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We report here a case of Sipple's syndrome, and we also analyze the relationship between the type of hypertension and urinary excretion of catecholamines in Sipple's syndrome based on the literature in Japan. One hundred and fourteen cases of Sipple's syndrome have been reported in Japan. The hypertension of patients with Sipple's syndrome shows a ratio of fitfull hypertension to continual hypertension of 6 to 1, whereas the ratio is 1 to 1.5 in patients whose pheochromocytoma is not accompanied by Sipple's syndrome. The patients with Sipple's syndrome, being pheochromocytoma can be classified into the adrenaline (U-AD) dominant type and noradrenaline (U-NA) dominant type based on the catecholamine excretion in the urine. The U-AD predominant (U-AD/U-NA greater than 0.4) patients mostly reveal fitfull hypertension, while patients with continual hypertension hardly show U-AD predominant.

CAPD歴約6か月の51歳, 男性が, 突然, 除水量低下と体重増加が出現し, 胸部X線検査で右側胸水貯留が認められたため, 精査加療目的で入院となった. 末梢の浮腫および炎症所見は認められず, 胸水中糖濃度が血糖より高かったため, 腹膜灌流液の胸腔への移行を疑い, 99mTc-MAAを用いて確定診断を施行した, 本症の治療として, 胸水排出後に自家血の胸腔内注入による胸膜癒着術を試みたところ, 単独では無効であったが, CAPDの短期間中断およびその後に1回注液量を減少させたCAPDを併用することによって効果が得られた. 本療法は, 副作用なしに施行できたが, 永久的な胸膜の癒着が得られるかどうかは不明であり, 今後長期的に経過を観察する必要がある.

The effect of intraperitoneal administration of heparin to patients on continuous ambulatory peritoneal dialysis (CAPD) remains obscure. We examined 8 patients on CAPD to investigate its effect. When 2.5 U/ml or 5 U/ml of heparin was given intraperitoneally, t1/2 of heparin activity in the dialysate was 0.5 to 2 hrs, and 6 hrs after administration its activity was 0.5 U/ml and 1.4 U/ml respectively. Whole blood clotting time was hardly affected because the transfer of heparin to the plasma was minimal. The plasma antithrombin III (AT -III) levels were comparable to patients on hemodialysis, but the AT-111level in the dialysate was only 1.5% of those in the plasma. We conclude that the intraperitoneal administration of heparin at these doses is effective in preventing fibrin precipitation when intraperitoneal AT -III levels are expected to be relatively increased such as at the start of CAPD or in the presence of peritonitis.

We investigated the basal levels and responses of cyclic GMP (cGMP) derived from perfused mesenteric arteries to acetylcholine (ACh) and sodium nitroprusside (SNP) in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) at different ages, in order to evaluate the basal and stimulated release of endothelium-derived relaxing factor (EDRF) from the resistance vessel during the development of hypertension. The mesenteric arteries were removed from 8-, 12- and 20-week-old WKY and SHR, and were perfused with Krebs-Henseleit solution containing 0.2 mM isobutyl methyl xanthine. The effluents from the perfused arteries were corrected before and after infusions of graded doses of ACh or SNP, and the levels of cGMP were measured. The basal levels of cGMP from the msenteric arteries in the 12- and 20-week-old SHR were significantly lower than those in age-matched WKY. A negative correlation was observed between the basal levels of cGMP and the systolic blood pressure in SHR, but not in WKY, among all ages. On the other hand, there were no differences in the responses of cGMP to infusion of ACh between the WKY and SHR at each age. Moreover, the responsiveness of cGMP to in-fusion of SNP in the 12-week-old SHR was much higher than that in age-matched WKY. These data suggest that the basal cGMP formation in the arteries which may reflect the basal release of EDRF is reduced in older SHR and is associated with the development of hypertension, and that the stimulated ralease of EDRF is not associated with the development of hypertension.

A sudden coronary thrombus formation was documented by chance during cardiac catheterization in a patient with postinfarction angina. The thrombus was successfully treated with intravenous urokinase and heparin infusions, and there after, coronary angioplasty was performed without any complication.

