to be stopped in nine instances. There was no pattern of hypotensive episodes preceding the arrhythmias. Mean serum K+ drawn at the time of the arrhythmias was 3.8 +/- 0.2 mEq/L. Mean plasma intact parathormone was 1128 +/- 417 pg/mL, compared to 454 +/- 58 pg/mL for our entire hemodialysis population (p = .0036). Subsequent echocardiograms showed abnormalities in 9/10 patients: five had left ventricular hypertrophy, six had left atrial enlargement, five had valvular lesions (four mitral regurgitation; one aortic incompetence), and three had ejection fractions <50%. There were four deaths in these patients over the next 14 months, but probably only one was cardiac. CONCLUSIONS: Serious atrial arrhythmias are common in a hemodialysis population. Risk factors for symptomatic atrial arrhythmias in hemodialysis patients may include hyperparathyroidism and echocardiographic findings of chamber enlargement, valvular lesions, or ventricular dysfunction.

Atrial Fibrillation↗
PubMed1996

Effect of oral L-carnitine on serum myoglobin in hemodialysis patients.

Oral L-carnitine has been reported to lower the elevated serum myoglobin of renal failure in chronic peritoneal dialysis patients, and intravenous L-carnitine can improve muscle fatigue and cramps in chronic hemodialysis patients. In this study oral L-carnitine, 1.98 g/day, was administered to 6 chronic hemodialysis patients for 8 weeks. Serum levels of myoglobin, creatine kinase, and aldolase, as well as skeletal muscle symptoms (cramps during dialysis, fatigue, and weakness) were monitored biweekly for 12 weeks. Mean baseline serum myoglobin level was 337 +/- 34 ng/mL. By 6 and 8 weeks mean serum myoglobin was 234 +/- 39 and 233 +/- 40 ng/mL, significantly lower by the Friedman test (p < 0.05). Four weeks after carnitine was discontinued, mean serum myoglobin had risen to 320 +/- 118 ng/mL. Serum creatine kinase and aldolase levels were normal throughout the study. All 6 patients noted improvement in muscular symptoms, with maximal effect at 8 weeks, although 2 patients did not improve until 2 to 4 weeks after carnitine was stopped. We conclude that oral L-carnitine may lower serum myoglobin and improve muscle cramps and weakness in hemodialysis patients. The maximal effect of carnitine on myoglobin occurs 2 weeks before the maximal improvement in muscular symptoms.

Administration, Oral↗
PubMed1985

Posttransplant diabetes in kidney transplant recipients.

We retrospectively reviewed the course of 1,000 renal transplants performed in 835 recipients (758 nondiabetics) to assess the incidence of new onset posttransplant diabetes in former nondiabetics. A total of 119 (15.7%) recipients manifested posttransplant diabetes, of whom 64 (53.8%) became hyperglycemic within 3 weeks of transplantation. Actuarial survival analysis indicated a statistically significant selection of blacks; 68 (57.1%) in the group of posttransplant diabetics contrasted with 30.4% of the overall series who were black (p = less than 0.01). Males comprised 73 (61.3%) of posttransplant diabetics, consistent with the male proportion of 66.6% in the entire series. The total dose of methylprednisolone administered before onset of posttransplant diabetes was less than 2.5 g in 86 (69%) and less than 5 g in 110 (92%) patients. Familial diabetes had been noted in 12 (10%) posttransplant diabetics and in 10 (9%) controls. New cases of posttransplant diabetes occurred at a relatively constant annual rate over the decade of study (+/- 15%/year). Patient survival in controls was greater than in posttransplant diabetics, reaching significance (83 vs. 67%) at 2 years. Kidney graft survival in controls and posttransplant diabetics was similar. We conclude that posttransplant diabetes is of greater prevalence in blacks, is not proportional to total dose or duration of intravenous methylprednisolone therapy, and imposes a threat to recipient survival.

Actuarial Analysis↗
PubMed1984

Hypertension jeopardizes diabetic patients following renal transplant.

