50 patients with clinical evidence of renal parenchymal disease underwent open renal biopsy, Gil-Vernet's posterior surgical approach was used in 33 cases, and the flank approach, in 12 cases. The posterior approach was found to be performed more rapidly, with adequate exposure and with diminished morbidity. The surgical indications and technique are reviewed and the advantages and limitations of the posterior surgical approach are discussed.

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Acute effects of antibiotics on the ultrastructure of rat renal tissue were studied. The alterations caused by tetracyclines were observed mainly as the degeneration of mitochondria in renal tubular cells. The changes caused by cephaloridine were noted in proximal tubules. They were the disappearance of brush borders and the increase of apical vesices. Myeloid bodies developed with the degeneration process in conjunction with mitochondria, lysosome, smooth endoplasmic retieulum and Golgi apparatus. The changes caused by other cephalosporins and penicillins were the increase of apical vesidles and lysosomes. Most remarkable changes were observed in animals injected aminoglycosides especially gentamicin. Numerous cytosegresomes containing polymorphous materials and membranous bodies were crowded in proximal tubular cells and tubular lumens of them.

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Nucleus locus coeruleus (LC) sensitivity was found to be diminished in the spontane-ously hypertensive rat (SHR). In order ascertain whether this is unique to the SHR or is also present in other forms of hypertension, LC responsiveness to electrical stimulation was determined in normotensive and in two-kidney, two-clip Goldblatt hypertensive (2-K, 2-C GH) Wistar-Kyoto (WKY) rats. The observations were compared with responses of sex- and age-matched normotensive (NR and WKY) rats using chloralose-urethane anes-thesia. The LC was stimulated electrically with biphasic pulses (50 Hz) to ascertain electrical threshold levels. Mean arterial pressure (MAP) was higher in the 2-K, 2-C GH than in the two normotensive groups (2-K, 2-C GH 154 ± 5 vs NR: 106 ± 4 or WKY 115 ± 2 mmHg; both p<0.001). Electrical, pressor threshold current (PTC) for the LC was greater in 2-K, 2-C GH (2-K, 2-C GH: 110 ± 10 vs NR: 79 ± 6 or WKY: 75 ± 7 μA; both p<0.025). Following pressure reduction (Venesection, 1 ml), only the PTC of WKY was decreased (p<0.05). Since these responses in the 2-K, 2-C GH were similar to those of the SHR, and since baroreceptor resetting is common to both forms of hypertension, these data suggest that baroreceptor resetting in chronic hypertension may involve peripheral as well as central mechanism

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In order to clarify the clinical and histological features of IgA nephropathy associated with impaired renal function, 91 patients with IgA nephropathy were studied. Renal biopsy specimens from 91 patients were examined by light and immunofluorescent microscopy, and 84 cases were examined by electron microscopy. At the time of renal biopsy, GFR was normal in 64 patients, and decreased in 27 patients. The patients with proteinuria more than lg/day and those with hypertension had decreased GFR at the time of renal biopsy, compared with those without such findings. The impaired renal function was found in the group of diffuse proliferative glomerulonephritis, compared with the group of other light microscopic findings. The patients with crescents and/or adhesions of glomerular tuft to Bowman's capsule had decreased GFR, compared with the patients without those histological findings. By electron microscopy, attenuation and splitting of the glomerular basement membrane (GBM) were frequently observed. There was tendency that the patients with marked attenuation of GBM had decreased renal function, compared with the patients without the findings. Subepithelial deposits, intramembranous deposits and subendothelial deposits were not rare findings. Those were found in nineteen, seven and five patients, respectively. The patients with subepithelial and/or intramembranous deposits had decreased GFR, compared with those without such findings. The mesangium was widened in some patients by marked increase in matrix containing a large amount of electron dense deposits. Most patients with such findings had decreased renal function. In conclusion, the clinical features associated with impaired renal function were heavy proteinuria and hypertension. The histological features which were associated with decreased renal function were diffuse mesangial proliferation, crescents and/or adhesions, marked attenuation of GBM, subepithelial and/or intramembranous deposits and diffuse mesangial widening by marked increase in matrix containing a large amount of deposits.

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Thirty-two renal biopsy specimens from 22 patients with definite Systemic Lupus Erythematosus (SLE) and 5 patients with probable SLE were studied by electron microscopy. The renal specimens from 160 patients with other renal diseases were also examined for the comparative study. In all cases of definite SLE and probable SLE the microtubular structures (MTS) were found in the endothelial cells of both glomerular and peritubular capillaries. These structures were not observed in other 160 comparative cases. Among the 5 cases of probable SLE, two cases treated with low dose corticosteroid and azathioprine and one case without treatment progressed definite SLE within one to 14 months. The remaining 2 cases treated with high dose corticosteroid were clinically improved. According to the results, it is concluded that the presence of MTS is one of the important morphological findings for the diagnosis of the early stage of SLE. The treatment with high dose corticosteroid seems to be preferable in the case of probable SLE showing MTS.

