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On the special occasion of the society's Golden Jubilee Conference in Cardiff, as a historical institution a short review of its own history was apposite.

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Realizamos un estudio sobre aspectos morfológicos de la laringe de la chinchilla. La laringe está compuesta por las porciones muscular, membranosa y cartilaginosa y tiene en promedio 9mm de longitud. En la pared lateral se localizan los plieges vocales y vestibulares; el ventrículo laríngeo es una pequeña depresión localizada entre estos pliegues. El epitelio laríngeo fue estudiado a travéz de la microscopía fotónica y electrónica de barrido. La superficie del espacio supraglótico está cubierto predominantemente por epitelio estratificado con aspecto de adoquín, mientras que, puede observarse un típico epitelio seudoestratificado compuesto por células ciliadas y no ciliadas en el área de la subglotis. Sin embargo, cerca de la parte caudal del pliegue vocal el epitelio cambia gradualmente de escamoso estratificado al tipo intermedio demostrando un aspecto de guardacantón. La capa subepitelial estaba compuesta por fibras elásticas y colágenas que contituían una intrincada malla

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We previously found that virtually all patients with nephrotic syndrome (NS) excrete supranormal amounts of urinary kallikrein; it is known that activity of the renin-angiotensin system (RAS) is increased in some such patients. We therefore studied the relationship between urinary kallikrein excretion (UKa) and plasma renin activity (PRA) in 16 patients with NS. Compared with healthy controls, PRA was normal in 8 subjects and elevated in 8; UKa was elevated in the high-renin group (40.4 +/- 5.2 nkat/24 h, normals 12.0 +/- 1.1). UKa was also elevated in the normal renin group (25.7 +/- 2.4 nkat/24 h) but to a significantly lesser degree. Significant activity in plasma against a specific substrate of glandular and renal kallikreins was observed in 8 of 10 patients with NS. Such activity was not found in plasma of 17 patients with glomerulonephritis without NS, or in 10 healthy controls. The results are in keeping with previous suggestions of a functional link between the renal kallikrein-kinin system (KKS) and the RAS, but indicate that the renal KKS is activated in NS, in some cases independently of the RAS. It is possible that renal kallikrein reaches the systemic circulation in some patients with NS.

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It is generally accepted that aluminium induces osteomalacia in chronic hemodialysis patients by binding to the calcification front, thereby inhibiting mineralization of osteoid. Because this form of osteomalacia is vitamin D resistant, the condition has often been assumed to be irreversible, although promising results have been achieved recently by using a chelating agent for removal of aluminium from the skeleton. In this paper we present four chronic hemodialysis patients with aluminium toxicity and histologic osteomalacia in whom the mineralization defect greatly regressed after the use of reverse osmosis treated-water for dialysis, but without further treatment. In three other patients, also with aluminium toxicity and histologic osteomalacia, similarly treated, the histological severity of the osteomalacia remained static. Those patients in whom bone mineralization status improved developed hyperparathyroidism after reverse osmosis water-treatment, whereas the static patients remained euparathyroid. The results suggest that resolution of aluminium related osteomalacia may occur with reduction in dialysis fluid aluminium, and that parathyroid hormone plays a role in the healing of aluminium related osteomalacia. The therapeutic implications are twofold: attempts to remove all traces of hyperparathyroidism may be detrimental to the bone mineralization status; and stimulation of the parathyroid glands by means of a mild reduction in dialysis fluid calcium may be of value in the management of those cases with persistent osteomalacia and low bone turnover.

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In a region with a relatively low incidence of aluminum toxicity water, dialysis fluid and plasma aluminum were monitored in hemodialysis patients before and after the introduction of reverse osmosis (RO) water. Before the use of RO water, there was a close correlation between plasma and dialysis fluid aluminum with exposure to aluminum being reflected equally by either water, dialysis fluid or plasma aluminum. Patients with clinical manifestations of aluminum toxicity were characterised by a plasma aluminum consistently greater than mumol/l and a dialysis fluid aluminum consistently greater than 1 mumol/l. No evidence of clinical toxicity was found in patients in whom the plasma aluminum was maintained up to 5 mumol/l. Following the introduction of RO water, the dialysis fluid aluminum was able to be maintained less than 1 mumol/l, the plasma aluminum fell and no new cases of clinical toxicity were identified over the following five years. An effect of aluminum hydroxide dosage on plasma aluminum could be identified only in patients in whom the dialysis fluid aluminum was less than 1 mumol/l. Plasma aluminum was found to be a poor guide to bone stores but appeared to correlate better with the presence of bone toxicity than total bone aluminum. Regular monitoring of dialysis fluid and plasma aluminum is recommended as a means of detecting exposure to aluminum as well as the source of exposure and as a guide to the risk of clinical toxicity.

