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Eleven hemodialyzed patients with uremia were examined for the effect of erythropoietin (EP) treatment carried out for 3 months on functions of different endocrine organs. EP treatment resulted in a decrease of the initial plasma levels of somatotropin, prolactin, follicle-stimulating and luteinizing hormones. EP treatment being over, there was a decrease in the plasma content of ACTH, cortisol and aldosterone. The treatment with EP was also associated with an insignificant rise of the plasma levels of parathyroid hormone and testosterone. EP treatment did not influence the plasma concentration of calcitonin and 25-OH-D. EP was found to exert no significant effect on the pituitary-thyroid reverse relationship. The 3-month treatment with EP eventuated in plasma renin activity inhibition as well as in an increase of the atrial level of natriuretic peptide in the plasma. EP treatment stimulated insulin secretion and reduced glucagon secretion. Finally, EP decreased the gastrin level and to a less degree the plasma level of pancreatic polypeptide.

In 16 children with steroid-responsive nephrotic syndrome (with minimal changes in the glomeruli) the plasma renin activity and aldosterone level were determined during recurrence of the nephrotic syndrome at the stage of oedema increase (FEN alpha 0.25%) and in early period of remission. Plasma renin activity was raised in all cases suggesting presence of hypovolaemia. Since it was not possible to establish a correlation between plasma renin activity and albumin level, as well as between this activity and aldosterone level, and aldosterone level and sodium excretion it may be surmised that the renin-angiotensin-aldosterone system has no decisive role in the pathogenesis of the nephrotic syndrome. The mechanism of oedema development is doubtlessly more complex.

Thirty-three cases of idiopathic IgA nephropathy were followed up for an average of 90.8 +/- 8.4 months. Four therapeutic regimens were applied: symptomatic therapy, immunosuppressive drugs, dipyridamole with acetylsalicylic acid and immunomodulating treatment with thymosin. Parameters of kidney function obtained during control and treatment periods were compared in each patient separately. In all cases but one, frequent fluctuations of serum creatinine levels were observed. Cumulative kidney survival ratio for 5, 10 and 15 years amounted to 1.00, 0.90 and 0.82, respectively. There was no apparent response to thymosin, aspirin and dipyridamole therapy. Immunosuppressive drugs are recommended in cases with steadily progressive disease, when serum creatinine concentration surpasses 2.5 mg/dl.

Fifty cases of idiopathic membranoproliferative glomerulonephritis were followed up for an average of 10 +/- 0.9 (SE) years. Forty of them, who presented a nephrotic syndrome, were treated by immunosuppressive drugs (prednisone, azathioprine, chlorambucil, cyclophosphamide) for 79 +/- 9.7 (SE) months. Cumulative survival ratio for 5, 10 and 15 years after enrollment was 0.90, 0.82 and 0.77 and after appearance of first symptoms or signs of kidney disease as determined by anamnestic data 0.97, 0.91 and 0.90 accordingly. Triple-drug therapy (prednisone and azathioprine combined with chlorambucil or cyclophosphamide) was more effective in improving proteinuria than other immunosuppressive regimens. No serious side effects were encountered.

Prolonged combined treatment with prednisone and immunosuppressive drugs can, if started early enough, significantly reduce the degree of proteinuria and preserve renal function. This is not necessarly associted with simultaneous histological improvement confirmed by renal biopsy. The proposed method of treatment deserve further evaluation.

Data presented in this study suggest existence of hyperendorphinism in uraemic patients. This hyperendorphinism may be regarded both as a primary beneficial compensatory mechanism counteracting disturbances of the internal environment, while causing secondary harmful side effects, which contribute to the uraemic state. Erythropoietin treatment of uraemic, haemodialyzed patients is followed by marked endocrine alterations (suppression of plasma levels of STH, ACTH, prolactin, glucagon, aldosterone, cortisol and plasma renin activity, elevation of plasma insulin and atrial natriuretic levels, lack of influence on plasma PTH, CT and AVP). It remains to be clarified whether the erythropoietin induced endocrine alterations are due to correction of the existing anaemia or reflect a specific effect of this hormone.

The functional outcome after the transplantation of 97 cadaveric kidneys stored up to 25 hours with simple hypothermia was analysed in relation to age of donor, extent of pre-agonal kidney damage, the length of warm, cold and standardised ischaemic times and the presence of multiple renal arteries. Analysis of various factors showed that the most important for function after transplantation were pre-agonal anoxic damage and the ratio of the cold/warm ischaemia time. Based on that observation, a diagram has been proposed which allows calculation of the safe cold storage time after retrieval of the kidney.

Peripheral blood lymphocytes from both normal subjects and kidney allograft recipients, before and on the 4th to 5th days after transplantation, were examined for antibody-dependent cellular cytotoxicity (ADCC) and lectin-induced cellular cytotoxicity (LICC). The graft recipients were treated with standard immunosuppression, which included azathioprine and prednisolone. 51Cr-labeled L1210 cells were used as targets for these two tests. ADCC and LICC activity were evaluated in the presence of rabbit anti-L1210 anti-serum and phytohemagglutinin (PHA), respectively. Comparison of the results obtained from healthy subjects with those of patients before grafting showed a significantly higher LICC activity in the latter group. The ADCC activity did not differ between the groups of healthy females and those awaiting transplantation but it was significantly decreased in the group of males awaiting transplantation as compared to healthy males. Four to 5 days after transplantation, the activity of ADCC and LICC remained unchanged in spite of the immunosuppressive treatment in 37 and 61% of the patients studied, respectively. In most of the patients, high ADCC and/or LIcC activity was followed by an accelerated acute rejection episode. A correlation between the ADCC and LICC activities, measured 4 to 5 days after transplantation, and the time of the first rejection episode was found. We conclude that double screening with ADCC and LICC tests in the 1st week after transplantation is valuable.

ADCC activity in 27 cadaver renal allograft recipients was studied. All the patients were given standard immunosuppressive treatment. Significant positive correlation between high ADCC activity during first 5 days after grafting and accelerated rjection crisis was found. The high positive ADCC test may signalize the possibility of acute accelerated rejection of renal allograft.

Using LDA test the presence of antibodies in patients prior to and post renal transplantation was studied. The relationship between the results of LDA test and graft rejection episodes, the treatment with large doses of prednisolone and CDC test performed simultaneously were analized. No correlation between results of LDA test prior to transplantation or its response to prednisolone treatment and acute rejection crises was found. The value of LDA test in predicting rejection episodes was not confirmed. LDA test detects antibodies 10 times more frequently than CDC test. The presence of cytotoxic antibodies CDC was not always connected with the presence of LDA and vice versa.