EXPERIMENTAL GLOMERULONEPHRITIS : THE PATHOGENESIS OF A LABORATORY MODEL RESEMBLING THE SPECTRUM OF HUMAN GLOMERULONEPHRITIS

Daily injections of any one of several foreign serum proteins produced in rabbits functional and morphological alterations similar to those seen in acute, subacute, and chronic human glomerulonephritis. The critical factor determining whether a rabbit would develop renal disease and the type of disease developed was the amount of antibody the rabbit formed. Those responding with much antibody were likely to develop an acute, self-limited glomerulonephritis and to be subsequently immune to further renal damage. Those responding with antibody barely sufficient to neutralize the antigen injected developed subacute and chronic glomerulonephritis. In the circulation of the rabbits with chronic glomerulonephritis, there was a daily recurring antigen-antibody reaction in the region of near antigen excess to near antibody excess which presumably led to the disease. Antigen apparently in the form of antigen-antibody complexes was deposited along the renal capillary basement membranes coincident with the development of subacute and chronic glomerulonephritis. Once developed, the morphologic stigmata of chronic glomerulonephritis persisted even after injections of antigen were stopped. However, in milder instances the renal function recovered in part after stopping antigen. This experimental model has several implications: first, the renal injury is precipitated by antigens with no known affinity for, or immunologic relationship to, kidney; second, antigen antibody complexes localize in the kidney, apparently on the basis of non-immunologic factors, and may be an etiologic agent of renal injury; third, severe hypersensitivity disorders can be related specifically to relatively poor as well as to good antibody responses; and finally, the pathogenesis suggested here offers an alternative to that of nephrotoxic serum nephritis for the experimental approach to the study of human glomerulonephritis.     

Intestinal perforation caused by magnetic toys

Accidental ingestion of foreign bodies is a common problem in children, but ingestion of magnets is rare. When multiple magnets are ingested, they may attract each other through the intestinal walls, causing pressure necrosis, perforation, fistula formation, or intestinal obstruction; as has been reported in 13 cases in the past 10 years. We report the fifth case in the literature of intestinal perforation and fistula caused by the ingestion of 2 small magnetic pieces of a toy by a 3-year-old boy. We find it necessary that sanitary authorities give more information to parents and physicians about the potential risks of these magnetic toys.     

Ophthalmoplegic migraine and infundibular dilatation of a cerebral artery

Ophthalmoplegic migraine (OM) is a childhood disorder of uncertain etiology manifesting recurrent unilateral headache associated with a transitory oculomotor (usually IIIrd nerve) palsy. Recent publications emphasize the finding on MRI of contrast enhancement in the IIIrd nerve suggesting that OM may be a recurrent inflammatory neuropathy. We report the case of a 7-year-old boy with typical symptoms of this disorder. Angio MR and Angio CT revealed the presence of an infundibular dilatation of a perforating branch of the posterior cerebral artery adjacent to the symptomatic IIIrd nerve. We speculate that this and perhaps other cases of OM may have a different pathophysiology related to compression of the IIIrd nerve by an adjacent vascular structure that could activate the trigeminovascular system and produce migrainous pain.     

Complex dorsal metacarpophalangeal joint dislocation caused by interosseous tendon entrapment: case report

We report a patient with open complex, dorsal metacarpophalangeal joint dislocation of the index finger with interposition of the first dorsal interosseous tendon and the transverse ligament of the palmar aponeurosis. To our knowledge, entrapment of the first dorsal interosseous tendon has not been reported to be the cause of irreducible dislocation of the metacarpophalangeal joint.     

Normothermic recirculation reduces primary graft dysfunction of kidneys obtained from non-heart-beating donors

Our aim was to analyze the short- and long-term function of kidneys procured from non- heart-beating donors (NHBD) by means of three techniques: in situ perfusion (ISP), total body cooling (TBC) and normothermic recirculation (NR). Fifty-seven potential NHBD were included. Mean warm ischemia time was 68.9 ± 35.6 min. Forty-four kidneys were obtained from donors perfused with ISP, 8 with TBC, and 8 with NR. Eighteen kidneys (32 %) started functioning immediately, 29 (52 %) showed delayed graft function (DGF) and 9 (16 %) showed primary non function (PNF). The actuarial graft survival rate was 76.4 % at 1 year and 56 % at 5 years. The patient survival rate was 89.3 % at 5 years. Incidence of DGF and PNF was significantly lower in kidneys perfused with NR than those with ISP or TBC (P < 0.01). Duration of DGF was shorter in kidneys obtained through TBC than in kidneys obtained with ISP (P < 0.05). In conclusion, NR reduces the incidence of DGF and may be considered the method of choice for kidney procurement from NHBD. Received: 21 July 1999 Revised: 11 January 2000 Accepted: 5 May 2000     

Developmental toxicity evaluation of gallium nitrate in mice

Gallium nitrate, a drug with antitumor activity, is presently undergoing clinical trials as a chemotherapeutic agent for the treatment of certain malignancies. Since there are very limited published animal toxicity data available, this study was conducted to investigate the potential adverse developmental effects of this drug. Pregnant Swiss mice were administered intraperitoneally gallium nitrate at 12.5, 25, 50, and 100 mg/kg/day on days 6, 8, 10, 12, and 14 of gestation. Monitors for maternal toxicity were body weight, food consumption and clinical signs. At sacrifice (day 18) maternal weight, liver and kidney weights, and gravid uterine weights were measured. Gestational parameters monitored were numbers of total implants, resorptions, postimplantation losses, and dead fetuses. Live fetuses were sexed, weighed, and examined for external, internal and skeletal malformations and variations. Maternal toxicity was noted in all the gallium nitrate-treated groups. Embryo/fetal toxicity was evidenced by a decrease in the number of viable implants, a reduction in fetal weight, and an increase in the number of skeletal variations (12.5, 25, 50 and 100 mg/kg). No significant increase in the incidence of malformations was observed at 12.5, 25, or 50 mg/kg. The no-observable-adverse-effect level (NOAEL) for both maternal and developmental toxicity of gallium nitrate was <12.5 mg/kg.