The primary aim of this multicenter, prospective, randomized cross-over study was to clarify whether a new model of hemodialysis (HD) potassium (K) removal using a decreasing intra-HD dialysate K concentration and a constant plasma-dialysate K gradient (treatment B) is capable of reducing the arrhythmogenic effect of standard HD, which has a constant dialysate K concentration and decreasing plasma-dialysate K gradient (treatment A). The secondary aim was to verify whether this new model is clinically safe. In treatment B, the initial dialysate K concentration had to be 1.5 mEq/liter less than the plasma K concentration, and exponentially decrease to 2.5 mEq/liter at the end of HD. Forty-two chronic HD patients with an increase in premature ventricular complexes (PVC) during dialysis were enrolled from 18 participating centers, and randomly assigned to either sequence 1 (ABA) or sequence 2 (BAB). A pool of 333 of 378 expected ECG Holter recordings were checked for signal quality; 269 (71%) from 36 patients (86%) had a satisfactory signal quality and 108 were selected for analysis (1 per patient per period). There was a difference in the natural logarithm of the increase in PVC/hr and PVC couplets/hr during HD between treatments A and B (1.70 +/- 1.59 vs. 1.09 +/- 1.76 and 0.94 +/- 0.86 vs. 0.64 +/- 1.01, a reduction of 36% and 32%, P = 0.011 and 0.047, respectively) without any carry over effect (P = 0.61 and 0.24, respectively). The fact that this decrease of one third is due to a lower plasma-dialysate K gradient is supported by the observation that it was more evident during the first than the last two hours of HD (a reduction in the natural logarithm of the increase in PVC/hr and PVC couplets/hr of 60% and 60%, P 0.002 and 0.009, vs. 26% and 17%, P = 0.098 and 0.332, respectively): the initial plasma-dialysate K gradient was 2.3 times lower during treatment B than during treatment A, without adversely affecting pre-HD plasma K levels. These results could have a considerably clinical impact not only because of the possibility of physiologically decreasing the arrhythmogenic effect of HD, but also because this effect can be considered a "marker" of the electrophysiological derangement induced by the administration of standard HD three times a week for years ("electric disequilibrium syndrome").
Four patients, stable on acetate hemodialysis (AHD), were switched to acetate-free biofiltration (AFB) which differs from AHD and bicarbonate hemodialysis (BHD) in that the dialysate contains no buffer, which is given intravenously as a hypertonic (1/6 M) Na bicarbonate solution. Within the 1st month the patients developed thirst and hypertension attributed to a positive Na balance. The aim of this investigation was to check this (1) by a study based on the predictable changes induced in the body compartments of 13 patients by the infusion and ultrafiltration (UF) of a hypertonic solution and (2) by direct determination and calculation of 28 Na mass balances in BHD and AFB. The theoretical model indicated that infusion of 4.87 liters of a 166.7 mEq/1 Na bicarbonate solution and UF of the same amount caused a positive balance of 233 mosm of Na. The Na mass balances showed a relationship between Na transmembrane gradient and loss or gain of Na in both methods (p < 0.0001). The slopes of the regression lines were not significantly different but there was a highly significant difference between the y axis intercepts (p < 0.0001), which indicates that the same Na transmembrane gradient that gives no net change of Na in BHD, induces a net gain of 240 mosm (120 mEq of Na) in AFB and that to obtain the same Na balance dialysate Na should be reduced by about 8 mEq/1 in AFB. These data are the same as the theoretical forecast which could be extended to all hemodiafiltration methods in which solutions of any tonicity have to be infused, in order to correctly predict the Na balance.
Abstract. IgD deposits have been investigated by an indirect immunofluorescence technique in 180 renal biopsies carried out on patients with various renal diseases. IgD was not present in nephrotic syndrome with minimal changes or focal glomerulosclerosis, in mesangial proliferative glomerulonephritis, in chronic advanced glomerulonephritis, in rheumatoid purpura and in other various nephropathies with predominant non‐glomerular lesions. Significant deposits of IgD were identified in 12 out of 16 cases of membranoproliferative glomerulonephritis, in 15 out of 23 cases of membranous nephropathy, in 11 out of 21 cases of focal proliferative glomerulonephritis with mesangial IgA deposits, in 2 out of 5 cases of proliferative glomerulonephritis with crescents and in 1 out of 6 cases of proliferative exudative glomerulonephritis. All cases of lupus nephritis and nephritis associated with mixed cryoglobulinaemia showed IgD deposits. In diabetic glomerulosclerosis, IgD was found in 1 out of 4 biopsies and only in the exudative lesions. In 5 out of 8 cases of amyloidosis anti‐IgD serum stained the amyloid substance irregularly. In such cases IgD was found in association with other immunoglobulins and complement with the same localization. These findings suggest that IgD may participate in the immunological processes which lead to the development of glomerular deposits, mainly in cases of chronic glomerular diseases.
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