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Biomedical subjects

F Ben Hamida

Publications and source records attributed to F Ben Hamida.

27 records · Page 2Linked to original sources
PubMed1993

Management of hyperphosphatemia in patients with renal failure.

Phosphate retention plays a major role in the pathogenesis of hyperparathyroidism at all stages of renal insufficiency. Dietary phosphate restriction is mandatory only for adults and is not advised for children because of the recommended diet allowance. Dietary restriction is usually not sufficient, and phosphate binders are almost always necessary when the glomerular filtration rate falls below 40 mL/min. Because long-term administration of aluminum phosphate binders is associated with risk of aluminum intoxication despite the use of so-called "safe doses", alternative phosphate binders should be used. Magnesium hydroxide and carbonate can be used only for dialysis patients because a low dialysate magnesium concentration is necessary to prevent the hazards of hypermagnesemia. Therefore, the major alternative is the use of alkaline salts of calcium. The most recently proposed salt, acetate, has a higher phosphate-binding capacity than carbonate but exposes patients to the same incidence of hypercalcemia despite the use of half the dose of elemental calcium. These salts should be taken with meals in order to complex more dietary phosphate and decrease calcium absorption and therefore the risk of hypercalcemia. Oral calcium alone, without 1 alpha OH-vitamin D3 derivatives, can prevent hyperphosphatemia and hyperparathyroidism in most uremic patients before dialysis and in about half of the patients dialyzed with a dialysate calcium of 1.5 to 1.65 mmol/L. 1 alpha OH-vitamin D3 derivatives, which increase intestinal absorption of phosphate, should be used only when hyperphosphatemia has been prevented by oral calcium and diet and when plasma parathyroid hormone levels increase above three times the upper limit of normal. To decrease hypercalcemic risk, patients should be given 1 alpha OH-vitamin D3 derivatives, preferably at night, as an intermittent bolus (intravenous or oral). In dialysis patients, the dialysate concentration of calcium may have to be further decreased in order to prevent hypercalcemia when high doses of oral calcium are necessary to control hyperphosphatemia.

Adult↗
PubMed1993

Long-term (6 months) cross-over comparison of calcium acetate with calcium carbonate as phosphate binder.

A previous short-term study of 10 weeks in 8 patients had shown us that with half the dose of elemental calcium, calcium acetate (CaAc) could control predialysis plasma phosphate (PPO4) as well as calcium carbonate (CaCO3) but that the incidence of hypercalcemia was not decreased. To better appreciate the value of CaAc in comparison to CaCO3, CaAc was given to 28 patients on chronic hemodialysis (6 men, 22 women, age 61 +/- 14 years; dialyzate Ca:1.5 mmol/l) for 6 months to replace CaCO3 at half the dose of elemental calcium (1,235 +/- 521 versus 2,375 +/- 1,470 mg/day). Because of gastrointestinal intolerance, CaAc had to be discontinued in 5 patients after 1-5 months. Magnesium hydroxide [Mg(OH)2] given in 18 of them in association with CaCO3 was discontinued and reintroduced in 6 patients in order to keep PPO4 < 2 mmol/l. Mean dosage of Mg(OH)2 was 2.09 +/- 1.4 g/day with CaCO3 and 0.9 +/- 0.5 with CaAc. Predialysis plasma concentrations of calcium and phosphate were monitored weekly during the 3 months of the control period under CaCO3 and during the 6-month administration of CaAc. Plasma calcium (PCa) was comparable with the 2 treatments (2.47 +/- 0.11 vs. 2.5 +/- 0.10 mmol/l), but PPO4 was significantly lower with CaAc (1.82 +/- 0.26 vs. 1.73 +/- 0.23 mmol/l). Plasma alkaline phosphatase remained constant (122 +/- 66 vs. 122 +/- 70; normal < 170 UI/l) as well as plasma intact PTH (121 +/- 153 vs. 121 +/- 146; normal < 54 pg/ml) and plasma aluminum (0.34 +/- 0.23 vs. 0.32 +/- 0.20 mumol/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1992

Use of alkaline calcium salts as phosphate binder in uremic patients.

