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In patients presenting with anti-glomerular basement membrane (GBM) disease with advanced isolated kidney involvement, the benefit of intensive therapy remains controversial due to adverse events, particularly infection. We aim to describe the burden of severe infections (SI) (requiring hospitalization or intravenous antibiotics) and identify predictive factors of SI in a large cohort of patients with anti-GBM disease. Among the 201 patients (median [IQR] age, 53 [30&ndash, 71] years) included, 74 had pulmonary involvement and 127 isolated glomerulonephritis. A total of 161 SI occurred in 116 patients during the first year after diagnosis. These infections occurred during the early stage of care (median [IQR] time, 13 [8&ndash, 19] days after diagnosis) with mainly pulmonary (45%), catheter-associated bacteremia (22%) and urinary tract (21%) infections. In multivariable analysis, positive ANCA ([HR] 1.62, 95% [95% CI] 1.07&ndash, 2.44], p = 0.02) and age at diagnosis (HR [95% CI] 1.10 [1.00&ndash, 1.21], p = 0.047) remained independently associated with SI. Age-adjusted severe infection during the first three months was associated with an increased three-year mortality rate (HR [95% CI] 3.13 [1.24&ndash, 7.88], p = 0.01). Thus, SI is a common early complication in anti-GBM disease, particularly in the elderly and those with positive anti-neutrophil cytoplasmic antibodies (ANCA). No significant association was observed between immunosuppressive strategy and occurrence of SI.

Resume Objectif Rapporter une serie d’hematomes surrenaliens spontanes sous Synacthene® et definir la prise en charge a court, moyen et long terme. Patients et methodes De janvier 2000 a decembre 2008, cinq patients (quatre hommes et une femme), d’âge moyen 47 ans, ont ete pris en charge pour hematomes surrenaliens spontanes chez des patients traites par Synacthene® pour lombosciatalgie documentee depuis 72 heures. La prise en charge associait une evaluation clinique, endocrinienne et radiologique. Resultats Quatre patients ont ete surveilles et un seul a necessite une prise en charge chirurgicale. Aucune tumeur surrenalienne n’a ete diagnostiquee lors du suivi avec un recul de deux ans (un a quatre). Deux patients etaient atteints d’un syndrome des antiphospholipides. Conclusion Les hematomes surrenaliens spontanes sont une pathologie rare, dont la prise en charge doit d’abord etre une surveillance clinique, biologique et morphologique. Le bilan endocrinien, immunologique et radiologique systematique doit rechercher une tumeur surrenalienne secretante ou non, et un syndrome des antiphospholipides.

Increased arterial stiffness and vascular calcification have been recognized as important predictors of cardiovascular mortality in patients with chronic kidney disease.In order to examine the precise temporal link between aortic stiffness and cardiovascular risk at the earliest stages of chronic kidney disease, we studied a cohort of 150 patients with chronic kidney disease (52 stage 2/3 patients, 51 stage 4/5 patients and 47 stage 5D patients). Each patient underwent a plain, lateral lumbar radiograph and an abdominal and thoracic multislice spiral computer tomography scan in order to identify and quantify aortic and coronary calcifications. Pulse wave velocity was used as a measure of arterial stiffness.Regardless of the disease stage, patients with chronic kidney disease had higher adjusted pulse wave velocity than controls with preserved renal function (14.6 +/- 3.8 vs. 10.7 +/- 1.7 m/s, respectively; P0.0001). Regarding aortic calcification, there was a gradual but significant rise in later chronic kidney disease stages. A similar trend was found for coronary calcification. In a multivariate analysis only age, mean arterial pressure, diabetes and the aortic calcification score were independent determinants of higher pulse wave velocity.We found that both vascular stiffness and vascular calcification appear early in patients with chronic kidney disease, but only vascular calcification worsens as the disease progresses. The increase of vascular stiffness in adult patients with chronic kidney disease seems to be more related to age, systolic blood pressure, diabetes and vascular calcification than to uremic toxicity.

