PubMed Health⌕ Search

Biomedical subjects

P Morinière

Publications and source records attributed to P Morinière.

At least 19 recordsLinked to original sources
PubMed2000

[Renal osteodystrophy (1): invasive and non-invasive diagnosis of its pathologic varieties].

1. Renal osteodystrophy is a general term encompassing all the disturbances of the phosphocalcic metabolism and their associated bone and soft tissue abnormalities, which progressively occur in chronic renal failure. In this article we detail their main histopathological and etiopathogenic aspects as well as their invasive and non invasive diagnostic approach. 2. Osteitis fibrosa is characterized by extensive medullary fibrosis and osteoclastic hyperresorption linked to PTH hypersecretion. 3. Adynamic bone disease is mainly related to iatrogenic oversuppression of PTH secretion. It is favored by aluminum overload which directly inhibits the osteoblasts. It is characterized by a low bone formation rate without primary mineralization defect so that the osteoid seam thickness is normal or low, in contrast to osteomalacia in which by definition osteoid thickness is increased. 4. Osteomalacia is mainly due to aluminum intoxication, vitamin D insufficiency, hypocalcemia, acidosis and exceptionally to hypophosphatemia. 5. The differential diagnosis between the histopathological entities may be oriented on clinical, radiological and biochemical means. Only the bone biopsy can make the diagnosis with certainty. This latter is however necessary for appropriate treatment only in the patients who have been exposed to aluminum and who are symptomatic or hypercalcemic in order to distinguish severe osteitis fibrosa from aluminic bone disease, and more particularly from mixed osteopathy. Indeed surgical parathyroidectomy in patients with mixed osteopathy associating bone hyperremodeling and mineralization defect with inappropriately thick osteoid seam may induce fracturing low turn over aluminic bone disease.

Bone and Bones↗
PubMed2000

[Renal osteodystrophy (2): its treatment in renal insufficiency before dialysis].

1. In the patient with renal insufficiency before dialysis, the phosphocalcic disorders appear insidiously. They are dominated by hyperparathyroidism which will be diagnosed on the initially yearly determination of plasma intact PTH as soon as creatinine clearance decreases below 60 ml/min, eventhough there is still no modification in plasma concentrations of calcium and phosphate. Its diagnosis should lead to initiate the therapeutic measures in order to prevent the irreversible thining of the corticals by endosteal resorption and later the occurrence of histological and radiological osteitis fibrosa favoring fractures. 2. Hyperparathyroidism prevention relies on two main measures: prevention of phosphate retention and hypocalcemia is implemented by progressive phosphate and protein restriction (from 1 g/kg/day when Ccr < 60 ml/min to 0.6 g/kg/day when Ccr < 20 ml/min) and administration of CaCO3 (1.5 g at lunch and dinner to better complex the phosphate) as soon as PTH is above normal; optimal vitamin D repeletion will be implemented by systematic supplementation of native vitamin D or 25OH vitamin D3 in order to bring P25OHD between 30-60 ng/ml (75-150 nmol/l) or more generally around the upper limit of the epidemiologic range of the laboratory; these measures should aim at maintaining plasma intact PTH in its optimal range variable with the degree of renal insufficiency: 0.5-1; 1-2.5 and 2-3 folds the upper limit of normal for creatinine clearance respectively at 60-30; 30-10 and < 10 ml/min. 3. Because of their hyperphosphatemic and hypercalcemic effect, 1 alpha-hydroxylated vitamin D derivatives will be regularly efficient and safe only when non-calcemic non-aluminic phosphate binder will be available and proven to be without side-effects. 4. Instrumental (surgical or by alcohol injection) parathyroidectomy should be considered when plasma intact PTH is > 5 to 7 times the upper limit of normal in the presence of hypercalcemia (> 2.60 mmol/l) and/or hyperphosphatemia (> 1.70 nmol/l) in spite of the above measures, the decision being reinforced by coexistence of bone radiologic abnormalities and metastatic calcifications. 5. Adynamic bone diseases are rare before hemodialysis in the absence of aluminum exposition by the drinking water or the aluminum-phosphate binders. In absence of aluminum it will be prevented by maintaining PTH in its optimal range. 6. Osteomalacia before hemodialysis is mainly due, in the absence of aluminum exposition, to vitamin D deficiency, hypocalcemia and acidosis. It is readily cured by physiological doses of native vitamin D or 25OH vitamin D3 bringing plasma 25 OHD above 16 ng/ml, in association with alkaline salts of calcium and if necessary of sodium bicarbonate.