In order to prevent aluminum toxicity induced by the association of aluminum phosphate binder with 1 alpha(OH) vitamin D3 derivatives and the use of deferoxamine with its own hazards to diagnose and treat this toxicity, we have shown in 1982 that it was possible to replace the iatrogenic association of aluminum phosphate binder with 1 alpha OH vitamin D derivatives by oral calcium carbonate taken with the meals in order to bind phosphate and correct the negative calcium balance. This led to the disappearance of the crippling aluminic osteomalacia and adynamic bone diseases in our center. The effectiveness of CaCO3 without 1 alpha(OH)D3 derivatives in the control of hyperparathyroidism in dialysis patients has been proven by the appearance in four patients of our dialysis population of an histological idiopathic adynamic bone disease associated with relative hypoparathyroidism, and by the finding that more than 50% of our dialysis population treated by this sole treatment have plasma concentration of intact PTH below twice the upper limit of normal (that is, the threshold above which only significant histological osteitis fibrosa is observed). Besides the compliance problem, the limit of CaCO3 is the occurrence of hypercalcemia which occurs in about 8% of the measurements. Since calcium acetate binds twice as much phosphate for the same dose of elemental calcium as CaCO3, its use has been recommended. However, clinical experience has shown that in spite of the fact that half the dose of calcium element given as acetate does actually control predialysis plasma phosphate as well as CaCO3, the incidence of hypercalcemia is not decreased, probably because calcium availability at the alkaline pH of the intestine is much greater with Ca acetate. When hypercalcemia is frequent (and not explained by autonomized hyperparathyroidism, adynamic bone disease, overtreatment with vitamin D, granulomatosis or neoplasia) it is necessary either to decrease the dose of calcium and complete the necessary binding of phosphate by adding small doses of Mg(OH)2 or Mg carbonate, provided the dialysate Mg is decreased to 0.2 to 0.35 mmol/liter to prevent hypermagnesemia or to decrease the dialysate calcium (DCa) concentration. The decrease of DCa can be made either just when hypercalcemia occurs or on a systemic basis according to the amount of CaCO3 used and to the necessity of associating 1 alpha(OH) vitamin D3 derivatives.(ABSTRACT TRUNCATED AT 400 WORDS)

Aluminum↗
PubMedDate not supplied

Impact of initial blood pressure on the mortality of diabetics undergoing renal replacement therapy.

The aim of this study was to determine the blood pressure (BP) profiles and their impact on mortality among a cohort of uremic diabetics treated by hemodialysis. The studied population includes all type II diabetics starting hemodialysis for end-stage renal disease between 1990 and 1996. There were 221 patients (144 men, 77 women) aged from 37 to 78 years, were all followed until death or December 2003 without any censored data. Survival analysis to identify predictors of death was performed using the actuarial method, Cox proportional model, including systolic, diastolic, mean, and pulse blood pressures (SBP, DBP, MBP, PP). One hundred seventy-eight patients (80.5%) were hypertensive at the start of dialysis. Hypertension preceded the diagnosis of diabetes in eight cases (4.5%); 154 patients (86.5%) received antihypertensive drugs and only 23 (14.9%) had well-controlled hypertension. Our population was subdivided into four groups according to their BP levels at the time of beginning of dialysis; G1 (19.5%): normal BP (SBP [90 to 140] and DBP [60 to 90]); G2 (30.3%): Hypertension stage 1 (SBP [140 to 160] and/or DBP [90 to 100]); G3 (32.1%): hypertension stage 2 (SBP [160 to 180] and/or DBP [100 to 110]); G4 (18.1%) hypertension stage 3 (SBP [180 to 220] and/or DBP [110 to 120]). Mean age and comorbidities were similar among the four groups. During a cumulative follow-up period of 872 patient-years, 191 patients died, representing a rate of 21.9 per 100 patient-years; 20.42% of these deaths occurred during the first 3 months of dialysis. Normotensive patients showed lower survival rates without any significant difference in comparison with those of other hypertensive groups. None of the initial BP parameters (SBP, DBP, PP, MBP, hypertension stages) seemed to influence early or global mortalities, which were rather related to the urgent onset of renal replacement therapy, to age, to serum albumin, and to the score of associated morbidities. We conclude that mortality of our hemodialyzed diabetics was not influenced by the blood pressure parameters recorded at the onset of dialysis.

Adult↗
PubMedDate not supplied

[Dominant polycystic renal disease. Study of 105 cases].

The study concerns 105 cases of dominant polycystic kidney disease. Affected relatives were observed in 65% of patients. The clinical features that leads to diagnosis were lumbar pain in 37.5% of cases, renal failure in 24.6% of cases and hypertension in 15.1% of cases. Hypertension was observed in 46.7% of cases and it seems that its onset is independent of chronic renal failure. Its frequency is of 55.1% when only kidneys were affected and of 21.4% when the liver was affected too. The progression of chronic renal failure is influenced by hypertension.

Adult↗