The incidence of uremic peripheral neuropathy and the effect of hemodialysis were evaluated in 35 non-dialysed patients with chronic renal failure (CRF) and 50 dialysed patients. Signs and symptoms of peripheral nerve dysfunction and motor nerve conduction velocity (NCV) were studied in both groups. The incidence of clinical neuropathy was 28.5% in CRF group and 18% in dialysed group, in-dicating that clinical neuropathy was improved by chronic dialysis therapy. The NCV in lower and upper extremities was almost equally affected, and this indicates the discrepancy of clinical neuropathy and electro-physiological neuropathy. The NCV in patients with terminal renal failure was significantly reduced, and statistical analysis showed an inverse relationship between NCV and serum creatinine or blood urea concentration, while this correlation was not shown in dialysed patients. No correlation was shown between NCV and methylguanidine (MG) or guanidino-succinic acid (GSA) of ECUM solution in terminal renal failure. It is suggested that uremic peripheral neuropathy might be influenced by substances other than creatinine, urea, MG and GSA. Chronic intermittent dialysis resulted in improvement of NCV, and this was shown more clearly in the group with frequent dialysis per week (3/W). Evidence of improvement of NCV was not observed within several months after starting dialysis therapy. Thereafter, gradual improvement was seen overr one year and NCV was maintained stationary in subnormal level by adequate dialysis therapy. It is suggested that the patho-physiological aspects of dialysis stage maybe influ-enced with the duration of dialysis therapy. In conclusion, subclassif ication of dialysis stage, i. e., introductory, intermediate and stabilized stage is necessary for evaluation of patho-physiologic study in dialysis stage. Introductory stage means the period of several months after starting dialysis therapy, intermediate stage the one within one year and stabilized stage the one over one year, respectively.

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Two patients of nephrotic syndrome with gastric carcinoma we presented. Examination of routine renal biopsy revealed the characteristic light, immunofluorescent and electronn microscopic features of membranous nephropathy. Subepithelial electron-dense deposits were corresponded to immunofluorescent deposits containing IgG and beta-l-c in the two cases. When tested by immunodiffusion, there was a line between the glomerular eluate obtained from the glomeruli of the patient's and carcinoembryonic antigen (CEA), prepared. And this eluate reacted specifically the surface of patients' tumor cells. The reactivity of the eluate was aboiisned by absorption of an extract of patient, s tumor tissue and CEA prepared. In addition, CEA was also demonstrated in the patients' urines. These events suggest that an immune mechanism related the gastric carcinoma is responsible for the glomerular lesion. Probably it is carcinoembryonic antigen-antibody complexes to have induced the nephropathy.

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Immunofluorescent studies were performed on the renal tissues obtained from 136 patients of various renal disease using FITC-labeled antibodies against kappa and lambda chain of immuno-globulins to compare with the deposition of heavy chains (gamma, alpha and mu), beta-1C and fibrinogen. Staining for both light chains (bitype) was positive in 84 cases. Twenty-two biopsy specimens showed positive staining for only one of the light chains (monotype). Thirty cases were revealed to be negative for light chain staining. No significant difference was observed in laboratory findings, light mrcroscopie timings, clinical courses and therapeutic effects between the monotypic deposition of light chains. There was also no significant difference in the staining pattern and localization between the deposition of light and heavy chains, except that the light chain deposition was observed almost exclusively on mesangial areas in certain cases in which the deposits of heavy chains were more prominent on mesangium than on capillary walls. No specific correlation was noticed between the kind of renal diseases and the type of light chains, but deposits in SLE were predominantly positive for lambda chains. Almost half of tre cases with monotypic staining of light chains were positive only for gamma chain without concomitant deposits of other heavy chains. Likewise, 19 of 30 cases with no demonstrable light chain deposits were found to be positive only for gamma chain.

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小児の急性糸球体腎炎(acute glomerulonephritis: 以下A.G.N.)および血管性紫斑病性腎炎(anaphyla-ctoid purpura nephritis:A.P.N.)の病初期の腎生検材料を用いて,一般に行われているようなIgG,IgA,IgM,Fibrinogenそして補体(β_1C/β_1A)の螢光染色を行うと共に,溶連菌抗原(type 12 group A strepto-coccus)の抗血清およびFITC標識患者血清を用いて組織内抗原の証明を試みた。A.G.N.においては,IgGおよび補体は主に糸球体基底膜にそってfine granularなdepositとして認められた。またIgAと溶連菌抗原ならびにFITC標識患者血清による三者の染色像パターンは非常によく似ており,各糸球体の5～20ヵ所のmesangial areaにfine granularなdepositの集合として見られた。一方,A.P.N.の場合には,これまでの報告とは異なりIgAおよびFibrinogenが主として糸球体基底膜にそってnodularなdepositとして認められ,またFITC標識患者血清による抗原の検索をも併せて試みてみたが,これでは残念ながら螢光染色を認めることが出来なかった。以上の事実より,A.G.N.の場合には,何らかの抗原(溶連菌の菌体成分)とその抗体の一つと考えられるIgAとの関係がこの腎炎発症の上で重要な役割を果していると考えられた。また一方A.P.N.の場合はで抗原の証明は困難であったがために,IgAをもってそのimmune complexと結びつけることはむずかしいが,先のA.G.N.の場合のIgAのdistributionとは全く異ったパターンであり,さらに両者の臨床経過の相違を併せて考えると,この病初期に認められたIgAは腎炎発症のみならず,その後の経過をも決定するような働きを持つ一因子となるのではないかと考えられた。

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