Hypertension is highly prevalent in both types I (87%) and type II (95) uremic diabetics at the time of kidney transplantation. Hypertension was diagnosed a mean of 16.9 yrs in type I, and 2.9 yrs in type II diabetics after the clinical diagnosis of diabetes was made. The majority (81%) of our patients were hypertensive postkidney transplant. Only 13% of hypertensive recipients became normotensive post-transplant. This group had a lower mortality rate (1/8, 12.5%), and all survivors (100%) had good graft function (mean creatinine = 1.6 +/- 0.6, range 0.9 to 2.5 mg/dl). By contrast, recipients who remained hypertensive post-transplantation had a much higher mortality rate (25/54, 48%), and loss of graft function necessitating dialysis occurred frequently (19/54, 35%). Of hypertensive diabetic recipients alive at a mean of 21 mos post-transplant, renal function was worse (mean creatinine = 3.1 +/- 3.0, range 1.0 to 13.7 mg/dl) than in nonhypertensive recipients. We conclude that while renal transplantation may be the treatment of choice in patients with diabetes mellitus, failure to control hypertension negatively biases the ultimate post-transplant course.

Diabetes Mellitus, Type 1↗
PubMed1980

Charcoal sorbent-induced hypolipidemia in uremia and diabetes.

Rats with hyperlipidemia associated with streptozotocin-induced diabetes or azotemia after subtotal nephrectomy were administered a diet containing 5% activated charcoal. Significant lowering of nonfasting serum cholesterol and triglyceride levels resulted. Charcoal-feeding also altered the abnormal high density lipoprotein electrophoresis pattern of diabetic rats toward normal.

Animals↗
PubMed1978

Relationship of plasma lipids to renal function and length of time on maintenance hemodialysis.

Significant hypertriglyceridemia, the most common lipid abnormality in renal failure, first occurs when the creatinine clearance falls to 50 ml/min. The prevalence of hypertriglyceridemia continues to rise as creatinine clearance falls further with the highest rate developing at a creatinine clearance less than 10 ml/min. Hypertriglyceridemia is correlated with plasma glucagon levels but not growth hormone or insulin. Plasma cholesterol values remain normal in the face of deteriorating renal function and show no correlation with any of the hormones measured. Although all three hormones became elevated as renal function diminished, none were directly correlated with glomerular filtration rate. There was a distinct decrease in the prevalence of hyperlipidemia after 5 years of maintenance hemodialysis therapy. Plasma growth hormone and glucagon through an effect on plasma triglyceride and plasma insulin by effecting plasma cholesterol may play a role in this decline of hyperlipidemia with duration of hemodialysis.

Adult↗
PubMed1978

Recurrent renal vein thrombosis consequent to membranous glomerulonephritis.

The diagnosis by inferior vena cavography of right renal vein thrombosis with extension into the vena cava was made in a 33 year old man with idiopathic membranous glomerulonephritis and multiple pulmonary emboli. After one year of continuous anticoagulant drug therapy with heparin and coumadin, venography showed absence of clots in the vena cava and therapy was discontinued. Proteinuria in excess of 4 g/24 hr continued. Six months later pulmonary emboli recurred and venography again demonstrated large clots in the vena cava and right renal vein. The potential for recurrence of renal vein thrombosis and pulmopnary embolism in the presence of active renal diseases is thus demonstrated.

Adult↗
PubMed1977

Iron absorption in experimental uremia.

Gastrointestinal absorption of radioactive iron (59Fe) was studied in uremic rats. Duodenal gut sac transport of 59Fe in a group of 12 rats with a mean BUN of 98+/-24.4 mg%, was 2.29+/-1.16. This was significantly lower (p less than 0.01) than the amount of 59Fe transported (4.88+/-1.87) across the duodenum of a group of control rats, mean BUN 22.9+/-3.2 mg%. We conclude that there is diminished absorption of iron in uremia.

Animals↗
PubMed1977

Sickle hemoglobinopathy and the kidney.

Individuals with sickle cell anemia manifest various functional and anatomic renal aberrations. Function of the renal medulla is uniformly affected as reflected in impaired urinary concentrating and acidifying ability. Disruption of normal blood flow patterns in the medulla with impairment of function of the loop of Henle (functional papillectomy), presumably because of sickling in the hyperosmolar and anoxic environment of the renal medulla, may mediate these abnormalities. Hematuria and frank papillary necrosis may result through the same mechanism. Nephrotic syndrome, glomerulonephritis, and progressive renal failure occur on occasion in sickle cell disease. Recent evidence strongly suggests an immune complex glomerulonephritis due to tubular injury with release of renal tubular antigen into the circulation of such individuals. Hemodialysis and renal transplantation appear to be reasonable modes of therapy for sickle cell patients in chronic renal failure.

Acidosis, Renal Tubular↗