The renin-angiotensin system and polycystic kidney disease.
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Biomedical subjects
Publications and source records attributed to A Martin-Malo.
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Calcitonin secretion is stimulated by acute hypercalcemia. Furthermore, in the rat, the calcemic response to parathyroid hormone (PTH) is decreased by calcitonin stimulation. However, in renal failure, it is not known if an increase in the serum calcium concentration within the physiologic range of serum calcium stimulates calcitonin and whether the increased calcitonin decreases the calcemic response to PTH. In the present study, four groups of pair-fed rats were evaluated: normals (N); parathyroidectomy (PTX); and two groups with renal failure (RF)--basal serum calcium less than 8.5 mg/dl (RFa) and basal serum calcium greater than 8.5 mg/dl (RFb). Hypocalcemia was induced by parathyroidectomy or in the RFa group, by a high phosphate diet. Increases in the serum calcium were produced by a 48 hour infusion of rat 1-34 PTH. In the RFa and PTX groups, stimulation of calcitonin was observed as the serum calcium increased from hypocalcemia to normal levels of calcium (P less than 0.01). In all four groups, increasing the serum calcium from normal levels to hypercalcemia increased the serum calcitonin level (P less than 0.05). The relationship between serum calcitonin and calcium was best expressed as a sigmoidal curve. In the two groups with basal hypocalcemia, PTX and RFa, the calcitonin-calcium curve was shifted to the left of the N and RFb groups.(ABSTRACT TRUNCATED AT 250 WORDS)
The calcemic response to parathyroid hormone (PTH) is decreased in renal failure. The reduction of hyperphosphatemia improves the calcemic response to PTH in animals with advanced renal failure. However, since low calcitriol levels in renal failure may also contribute to the decreased calcemic response to PTH, the improved calcemic response observed during the reduction of serum phosphorus may be partially mediated by an increase in serum calcitriol levels. The present study evaluated the calcemic response to PTH in rats with moderate and advanced renal failure and how this response was modified by a high and a low phosphorus diet. In addition, the effect of a change in dietary phosphorus on calcitriol levels was also evaluated. A 48-hour continuous infusion of 1-34 rat PTH increased the serum calcium level to 18.2 +/- 0.4 mg/dl in normal rats, versus 13.7 +/- 0.9 and 12.1 +/- 0.2 mg/dl in rats with moderate and advanced renal failure, respectively. During the PTH infusion, a high phosphorus diet increased the serum phosphorus and resulted in a reduced calcemic response to PTH at each level of renal function; respective serum calcium levels were 13.8 +/- 0.6 mg/dl in normals, 11.2 +/- 0.2 mg/dl in moderate renal failure and 9.6 +/- 0.5 mg/dl in advanced renal failure. In normal rats and in rats with moderate renal failure, dietary phosphorus restriction during the PTH infusion increased serum calcitriol levels. In rats with advanced renal failure, serum calcitriol levels were lower than in the other two groups and were not affected by changes in dietary phosphorus.(ABSTRACT TRUNCATED AT 250 WORDS)
White blood cell counts and plasma C5a anaphylatoxin values were studied during haemodialysis with cuprophane, ethylenevinylalcohol, polycarbonate, polymethylmethacrylate, acrylonitrile, polysulphone and polyacrylonitrile membrane dialysers. Cuprophane induced marked leukopenia with striking plasma generation of C5a. Ethylenevinylalcohol, polycarbonate, polymethylmethacrylate and acrylonitrile promoted an intermediate degree of leukopenia with mild but significant complement activation; however, leukopenia and C5a generation were not time-related with some of these membranes. In contrast, polysulphone and polyacrylonitrile showed neither leukopenia nor C5a increase. These data suggest that although there must be further factors involved, complement-derived anaphylatoxin C5a generation may have a relevant role in the mechanism of haemodialysis-induced leukopenia. At the present time evaluation of the leukopenic effect and the C5a generation capability of a membrane seem worthwhile for estimating its degree of biocompatibility.
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We studied ten patients on hemodialysis (HD) treated in sequence with cuprophan (CU), ethylenevinylalcohol (EVAL), polyacrylonitrile (A-69) and polysulphone (PSP) membrane dialyzers. beta 2-microglobulin (beta 2m) was measured by radioimmunoassay in plasma and dialysate samples. Plasma concentrations were corrected for changes in extracellular volume (ECV). We also studied adsorption in vitro by incubating the above membranes with I-125-labelled beta 2m. There were no changes in beta 2m plasma concentration after HD with CU dialyzers, but a significant decrease was observed with the other membranes tested. Filtration of beta 2m across the dialyzer was absent with CU and minimal with EVAL. However, large amounts were recovered from dialysate with the high-permeability dialyzers, AN-69 and PSP. In vitro studies showed that maximal adsorption capacity was obtained with AN-69 (13%) compared to 9% with CU, 4% with EVAL and 7% with PSP. In summary, beta 2m clearance with PSP is achieved through greater removal of this protein by mass transport across the membrane. The mechanism by which beta 2m is removed from blood during AN-69 dialysis seems to include both adsorption to and filtration by the membrane itself.
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We have investigated the usefulness and practicability of the so-called sequential hypertonic dialysis in 2 selected patients with severe hemodialysis-induced hypotension; 190 mmol/l of sodium dialysate during the 1st and 3rd h and 132 mmol/l throughout the 2nd and 4th h were used, with a Drake-Willock-Bi proportionating unit, which was electronically modified for the purpose of the study. Crossover was made, patients serving as their own controls in two consecutive cycles: 3 weeks conventional hemodialysis followed by 4 weeks sequential hypertonic dialysis, using high-flux dialyzers. At the end of sequential hypertonic dialysis a greater weight loss was achieved (p less than 0.001) with absolute stability of blood pressure. There were no significant changes in plasma osmolality and plasma volume during sequential hypertonic dialysis when compared with conventional hemodialysis. Dialysis symptoms and complications were less frequently recorded during sequential hypertonic dialysis (p less than 0.001). At the end of each sequential hypertonic dialysis period, hemoglobin, potassium, and phosphate plasma levels improved significantly and plasma sodium concentrations remained within the normal range. We conclude that sequential hypertonic dialysis is an easy and routine feasible procedure with our methodology. It is possible to achieve the ideal dry weight with no symptomatic hypotension. Sequential hypertonic dialysis constitutes an alternative to sequential ultrafiltration in selected patients, as it minimizes the falloff in plasma volume and osmolality observed during conventional hemodialysis.
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