Patient T.S., a 51-year-old woman, suffered from rheumatoid arthritis at 25 years old and got a remarkable deformity of her fingers at 40 years old. At that time, She was noticed to have hypertension andd proteinuria. On, She suffered from acute tonsillitis and then got a high fever and general edema. On, She was admitted to our hospital. On admission, BP was 186-104 mmHg, BT was 38.8°C, general edema and pericardial-and pleural effusion and ascites was found. The laboratory data were as follows; WBS 2100/mm³, ESR 120 mm (1°) IgG 2300 mg/dl, RA test positive, ANF positive (diffuse pattern) and marked hypocomplementemia. She had a profound proteinuria (4-5g/day) and showed the nephrotic syndrome. Her renal function was severely decreased (GFR 15.3ml/min, RPF 171.7ml/min). The renal biopsy specimens showed active lupus nephritis (MPGN type) by light microscopy and subendotherial dense deposit and segmental circumferential mesangial interposition by electron microscopy. By immunofluorescent microscopy, IgG, IgA, β₁C, C_1q and C₄ was stained granular along the capillary walls and mesangium. We reported a rare overlaping case who suffered from calssical RA which satisfied the criteria of BRA, suffered about 26 years later from lupus nephritis which also satisfied the criteria of ARA.

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Hemodialysis is widely used in the treatment of patients with chronic renal failure m Nevertheless morbidity and mortality among these patients is significant. Thus, it is important to study the effects of hemodialysis in such patients. In this report, 13 autopsy cases of patients treated with hemodialysis were histopathologically studied and compared with 15 autopsy cases of non-hemodialyzed patients with chronic renal failure, In the patients treated with hemodialysis, there were significant findings in many organs. Causes of death in the non-hemodialysis cases were mostly uremia, but in hemodialysis cases they consisted of 4 cases of massive bleeding from multiple gastric and duodenal ulcers, 3 cases of circulatory failure, 3 cases of severe infection and one case of cerebral bleeding. In hemodialysis cases the kidneys were strongly atrophic, and these surfaces showed a fine granular appearence. Microscopically, hyalinized glomeruli, tubules filled with colloid-like material, interstitial fibrosis, small round cell infiltration and arteriolar sclerosis were frequently observed. Common pathological changes of other organs in hemodialysis cases included multiple gastric and duodenal ulcers (69%), hepatic centrolobular fatty changes (77%) and chronic pancreatitis (31%). The frequency of these findings was higher than in non-hemodialysis cases. In the patients treated with long term hemodialysis, atherosclerotic changes of aorta and of the arterioles in several organs were more severe than those in the same-aged patients not on hemodialysis.

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Of 120 cases with primary, fatal glomerular lesions revereled in 7000 serial autopsy materials during the past 15 years, only 3 patients had died from membranous glomerulonephritis. The first patient had suffered for severe nephrotic syndrome for 3 years before his death, and rapidly developed fatal outcome due to acute renal failure. The autopsy revealed severe cellular cresentic glomerulonephritis superimposed on the membranous glomerulonephritis. GBM were electron microscopically diffusely thickend by large number of dense and/or translucent deposits in epimembraneum, without mesangial cells proliferation. The rapidly progressed renal failure had been followed these severe extracapillary (crescentic) glomerulonephritis. The second patient died from complicating pyelonephritis after 7 years from initial manifestation of membranous glomerulonephritis. Necropsy revealed considerable, inflammatory cell infiltration in interstitum, and about 51% obsolescent glomeruli concentrating on the outer cortex in which they may be induced by ischemic renal flow. Residual glomeruli electron microscopically revealed number of dense and/or translucent in the epimembraneum. Mesangial cells, however, did not increase in number. The third patient had had a history of nephrotic syndrome, DM and hypertension, since 111 years, and was admitted with fever, icterus and anasarca. She was suddenly developed fatal renal failure after drip inf usioncholangiography. Autopsy findings comprised diabetic and hypertensioe glomerular lesions overlapped membranous glomerulonephritis which was also electron microscopically comfirmed. Causes of the death of all three patients were not of membranous glomerulonephritis itself, but their complications may lead to fatal outcome, that is, superimposed severe crescentic glomerulonephritis, pyelonephritis or jaundice, DM and hypertension, as aggravating factors. Thus, the prognosis of membranous glomerulonephritis itself seems to be very favorable.

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Serum lipids were studied in onehundred and two non-nephrotic patients with chronic renal failure (CRF). Serum triglyceride (TG) values (mean ± SD) of the patients with CRF were significantly higher (p<0.001) than those of normal controls (103 ± 35 mg/dl) during both pre-dialysis (144 ± 67 mg/dl) and dialysis (202 ± 107 mg/dl) stages. Elevated serum cholesterol level (237 ± 44 mg/dl versus 193 ± 34 mg/dl of controls) was found in post-transplant patients. Eight pre-dialysis patients were fed carbohydrate-rich (64% of total calories) and .poor (47%) diets, each for one week successively, while maintaining an isocaloric level of 1800 Cal and similar polyunsaturated to saturated fatty acid ratio (0.90 versus 0.76). Mean fasting plasma TG level on the carbohydraterich diet was 158 ± 35 mg/dl and decreased to a mean of 118 ± 24 mg dl on the carbohydrate-poor diet. This difference was significant (p<0.02). However, the plasma hepatic and extra-hepatic post-heparinic lipolytic activities showed constant decreased levels through the diet therapy. In conclusion, hypertriglyceridemia may be due to enhanced TG production caused by carbohydraterich diet, which is customary in these patients, superimposed on potentially defective TG-clearing ability in the patients with CRF.

