PubMed Health⌕ Search

Biomedical subjects

M Ekberg

Publications and source records attributed to M Ekberg.

13 recordsLinked to original sources
PubMed1978

Combination of fibromuscular hyperplasia, renal aplasia, hypoplasia or dysplasia and otosclerosis occurring in the same individual or the same family.

We have found 3 reports of fibromuscular hyperplasia (FMH) of the renal arteries with hypertension occurring in 2 siblings as well as a few instances of renal agenesis and unilateral renal aplasia occurring in the same family. In this paper we report on FMH of the renal arteries in 2 women, one giving birth to a child with renal agenesis, the other to a child with a focally dysplastic hypoplasia of the kidneys. A third family is reported, heavily loaded with hypertension and otosclerosis, in which 2 siblings with FMH and otosclerosis were found. Another 4 patients without known heredity for hypertension, but with FMH combined with renal or urinary tract anomalies, are also reported. The findings are discussed, particularly in relation to the findings in a large material of chronic non-obstructive pyelonephritis, where in those with well maintained renal function, hypertension below the age of 40 was found predominantly in females with a positive family history of hypertension and signs highly suggestive of infected hypoplasia or dysplasia of the kidney.

Abnormalities, Multiple↗
PubMed1978

Pharmacokinetic and therapeutic studies of pivmecillinam in patients with normal and impaired renal function.

Pivmecillinam which is the oral form of mecillinam was evaluated by treatment of 26 patients presenting various types of urinary tract infections and by prophylactic treatment of 12 patients. Pivmecillinam given in a daily dosage of 1.2 g for periods of 1 to 56 weeks was well tolerated in all of the patients including those with impaired renal function without any dose reduction. The original bacterial strain in the urine was eradicated in 100% of the cases. Two patients had a superinfection and 4 had a recurrence during a 3-month follow-up period. The oral absorption of pivmecillinam was investigated in 15 patients with normal or slightly reduced renal function and in 5 patients on maintenance hemodialysis. High serum levels were achieved within 1 to 2 h after administration. Patients with reduced renal function showed retarded elimination rates, suggesting that the dose should be adjusted in this category of patients.

Acute Kidney Injury↗
PubMed1977

Hemolytic uremic syndrome. Results of treatment with hemodialysis.

The characteristics of the hemolytic-uremic syndrome in 7 children living in a well defined area in the south of Sweden are described. All the patients had a severe form of the disease and were critically ill. The clinical activity could best be followed by measuring blood platelets and urinary FDP. Early institution of hemodialysis treatment, given almost daily until normalisation of platelet count and urinary output, is the most important live-saving measure. Full dosage heparin seems not to be necessary. Six patients survived and were followed-up for 1-7 years. When last seen they all had normal renal function and blood pressure.

Blood Cell Count↗
PubMed1977

Proteinuria following renal arteriography. Report of two cases.

Two patients reacting with transitory, massive proteinuria after diagnostic renal arteriography with a commonly used non-ionic contrast medium, metrizoate, are described. One of them developed temporary renal failure; the concentration of urinary albumin reached 330 g/g creatinine. It is suggested that intratubular precipitation of proteins, obstructing urinary flow, might be one factor in the development of her renal failure.

Acute Kidney Injury↗
PubMed1976

Cytomegalovirus hepatitis in an artificial kidney unit.

Serum hepatitis is a dreaded risk in connection with regular dialysis treatment (RDT). Liver damage, however, can be cuased by other diseases, such as infection with cytomegalovirus (CMV). Two cases in our artificial kidney unit revealed signs of liver damage with increased liver enzyme activity. Case 1, a woman, was on RDT after an unsuccessful renal transplantation, and Case 2, a man, belonged to the staff. Serum hepatitis was initially suspected in both cases, but repeated examinations of the sera revealed no hepatitis B antigen or antibodies (HbAg and HbAb). Later on, both showed a significant increase in antibodies in complement fixations reaction (CF) to CMV-antigen. CMV could be isolated from urine in Case 2. Case 1 had been bilaterally nephrectomized. The symptoms (tiredness, muscle pain and headache) and the course of the disease were mild in both cases and liver enzymes became normal within 1-2 weeks. Twenty out of 31 examined patients and staff had antibodies in CF to CMV-antigen, but in none was there any significant increase. The source of infection may have been transfusion of fresh blood in Case 1, but in Case 2 no particular source could be suspected. Thus, in liver damage CMV-infection may be an etiological alternative. In routine work at artficial kidney unite patients and personnel are regularly examined in respect of bilirubin, liver enzymes, HbAg and HbAb in serum. We recommend also examination of serum for antibodies in CF to CMV-antigen. Until a firm differential diagnosis has been established the patient should be isolated and the dialysis equipments used only by that patient.

