Plasmapheresis and peritoneal dialysis in the management of rapidly progressive glomerulonephritis.

Six patients with rapidly progressive glomerulonephritis were given plasmapheresis and peritoneal dialysis by manual technique. At the start of treatment the patients were in renal failure and all but two were practically anuric. Renal biopsy revealed glomerular sclerosis in 4 cases. One of the patients in whom segmental focal fibrosis was found, went into remission. In the other three cases extensive hyaline degeneration was present. One of them was placed on a dialysis program, two died with circulatory failure. In two cases no glomerular sclerosis was found, though extensive changes of the tissues were present. One of these patients went into remission, the other died from respiratory failure consequent upon recurrent pneumothorax and gross pulmonary infiltration. The only chance of success in the management of rapidly progressive glomerulonephritis is offered by the earliest possible diagnosis. In cases of glomerular sclerosis the chances are very poor.

Effect of hyperosmolar peritoneal dialysis fluid on the elimination of small- and medium-molecular substances.

The efficiency of peritoneal dialysis by the use of hyperosmolar dialyzing fluid (680 mOsm/1) was studied in 7 patients with chronic renal failure. The results were referred to the control values obtained in the first and in the terminal periods. In the course of treatment by means of the solution of high osmolarity the clearance of small- and medium-molecular substances increased. A significant increase in ultrafiltration was demonstrable. Protein loss and elevation of the blood glucose levels were noted as side-effects.

Effect of haemo- and peritoneal dialysis on the cell-mediated immune response in chronic uraemia.

Lymphocytopenia, decreased spontaneous rosette formation, and a decreased T lymphocyte count have been found in patients with non-uraemic glomerulonephritis (71 cases) and in different stages of uraemia (68 cases). In chronic glomerulonephritis and in the early stage of uraemia, cell-mediated hypersensitivity (lymphocyte migration inhibition) to glomerular basement membrane (GBM) characteristic of glomerulonephritis could be demonstrated. Hypersensitivity disappeared in the terminal stage of uraemia indicating endogenous immunosuppression.

Blood coagulation and hereditary nephritis.

Nineteen patients with hereditary nephritis - members of six families - were studied for haemostasis on 11 occasions by the use of four capillary tests, 14 different blood coagulation tests and two different platelet function tests. Systemic capillaropathy was demonstrable in 8 out of 15 cases of the non-uraemic, and in all the 5 cases of the uraemic group. No completely normal blood coagulation was found in any of the cases and the coagulation disorders were never of exclusively haemorrhagic pattern. On the evidence of the complex studies, hypercoagulability as well as hyper-hypocoagulability were found in the uraemic and non-uraemic groups alike. Reduction in plasma fibrinolytic activity, elevation of the fibrinogen level and a shift of the thrombelastogram in the direction of thrombosis were demonstrable in the majority of the cases.

Blood coagulation abnormalities in the Schönlein-Henoch syndrome in adults.

23 adult patients with Schönlein-Henoch's syndrome were observed between 1965 and 1976. Nephropathy was noted in 18, gastrointestinal bleedings in 13, thrombosis of legs in 4, cases. Haemostasis was studied in the successive phases of the process on 185 occasions altogether. The studies included four different capillary tests, thromboelastography, the Gerendás coagulogram, determination of partial thromboplastin time and two platelet-function tests. Additional renal biopsy was performed in 10 cases, mesocolon and skin biopsy in one case each. The results of at least one of the capillary tests were found positive in each of the patients in some stage of the process. The coagulation status was marked by hyperocagulability either in itself or combined with laboratory signs of hypocoagulability. Immunohistological study of the biopsy specimens revealed glomerular fibrin deposits in 7 cases. On the evidence of the follow-up studies the laboratory tests may be used for the assessment of the activity of the process. The alternatives of local intravascular coagulation (LIC) or of compensated diffuse intravascular coagulation (DIC) are offered for the interpretation of hypercoagulability.

Hereditary nephritis and the heart.

Eleven cases of hereditary nephritis were studied for cardiac abnormalities by means of ECG and BCG. With the exception of two cases no significant abnormalities were demonstrable, which indicates that this genetically transmitted process generally leaves the heart unaffected. It is thus to be expected that intermittent haemodialysis, as far as the heart is concerned, will be well tolerated by these patients.

Blood coagulation defect in Masugi nephritis.

The platelet count and the coagulation pattern have been studied on the basic of nine laboratory tests in Masugi nephritis of the delayed type. Platelet consumption was found to constitute the initial manifestation of Masugi nephritis. The prenephritic stage and the manifestation of nephritis were invariably associated with hypercoagulability, as reflected by a loss of the spontaneous fibrinolytic activity of plasma, together with an elevation of the fibrinogen level and an increase in maximal thrombus elasticity. At the onset of nephritis the platelet count declines again. The hypercoagulability is attributed to intravascular coagulation in the kidney.

Haemorrhagic pericarditis and cardiac tamponade during chronic haemodialysis.

Three cases of uraemic haemorrhagic pericarditis observed during haemodialysis treatment are described. The condition is explained with uraemic toxicosis, cyclic heparinaemia resulting from dialysis, deficient thrombocyte function, and decreased capillary resistance. The clinical appearance of haemorrhagic pericarditis was not typical in any of the cases. Two patients died, while in one patient partial pericardiectomy was performed with success.

Care of the patient in autoimmune renal disease. Assessment of clinical and immunological activity.

174 patients suffering from various autoimmune and renal diseases have been followed up for periods of one to four years. Repeated assessment of clinical and immunological activity is indispensable for therapy, prognosis and rehabilitation. Determination of microscopic haematuria by the Addis count proved to be the best indication of clinical activity. Immunological activity was assessed by the CH50, C3 and immunoconglutinine tests, the titer of the anti-glomerular basal membrane antibodies and the inhibition of leucocyte migration. Depending upon the nature and stage of the disease one or more positive tests indicated activity of the pathological process. Consequently, the simultaneous application of several methods is recommended for assessment of immunological activity in autoimmune renal diseases.

Changes in the electrocardiogram, vectorcardiogram and ballistocardiogram after hemodialysis in chronic uremia.

In 12 cases with uremia, the electrical activity and form and amplitude of Bcg (displacement) were investigated before and after hemodialysis. The uremia was secondary to chronic glomerulonephritis (9 cases), familial nephritis (1 case), polycystic kidney disease (1 case) and chronic pyelonephritis (1 case). During the study digitalis was not given to the patients. The ECG and Bcg abnormalities were irreversible in most cases. In 9 cases the VCG showed hypertrophy of the left ventricle. Considering these facts it is assumed that myocardial hypertrophy might play an important part in the development of irreversible pathological repolarization and hemodynamic troubles in chronic uremia.