The objective of this study were (1) to evaluate the prevalence of anti-annexin II antibodies in patients with various autoimmune diseases and antiphospholipid syndrome and (2) to correlate anti-annexin II antibodies with anti-phospholipid antibodies. Anti-annexin II antibodies and anti-phospholipid were detected, using an enzyme-linked immunosorbent assay, in the serum of patients with primary antiphospholipid syndrome (n = 16), systemic lupus erythematosus (n = 53), primary Sjogren syndrome (n = 71), systemic sclerosis (n = 17), systemic vasculitis (n = 18), and rheumatoid arthritis (n = 119). Healthy blood donors (n = 99) were used as controls. Anti-annexin II antibodies were significantly more prevalent in patients with connective tissue diseases (8.5%), especially antiphospholipid syndrome (14.8%) and rheumatoid arthritis (10%), than in controls (2%). An inverse correlation was observed between anti-annexin II antibodies and antiphospholipid antibodies. Annexin II can be recognized by antibodies in serum from patients with systemic autoimmune disorders. Further studies are required to determine the clinical significance of anti-annexin II antibodies in rheumatoid arthritis and to determine their diagnostic value in discriminating clinical subgroups of patients with antiphospholipid syndrome.

AimsTo evaluate vascular expression of annexin A2 (ANXA2) and its subunit S100A10 in lupus nephritis (LN).MethodsThe present histological study included 14 patients with LN and 11 controls (patients with non-lupus kidney diseases). Kidney biopsies from patients with lupus were scored for lupus glomerulonephritis (according to the International Society of Nephrology/Renal Pathology Society 2003 classification) and vascular lesions (such as microthrombi and antiphospholipid syndrome nephropathy (APSN)). ANXA2 and S100A10 expression in glomerular and peritubular capillaries was evaluated by immunohistochemistry on tissue sections. The staining intensity score ranged from 0 (no expression) to 4 (intense expression).ResultsIn patients with LN, the median age (range) at first kidney biopsy was 36 (18–49). Vascular lesions were observed in six patients (including two with APSN). We observed intense expression of ANXA2 in glomerular and peritubular capillaries while expression of S100A10 was weaker. However, one of the patients with APSN showed strong S100A10 expression. Patients with LN and controls differed significantly in terms of S100A10 expression in peritubular capillaries. We also observed a statistical difference between patients who had LN with renal vascular lesions and those without renal vascular lesions in terms of ANXA2 expression in peritubular capillaries.ConclusionsThe presence of vascular lesions in LN appears to be associated with significant differences in the vascular expression of ANXA2. Vascular expression of ANXA2 was somewhat higher in LN. Vascular expression of S100A10 was somewhat lower in LN (except one of the two patients with APSN). Further studies of ANXA2's putative value as a biomarker of active LN or of vascular lesions in LN are required.

Resume Introduction. – Le purpura rhumatoide est une des vascularites systemiques les plus frequentes. L’atteinte musculaire est rare, en particulier chez l’adulte et sa physiopathologie mal elucidee. Nous rapportons une observation au cours de laquelle les donnees histologiques et radiologiques mettent en evidence un hematome intramusculaire secondaire a une vascularite leucocytoclasique revele par une deglobulisation profonde. Exegese. – Un homme âge de 68 ans, traite par antivitamine K pour une maladie thromboembolique veineuse recidivante, presente un purpura rhumatoide caracterise par une glomerulonephrite segmentaire a depots d’immunoglobulines A, une vascularite necrosante cutanee et des douleurs abdominales. Les lesions dermatologiques et digestives evoluent favorablement sous corticotherapie, mais on constate une deglobulisation severe au onzieme jour de traitement rapidement rattachee a de volumineux hematomes intramusculaires bilateraux des membres inferieurs. L’examen histologique confirme que la vascularite est responsable des suffusions hemorragiques. L’echographie et l’imagerie par resonance magnetique ont permis de mieux preciser morphologiquement l’etendue des hematomes. Conclusion. – Les hematomes intramusculaires sont exceptionnels au cours du purpura rhumatoide. Ils sont la consequence d’une vascularite a complexes immuns dont le traitement est difficile. Dans notre observation, la corticotherapie a forte dose a ete insuffisante a en juguler l’evolution.