Chronic Kidney Disease-Mineral and Bone Disorder↗
PubMed2000

[Renal osteodystrophy (3); its treatment in dialysis patients].

The prevalence and the clinical gravity of the various histopathological varieties of renal osteodystrophy in dialysis patients depends on the severity of both the aluminium intoxication and that of hyperparathyroidism. The prevalence of bone pains, fractures and hypercalcemias are the highest in adynamic bone diseases (ABD) with severe aluminium intoxication, then in osteitis fibrosa and mixed osteopathy, in the ABD with moderate aluminium intoxication and rare in the mild lesion in spite of similar moderate aluminium intoxication. In the absence of aluminium intoxication, hypercalcemia and hyperphosphatemia prevalence is higher only when intact PTH is more that 4 times the upper limit of normal. When PTH is between 1 and 2 folds the ULN this prevalence is null and bone mineral density is the highest. 2. The low turnover aluminic bone diseases (osteomalacic or adynamic) will be cured by long term deferoxamine treatment. The hazards of such treatment justify the performance of a bone biopsy to ensure the diagnosis. Their prevention relies on adequate treatment of tapwater and definitive exclusion of long term administration of aluminum phosphate binders. 3. Non aluminic osteomalacia will be treated according to the same guidelines given for the uremic patients before dialysis. 4. Non aluminic adynamic bone disease will be cured by means aiming at stimulating PTH secretion as discontinuing 1 alpha hydroxylated vitamin D derivatives, and, if there is no hyperphosphatemia by discontinuation of calcium supplement. In case of hyperphosphatemia in dialysis patients CaCO3 doses have to be nevertheless increased after the dialysate calcium concentration (DCa) has been decreased in order to induce a negative perdialytic calcium balance for PTH secretion stimulation. In the near future substitution of CaCO3 by non calcemic non aluminic phosphate binders will suffice. 5. Osteitis fibrosa due to hyperparathyroidism will be treated first by securing an optimal vitamin D repletion (bringing plasma 25OH vitamin D around 30 and 60 ng/ml or 75-150 nmol/l) and by correcting hypocalcemia and hyperphosphatemia by CaCO3 at high doses (3-12 g/day) taken with the meals. In case of hypercalcemia dialysate calcium concentration will be decreased to correct it or, in a near future, CaCO3 will be decreased to 3 g/day and hyperphosphatemia will be controlled by non calcemic, non aluminic phosphate binders. When hyperphosphatemia is controlled whereas plasma calcium is normal or low, 1 alpha hydroxylated vitamin D derivatives can be administered. 6. Instrumental parathyroidectomy should be considered when plasma levels of intact PTH remain above 7 folds the upper limit of normal whereas hyperphosphatemia persists and hypercalcemia occurs in order to prevent thining of the corticals and subsequent fracture risk. In case of previous exposition to aluminum, a deferoxamine test and/or a bone biopsy will be performed to decide a long term DFO treatment before the parathyroidectomy in order to prevent the transformation of a mixed osteopathy into an aluminic adynamic bone disease. 7. The difficulty of hyperparathyroidism control in dialysis patients is due to poor compliance to phosphate binders and to irreversible parathyroid hyperplasia with occured before the dialysis stage. This stress the primary importance if its early prevention without iatrogenia by first CaCO3 and vitamin D repletion, as soon as the creatinine clearance decreases below 60 ml/min/1.73 m2.

Aluminum↗
PubMed1999

Is low plasma 25-(OH)vitamin D a major risk factor for hyperparathyroidism and Looser's zones independent of calcitriol?