We studied, prospectively, the predictive value of late potentials to cardiac sudden death and sustained ventricular tachycardias in 385 patients with myocardial infarction surviving over 4 weeks. Signal averaged electrocardiogram was performed over a 4 week period from the onset of acute myocardial infarction in all patients. Late potentials were observed in 118 of 385 patients. During the mean follow up period of 24.3 months, 17 patients had cardiac sudden death and 15 patients had symptomatic sustained ventricular tachycardias. In 16 of 17 patients with cardiac sudden death and 14 of 15 patients with sustained ventricular tachycardias, late potentials were observed. Sensitivity, specificity, positive predictive value, negative predictive value, and predictive accuracy of late potentials to cardiac sudden death in these 385 patients were 94.1%, 72.3%, 13.6%, 99.6% and 73.2% respectively. Also, these predictive values of late potentials to sustained ventricular tachycardias in the group of patients were 93.3%, 71.9%, 11.9%, 99.6% and 72.7%, respectively. We concluded that the clinical usefulness of late potentials in patients with myocardial infarction surviving over 4 weeks in the negative predictive value to cardiac sudden death and sustained ventricular tachycardias is superior to that of positive predictive value. Sensitivity of late potentials to these events is also higher.

It is known that membranoproliferative glomerulonephritis (MPGN), hypocomplementaemia and C3 nephritic factor (C3NeF) are closely related to each other, and the presence or absence of C3NeF in the serum is important for evaluating the nature of MPGN. However, some difficulties have been encountered in detecting this factor and therefore a new assay permitting the direct detection of C3NeF without purifying IgG from the patient's serum has been devised. Using this assay method, C3bBb-stabilizing activity was observed even in sera from MPGN patients who were non-hypocomplementaemic. Furthermore, among 98 cases with hypocomplementaemia. C3NeF was found to be absent in 66 cases.

In the present study, hog pancreatic kallikrein (HPK, 2,000 KU/kg body weight) was intramuscularly injected into male rabbits and several plasma hormones [kinin, prostaglandin E (PGE), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), thromboxane B2 (TXB2), plasma renin activity (PRA), aldosterone, and ACTH] were measured before and after the HPK administration, in order to clarify the role of glandular kallikrein in the blood. The plasma kinin concentrations were significantly (p less than 0.001) increased from 1 +/- 1 (mean +/- SE), the baseline level, to 230 +/- 22, 288 +/- 36 and 130 +/- 9 pg/ml at 30, 60, and 120 min, respectively, after HPK administration. The plasma level of PGE were slightly increased after HPK administration, but the change was not significant compared to the mean baseline level. The plasma levels of 6-keto-PGF1 alpha were significantly increased from 229 +/- 38, the baseline level, to 594 +/- 131 (p less than 0.05) at 30 min after the administration of HPK and tended to increase (378 +/- 67) at 60 min after the HPK administration, but fell to 278 +/- 37 pg/ml at 120 min after the administration of HPK. On the other hand, the changes in plasma TXB2, aldosterone, ACTH, and PRA before and after HPK administration were not significant. The present results showed that exogenous intramuscular administration of HPK increased the plasma levels of kinin and prostacyclin, but caused no elevation in the plasma levels of other hormones including PRA. It is concluded, therefore, that in this acute experiment, there was a close relationship between the kallikrein-kinin system and prostaglandins.

A 29-year-old Japanese male with a 19-year history of subcutaneous eosinophilic lymphoid granuloma (Kimura's disease) was referred to the Nephrology Service of the Nihon University Hospital for evaluation of edema and massive proteinuria. The renal biopsy disclosed minimal glomerular lesions. In this paper a case of nephrotic syndrome associated with eosinophilic lymphoid granuloma is reported.

