[Extracapillary glomerulonephritis with anti-myeloperoxidase antibodies in 2 patients with systemic scleroderma treated with penicillamine D]. / Glomérulonéphrite extracapillaire avec anticorps anti-myéloperoxydase chez 2 malades ayant une sclérodermie systémique traitée par D-pénicillamine.

BACKGROUND: Side-effects, including autoimmune disorders, are frequent with D-penicillamine therapy. Proteinuria is observed in 10% of the patients, often secondary to extramembranous glomerulopathy. Necrotizing extracapillary glomerulonephritis is however exceptional. CASE REPORTS: Two patients with systemic sclerodermia were treated with D-penicillamine for 7 and 14 years. Both developed necrotizing extracapillary glomerulonephritis with anti-myeloperoxidase antibodies (anti-MPO), associated with hemorrhagic alveolitis in one case. Partial regression of the renal failure was obtained after withdrawal of D-penicillamine and combination treatment with prednisone and cyclophosphamide. DISCUSSION: Extracapillary glomerulonephritis or a lung-kidney syndrome are frequently associated with anti-MPO antineutrophil cytoplasm antibodies (ANCA). In systemic sclerodermia, the presence of anti-MPO appears to define a group of patients at risk of pauci-immune extracapillary glomerulonephritis or a lung-kidney syndrome. In addition, the presence of ANCA in patients with renal failure would suggest extracapillary glomerulonephritis rather than sclerodermic microangiopathy. Development of extracapillary glomerulonephritis with anti-MPO in patients who are taking D-penicillamine suggests that inductor mechanisms other than D-penicillamine are involved in the pathogenesis of these glomerulopathies.

[Chronic interstitial nephritis and mesalazine: 3 new cases?]. / Néphrite interstitielle chronique et mésalazine: 3 nouveaux cas?

We report three new cases of chronic interstitial nephritis occurring in two patients with Crohn's disease and one patient with ulcerative colitis treated with mesalazine. In the three cases asymptomatic renal disease was revealed by an increase in serum creatinine which was normal before treatment. Renal biopsy showed features of severe chronic interstitial nephritis. Mesalazine withdrawal and administration of steroids in two cases led to partial improvement of renal function. Mechanism of renal toxicity of mesalazine is unknown. These observations stress the need for monitoring renal function in patients with inflammatory bowel disease treated with mesalazine.

Improvement of severe secondary hyperparathyroidism in dialysis patients by intravenous 1 alpha(OH) vitamin D3, oral CaCO3 and low dialysate calcium.

Seventeen patients (9 men, 8 women; aged 27 to 75 years) who were on chronic hemodialysis for 1 to 14 years were included in the study because they had severe hyperparathyroidism diagnosed by elevated plasma alkaline phosphatase and on plasma intact PTH levels more than twice the upper limit of normal. They had been previously treated with various combinations of oral calcium and/or Al(OH)3 as phosphate binders, oral 1 alpha(OH) vitamin D3 metabolites and a dialysate calcium concentration (DCa) of 1.6 to 1.75 mmol/liter. When i.v. alpha calcidol was introduced DCa was reduced to 1.25 mmol/liter and CaCO3 taken with the meal was used as the sole phosphate binder. alpha calcidol was i.v. injected after the third dialysis of the week at a dose up to 4 micrograms per dialysis in order to obtain a predialysis plasma concentration of Ca at 2.5 +/- 0.2 and PO4 between 1.5 and 2 mmol/liter. All the other treatments were discontinued. During the six months of follow-up, the mean weekly dose of alpha calcidol was 6 micrograms and CaCO3 700 +/- 50 mmol. Plasma calcium (PCa) increased moderately from 2.35 to 2.47 mmol/liter (P < 0.05) whereas plasma PO4 (PPO4) did not significantly increase (1.56/1.64 mmol/liter). Total alkaline phosphatase and its bone isoenzyme activity decreased significantly to normal values [respectively from 186 to 83 IU (normal: 135) and from 102 to 32 IU (normal < 33)] whereas plasma intact PTH decreased from 485 to 125 pg/ml (normal < 55).(ABSTRACT TRUNCATED AT 250 WORDS)

[Destructive spondylarthropathy with amyloid deposits in 3 patients on chronic hemodialysis]. / Spondylarthropathie destructrice avec dépôts amyloïdes chez 3 patients en hémodialyse chronique.

Destructive spondyloarthropathy is a recently described complication of chronic hemodialysis. Three patients presenting spondyloarthropathy with destructive discovertebral lesions of the cervical or lumbar sections of the spine underwent surgery due to neurologic complications: persistent radiculalgia (two cases), regressive tetraparesis (one case). Discal lesions were associated with dislocation of the posterior intervertebral articulations and slipping of vertebrae. These patients had been receiving chronic hemodialysis for more than ten years; two presented hyperparathyroidism and blood aluminum was markedly increased in all cases. Two patients had undergone surgery for bilateral carpal tunnel syndrome. Anatomopathological examination of surgical specimens demonstrated the presence of amyloid deposits in the intervertebral disc. This suggests that amyloidosis, which is frequently seen with carpal tunnel syndrome in patients receiving prolonged hemodialysis, also plays a role in the development of spondyloarthropathy.

Effect of propranolol and metoprolol on parathyroid hormone and calcitonin secretions in uraemic patients.

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.