BACKGROUND: Recent reports suggest that calcitriol might not be the sole active metabolite of vitamin D and that plasma concentrations of 25-(OH)vitamin D (25OHD) are often abnormally low in hemodialysis patients. We have therefore evaluated plasma 25OHD as a risk factor for parathyroid hormone (PTH) hypersecretion and radiological bone disease. We carried out a cross-sectional study during the month of September in an Algerian dialysis center of 113 patients who were not taking supplements of alphacalcidol or calcitriol. METHODS: Plasma 25OHD, calcitriol, PTH, calcium, phosphate, bicarbonate, and aluminum were measured, and x-rays of the hands and pelvis were obtained for evaluation of subperiosteal resorption and Looser's zones. RESULTS: The median plasma 25OHD was 47.5 nmol/liter (range 2.5 to 170.0). Univariate analysis showed that plasma PTH was correlated positively with months on maintenance dialysis and negatively with plasma 25OHD, calcitriol, calcium, bicarbonate and aluminum, but not with that of phosphate. plasma 25OHD was positively correlated with calcium and calcitriol. Using multiple regression analysis, only plasma 25OHD (negative) and the duration on maintenance dialysis (positive) were independently linked to plasma PTH. The prevalence of isolated subperiosteal resorption (ISR) was 34%, and that of the combination of resorption with Looser's zones (CRLZ) was 9%; thus, only 57% of the patients had a normal x-ray appearance. These groups were comparable with regards to age, gender, and duration on dialysis. When the biochemical measurements of the patients with CRLZ were compared with those from patients without radiological lesions, plasma 25OHD was the only parameter to show a statistically significant difference, being significantly lower in the CRLZ group (26 +/- 18 vs. 57 nmol/liter, ANOVA, P < 0.004). Plasma 25OHD was also significantly lower in the ISR group (44, P < 0.05) than in the normal x-ray group, and plasma Ca (P < 0.003) and bicarbonate (P < 0.02) were lower. Logistical analysis showed that the presence of resorption was independently linked only with plasma PTH. Looser's zones and subperiosteal resorption were not seen in patients with plasma 25OHD of more than 40 (Looser's zones) and more than 100 nmol/liter (subperiosteal resorption). The optimal range for intact PTH in hemodialysis patients with mild aluminum overload is 10 to 25 pmol/liter. We found that plasma PTH was inappropriately high only when plasma 25OHD was less than 100 nmol/liter. With a plasma 25OHD of between 100 and 170 nmol/liter, hypercalcemia was present with a plasma PTH of less than 10 pmol/liter in only one case. CONCLUSIONS: This cross sectional study shows that low plasma 25OHD is a major risk factor for hyperparathyroidism and Looser's zones. In dialysis patients, we suggest that the plasma levels of 25OHD are maintained around the upper limit of the reference range of sunny countries.

Adult↗
PubMed1999

[Factors in the progression of renal insufficiency during the 2 years preceding the use of dialysis].

UNLABELLED: The respective contribution of sex, type of nephropathy, degree of proteinuria, blood pressure, protein and sodium daily intake, lipid profile, protidemia, hemoglobinemia, acidosis and CaPO4 product on the rate of renal failure progression is debated. The link between these parameters and the decrease of creatinine clearance, delta Ccr (according to Cockroft) was assessed in uni and multivariate analysis in a population of 49 patients (26 men, 23 women; age 60 +/- 15 years, weight 73 +/- 15 kg) selected out of 173 presently treated hemodialysis patients on the basis of availability of a quarterly follow-up for two years before starting dialysis. The patients were advised a moderate protein and salt restriction which could be retrospectively assessed (on urinary excretion of urea and sodium) at respectively 0.82 g/kg/day and 6.5 g/day. The two years delta Ccr was 14 +/- 14 ml/min. It was not different in men and women (specially when expressed in % of initial value). This decrease in Ccr was neither significantly different in glomerular disease (17 +/- 8, n = 14), diabetic nephropathy (12 +/- 6, n = 7), nephroangiosclerosis (15 +/- 8, n = 5), interstitial nephritis (12 +/- 10, n = 14), and PKD (11 +/- 12, n = 9). Patients with antihypertensive drugs (n = 42) had a faster progression than those without drugs (n = 7): delta Ccr = 15 +/- 14 vs 7 +/- 7 ml/min (p < 0.05) in spite of comparable blood pressure but with higher proteinuria. Linear regression of delta Ccr with the initial and two year averaged values of the quantitative parameters showed a significant positive link for both values with cholesterol, hemoglobin and proteinuria and a negative one with protidemia. A positive link was observed with the initial value of bicarbonate and the two year mean of diastolic and mean blood pressures. No link at all was observed with urea and Na excretion, CaPO4 product and triglycerides. Multiple regression disclosed a significant link only for protidemia (negative with both initial and two years averaged value), diastolic BP (only for the two year averaged value and hemoglobinemia (for the initial value). When the patients were classified according to a threshold value of their protidemia, DBP, hemoglobinemia, and cholesterolemia those with the combination of two risk factors of progression (pro-tidemia < 66 g/l, DBP > or = 90 mmHg, hemoglobinemia > 11 g/dl, proteinuria > 3g/d, CT > 5 mmol/l) had a significantly greater decrease of Ccr than those with the three other combinations at the exception of the association of low protidemia with DBP. CONCLUSION: 1. diastolic hypertension and low protidemia are the two most important factors predicting progression of renal failure; 2. a predictive synergy was furthermore pointed out between on one hand low protidemia and diastolic hypertension and on the other hand proteinuria and cholesterol; 3. on the contrary, anemia attenuates progression linked to low protidemia, diastolic hypertension, proteinuria and high cholesterol.