Resume Introduction Le syndrome primaire des antiphospholipides est une cause tres rare d’hemorragie surrenalienne. Observation Un patient de 51 ans a eu une hemorragie surrenalienne unilaterale, favorisee par la prescription de Synacthene® pendant les 4 jours precedents. Il n’avait pas d’insuffisance surrenalienne, mais le bilan immunologique a revele la presence d’anticorps anti-phospholipides. Apres un recul de 2 ans, la surveillance des surrenales n’a montre ni tumeur sous-jacente, ni insuffisance endocrinienne. Commentaires L’atteinte surrenalienne est bien decrite dans le syndrome des anti-phospholipides et peut se presenter sous la forme d’une insuffisance surrenalienne en cas d’hemorragies bilaterales parfois seulement microscopiques. De plus, Synacthene® est connu pour pouvoir declencher des hemorragies surrenaliennes, mais cette complication reste rare. Par ailleurs, toute hemorragie surrenalienne unilaterale necessite une surveillance ulterieure de plusieurs mois a plusieurs annees pour eliminer une tumeur sous-jacente et pour controler l’absence de survenue d’une insuffisance surrenalienne si l’atteinte est bilaterale.

Resume Introduction Le mycophenolate de sodium (Myfortic ® ) est une formulation gastroresistante de l’acide mycophenolique utilise comme agent immunosuppresseur. Nous rapportons le cas d’une femme ayant eu des ulcerations buccales multiples associees a la prise de mycophenolate de sodium avec recidive des ulcerations lors de la reintroduction de ce traitement. Observation Il s’agissait d’une femme de 26 ans suivie depuis 1993 pour un lupus erythemateux dissemine, traite initialement par corticotherapie et mycophenolate mofetil (Cellcept ® ). Ce traitement avait ete arrete en raison de la survenue d’un zona plurimetamerique et d’une leucopenie. Elle consultait pour des ulcerations buccales invalidantes survenues 15 jours apres l’introduction d’un traitement par mycophenolate de sodium. Il n’y avait aucun argument pour une infection opportuniste ou une poussee lupique. L’arret du medicament permettait une disparition des lesions. La reintroduction de mycophenolate de sodium quelques semaines plus tard entrainait une recidive des ulcerations buccales, regressant 72 heures apres l’arret definitif du medicament. Discussion Le mycophenolate de sodium est une formulation recente, gastroresistante de l’acide mycophenolique, developpee pour reduire les effets indesirables digestifs du mycophenolate mofetil. Des cas isoles d’ulcerations buccales apres prise de mycophenolate mofetil ont ete rapportes. Une toxicite directe du medicament etait alors evoquee. Cet effet indesirable n’avait jamais ete decrit avec le mycophenolate de sodium. Dans notre observation, le fait que la malade avait prealablement pris un traitement par mycophenolate mofetil, sans toxicite muqueuse, alors qu’elle etait exposee a une concentration en acide mycophenolique au moins equivalente, est d’autant plus particulier.

We report a case of a retroperitoneal hematoma occurring in a patient under anticoagulation therapy for deep-venous thrombosis and presenting as an anuric acute renal failure. A coexisting polycythemia vera led to misdiagnosis that could have been life-threatening. A woman, known for polycythemia vera and a single functioning right kidney, was admitted with mild abdominal pain in a context of recent deep venous thrombosis under low-molecular weight heparin. Clinical examination revealed hepatomegaly associated with polycythemia vera. Biochemical evaluation disclosed an acute renal failure, and renal ultrasonography showed no dilation of the renal pelvis. Retroperitoneal hematoma resulted in shock, progressive anemia and obstructive renal failure, related to renal pelvic compression. A right renal indwelling catheter was introduced to restore urine flow after one hemodialysis session, and an inferior vena cava filter was placed because of anti-coagulation contra-indication. However, pulmonary embolism occurred, so that oral anticoagulants were introduced. The hematoma resorbed spontaneously, and a year after this episode, the patient is still alive and well. Retroperitoneal hematoma is a rare cause of obstructive acute renal failure and a life-threatening complication of anti-coagulation therapy.