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To assess the possible role of the renal kallikrein-kinin system in the pathogenesis of glomerulonephritis (GN), 24 h urinary kallikrein excretion (Uka) was measured in normal controls and in 32 patients with GN, 16 of whom had nephrotic syndrome. Compared with controls, Uka was decreased in GN without nephrotic syndrome (4.6 +/- 2.8 nkat day-1, controls 11.5 +/- 3.5 nkat day-1) but was markedly increased in patients with nephrotic syndrome (26.7 +/- 9.9 nkat day-1). The increased kallikrein excretion in nephrotic syndrome was not explained by leakage from plasma, protein binding of active kallikrein, passive 'washout' due to changes in sodium and water excretion, or by increased activity of the renin-angiotensin-aldosterone system, but may relate to changes in extracellular volume, plasma oncotic pressure and volume, or other intrarenal haemodynamic or hormonal factors. Increased activity of the renal kallikrein-kinin system is not a uniform finding in glomerulonephritis, but may be an important aspect of nephrotic syndrome.

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Exposure to organic solvents was compared by interview and questionnaire in 50 patients with biopsy-proven proliferative glomerulonephritis in whom there was no evidence of systemic disease or preceding infection with that of 100 control subjects matched for age, sex and social class. The interview was conducted by a lay person who did not know whether the interviewee was a patient with glomerulonephritis or a control subject. The exposure scores derived from the results of the questionnaires were significantly greater in the patients with glomerulonephritis than the control subjects (13,186 +/- 3,716 vs. 3,030 +/- 1,152, p less than 0.01). The degree of exposure was higher in those patients with the more severe diffuse endocapillary proliferative glomerulonephritis than in those with mesangial proliferative glomerulonephritis. In the glomerulonephritis patients solvent exposure was mainly occupational in origin and involved fuels, paints and degreasing agents in most cases. This occupational exposure was significantly greater than in the control subjects (13,061 +/- 3,858 vs. 2,878 +/- 1,146, p less than 0.01). It is suggested that exposure to organic solvents may participate in the pathogenesis of non-systemic proliferative glomerulonephritis.

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Serial estimations of plasma prekallikrein in four critically ill patients in intensive care showed reduced values in each case, suggesting activation of the plasma kallikrein kinin system. In contrast, samples taken early from 15 patients attending an accident and emergency department with multiple trauma showed significantly elevated plasma prekallikrein concentrations; the significance of this observation is at present unclear.

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Forty cases of mesangiocapillary glomerulonephritis are reviewed for whom both light and electron microscopy and full clinical data were available. Immunofluorescence microscopy (IF) was performed on 23 cases and complement screening (CH50, C4 and C3) on 25 cases, with follow-up period of 5-22 y. The results of EM revealed 17 cases (42 per cent.) of Type I and 23 cases (58 per cent.) of Type II MCGN but only 52 per cent. of Type II cases were correctly identified by light microscopy. Epimembranous deposits were seen as frequently in Type II as in Type I (26 per cent. and 30 per cent.) and fragmentation of glomerular capillary basement membranes (GBM) was seen in 27 per cent. of Type I cases. Overall patient survival was 49 per cent. at 10 y and that of patients who presented with nephrotic syndrome was poor (39 per cent. at 10 y). Persistent hypocomplementaemia with C3 Nephritic Factor was present in 40 per cent.; the survival of these patients was less than those with normal complement levels (70 per cent. vs 100 per cent. at 5 y) and they were also more likely to develop renal failure. Renal failure was more likely to develop in those with a creatinine clearance of less than 100 ml/min at presentation and where the biopsy showed substantial crescents in greater than 20 per cent. of glomeruli. Mean CH50, C3 and C4 was lower in the hypocomplementaemic as compared to normocomplementaemic patients, and there were no differences between Type I and Type II. IF showed immunoglobulins and fibrin as well as C3 in both Type I and Type II cases. Our results support the concept of an immune-complex mediated phase in both types of MCGN, and we further suggest that (a) epimembranous deposits are common in both Type I and Type II and (b) cases with fragmentation of the GBM should be designated Type Ia.