Adult↗
PubMed1976

Determination of urinary fibrin/fibrinogen degradation products by radioimmunoassay.

Glomerular fibrin/fibrinogen related material is often found in the early stage of especially proliferative types of glomerulonephritis and during rejection of renal grafts after transplantation. The presence and concentration of urinary fibrin/fibrinogen degradation products (FDP) have been found to be correlated to the extent of glomerular fibrin deposits. Most methods for FDP determination hitherto available are not sensitive enough to detect such small amounts of the fibrin/fibrinogen related material in the urine as are found in early glomerulonephritis. A radioimmunoassay for determining urinary FDP is described, in which the high molecular weight degradation products (HMWDP) are first converted into end degradation products (D and E) by addition of plasminogen and streptokinase to the urine sample. In the test an antiserum against purified D-products is used, which avoids the influence of varying binding properties and therefore makes the method more specific.

Cross Reactions↗
PubMed1976

The determination of fibrinolytic degradation products in concentrated urine after renal transplantation.

Fibrin/fibrinogen degradation products (FDP) were determined in concentrated as well as unconcentrated urine in 29 patients undergoing renal transplantation. When determined in unconcentrated urine, FDP was found for 3-4 weeks after an uneventful transplantation, compared with 12 weeks when determined in concentrated urine. After acute rejection episodes FDP was found in unconcentrated urine, but remained in the concentrated urine for 8 weeks longer when concentrated urine was used for determination. In early chronic rejection and glomerulonephritis, FDP appeared as a sign of glomerular lesion in concentrated urine before it was found in unconcentrated urine. It was concljded that the presence of FDP in concentrated urine is a diagnostic tool of value particular in detecting early glomerular lesions caused by chronic rejection or glomerulonephritis.

Creatinine↗
PubMed1976

Co-trimoxazole in the long-term treatment of pyelonephritis with normal and impaired renal function.

The effect of co-trimoxazole was studied in 29 cases of acute or chronic pyelonephritis. The therapy produced the desired effect in 22 out of 23 cases and in the 6 cases treated prophylactically. We used a special dosage schedule for the combination of sulphamethoxazole and trimethoprim in the treatment of patients with normal renal function and with varying degrees of renal impairment. The results show that the plasma concentrations were at satisfactory therapeutic levels, with no accumulation of the three substances and without causing any toxic side effects, even in patients with severe impairment of the renal function. The mean duration of the treatment was 12.3 months. The material is, however, not largelu enough to warrant the recommendation of standardized treatment according to the schedule described, in spite of the favourable experience gained. It does, however, permit us to recommend that the plasma concentrations should be determined, particularly of the total sulphamethoxazole in patients with severely impaired renal function.

Acute Disease↗
PubMed1975

Factor VIII and glomerulonephritis.

To find out if determination of factor VIII,which most probably is synthetised in the intima of blood-vessesls, is of value for predicting the severity of vessel damge in glomerulonephritis, factor-VIII activity, factor-VIII-related antigen, and glomerular filtration-ratewere esto,ated om 85 patients with early glomerulonephritis on admission, and in 70 of these at follow-up for up to 4 years. The levels of factor-VIII activity and factor-VIII-related antigen on admission were normal in those patients who recovered. Where renal function was impaired on admission or becaome so during follow-up, factor VIII was high. Determination of factor VIII might thus be of prognostic value in early glomerulonephritis.

Antigens↗
PubMed1975

Origin of urinary fibrin/fibrinogen degradation products in glomerulonephritis.

To elucidate the origin of the fibrin/fibrinogen degradation products (F.D.P.) occurring in the urine in glomerulonephritis 28 patients with glomerulonephritis were examined for renal fibrinolytic activity, F.D.P. in urine and serum, and blood fibrinolytic activators and blood fibrinolytic activators and inhibitors. Unlike the glomerful of healthy kidneys, which were fibrinolyticly inactive, those of kidneys with glomerulonephritis constantly showed fibrinolytic activity. The presence or absence of fibrin in the glomeruli was almost always accompanied by, respectively, the presence or absence of urinary F.D.P., which suggested a renal origin of urinary F.D.P. in glomerulonephritis. The low fibrinolytic activity of the blood and the absence of F.D.P. in the serum of these patients make it unlikely that the urinary F.D.P. in glomerulonephritis result from glomerular filtration.

Alpha-Globulins↗