Renal involvement in sarcoidosis displays a wide range of manifestations, and kidney dysfunction may involve all three mechanisms of renal failure. We report a new case of systemic sarcoidosis presenting as a severe renal failure due to hypercalcemia, sarcoidosis-related bilateral nephrolithiasis and granulomatous interstitial nephritis. A prostate adenocarcinoma was also diagnosed, but has to be regarded as an unrelated disease.

In normal pregnancy, cross-sectional clinical data do not consistently show plasma ANF concentration differences between early pregnancy and the nonpregnant state. Sequential data in the baboon (but not in rat) show a significant decrease in plasma ANF concentration and in cardiac filling pressures in early pregnancy. The latter data support the view that pregnancy is an underfill state secondary to a primary vasodilatation. Cross-sectional and longitudinal studies in normal pregnancy in humans show that plasma ANF levels tend rise to values that are, in the third trimester, higher than in the nonpregnant state. However, late postpartum sequential data (1.5–3 months) in humans do now show a significant drop in plasma ANF concentrations, suggesting that plasma ANF is not actually increased in normal pregnancy. In the baboon (but not in the rat) there is a steady rise in plasma ANF levels to values that are significantly higher in third trimester than before pregnancy. These data suggest that in human pregnancy, in contrast with the baboon, the plasma volume expansion induced by normal pregnancy is not sensed as such by the atria probably because of an isopressive adaptation of plasma volume to an enlarged vascular bed. However, acute decrease or increase of venous return induced by low sodium diet, changing position or infusion of isotonic saline are sensed as such by the atria in normal pregnancy as in the nonpregnant state. In humans and rats, a steady rise in plasma ANF concentration is observed during the first few days after delivery suggesting that at this time the atria sense an effective hypervolemia; the latter occurring through a decrease in the functional size of the intravascular compartment owing to the elimination of the placenta as well as by the autotransfusion carried out by the emptied uterus. The resulting increase in central venous pressure may stimulate ANF release that, together with a decrease in renin and aldosterone secretion, may thus contribute to the diuretic crisis observed after delivery. In pregnancy-induced hypertension, plasma ANF levels are usually increased but may remain normal in mild hypertension. In preeclampsia, plasma ANF concentration is more consistently increased, specially in the severe form. Plasma ANF decreases to normal levels after delivery when hypertension has disappeared. Plasma ANF concentration is directly correlated to blood pressure. A deficiency in ANF secretion can not, therefore, be the primary cause of pregnancy-induced hypertension or preeclampsia. On the contrary, ANF may play a compensatory role preventing further increase of blood pressure. However, because of the suppressive effect of ANF on renin and aldosterone secretion and by promoting a shift of the plasma fluid into the interstitial space, ANF elevation in preeclampsia may actually contribute to worsen the hypovolemia and explain the paradoxical association of hypovolemia with the hypostimulation of the renin–aldosterone system. The mechanism underlying the increased ANF secretion in preeclampsia is not clear since cardiac filling pressures in untreated preeclampsia are decreased and hence increased ANF release through atrial stretch seems unlikely. It is possible that neuroendocrine mechanisms yet to be identified are responsible for this observation.Key words: atrial natriuretic factor, pregnancy, preeclampsia, pregnancy-induced hypertension.

Drug rash with eosinophilia and systemic symptoms (DRESS) is a severe cutaneous drug reaction with a long duration of eruption and serious organ involvement. The mortality rate has been estimated at about 10%. Aromatic anticonvulsants, sulphamides, minocycline and more rarely carbamazepine are the principal responsible drugs. We report the first case of chlorambucil-induced DRESS syndrome in a 70-year-old man recently diagnosed with chronic lymphocytic leukaemia. He developed recurrent skin rash, fever, hypereosinophilia, and acute renal failure after rechallenge with chlorambucil. The condition improved slowly after stopping medication and systemic steroids. Prompt recognition of a chlorambucil drug reaction is essential in patients receiving chemotherapy.