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Plasma exchange (PE) and immunosuppression was used in the treatment of 17 patients with severe glomerulonephritis and 17 acute rejections in transplant recipients. No response occurred in crescentic nephritis with anuria; a temporary improvement occurred in other nephritis patients but half of these relapsed on immunosuppression alone. Seven rejection episodes responded. Responses always occurred promptly and prolonged PE did not improve the results. Histology, serum complement or immune complex results did not predict a successful outcome.

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Severe renal failure caused by the mushroom Cortinarius speciosissimus was first recognised in 1972 and has been reported only from Scandinavia. In the summer of 1979 and following the consumption of the wild mushroom in Scotland, three previously healthy young adults developed the recognised features of cortinarius poisoning-namely, gastrointestinal upset after 36-38h, followed by nausea, anorexia, headache, rigors, severe burning thirst, muscle aching, and oliguria. One patient had a diuresis after 8 days and recovered completely. The two other patients did not present to hospital until 10 days after ingestion and severe renal failure had already developed. Both had a severe interstitial nephritis and neither recovered renal function. They were maintained on intermittent haemodialysis until they received renal transplants 9 months later. This form of mushroom poisoning has not so far been reported in the British Isles. With the increasing popularity of wild-mushroom eating, posters and publications on wild edible foods should contain warnings about the toxic nature of species of the genus Cortinarius.

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Twelve patients being treated by intermittent haemodialysis developed a severe microcytic hypochromic anaemia despite adequate iron supplements. Serum ferritin concentration was normal or high. Seven patients later developed histologically proven fracturing osteomalacia and one a fatal encephalopathy. Plasma aluminium concentration was high in all twelve patients and the source was the water used to make up dialysis fluid. Following dialysis with aluminium free dialysis fluid, plasma concentrations of aluminium fell, red cell morphology returned to normal and haemoglobin rose. We believe that in addition to causing encephalopathy and osteomalacia, aluminium causes a microcytic hypochromic anaemia. This anaemia appears to be the first manifestation of aluminium intoxication and is reversed by removing the source of aluminium.

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Three cases of Goodpasture's disease are described who were treated with intensive plasma exchange and immunosuppression. There was no improvement in renal function and the patients required chronic haemodialysis, but renal function did recover with treatment for recurrence of disease in a transplanted kidney. Anti-GBM antibody levels were not controlled and substantial reduction in fibrinogen and complement were only achieved with daily treatment. A controlled trial of this regime is urgently required.

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The response of hyperparathyroidism and skeletal calcium loss in haemodialysis patients to treatment with 1alpha-hydroxyvitamin D3 and a dialysate calcium concentration of 1.375 mmol/l was compared with the response to treatment with a dialysate calcium concentration of 1.375 or 1.75 mmol/l alone over a 6 month period. In patients treated with 1alpha-hydroxyvitamin D3 there was a significant rise in plasma calcium associated with a significant fall in plasma alkaline phosphatase and plasma parathyroid hormone as well as resolution of sub-periosteal erosions. In these patients there was a significant rise in the calcium content of the forearm assessed by neutron activation analysis in comparison to patients treated with a dialysate calcium concentration of 1.75 or 1.375 mmol/l alone. In patients treated with a dialysate calcium concentration of 1.375 or 1.75 mmol/l alone there was no significant change in the plasma calcium, alkaline phosphatase or parathyroid hormone after 6 months and in these patients subperiosteal erosions either did not change or became worse. No significant difference in the response in these two groups was observed. This study indicates that treatment of haemodialysis patients with 1alpha-hydroxyvitamin D3 is significantly more effective than treatment with a dialysate calcium concentration of 1.375 or 1.75 mmol/l alone in preventing progression of hyperparathyroidism and skeletal calcium loss.

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