Acidosis↗
PubMed1999

[Role of the time of administration of calcium carbonate (before or during mealtime) in the control of hyperphosphatemia in patients on maintenance hemodialysis].

UNLABELLED: A study has claimed that at equal elemental calcium dose, CaCO3 was not less but equally efficient in controlling predialysis hyperphosphatemia as calcium acetate provided both calcium salts were given five minutes before the meals instead of during the meals because the higher acidity of a fasting gastric juice would allow a better dissociation of CaCO3. To examine the point that CaCO3 is more efficient if it is taken five minutes before compared to during the meal, we performed a two month randomised cross-over trial in twelve reliable and stable patients maintained on chronic hemodialysis while their treatment and diet remained constant. Comparison of the plasma concentrations measured during the two modes of administration showed no significant difference in creatinine, urea, bicarbonate, intact-PTH. Mean (+/- SD) plasma PO4 was significantly higher (1.93 +/- 0.50 versus 1.72 +/- 0.40 mmol/l; p = 0.02) whereas corrected plasma Ca was significantly lower (2.30 +/- 0.15 versus 2.38 +/- 0.17 mmol/l; p = 0.01) when CaCO3 was given before the meals than during the meals. CONCLUSIONS: a) administration of CaCO3 before the meal decreases its efficiency in controlling hyperphosphatemia since plasma PO4 was actually slightly higher with this timing of administration; b) administration of CaCO3 before the meal is associated with significantly lower plasma corrected calcium suggesting a smaller absorption of calcium which may be an advantage but only in hypercalcemic patients; c) there is no reason other than the prevention of its hypercalcemic effect to recommend the administration of CaCO3 just before the meals than during the meals.

Aged↗
PubMed1999

[Inhibition of gastric secretion by omeprazole and efficacy of calcium carbonate in the control of hyperphosphatemia in patients on maintenance hemodialysis].

UNLABELLED: Apparent contradictions exist in the literature regarding the effect of gastric secretion inhibition on phosphatemia. In healthy adults, omeprazole has been reported to prevent the increase of plasma phosphate or of phosphaturia observed after an acute phosphate load suggesting an inhibition of phosphate absorption. In patients on chronic hemodialysis their hyperphosphatemia is associated to gastric hypersecretion but the inhibition of this latter by ranitidine in patients taking CaCO3 has been reported to increase their plasma phosphate. Because of this contradiction, we have made an open cross-over study in 16 stable and compliant patients in chronic hemodialysis taking a mean daily dose of 9.4 +/- 4 g of CaCO3 and compared their predialysis plasma concentration of phosphate, calcium, protides, bicarbonates, intact PTH, urea and creatine for two successive periods of two months without or with 20 mg of omeprazole. Plasma phosphate did not increased significantly with omeprazole (from 1.80 +/- 0.38 to 1.89 +/- 0.42 mmol/l) whereas plasma corrected calcium significantly decreased from 2.41 +/- 0.18 to 2.36 +/- 0.16 mmol/l (p = 0.04) and plasma bicarbonate decreased significantly from 26.7 +/- 3.5 to 25.7 +/- 3.1 mmol/l (p < 0.05). No significant change was observed in plasma creatine and urea suggesting stability of dialysis efficiency and of protein and therefore phosphate intake. CONCLUSION: These data do not support that CaCO3 efficiency as phosphate binder is decreased with inhibition of the gastric secretion by omeprazole.

Adult↗
PubMed1999

[Hemodialysis and strongyloidiasis: a presumed cause of eosinophilia able to mask the other].