Plasma renin activity (PRA) was measured in 14 control subjects and 27 patients with essential hypertension (EH) (low renin group: 9, normal renin group: 11, and high renin group: 7) before and after the following stimulation tests. Test procedures: 1) Circadian rhythm (0600, 1600 and 2400h). 2) Adrenal stimulation test (ACTH: 12.5 I.U.). 3) Adrenal suppression test (Dexamethasone: 1.0 mg). 4) Metopirone test (1.5 g). 5) Angiotensin II infusion test (8 ng/kg/min). 6) Saline infusion test (1000 ml/hr). Patients with low PRA showed significantly lower levels of PRA than those of other two groups in circadian rhythm, after 2 hours of ACTH infusion and after angiotensin II infusion. Furthermore, these patients showed significantly higher responses of PRA than other two groups after furosemide test under dexamethasone and after metopirone test. In case of saline infusion test, patients with low and normal PRA did not show significantly decreased levels of PRA after the infusion, though all patients with high PRA and all control subjects showed significantly decreased levels of PRA. From the present studies, it might be concluded that patients with low PRA has an unknown mineralocorticoid excess which is ACTH dependent and 11 hydroxylated and some of hypertensive patients have an abnormality in their renin-angiotensin-aldosterone volume feed back loop as a factor for hypertension.

Spironolactone was administered to spontaneously hypertensive rats (SHRs) in order to examine the urinary excretions of prostaglandin E2 (PGE2) and kinin. Thirteen SHRs were divided into 2 groups, and 0.1 ml of sesame oil was administered to one of 2 groups (spironolactone-untreated group) (n = 6) and 20 mg of spironolactone in 0.1 ml of sesame oil was administered to the other group (spironolactone-treated group) (n = 7) by the subcutaneous route for 10 days in succession, followed by the determination of body weight, blood pressure, urine volume, excretion levels of Na, K, kinin and PGE2 in 24-hour urine. Blood samples were drawn after these animals were killed by decapitation for determining plasma renin activity (PRA). In consequence, decreased blood pressure and increased urinary Na excretion were observed in the spironolactone-treated group. On the other hand, PGE2 excretion level in 24-hour urine markedly decreased immediately after administration of spironolactone (p less than 0.05) and was maintained at lower levels up to the end of experiment. However, 24-hour urinary kinin levels showed similar changes in the spironolactone-treated group and the untreated group with no significant difference between the two groups. These results indicate that spironolactone has a suppressive effect on urinary PGE2 excretion, the activity of which is not mediated by kinin production in the kidneys but produced by a direct action of spironolactone itself.

Cell-mediated immunity (CMI) was evaluated in 26 patients with lipoid nephrosis (LN), 50 patients suffering from chronic diffuse proliferative glomerulonephritis (CGN) without renal sufficiency and 24 healthy controls. The following parameters were measured: delayed hypersensitivity skin test responses to purified protein derivative (PPD) and candida, circulating lymphocytes. T lymphocytes and T lymphocytes with receptors for the Fc portion of IgG (T gamma cells) or IgM (Tmu cells). Patients with LN in relapse had less mean induration of skin reactivity and a smaller proportion reacting to both antigens as compared with the control subjects. In contrast, the intensity of skin reactivity and the frequency of negative reactions in patients with LN in remission and CGN were similar to those of the control subjects. It was also found that the LN patients in relapse had a significant T lymphocytopenia as well as a significant decrease in absolute numbers of Tmu and T gamma cells, whereas the patients with LN in remission and CGN did not differ significantly from the control population. Thus, the majority of patients with LN in relapse demonstrated an impaired response in a CMI assay system. The disturbed CMI may be secondary to hypoproteinemia and other nutritional factors induced by the nephrotic syndrome.

Forty-eight patients with a variety of primary renal diseases and systemic lupus erythematosus (SLE) were examined for the proportion of circulating T lymphocytes bearing receptors for IgM (T mu cells) or IgG (T gamma cells). Although the control group showed strikingly similar mean values for both T mu and T gamma cells, the whole group of patients with primary renal diseases and SLE showed a wide scatter of values. Sixteen patients with primary renal diseases and SLE had higher proportions of T gamma cells than the control group, whereas seven patients with chronic glomerulonephritis (CGN), membranoproliferative glomerulonephritis (MPGN), lipoid nephrosis (LN), and SLE showed very marked decrease in the proportions of T gamma cells in the peripheral blood. On the other hand, six out of the total group of patients had low proportions of T mu cells in the peripheral blood. However, no consistent relationship between the proportion of T mu and T gamma cells was found in our study. These findings indicate that there exists a heterogeneity of T-lymphocyte subpopulation distribution in some patients with primary renal diseases and SLE. The possible significance of these phenomena in the pathophysiology of renal diseases is discussed.