Renal osteodystrophy becomes clinically significant when the following features are present: clinical symptoms (pain, muscle weakness, pruritus), radiological signs (subperiosteal erosions, osteopenia, fractures or pseudofractures, slipped epiphysis with coxa vara or genu valgum in children, metastatic calcification) and marked plasma abnormalities, particularly uncontrollable hyperphosphatemia. Clinically significant bone disease is not usually seen in adults until they have been on dialysis for several years but may be seen earlier (even before dialysis has been started) in children. Such bone disease may be due either to hyperparathyroidism or to aluminum (Al) bone disease. In favor of hyperparathyroidism are the following features (1, 2): rarity of pain and fractures, greater elevation of alkaline phosphatase, greater elevation of parathyroid hormone (PTH) plasma concentration and lower basal plasma concentration of Al (

Cholesterol microembolism may produce a variety of signs and symptoms mimicking systemic vasculitis. We report five patients with the syndrome of multiple cholesterol emboli suggesting a polyarteritis nodosa (PAN): four patients out of five presented the international criteria for PAN and only the biopsy or ocular fundi permitted the diagnosis, showing cholesterol microemboli.

Neurologic and cardiac involvements are uncommon in Relapsing Polychondritis. Moreover frontiere forms with Behcet's disease are very rare and they are called MAGIC syndrome. We describe a case of a 43 year-old patient with severe trivalvular heart involvement and auriculoventricular heart block. Only one case was previously reported. Hence physical examination revealed a pyramidal syndrome and a weak palsy of the VIIth cranial nerve. The performed pathergic test was positive suggesting MAGIC syndrome diagnosis.

During the following of 300 cases of Systemic Necrotizing Vasculitis, between November 1980 and January 1992, the authors describe the association of a crescentic glomerulonephritis and Systemic Necrotizing Vasculitis (Kussmaul-Maier disease) ; a rare association never described before.

Nineteen patients who had been on maintenance hemodialysis for 33 months ,(± 13) with conditions optimized to prevent renal osteodystrophy (3 times week, a dialysate calcium of 7.0 mg/dl, oral calcium supplement and aluminum hydroxide to correct hypocalcemia and hyperphosphatemia, but with no vitamin D supplement) were treated with 1-alpha-HCC and 25-HCC (daily dosage of 1 and 50 μg respectively) for one year. This treatment was stopped every time the predialytic plasma levels of calcium and/or phosphate rose above 11.0 and 7.0 mg/di respectively in spite of an Increase in the prescribed dosage of aluminum hydroxide, and was resumed after normalization of plasma calcium and/or phosphate at reduced doses. The effect of vitamin D therapy was mainly assessed by histomorphometric evaluation of bone biopsies performed before initiating the treatment and 6 to 12 months later. Initially, no patient had histological evidence of osteomalacia as assessed by osteoid thickness Index, in spite of low plasma 25-HCC levels in 10 15 patients. 14 19 had hyperparathyroidism with extended active resorption surfaces (ARS) which were positively correlated with plasma PTH levels. During treatment, no patient developed osteomatacia. ARS Improved in 6 patients, worsened in 7 and remained unchanged In the 6 others, including 3 with initially normal values. When comparing worsened versus Improved patients, the aggravation of osteltis fibrosa was associated with increasing levels of plasma phosphate and pPTH. It is concluded that addition of vitamin D derivatives to optimal dialysis condlitions seems of questionable value because : 1) optimal dialysis conditions alone adequately prevent osteomalacla and most radiological osteitis fibrosa ; 2) vitamin D metabolite therapy may make plasma phosphate control more difficult which contributes to worsening of residual hyperparathyrodism.

