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Biomedical subjects

A J Matas

Publications and source records attributed to A J Matas.

At least 361 records · Page 20Linked to original sources
PubMed1977

Acute renal failure following blunt civilian trauma.

Renal failure developed in 20 patients following blunt civilian trauma. Ten recovered normal renal function; 8 currently survive. Survivors and nonsurvivors did not differ in age, time from trauma to anuria, mean blood urea nitrogen or creatinine level prior to the first or to subsequent dialyses. However, there was an increased incidence of sepsis and liver failure in those who died. When outcome was related to site of injury, patients with closed head injury and/or intra-abdominal injury had a worse prognosis than those with thoracic or extremity injury only. Only 2 patients with perforated bowel survived; both had peritoneal dialysis combined with peritoneal lavage with antibiotic solutions. Mortality in patients with posttraumatic renal failure remains high; however, death is usually a result of associated complications rather than a result of the renal failure. Aggressive management of other complications of the trauma, especially sepsis or potential sepsis, is necessary. We recommend peritoneal dialysis combined with peritoneal antibiotic lavage where there is a potential for posttraumatic intra-abdominal sepsis associated with renal failure.

Acute Kidney Injury↗
PubMed1977

Pseudorejection: factors mimicking rejection in renal allograft recipients.

Serum creatinine level is used as a major measure of post-transplant renal function at most centers. A significant elevation of creatinine level suggests allograft rejection. However, other factors affect renal function in the transplant recipient and each may cause an elevation in serum creatinine level, suggesting a rejection episode. It is important to make the correct diagnosis and not treat these episodes with anti-rejection therapy. We reviewed the course of patients transplanted between 1969 and 1974 to determine the pathogenesis of creatinine elevations retrospectively found to be due to causes other than rejection. Six distinct causes were found: hyperglycemia, ureteral obstruction, infection, lymphocele, arterial stenosis, and recurrence of the original disease. Each of these is discussed individually. In order to make the diagnosis of pseudorejection, a high index of suspicion is necessary.

Adolescent↗
PubMed1977

When should the third renal transplant rejection episode be treated?

Recent reports cite better survival when repeatedly rejecting renal allografts are removed and patients returned to hemodialysis. However, the criteria for graft removal remain undefined; although some reports recommend removing all kidneys undergoing a third rejection. In our series (1968-1973) of 316 patients with technically successful first grafts followed 2(1/2)-8 years, graft survival was inversely related to the number of rejection episodes. One hundred per cent of kidneys without rejection are currently functioning or functioned at the time of death compared to 90% with one rejection, 67.4% with two and 21% with three. However, 40% of kidneys having three rejection episodes functioned longer than one year after treatment of the third rejection episode. In an attempt to determine the predictability of one year graft survival or failure following treatment of the third rejection, a formula was developed that correctly predicted in 33 of 38 (87%) patients. The formula was based on information available prior to treatment of the third rejection episode, and represents an index of baseline renal function (serum creatinine after second rejection episode) and two indices of the severity of rejection episodes (serum creatinine change between the first and second rejection episodes; rapidity of sequential rejection).Following its derivation, the formula was applied to a second group (1974) of 19 patients having had three rejection episodes. The formula correctly predicted one year allograft survival or failure following treatment of the third rejection episode in 68% of these patients. A striking finding of our review was a significant difference in current patient survival between those having no rejection episodes (89%) and those having one or more rejection episodes (65%) (p < .00001). There was no significantly greater long-term curtailment in survival if more than one rejection eipsode was treated. Patients having one rejection eipsode seemed to die from varying causes and at varying time periods. Patients dying after two or more rejection episodes had an increased incidence of deaths due to bacterial infection.

Creatinine↗
PubMed1977

Portal versus systemic transplantation of dispersed neonatal pancreas.

It is not known whether the advantage of the portal vein as a transplant site for islet transplantation is caused by the immediate availability of a blood supply or by the localization of the islets in the portal circulation. We transplanted minimal quantities of islet tissue from neonatal rat donors to isogeneic adult rats with streptozotocin-induced diabetes. Transplants were performed to three sites, i.p., portal vein, and systemic vein (i.v.). When four neonatal donors were used for each recipient there were no i.p. cures but 90% i.v. and 100% portal vein cures, which suggests that access to a blood supply is important. As the amount of tissue transplanted was decreased, there were significantly more cures with the portal vein route, which suggests that localization of the islets in the portal circulation is also important to graft survival.

Animals↗
PubMed1977

Autotransplantation of pancreatic islets without separation of exocrine and endocrine tissue in totally pancreatectomized dogs.