The locus coeruleus was subjected to biphasic electrical stimulation, and a group of deoxycorticosterone acetate (DOCA)-salt hypertensive rats revealed a greater pressor response than a group of normotensive control rats. The pressor threshold current (i.e. minimum current to raise the arterial pressure by 10 mm Hg) of DOCA-salt hypertensive rats was also lower. The threshold current was low even in the prehypertensive stage of DOCA-salt treated rats. During arterial pressure fall, the pressurethreshold current lowered only in normotensive rats and neither group underwent a change during pressure rise. These data indicated that the locus coeruleus had a pressor role and it had been accelerated in DOCA-salt treated rats before hypertension was evident. Following bilateral electrical lesions of the locus coeruleus no significant differences were observed in the arterial pressure changes, while vascular reactivity to norepinephrine did not differ between the two groups. The results suggest that the locus coeruleus may be involved in the development of hypertension but may not be important in the maintenance of it.

The effects of somatostatin on plasma renin activity (PRA) and blood pressure were evaluated in patients with essential hypertension (EH) and in normotensive subjects. All subjects examined were hospitalized and placed on a diet containing 7-8 g/day sodium chloride and received an intravenous infusion of somatostatin (500 microgram/20 ml of saline, for 60 min) in the basal condition. During somatostatin infusion, the mean blood pressure (MBP) remained unaffected in all patients with EH and the normotensive subjects, while the PRA decreased slightly in the EH group. When the patients with EH were classified according to their renin levels (low, normal and high), parallel significant decreases in MBP and PRA were found only in the high renin group during the somatostatin infusion. No significant change in MBP and PRA was observed in the other groups including the normotensive subjects. To assess the activity of synthetic somatostatin, the plasma levels of growth hormone (GH) and cyclic AMP were measured. These levels were lowered significantly during the infusion and the GH levels showed a rebound 15 min after cessation of the infusion. The cyclic AMP returned to the basal levels, but no rebound was observed. The above data indicate that the fall in blood pressure in the high renin group in the basal condition was probably due in part to reduced renin release by somatostatin, and the maintenance of high blood pressure especially in high renin EH.

Although mucolipidosis, a fatal metabolic storage disorder, is associated with cardiovascular abnormalities, detailed, non-invasive cardiac examinations have not been well documented. We studied 4 children with type II and type III mucolipidosis, 3 of whom had unequivocal evidence of aortic regurgitation characterized by phonocardiography and M-mode echocardiography. Two-dimensional echocardiography showed an aortic valve prolapse in 3, a mitral valve prolapse in 2 and a tricuspid valve prolapse in 1. The QT interval was prolonged in 2 cases. In 1 autopsy case, we found considerably thickened and retracted aortic, mitral, and tricuspid valves, and accumulation of the foam cells in the myocardium. Echocardiography revealed similar findings in another 3 cases. We conclude that cardiac manifestations in this disorder should be examined carefully particularly by the use of echocardiography which is an excellent technique for detecting cardiovascular abnormalities in mucolipidosis.

When the ventricle is electrically stimulated at a faster rate, the cessation of the drive is followed by a temporary suppression of automaticity (overdrive suppression). The effects of lidocaine and verapamil on overdrive suppression were studied in dogs. Lidocaine slowed the ventricular escape rate and prolonged the pause following overdrive; occasionally, it was about twice the next succeeding RR interval. On the contrary, verapamil influenced neither the ventricular escape rate nor the pause following overdrive. It is suggested that lidocaine not only suppresses the automaticity of ventricular escape pacemaker but also induces exit block and that the spontaneous depolarization of the ventricular pacemaker is not slow channel-dependent.