We have measured simultaneously plasma renin activity (PRA), aldosterone and catecholamines in the plasma of 3 groups of pregnant women after the 20th week: group 1 of 16 normotensive controls, group II of 17 women with rest responding hypertension (RRH), group III of 18 women with permanent hypertension (PIH). All the patients were ambulatory on a normal salt diet. PRA was significantly higher in the RRH than in the control and PIH groups (15,8 +/- 2,3ng/ml/l versus 6,7 +/- 0,5 and 8,9 +/- 0,9 respectively). Plasma epinephrine (PE) and norepinephrine (PNE) were significantly higher in the PIH than in the control and RRH groups (respectively 135 +/- 28 pg/ml versus 56 +/- 13 and 63 +/- 17 for PE and 387 +/- 91 versus 206 +/- 32 and 200 +/- 47 pg/ml for PNE). In the PIH group there was a negative correlation between PRA and blood uric acid. It is concluded that the adrenic system is activated in PIH whereas the renin angiotensin system is activated in RRH of pregnancy.

Plasma immunoreactive atrial natriuretic factor 99-126 (ir ANF), plasma volume, plasma renin activity, and plasma aldosterone were measured during pregnancy in 14 normotensive nonpregnant women, 15 normotensive pregnant women, 35 patients with pregnancy-induced hypertension (PIH), and in ten patients with preeclampsia (PE). Repeated measurements were carried out 2 months after delivery in a subgroup of the same patients. The plasma levels of ANF were found to be higher in pregnant normotensive women than in nonpregnant normotensive women, but the decrease of plasma ANF 2 months after delivery was not significant on the basis of seven paired data, so that it cannot presently be stated with certainty that pregnancy per se stimulates ANF secretion. Still higher levels of ANF were found in PIH and, especially, in PE. A positive correlation was found in the pooled population of normotensive and hypertensive pregnant women between plasma ANF and mean arterial pressure. A greater decrease of plasma ANF was found after delivery in the hypertensive patients than in the normotensive controls. This excludes an absolute deficiency of ANF secretion in the pathogenesis of hypertension. These findings suggest a compensatory role of ANF in the prevention of blood pressure increase. Plasma renin activity (PRA) and plasma aldosterone concentrations were higher in normotensive pregnant women than in normotensive nonpregnant women. Compared to normal pregnancy, plasma volume was decreased in PIH (-17%) and in PE (-25%), whereas PRA was less increased in both groups and plasma aldosterone concentration was less increased only in the PE group. The simultaneous high levels of plasma ANF may explain this inappropriate hypostimulation of renin secretion by hypovolemia in these hypertensive states.

1. The technique of combined intravenous renal arteriography and pyelography is described and results in 848 hypertensive patients are reported. 2. The procedure was tolerated better than Seldinger arteriography and the diagnostic accuracy for renal artery stenosis was 95%. 3. The prevalence of renovascular disease was 7%. 4. Cost-effectiveness calculations favour combined intravenous arteriography and pyelography rather than the usual approach based on assessment of the indications for Seldinger arteriography from clinical and urographic signs.

1. In four patients, whose hypertension was not controlled (supine blood pressure > 150–90 mmHg) by addition of 5 mg/day of prazosin to previous treatment (diuretics and β-blockers), clonidine (150–450 μg/day) led to control of hypertension in three cases. 2. In ten patients whose hypertension was not controlled by a treatment including clonidine (300–450 μg/day), the progressive addition of prazosin to a maximal dose of 4–22.5 mg/day led to control of hypertension in nine cases (mean supine blood pressure decreased from 174–102 to 144–88 mmHg). 3. In 13 hospitalized patients, clonidine was abruptly interrupted whereas prazosin was continued. Mean blood pressure (± sem) rose from 145 ± 1/85 ± 2 to 169 ± 7/104 ± 5 mmHg 48 h after clonidine withdrawal whereas plasma noradrenaline and adrenaline rose from 328 to 758 pg/ml and from 75 to 137 pg/ml. No subjective symptoms were noted. There was a negative correlation between blood pressure increase and the dose of prazosin. 4. It is concluded that (a) there is no antagonism between clonidine and prazosin in their antihypertensive action in man when used at usual clinical doses, (b) a protective effect of prazosin against an eventual clonidine withdrawal syndrome is suggested by the negative correlation between blood pressure increase and the dose of prazosin.