The aims of this study were to determine whether diabetes could be ameliorated in dogs by autotransplantation of pancreatic fragments to the spleen and to determine the optimal time of collagenase digestion for pancreatic tissue dispersal. Forty-eight dogs were made diabetic by total pancreatectomy. Fifteen dogs not further treated survived 7.0+/-1.1 (SE) days with a mean plasma glucose of 401+/-5 (SE) mg/100 ml 2 days after pancreatectomy. The pancreases of 33 dogs were distended with Hanks' solution, minced, digested with collagenase (600 microns/ml of tissue), for 0 to 25 minutes, and autotransplanted to the splenic pulp. The incidence of permanent normoglycemia (fasting plasma glucose less than 150 mg/100 ml) and the K value of glucose tolerance tests (GTT) performed 2 and 10 weeks after transplant were determined in experimental groups divided according to the length of collagenase digestion. All five dogs receiving undigested tissue remained hyperglycemic. One of seven dogs receiving tissue digested for 10 minutes became normoglycemic. In contrast, seven of eight, seven of seven, and six of six dogs receiving tissue digested for 15, 20, and 25 minutes, respectively, became normoglycemic (followed for 6 months). K values at 2 weeks were 1.20+/-1.19 (SE)% 1.60+/-0.25 (SE)%, and 0.78+/-0.08 (SE)% in the normolgycemic dogs of the 15, 20, and 25 minute digestion groups, respectively. The K value of normal dogs was 3.30+/-0.27 (SE)%. The glucose tolerance curves of the 20 minute group at 2 and 10 weeks most nearly approximated the curves of normal dogs. K values improved in all recipient dogs. Diabetes recurred immediately and death occurred at a mean of 4.8+/-1.5 days in 12 recipient dogs following splenectomy. We conclude that pancreatic fragments can be successfully autotransplanted to the spleen without separation of endocrine and exocrine tissue and that 20 minutes is the optimal period of collagenase digestion for tissue preparation.

Animals↗
PubMed1977

Clinical characteristics of the lethal cytomegalovirus infection following renal transplantation.

An ongoing prospective study of the role of viruses in renal transplant recipients has provided identification of two patterns of cytomegalovirus (CMV) infection. In both patterns, fever and leukopenia occur within 6 months after transplant. In addition, the benign form is characterized by renal biopsy evidence of rejection and brisk Antibody responses to CMV. The lethal syndrome runs a typical 4 week course, beginning with prostration, orthostatic hypotension, mild hypoxemia and progressing to severe pulmonary and hepatic dysfunction, muscle wasting, central nervous system depression, and death. antibody responses to CMV are minimal, and renal biopsy does not show rejection despite elevation of serum creatinine. At autopsy, CMV is found in lung, liver, kidney, gastrointestinal tract, and brain. Successful management of the potentially lethal kidney, gastrointestinal tract, and brain. Successful management of the potentially lethal CMV syndrome requires rapid clinical recognition and immediate reduction of immunosuppressive therapy. future prospects for control include development of a CMV vaccine and specific antiviral chemotherapy.

Antibodies, Viral↗
PubMed1977

Hepatocellular transplantation in acute liver failure.

Acute liver failure carries a high rate of mortality, but if metabolic support can be maintained for a critical period, liver healing and recovery are possible. Current techniques of temporary hepatic support are cumbersome and inconsistently effective. We studied the ability of dispersed hepatocytes to provide metabolic support when transplanted to rats with liver failure induced by dimethylnitrosamine (DMNA), a rapidly metabolized agent that is selectively toxic to liver cells. DMNA (20 mg/kg) was administered intravenously to 92 Lewis rats. Animals were divided into four groups receiving the following treatments 24 hours after DMNA administration: group I-intraperitoneal transplantation of hepatocytes prepared from 2.0 gm of normal isologous rat liver; group II-infusion into the portal vein of hepatocytes prepared from 1.5 gm of liver; group III-infusion of saline into the portal vein; group IV-no further treatment. The percentages surviving in each group 3 weeks after DMNA administration were 63%, 71%, 17%, and 6%, respectively. Mean serum glutamic oxaloacetic transaminase (SGOT) levels 3 days after DMNA administration were similar in the four groups, indicating that the degree of liver damage was equivalent. A significantly higher proportion of hepatocyte treated rats survived. Liver histology after DMNA administration showed hemorrhagic central lobular necrosis. A return to near-normal architecture occurred by 3 weeks in surviving animals. In group II hepatocytes were seen in portal venules, sinusoids, and central veins. We conclude that dispersed hepatocytes, transplanted either intraperitoneally or via the portal vein, can provide sufficient metabolic support to allow for recovery from drug-induced hepatic necrosis.

Acute Disease↗