In order to elucidate a participation of the mesangiolysis in the formation of diabetic nodular lesions, 355 kidney specimens obtained from 327 patients with primary diabetes mellitus were studied. Mesangiolyses begun by focal and segmental disintegration of the pivotal structure of the mesangium ("torn off phase"), resulting in cystic or aneurysmal dilatation of the involved tuft, were found in 56 specimens (16%). The dilated tufts were filled with lysed mesangial matrix, which showed a reticular or fibrillar arrangement ("structureless phase"), being followed by a concentrical re-arrangement ("reconstructive phase") and by the ultimate formation of diabetic nodules. The mesangiolysis of various phases was frequently found concomitant with severe diabetic arteriolosclerosis and, in the reconstructive phase, the lysed mesangial matrix near the recanalized capillary along the inner aspect of glomerular basement membrane was observed to be rearranged in a layered structure. These results suggest the hypothesis that: 1) the mesangiolysis is the initial lesion occurring in glomeruli in the process of diabetic nodule formation, and disturbed blood flow into glomeruli, caused by diabetic arteriolosclerosis, may be implicated in the development of the mesangiolysis; and 2) concentric compression of the lysed mesangial matrix by recanalized capillaries forms layered structures and ultimate completed diabetic nodules.

SUMMARYGlomerular injury caused by injection of heterologous anti-glomerular basement membrane antibodies (anti-GBM Ab) is increased in rats pretreated with small doses of bacterial lipopolysaccharide (LPS). We have Investigated the involvement of tumour necrosis factor-alpha (TNF-a), IL-la and IL-l^in this phenomenon by passive immunization against these cytokines. Anti-TNF-«oranti-IL-l/i antibodies given 15 h before the induction of nephritis significantly decreased injury in this model, whether assessed by the magnitude of albuminuria. the prevalence of giomerular capillary thrombi or the intensity of glomerular neutrophil infiltrate. Aibuminuria in anti-GBM Ab alone was U ±3. LPS/anU-GBM Ab 87 + 22. and anti-TNF-a antibodies/LPS/anti-GBM Ab 21 ±6 mg/24 h (mean + s.e.) /*<0-05. Passiveimmunization with antibodies to IL-l/f had a similar effect (anti-GBM Ab.O-6 + 0-l,LPS/anti-GBM Ab.92+19.anti-IL-l/fantibodies/LPS./anti-GBM Ab39±8mg/24h. P<{)QS). The prevalence of glomerular capillary thrombi was also reduced significantly by these Ircatmcnts; from 22±5% to 4±1% in the case of anti-TNF-a antibodies and 28±5% to 13 ±4% with anti-IL-1 ^antibodies, Similarly, the glomerular neutrophil infiltrate was also reduced by these treatments; from 42 + 3 to 25±1 In the case of anti-TNF-D; and 47±2 to 30+1 with anti-IL-lâ ntibodies. In eontrast, passive immunization againsi IL-la had no effect on either albumin excretion {4 + 3, 83 + 22 and 77 + 24 mg/24 h), glomerular capillary thrombi (2+1; I9±5 and !6±3) or glomerular neutrophil infiltrate (22 + 3; 47 + 5 and 48 + 5 from the three groups respectively). These results demonstrate that enhanced antibody mediated injury in the kidney is modulated by TNF-a and \L-\(i but not by IL-la.Keywords nephrotoxic antibody lipopolysaccharide tumour necrosis factor-alpha interleukin-1 a and P aipha 2-macroglobulln

A case of vitamin D resistant hypophosphatemic osteomalacia associcated with osteosarcoma of the mandible is presented. The patient complained of lumbar, knee and foot pain and muscle weakness of two years' duration. Serum phosphorus was 1.0-1.6 mg/dl, tubular reabsorption of phosphorus was 47 to 58%, TmP04/GFRwas 0.7-1.2mg/dl. Aminoaciduria was noted. Bone biopsy confirmed the diagnosis of osteomalacia. He partially responded to the treatment with 1«(OH)D3and sodium phosphate. After removal of sarcoma of the mandible, symptomsremitted and pertinent laboratory data became normal except serum alkaline phosphatase for more than one year without treatment. It is suggested that an impaired response of the tubule and bone to active vitamin D3, caused in some way by the osteosarcoma might be one of the causes of osteomalacia in this case.

[Purpose] This study assessed changes in body composition before and after dialysis in chronic hemodialysis patients and determined the relationships between various body composition parameters and blood lipid levels in these patients. [Subjects] The cross-sectional study included 19 dialysis outpatients (17 men and 2 women, aged 35–82 years). [Methods] Body mass index, body weight, percent body fat, and percent skeletal muscle were measured before and after dialysis by using body impedance analysis. Blood lipid levels were obtained from patients’ clinical records. The body composition parameters before and after dialysis were compared using paired t-tests. Spearman’s rank correlation coefficients were calculated to determine relationships between the body composition parameters, before and after dialysis, and the blood lipid levels. [Results] All body composition parameters differed significantly before and after dialysis. High-density lipoprotein cholesterol level significantly correlated with all the body composition parameters, whereas total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels significantly correlated with some of these parameters. The correlation coefficients revealed no major differences in the relationships between blood lipid parameters and body compositions before and after dialysis. [Conclusion] Our findings suggest that body composition parameters, whether measured before or after dialysis, can be used to evaluate obesity in longitudinal studies.