The authors report a case of recurrent strongyloidiasis in a former French soldier of the Indochina colonial war (1946-54). Strongyloidiasis was associated with inaugural renal failure (acute steroid-resistant interstitial-type), requiring permanent hemodialysis. Despite antiparasitic treatment, relapse with digestive and pulmonary symptoms occurred 10 years later, following chronic eosinophilia. This observation emphasises that in dialysed subjects, eosinophilia should always stimulate a search for parasitic etiologies before incriminating dialysis-material allergy. Strongyloidiasis is a self-perpetuating helminthiasis whose distribution area is far greater than the intertropical zone. It can be completely asymptomatic, appear as late digestive complications and be responsible for bacteraemic peaks with septic visceral localizations. It causes a chronic oscillating eosinophilia. Diagnosis is usually performed by iterative stool examinations by Baermann technique in order to detect Strongyloides stercoralis rhabditoid larvae. In dialysed patients with unexplained eosinophilia awaiting renal transplant, the options of systematic thiabendazole (50 mg/kg) or ivermectine (0.2 mg/kg) single-dose to overcame the risk of disseminated strongyloidiasis induced by immunosuppressive post-transplantation therapy could be debated.

Aged↗
PubMed1998

[Percutaneous recanalization of proximal venous thromboses in chronic hemodialysis patients].

Occlusion of the proximal vein in chronic hemodialysis patients results in vein hypertension and a "swollen arm". The usual treatment for this "swollen arm" consists in closing up the fistula and making another access on the contralateral member. But this is not always possible and, with some patients, recanalization is the only solution. We have performed 4 recanalizations successfully: 2 accesses remain permeable after 10 and 24 months, another patient needed to be fitted with two endoprosthesis just after recanalization and access, in his case, remained permeable until he died of intestinal ischemic syndrome six months later. The fourth patient presented a reocclusion two months later but could not be reoperated on because of bad general state of health. An attempt to perform recanalization on a fifth patient was a failure. Such results show that recanalization of a thrombosed proximal vein is worth attempting before closing access for good.

Adult↗
PubMed1997

Percutaneous recanalization of occlusion of central and proximal veins in chronic hemodialysis. Technical note.

Occlusion of the central and proximal veins in chronic hemodialysis patients results in considerable edema of the arm of the vascular access that is unable to drain normally. This is a formidable problem because it is very often necessary to close the vascular access, which is sometimes the last available one. To avoid resorting to this disastrous solution, recanalization of the occluded vein by percutaneous recanalization followed by endoluminal angioplasty was successfully performed in five patients (4 innominate veins and one axillary vein). Immediate failure occurred in a sixth patient, and delayed failure after two months of patency (innominate vein) in another patient for whom there had been no systematic stent placement. Recanalization was still patent in four other patients at 3, 6, 12 and 26 months. These results are an encouragement to attempt percutaneous recanalization by angioplasty of occluded central veins because, when successful, this technique makes it possible to preserve the vascular access and to avoid onerous surgery. We believe that this technique should therefore become better known.

Adult↗
PubMed1997

Invasive versus non-invasive diagnosis of renal bone disease.

At present, bone histomorphometry remains the gold standard for the diagnosis of the various types of renal bone disease. In the search for a non-invasive method of diagnosis, biochemical serum markers of bone remodelling, in addition to serum intact parathyroid hormone and aluminium determinations, have been proposed as the most reliable tools and are at present widely used in clinical practice. Their respective diagnostic values, as separate items and in combined analysis, are thoroughly discussed in the present review.

Aluminum↗
PubMed1997

[Relative depletion in native vitamin D: a potential risk factor in Algerian hemodialysis patients with radiological evidence of hyperparathyroidism and osteomalacia independent of calcitriolemia].

Looser striae on the ischio-pubian branches and subperiosteal resorption of the phalanges were looked for in 113 chronic hemodialysis patients at the University Hospital of Annaba (Algeria) and were found in respectively 14 and 48 patients. Comparison of patients with and without radiological complications showed no significant difference in their age, sex ratio, nature of initial kidney disease and duration on dialysis. The patients with Looser striae had lower plasma levels of 25OHD3 than those without striae, whereas all other plasma parameters were similar. The plasma concentrations of intact PTH were higher in patients with resorption; these patients had lower plasma concentrations of calcium, bicarbonate, aluminum and 25OHD3 but similar plasma concentrations of phosphate and 1,25(OH)2D3. Multivariate analysis showed that PTH concentrations were independently linked only to plasma 25OHD3 (negatively) and duration on dialysis (positively). The results of this transversal study are in agreement with the well established pathophysiological roles of PTH hypersecretion, hypocalcemia and acidosis in the appearance of radiological hyperparathyroidism in hemodialysis patients. Furthermore they suggest that a relative native vitamin D deficiency may have a calcitriol independent role in favoring the occurrence of both osteitis fibrosa and osteomalacia.

Adult↗