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Focal glomerulosclerosis in patients with unilateral nephrectomy. To investigate whether proteinuria and focal glomerulosclerosis (FSG) might develop in humans as well as in experimental models following a reduction in renal mass, we performed a retrospective study of 24 patients previously nephrectomized for unilateral renal disease. None of the patients presented signs of systemic diseases, Alport syndrome, essential hypertension, reflux nephropathy, and other abnormalities on intravenous pyelography. At the time of the first observation seven patients had pathological proteinuria (group 1) while 17 presented a normal protein excretion (group 2). All patients in group 1 and only 4 of 17 in group 2 were male. No other significant differences were found between the two groups. The median age at nephrectomy of the proteinuric patients was 22.3 years, and proteinuria developed after a mean period of 12.2 years. A renal biopsy was performed in four patients and showed a constant pattern of FSG. After a mean follow-up period of 7.3 years from the onset, proteinuria remains unchanged and renal function is well preserved in all the patients. In conclusion our series suggests that also in humans proteinuria and FSG might appear in solitary kidneys due to nephrectomy. This glomerular damage may result from the association of glomerular overload with other unidentified factors. Glomerulosclerose focale chez des malades avec une nephrectomie unilaterale. Afin de rechercher si une proteinurie et une glomerulosclerose focales (FSG) peuvent se developper chez les humaines et dans des modeles experimentaux apres une reduction de la masse renale, nous avons effectue une etude retrospective de 24 malades nephrectomises auparavant pour une maladie renale unilaterale. Aucun de ces malades n'avait de signe de maladie systemique, de syndrome d'Alport, d'hypertension essentielle, de nephropathie de reflux ou d'autre anomalie a l'urographie intraveineuse. Au moment de la premiere observation, sept malades avaient une proteinurie pathologique (groupe 1) tandis que 17 avaient une excretion proteique normale (groupe 2). Tous les malades du groupe 1, et seulement 4 de 17 du groupe 2 etaient des hommes. Aucune autre difference significative n'a ete trouvee entre les deux groupes. La mediane de l'âge au moment de la nephrectomie des malades proteinuriques etait de 22,3 ans et la proteinurie se developpait apres une periode moyenne de 12,2 ans. Une biopsie renale a ete effectuee chez quatre malades et a montre un aspect constant de FSG. Apres un suivi moyen de 7,3 annees a partir du debut, la proteinurie reste inchange et la fonction renale est bien preservee chez tous les malades. En conclusion, nos series suggerent que chez les humaines egalement une proteinurie et une FSG peuvent apparaitre dans des reins solitaires apres nephrectomie. Cette lesion glomerulaire pourrait resulter de l'association d'une surcharge glomerulaire avec d'autres facteurs non identifies.

Model-based study of the effects of the hemodialysis technique on the compensatory response to hypovolemia.BackgroundHemodialysis technique (dialysate composition, filter, convection/diffusion ratio, etc.) can have an impact on the patient's tendency to acute hypotension. We have examined the hypothesis that the dialysis technique affects the hypotension risk by altering the cardiovascular compensatory response to hemodialysis-induced hypovolemia.MethodsTwelve hypotension-prone subjects were studied during six sessions of conventional bicarbonate dialysis (BD) and six sessions of acetate-free biofiltration (AFB). Blood volume (BV) control system was used in AFB to provide a BV change equivalent to the BV change observed in BD. The efficacy of reflex compensatory mechanisms was assessed by a model-based computer analysis of the BD and AFB sessions.ResultsBD sessions were complicated by hypotension more frequently than the AFB ones (34/66BD vs. 18/66AFB). Hypotension arose about 60 minutes earlier in BD (123 ± 41 minutes in BD vs. 183 ± 25 minutes in AFB, P < 0.01), and after a smaller BV reduction (hypotension BV 7.9%± 2.0% in BD vs. 10.9%± 2.6% in AFB, P < 0.05). Model-based computer analysis of the sessions without hypotension revealed differences in peripheral resistance adaptation (9%± 9% BD vs. 19%± 7% AFB, P < 0.05) as well as in the stroke volume reduction (19%± 8% BD vs. 10%± 8% AFB, P < 0.001). Model analysis of sessions with hypotension indicated that compensatory mechanisms were almost inoperative in BD, whereas a residual capacity to control peripheral resistance and cardiac contractility was present in AFB. Model simulations demonstrated that hypotension occurred later in AFB since the residual compensatory capacity in AFB was able to sustain the arterial pressure for larger BV reductions (8.3% BD vs. 11.2% AFB).ConclusionThe increased risk of acute hypotension in BD compared to AFB is caused by a therapy-induced inhibition of reflex compensatory response to hypovolemia.

B and T cell abnormalities in patients with primary IgA nephropathy. The in vitro function of B and T cells was studied in 16 patients with primary IgA nephropathy (PIgA-N). The distribution of OKT3 + cells (total peripheral T cells) and of regulatory T cell subsets (helper OKT4 + and cytotoxic/suppressor OKT8+ cells) was evaluated and a testing for 47 HLA-A, B, C, DR, and DQ antigens was carried out in the 16. B lymphocyte IgA production, after stimulation by poke weed mitogen in the presence of T cells from normal donors treated with mitomycin C, was significantly greater in patients than in controls. T lymphocytes from patients with PIgA-N were more efficient than T cells from controls in providing IgA specific helper activity for normal B cells. The analysis of the individual data showed that the overactivity of B cells and the T cell operational dysfunction was present in about 50% of the patients and did not correlate. No numerical imbalance between T lymphocyte subsets nor any association between lymphocyte behavior, HLA antigen distribution, and a number of clinical, laboratory, and immunohistological findings was observed. Our data, therefore, suggest that PIgA-N is an immunologically heterogeneous disease and that an IgA-specific B cell overactivity and/or overall IgA-specific T cell helper activity may be present in some patients.