Alterations in the concentration of plasma dehydroepiandrosterone sulfate (DHEA-S) and cortisol in patients with essential hypertension (EH) were investigated. The subjects were 25 patients with EH: 7 of low plasma renin activity (PRA) group, 10 of normal PRA group and 8 of high PRA group; 7 normal subjects were used as the controls. Plasma DHEA-S and cortisol were measured before and after the following tests: (1) circadian rhythm (6:00, 16:00 and 24:00), (2) furosemide (0.7 mg/kg) test, (3) ACTH (12.5 IU/4 hr) infusion test, (4) dexamethasone (1.0 mg) test, (5) furosemide (0.7 mg/kg) test under dexamethasone (1.0 mg) treatment, (6) metopirone (1.5 g) test, (7) angiotensin II (8 ng/kg/min, 30 min) infusion test and (8) saline (1000 ml/hr) test. The alterations of the endogenous ACTH-adrenal hormone system as well as the renin-angiotensin-aldosterone system induced by these tests did not cause significant changes of plasma levels of DHEA-S in the 3 groups with EH. However, significant enhancement of plasma DHEA-S was observed after both the administration of exogenous ACTH and angiotensin II. It is considered that the responsiveness of DHEA-S to ACTH may increase in the low and normal PRA groups and that the responsiveness of DHEA-S to angiotensin II may increase in the high PRA group. Based on these results, it is suggested that plasma DHEA-S hardly or only partially participates as a causal factor of EH.

To determine whether patients with systemic lupus erythematosus (SLE) and active nephritis have more profound defects in suppressor cell activity, we studied concanavalin A (Con A)-induced suppressor cell activity (SCA) in 12 patients with lupus nephritis (LN) and 11 patients with chronic mesangial proliferative glomerulonephritis (CGN) without renal insufficiency. The levels of Con A-induced SCA were decreased in patients with LN compared with those in normal controls and those in CGN patients and lower in LN patients with the nephrotic syndrome (NS) than in those without NS. In contrast, the mean responses of Con A-induced SCA in CGN patients with or without NS did not differ from normal subjects. These findings may lend further insight into the understanding of the immunoregulatory defect in LN.

症例は21才男性.減量を目的に6カ月間に約50kg体重を減少させ,全身倦怠感,意識消失発作を来したため入院となった.入院時,心電図上心拍数36回/分の洞性徐脈を認め,心エコーでは心膜液貯留を認めた.また頭部CTスキャンでは脳萎縮を認めた.血液検査では甲状腺機能検査においてlow T3 syndromeを呈し,さらに経過中, GH値の高値,一過性のGOT, GPT値の上昇等を認めた.本症例は著しい体重減少をきたしているものの,入院時,標準体重を示していることから,我国における神経性食欲不振症の診断基準にあてはまらないが,臨床経過等を総括すると,多彩な臨床症状を呈した神経性食欲不振症の男性例と考えられた.

Fibrinopeptide A (FPA) in both urine and plasma was measured using radioimmunoassy in order to confirm the presence of intrarenal coagulation in renal disease. Patients were divided into 2 groups according to the urinary FDP (mg)/urinary protein (g) ratio: Group A, patients with above 1.0 of the ratio. Group B, patients with less 0.5 of the ratio.The results were as follows: (1) Urinary FPA did not correlate to plasma FPA. (2) Urinary FPA were significantly high in group A, but were normal in group B. (3) The renal functions of group A were all markedly deteriorated. But, the renal functions of group B showed widely spread values. (4) Heparin administration on group A patients reduced their urinary FPA with improvement of renal functions and azotemia.These results indicate: (1) Above 1.0 of urinary FDP (mg)/urinary protein (g) ratio and high urinary FPA reflect the presence of extensive intrarenal coagulation. (2) Extensive intrarenal coagulation was occured only in the patients with markedly deteriorated renal functions. (3) These patients were only a few in renal disease patients. (4) It might be difficult to get good clinical improvement in chronic patients even when intrarenal coagulation is both accuratetly detected and completely eliminated by anticoagulants. (5) However, anticoagulant therapy has proved to be benificial in acute pacients with extensive intrarenal coagulation.