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In order to clarify the hypotensive mechanisms of converting enzyme inhibitor, captopril (50mg) was administered orally in 11 hypertensive patients, of whom 9 had essential hypertension, one had primary aldosteronism, and one had glucocorticoid responsive hyperaldosteronism. There was a significant correlation between fall in mean blood pressure (MBP) and pretreatment levels of plasma renin activity (PRA) at 30 min after captopril in 9 patients with essential hypertension (r=-0.687, p<0.05). On the other hand, there was also a significant correlation between the fall in MBP and changes in plasma bradykinin (BK) levels in response to captopril at 15 min (r=-0.753, p<0.02) and 120 min (r=-0.754, p<0.02) in essential hypertensives. In essential hypertensives with PRA above 1.5 ng/ml/h (group I), the decrease of plasma aldos-terone concentration (PAC) was significantly greater than those with PRA below 1.5 ng/ml/h (group II) at any time after captopril administration, while the increments in plasma BK of group I was lesser than those in group II. In a patient with primary aldosteronism, and also in a patient with glucocorticoid responsive hyperaldosteronism, captopril lowered markedly their blood pressures with a significant elevation of plasma BK, while both PRA and PAC were unchanged. From these findings, it is suggested that the hypotensive effect of captopril is mainly due to the inhibition of the renin-angiotensin-aldosterone system rather than that of the kallikrein-kinin axis in high-renin hypertension. Conversely, in low-renin hypertension, the hypotensive action may contribute to its inhibitory effect on the kallikrein-kinin system rather than that on the renin-angiotensin-aldosterone system.

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Urinary kallikrein (U-Kal) excretion was measured by MCA fluorometric method in 43 hyperten-sive patients on arbitrary sodium intake and compared with those of 44 normotensive volunteers. U-Kal excretion was significantly reduced (P>0.05) in hypertensive patients with normal renal function. There was a significant correlation between 24 hour U-Kal and urinary sodium excretion (P<0.01) and potassium, excretion (P<0.01) in normotensive subjects, but not in hypertensive patients. There was no correlation between U-Kal and PRA, plasma or urinary aldosterone either in hyperten-sives or in normotensives. When subjects were divided by age range, younger (20-39 yr) age hyperten-sive group showed significantly (P<0.05) lower U-Kal excretion compared with younger normotensive group. U-Kal showed a tendency to decrease with age but this did not reach statistical significance in our outpatient study. There was no significant difference in U-Kal excretion both in middle (40-59 yr) and in older age (60-79yr) groups. These results demonstrate that U-Kal decreased in younger hypertensive patients in situations where sodiumm intake was given arbitrary and may suggest an abnormal urinary kallikrein excretion in hypertension.

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Brain angiotensin-converting enzyme activity was determined in six areas of the brain (cerebral cortex, midbrain, thalamus, hypothalamus, striatum and cerebellum) of normotensive and experimental hypertensive rats (1-clip, 1-kidney Goldblatt hypertensive, 1-clip, 2-kidney Goldblatt hypertensive and 2-clip, 2-kidney hypertensive rats). The systolic blood pressure markedly elevated in each experimental hypertensive rat. Angiotensin-converting enzyme activity was relatively high in the thalamus and relatively low in the cerebellum of normotensive and experimetal hypertensive rats. However, the enzyme activity in the hypothalamus of 1-clip, 2-kidney Goldblatt hypertensive rats was significantly higher than that of normotensive rats, while there was no significant difference in the enzyme activity among normotensive, 1-clip, 1-kidney Gold-blatt hypertensive and 2-clip, 2-kidney hypertensive rats. These results suggest that in 1-clip, 2-kidney Goldblatt hypertensive rats, increased brain angio-tensin-converting enzyme activity may play a possible role in the hypertension through much more conversion of angiotensin I into II in the brain.