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In order to more fully clarify the suppression of plasma renin activity (PRA) in essential hypertension with low PRA, PRA, plasma aldosterone, serum and urinary sodium, potassium and osmorality were measured in patients with low, normal and high PRA before and after the intravenous administration of furosemide (0.7mg/kg) and 2 hours of ambulation. Before the above test, patients with low PRA showed lower levels of hematocrit, significantly higher levels of serum sodium and serum osmorality than other two groups. After the above test, the same group showed lower blood pressure, more increased urinary volume, more decresed urinary sodium and potassium excretion, higher reabsorption of sodium, and lower reabsorption of free water than other groups. Therefore, it might be concluded that patients with low PRA have abnormalities in renal tubular sodium reabsorption and urinary concentration mechanism as a factor for the suppression of PAR, as compared with other two groups.

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The therapeutical effect of dipyridamole (Dp) on chronic glomerulonephritis and nephrotic syndrome in large administration (300 mg/day and 450 mg/day for 4 weeks) was investigated in a double blind group comparison method This study was started with 34 patients at first, but 6 patients dropped out afterwards. Therefore, 28 patients were finally subjected to our analysis. Among them, 8 were patients with chronic glomerulonephritis (urinary protein : over 2 g/day) and 20 patients with nephrotic syndrome (primary : 15 patients, diabetic : 5) On the average, the decrease rate of urinary protein (D) was 48% in all 28 cases, 41% in 300 mg/day administration group (Group I, 13 cases) and 48% in 450 mg/day administration group (Group II, 15 cases). Average D was also observed 40% in 21 cases who were administered Dp alone (50% in 10 cases of Group I, 30% in 11 cases of Group II ), 78% in 6 cases who were administered a steroidal agent concomitantly (36% in 2 cases of Group I, 99% in 4 cases of Gouup II), and 0.8% in 1 case who was administered a steriodal agent and an immunosuppressive agent concomitantly. The urinaryprotein-decreasing effect of Dp was categorized into "remarkable improvement" (A) in case of D 50/, "slight improvement" (B) in case of 25% < D < 50% and "effective" for A+B, It was found ont that 15 cases fell under A and 4 cases under B in all 28 cases (effective rate : 68%) By groups, 6 cases fell under A and 3 cases under B in Group I (effective rate : 69%), and 9 cases fell under A and 1 case under B in Group II (effective rate : 67%). In other examinations, serum albumin and total cholesterol improved and plasma fibrinogen tended to improve. As a result of histological investigations, effective rates of Dp were obsereved to be high on prolif rateive glomerulonephritis and diabetic nephropathy. Thus, significant difference was not observed in therapeutical effect of Dp on chronic glomerulo nephritis and nephrotic syndrome between administration by 300 mg/day and 450 mg day, so that the 300 mg day administration of Dp seems sufficient for the treatment of renal disease. In case any effect is not produced by the 300 mg/day administration, dose should be increased. Also a great hope can be laid on the effect of the concomitant use of Dp with steroidal agents on steroid-resistant nephrotic syndrome.

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A case of pseudo Bartter syndrome in furosemide abuse was described. The case was 24 year-old female, a nurse, who was admitted because of persistent hypokalemia on, she noted pretibial edema for which furosemide was prescribed by a local doctor. Since then, she had taken about 80 mg of furosemide daily until, when transient cardiac and respiratory arrest developed and serum potassium was found to be 2.0 mEq per liter. The patient was advised to discontinue furosemide. Serum potassium, however, remained inn hypokalemic range in spite of potassium supplementation. At admission she appeared healthy and denied using furosemide, diuretics and laxatives. Serum potassium was 2.4, sodium 143, chloride 90 mEq per liter. Arterial blood pH was 7.477 and plasma bicarbonate 31.3 mEq per liter. Diagnosis of pseudo Bartter syndrome was suspected because of 1) persistent hypokalemia with increases in potassium clearance, plasma renin activity, plasma aldosterone concentration 2) low response of blood pressure to angiotensin II 3) minimal to moderate hyperplasia of J-G apparatus 4) no improvement of clinical condition with indomethacin. After discharge, the patient had been well with persistent hypokalemia until, when she became unconscious abruptly followed by generalized convulsion. Serum potassium was 1.5 mEq per liter. Incidentally it was discovered that she had obtained a lot of furosemide from pharmacy without doctor's prescription. At first she insisted not to take furosemide but finally admitted taking furosemide 280 mg daily. It was quite surprising that she had been taking furosemide continuously even though having episodes of cardiac and respiratory arrest, generalized convulsion which, she should know, might be deeply related to f urosemide usage. It is strongly suggested that furosemide abuse would be one another etiologic condition for pseudo Bartter syndrome and furosemide should not be prescribed without careful supervision.

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