To evaluate the adequacy of simple calcium restriction for patients with idiopathic calcium stones the effect of 5 days of calcium restriction without oxalate restriction on renal excretion of calcium and oxalate, and the corresponding probability of stones were assessed in 50 controls and 48 patients. Renal excretion of calcium decreased and that of oxalate increased significantly in all groups but the importance of the changes was critically dependent upon the underlying pathophysiological condition. The probability of stones decreased only in patients with absorptive hypercalciuria type II owing to the usual excessive calcium intake and increased in those with absorptive hypercalciuria type I and renal hypercalciuria, which are associated with true hyperabsorption of calcium and represent the 2 forms of idiopathic hypercalciuria. We believe that simple calcium restriction is beneficial for patients with idiopathic calculi only when the hypercalciuria is caused by exaggerated intake of calcium, since it increases the probability of stones in patients with idiopathic hypercalciuria. Calcium restriction always is associated with an increase in oxalate excretion, suggesting that simultaneous oxalate restriction should be added in all cases to decrease the probability of stones.

Magnesium accounts for about 20% of the total inhibitory activity of urine with respect to calcium stone formation1. Magnesium depletion has been shown to cause calcification in the proximal tubule cells and in the tubular lumen in rats2 and to be responsible for nephrocalcinosis in children. Based on these data, magnesium deficiency has been suspected as a factor in the pathogenesis of calcium stone formation although it has been observed only rarely3. Moreover, the data on magnesium excretion in stone formers are conflicting, and may even be normal4 or increased5. These discrepancies may be explained by the fact that dietary calcium and calcium excretion were not taken into account, despite the fact that in normal individuals magnesium excretion is directly correlated with calcium excretion6. For these reasons it seemed interesting to us to study magnesium metabolism in various groups of idiopathic calcium stone-formers classified according to calcium excretion during a controlled calcium diet.

Reports concerning the effects of Cimetidine on parathyroid hormone levels in primary hyperparathyroidism (1–4) and in secondary hyperparathyroidism of renal failure (5–8) are increasing in number, but lead to disagreeing conclusions. These discrepancies are unclear and could be possibly explained by: 1) a variable compliance to treatment, since no measurement of plasma levels of Cimetidine has been made in these reports, 2) differences in specificity of parathyroid hormone immunoassays, since, in a studied group of hemodialysed patients, the lowering effect of Cimetidine on parathyroid hormone levels previously observed using a carboxyterminal antiserum (5), was not confirmed when the same samples were assayed a second time using an aminoterminal antiserum (9). It has also been suggested (8) that Cimetidine could act on the metabolic fate of circulating parathyroid hormone rather than on its secretion, thus explaining differences between results derived from either carboxy or aminoterminal immunoassays.

Secondary hyperparathyroidism is a constant and not yet resolved complication of chronic renal failure. Current therapeutic methods for parathyroid gland suppression in uremic patients are mainly based on the use of phosphate binders, oral calcium supplementation and eventually on administration of vitamin D metabolites (1). Since these measures are not always quite successful, it is interesting to evaluate other measures suggested by recent physiological data on the regulation of PTH secretion. As a matter of fact, beside the circulating levels of ionized calcium and magnesium (2), PTH secretion appears to be regulated by substances such as dopamine, histamine (via H2 receptors), secretine, glucagon, PgE2 and catecholamines (3).

Nine uraemic patients not being treated by dialysis received intravenous propranolol 1 microgram/kg/min for 85 minutes after a priming dose of 1 mg. Fifteen days later, six of them received intravenous metoprolol 1.2 microgram/kg/min after a priming dose of 1.2 mg. Plasma concentrations of parathyroid hormone (PTH) and calcitonin fell significantly after propranolol but not after metoprolol, whereas no change in plasma concentrations of ionised calcium and phosphate occurred with either drug. Heart rate fell similarly with both drugs. The fact that propranolol acutely suppressed PTH and calcitonin secretion in uraemic patients indicates that further studies are warranted to assess the long-term effects of the drug on the secretion of these hormones and on renal osteodystrophy. The contrast between the responses to propranolol and metoprolol supports the concept that PTH and calcitonin secretion is modulated through specific beta 2-receptors.