A man, now 26 years old, received a ventriculo-atrial shunt at the age of 23 years for hydrocephalus caused by the obliteration of aquaeductus mesencephali which followed the traffic accident. At that time the urine was normal. 6 months after the insertion of the shunt, he became febrile, and at this time proteinuria and hematuria were first pointed out. After the shunt revision the patient became afebrile and hematuria disappeared, but proteinuria persisted. Several months later, spiking fevers developed again and hematuria recurred. At the age of 26 years, on admission to this hospital, he had mild anemia, proteinuria and hematuria. BUN levels, serum creatinine levels and serum electrolytes values were normal. There were hypergammuglobulinemia and increase in serum immunoglobulin concentrations of IgG and IgM. Serum β_1C-1A globulin concentrations were low. CRP and RA were persistently positive. The ASO titers were 50 to 125 units. Throat cultures were negative for streptococci. Tests for lupus erythematosus and antinuclear antibodies were negative. Four blood-cultures were taken, and all yielded a growth of coagulase-negative Staphylococcus albus. Renal function test showed a slight decrease in PSP excretion and a moderate reduction in GFR and concentrating ability. After the antibiotics were discontinued, proteinuria and hematuria increased and the creatinine clearance was deteriorated. By the administrations of antibiotics proteinuria, hematuria and the creatinine clearance were improved, and serum β_1C-lA globulin concentrations returned to normal values, but thereafter were reduced again. Renal biopsy revealed diffuse intra-and extracapillary glomerulonephritis. On electronmicroscopy, fine granular subendothelial electron-dense deposits were found in the glomerular basement membrane. Immunofluorescence studies revealed positive staining in a granular pattern against IgG and β_1C globulin. A culture of blood from the biopsy needle was negative. In this case an immune pathogenesis of the antigen-antibody complex type was suggested strongly by the presence of 1) IgG and β_1C globulin in the glomeruli, 2) subendothelial electron-dense deposits in the glomerular basement membrane, and 3) hypocomplementemia.

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Twelve male Wistar rats were infected with Pseudomonas aeruginosa and then subjected to bilateral nephrectomy. Electron microscopic examination of proximal tubules of the extirpated kidneies yielded the following findings. I. Kidneies extirpated on the 7 th day after intravesical infusion of 1.0 ml of a suspension of Pseudomonas aeruginosa (containing 10¹⁰ cells per milliliter) : There were noted generalized, mild atrophy of cytoplasm, an increase in the number of cytosomal vacuole and cytosomal dense body obviously. II. Kidneies extirpated at 24 hours after infusion of 0.5 ml of the same bacterial suspension into vena cava inferior of the rats preceded by ligation of the left ureter : Marked atrophy of cytoplasm, vesicular dense bodies occuring sporadically or intensively in the apical area, and relative small size of cytosomal vacuoles prominently. In area with advanced degeneration, severe destruction or disappearance of mitochondriae and appearance of a cytosomal myelin figures-like body were observed. III. Kidneies, at 24 hours after infusion of 0.5 ml of the bacterial suspension into the left renal pelvis, preceded by ligation of the left ureter : Distinct atrophy of the cytoplasm, vesicular dense bodies appearing intensively or sporadically in the apical area, appearance of cytosomal vacuoles and cytosomal dense bodies of relative small size, and low electron densities of the membranes of the organelles generally. From these results it may follow that vesicular dense bodies are considered to represent hemoglobin droplets, generally tend to increase in number in association with chronic inflammatory diseases rather than acute ones, and thus not be specific for infection with Pseudomonas aeruginosa. Cytosomal vacuoles and cytosomal dense bodies are considered to reflect an autolytic action in response to endotoxin, a phenomenon occuring not only in infection with Pseudomonas aeruginosa but also in other types of infection in general, and might possibly provide histological diagnostic evidence for celluar degeneration.

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In the preceding paper the author reported a method for qualitative and quantitative analysis of urinary acids using the automatic recording titrator. This paper reports the results of investigations by this method in patients with chronic nephritis and chronic pyelonephritis. The material used was early-morning urine.(1) Control subjects Out of 29 healthy subjects, the titration curve was of JJJ-type in 16 and of JJ-type in 13. In the tests of 10 cases, HCO₃-was not detected. Urine pH had a mean of 6.02±0. 31. NH₄⁺ showed the highest concentration, followed by TA and OA in this order. OA/TA was under 0. 30, and NH₄⁺/TA was over 1.8. (2) Chronic nephritis Out of 22 cases, the titration curve was of JJJ-type in 16 and of JJ-type in 6. The curves with the pH-jump of OA (i. e. JJJ-type and JJ-O⋅P type) were found in as high as 82% of the cases. In 11, three abnormal types (i. e. A(-), A(±) and O(_??_) type) were found, indicating no excretion of NH₄.+, a marked reduction of NH₄⁺ concentration and an increase of OA concentration, respectively. Urine pH was low with a mean of 5, 63. TA concentration was well preserved compared to the marked reduction of NH₄+ concentration, resulting in the reduction of NH₄⁺/TA. These results were similar to those of previous studies in the literature. OA concentration and OA/TA were increased. In every one of the 11 cases of abnormal types, renal functions declined markedly, and most of them developed metabolic acidosis. (3) Chronic pyelonephritis Among 14 cases, only 2 showed abnormal titration curve. Both TA and NH₄⁺ concentrations were reduced to a marked degree, but in most cases NH₄⁺/TA was not reduced. Increase of OA/TA or reduction of NH₄⁺/TA was not caused by the decline of glomerular functions. These results differed from those in chronic nephritis. Urine pH approximated that of the controls with a mean of 5.95. In the tests of 6 cases, HCO₃-was not detected. Glomerular functions were impaired in only 1 of 14, but out of 9 cases examined for metabolic acidosis, it was observed in 3. (4) From these observations it is concluded that the pattern of acid excretion in early-morning urine represents the renal functions in maintaining the acid-base balance.

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This paper reports the pattern of acid excretion in patients on chronic hemodialysis and with renal tubular acidosis examined by the method for qualitative and quantitative analysis of urinary acids which was reported in a previous paper. The specimens were early-morning urine and the titration curve with alkali was drawn by the automatic recording titrator. (1) Chronic hemodialysis cases In 10 cases, there were 1 of JJJ-type, 6 of JJ-type and 3 of J-type. Every case showed an abnorml type of titration curve, i. e. A(±) or A(-) type. Especially in the A(-) type, H₂PO₄-showed a pH-jump, i. e. the type was J-P. There was no significant relation between the type and the duration of dialysis. Urine pH was high, except in 1, with a mean of 7.00. This is presumably due to the excretion of HC0₃- caused by an increase of its concentration in the blood by importation from dialysate. TA and NH₄.+ concentrations were markedly reduced. In 5 cases examined for HCO₃-excretion, it was found in every case. (2) Cases of renal tubular acidosis In all the 3 cases studied, the titration curve was of JJ-P⋅AB type, but the proximal RTA case represented JJJ-type in an advanced stage. Urine pH was over 6.00 in spite of the presence of metabolic acidosis, with a mean of 6. 79, TA concentration was reduced in every case. NH₄+ concentration was reduced in two cases with distal RTA, but within the normal range in the case with proximal RTA. HC0₃- was detected in every case. But in an advanced stage of acidosis in the proximal RTA case, TA and NH₄⁺ concencentions markedly increased and HC0₃- disappeared. The causes of this are discussed.

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