Hydronephrosis was produced experimentally by ligating the left ureter in 23 male Wistar rats and the kidneies were removed bilaterally at varying intervals after the operatton. Microscopic examination was then made of the renal tissues, proximal tubules being particularly examined electron microscopically, with the following results.1. Photomicroscopically, there were noted slight changes in the interstitium of renal tubules occurring relatively early after ligation of the ureter, followed by degeneration of cells of the tubules and lastly by a decrease in number, destruction and atrophy of glomeruli.2. Significant electron microscopic findings of renal tubules were as follows: At one week of ligation swelling and atrophy of brush border, transformation of apical tubular invagination, atrophy of apical dense tubules, transformation and atrophy of mitochondria, thickening of basement membrane and appearance of vesicular dense body, at 2 weeks appearance of vacuoles and their arrangement adjacent to microvilli, conspicuous deposition of granular substance on the membrane of vacuoles, and appearance of vesicular dense body, at 6 weeks fragmentation, and bending of brush border, indistinctness of vesicular dense body, apical tubular and apical dense tubules, prominent tubular structure, and atrophy and thinning of basement membrane, at 8 weeks a high degree of cytosomal atrophy, at 12 weeks : an ncrease in vesicular dense body and appearance of lysosome, at 18 weeks a high degree of atrophy of and formation of collagen fibers in cytoplasm, fragmentation, destruction and disappearance of brush border, and marked atrophy, transformation and disappearance of mitochondria. Golgi zone and endoplasmic reticulus were found relatively well preserved up to 12 weeks after operation.

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Chronic intermittent hemodialysis is now well established as an effective form of treatment in patie-nts with chronic renal insufficiency. With increasing longevity however, a number of metabolic abnorma-lities have been described in patients on this form of therapy. One of these involves disturbances in lipid metabolism, and hypertriglyceridemia often appears in patients on chronic hemodialysis programs. In present studies, we examined plasma lipids in 25 patients with chronic renal disease prior to the time they were begun on dialysis. Patients with the nephrotic syndrome and diabetes were excluded from this group. Serum cholesterol levels in these patients averaged 143.1±78.4 mg% whereas age-paired co-ntrols had cholesterol levels which averaged 192.5±42.8mg%. Phospholipid levels in these uremic pa-tients were also lower than those found in normal control subjects (141.4±30.4mg% and 178.7±31.5 mg% respectively). Triglyceride concentrations and free fatty acid concentrations were within normal limits. By contrast, plasma cholesterol and phospholipid levels in 17 patients on chronic hemodialysis were consistently elevated. Free fatty acids remained within normal limits but triglyceride levels gradually increased as the hemodialysis program continued. Thus, 9 patients who had been on hemodialysis for 2 years had hypertriglyceridemia with average levels of 189.8±55. 3 mg%. Plasma insulin levels in these patients were either normal or slightly increased both before and after the institution of the chronic hemodialysis program. Moreover, lipoprotein lipase activity was decreased in uremic patients whether or not they were on dialysis. Thus the hyperlipidemia which develops in patients on chronic hemodialysis appears to relate to whether increased synthesis, decreased utilization, or both.

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Glomerular changes characterized by the crescent forming glomerulonephritis in a family of Alport's syndrome were reported (26 yrs._??_, 33 yrs._??_). Serial kidney sections with PAS and PAM stainings revealed that the extracapillary proliferation was based on the damage of the glomerular basement membrane (GBM). The development of extracapillary glomerulonephritis was discussed with special reference to the lesion of the GBM.

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It is well known that patients with acute renal failure have urinary concentrating defect even after clinical recovery. However, few attemps were made to study the mechanisms responsible for the defect and its improvement in acute renal failure. In the present work, urinary concentrating ability and intrarenal hemodynamics were studied in acute renal failure in previously uni-nephrectomized rabbits, caused by 2-hr clamping of the contralateral renal artery. Arterial clamping resulted in acute oliguric renal failure comparable to that in man. Directly meas-ured renal blood flow restored fairly well immediately after release of clamping. Superficial cortical blood perfusion, estimated by an isotope-labelled microsphere technique, was slightly reduced for the first several days following the occlusion, whereas deep cortical perfusion increased. During the oliguric stage, medu-llary osmolality was markedly diminished, concomittently with reduced (U/P) osm. C_IN, EPAH and fractional sodium reabsorption were tremendously decreased. Light microscopic observations revealed tubular necrosis and intratubular cast formation. During the early diuretic stage, which uniformly followed the oliguric stage, C_IN, medullary osmola-lity and (U/P)osm were reduced. Intratubular casts disappeared while regenerated tubular cells were focally observed. In 2 weeks after the occlusion, fairly well improved C_IN, EPAH, sodium reabsorption, medullary osmolality and (U/P)osm, and a remarkable regeneration of tubular epithelium were found. In 7 weeks, C_IN and EPAH returned to the preclamping values whereas medullary osmolality decreased again with an appearance of medullary fibrosis. Also, (U/P)osm did not completely restore. The findings indicate that urinary concentrating ability restores slowly as compared with other renal functions in ischemic acute renal failure of rabbits.

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