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The appearance of placental type (Shiba-isozyme) of aminopeptidase N (EC 3. 4.11.2.) was examined in 14 patients with renal cell carcinoma. All cancerous tissues were histopathologically diagnosed as clear cell type. The enzyme was solubilized from the membrane fraction with trypsin. Shiba-isozyme was found in 11 of 14 patients (78.5%). Among them, 5 cancerous tissues showed Shiba-isozyme and normal kidney aminopeptidase N, but the remaining 6 ones showed only Shiba-isozyme. A cell line established from renal cell carcinoma that was 50-th passage had only shiba-isozyme. Shiba-isozyme differed from normal kidney enzyme, but was identical with placental enzyme with respect to electroporetic mobility, isoelectric point, SDS-denaturation and heat stability. Anti-kidney and anti-placental aminopeptidase N antibodies showed similar titration curves against Shiba-isozyme. Double immunodiffusion tests revealed that Shiba-isozyme, kidney and placental enzymes were immunologically identical. These results that Shiba-isozyme is a carcinoplacental isozyme and Shiba-isozyme may be a valuable tumor-marker-enzyme of renal cell carcinoma.

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Platelet serotonin, plasma serotonin, beta-thromboglobulin (β-TG), platelet factor 4 (PF4) and platelet aggregation were studied in 89 patients with renal diseases, in 10 healthy subjects and in 12 diabetes mellitus (without nephropathy) with a proposal to identify platelet involvement in these subjects. Depressed platelet serotonin and raised plasma serotonin, β-TG and PF4 levels were observed in patients with membranous nephropathy (non-nephrotic), proliferative glomerulonephritis with crescents, lupus nephritis (especially diffuse proliferative lupus nephritis) and diabetic nephropathy. However, increases of platelet aggregation were not so remarkable in these patients, moreover, patients with diabetic nephropathy showed decrease platelet aggregation. In the patients with diabetes mellitus, depressed platelet serotonin and raised plasma β-TG were also observed. In comparison with the patients with diabetic nephropathy to diabetes mellitus without nephro-pathy, the levels of plasma β-TG, PF4 and serotonin were higher in diabetic nephropathy, and depre-ssion of platelet serotonin was more remarkable in diabetes mellitus. Therefore, it is considered that there is some difference in degree of platelet activation on these two groups. In our study, patients with lipoid nephrosis have not showed increased platelet aggregation and serotonin release from platelets. The levels of β-TG and plasma serotonin may be modified in severe renal dysfunction because these two parameters were affected by severe renal dysfunction. These results suggest that activated platelet release reaction may play important role on progression of renal diseases.

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Histological findings of the kidney in a case which presented Imerslund's syndrome are reported in this paper. A patient in this case is a boy of 16 years old with chief complaints of proteinuria and anemia. Peripheral blood examination revealed macrocytic-hyperchromic anemia and appearance of megaloblasts in the bone marrow. Activation of intrinsic factors (IF) in the gastric juice was found to be normal, while vitamin B₁₂ as well as vitamin B₁₂-IF compound absorption tests showed low levels of them in the blood. Daily urine protein excretion was 0.3-0.6g with 78.2% of the total being albumin and without hematuria and pyuria. Urineβ-microglobulin increased slightly. Renal functions were normal as well as pyelographical findings. Renal biopsy study showed focal, segmental mild proliferation alone in the mesangial matrix and normal capillary walls, tubules and blood vessels, which were diagnosed as minimal change. Mild deposition of IgM in the mesangial region was observable by immunofluorescent antibody method, while other immunoglobulins, complements and fibrinogen were negative. Electronmicroscopic study showed normal mesangium and glomerular basement membrane. Eighteen researches that had been made abroad on Imerslund's syndrome cases by 1979 described that histological findings of kidneys clarified by lightmicroscopic studies were mostly minimal change. Rumpelt et al. reported based on electronmicroscopic study that there were dilatation of the rough endoplasmic reticulum in the podocytes with accumulation of a finely fibrillar material within the widened cisternae while Collan et al. described that they confirmed appearance of dark deposit in the mesangium.

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One hundred and forty-three patients were treated at the Kidney Center in the Fukuoka University Hospital from December 1974 to September 1981. Seventy-eight patients were treated for end-stage renal disease (ESRD), 14 for acute renal failure, 22 for medical complications of chronic renal failure, 20 for surgical complications and 9 for other reasons including paraquat poisoning and intractable ascites. ESRD group was evaluated just before the initiation of dialysis with respect to age, sex, underlying renal diseases, clinical features, laboratory data and the methods of dialysis. As for blood pressure, 13% was normotensive and 72% hypertensive, of which 13% was resistant to ultrafiltration and required the antihypertensive drugs. Plasma renin activity of the uncontrollable hypertension group was significantly higher that of contrnllable one. The number of the patients with surgical complications requiring operations is increasing, especially those with ophthalmological complications.

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