A simplified screening test for differentiating primary aldosteronism (PA) from low renin essential hypertension (LREH) is presented. Nine patients with LREH and 5 patients with PA due to adrenal adenoma were studied. In the patients with LREH, the levels of plasma renin activity (PRA) before and after treatment with furosemide (0.7 mg/kg, i.v.) and a 2-hour ambulation under treatment with dexamethasone (1.0 mg) (dexamethasone + furosemide test) increased briskly, compared to the levels of PRA before and after treatment with furosemide (0.7 mg/kg, i.v.) and a 2-hour ambulation (furosemide test). In patients with PA, there was no significant difference between the mean levels before the furosemide test and before the dexamethasone + furosemide test, or between the mean levels after the furosemide test and after the dexamethasone + furosemide test. These results suggest that the suppression of PRA in patients with LREH may be related to a factor controlled by dexamethasone. It is concluded that the dexamethasone + furosemide test is useful for differentiating PA due to adenoma from LREH.

To clarify the vasoconstrictory action of leukotriene D4 (LTD4) on the injured coronary arteries, 8 mongrel dogs were denuded by basket balloon catheter (denuded group) and LTD4 (0.33μg) was directly administered into left anterior descending coronary artery. Hemodynamic parameters as well as epicardial ECG were recorded after LTD4 administration. Another 8 non-denuded dogs were served as control.Furthermore, the influence of denudation to LTD4-induced coronary spasm was determined by coronary arteriography (CAG) . In results, a significant reduction of coronary blood flow (from 1.03±0.13 to 0.49±0.05 ml/kg/min. P

The influence of a Mg-deficient diet on blood pressure and various hormonal systems was examined in Wistar rats (WR) and spontaneously hypertensive rats (SHR). The WR and SHR were individually divided into 2 groups. The Mg-deficient diet was given to one group, and a Mg-containing diet was given to the other group for 3 weeks. During this experimental period, the body weight, blood pressure, urine volume, blood and urinary electrolytes, plasma steroid hormones, plasma renin activity (PRA), and urinary hormones [kinin, prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and noradrenaline] were examined. Although no significant difference in body weight was observed between the Mg-deficient and Mg-containing diet groups in either the WR or SHR (because the experiments were performed in a pair-fed fashion in both kinds of rat), the blood pressure was increased in the Mg-containing diet group but was unchanged in the Mg-deficient diet group. As regards changes in electrolytes, a decreased urinary excretion of Mg and significantly increased urinary excretion of P were observed in the Mg-deficient diet group in both the WR and SHR. Furthermore, decreased levels of serum Mg and P and increased levels of serum Ca were also noted. In the WR group, the urinary excretion of noradrenaline was significantly increased in the Mg-deficient diet group as compared to the Mg-containing diet group. However, the change was reversed in the SHR group. The plasma steroid hormones and PRA were both significantly low in the Mg-deficient diet group in both the WR and SHR. The urinary excretions of PGE2, 6-keto-PGF1 alpha, and kinin showed no significant differences between the two diet groups. The above results indicate that blood pressure is not affected by the Mg-deficient diet in either the WR or SHR, and the possible participation of the sympathetic nervous system in the mechanism of control of blood pressure may differ somewhat between the WR and SHR. In addition, Mg ion was found to play an important role in the biosynthesis of renin and steroid hormones but to have no such significant role in the urinary excretions of kinin, PGE2, and 6-keto-PGF1 alpha.

The pituitary-adrenocortical response to ovine corticotropin-releasing factor (CRF) was investigated in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) anesthetized with pentobarbital. After intravenous administration of various doses of CRF (0.1, 1.0 and 10 micrograms), the plasma levels of ACTH were significantly increased in both groups. ACTH increments after various doses of CRF were dose-dependent in WKY. ACTH increments after injections of 0.1, 1.0, and 10 micrograms of CRF in SHR were 123.2 +/- 36.5 (SE), 123.0 +/- 52.2 and 60.3 +/- 48.5 pg/ml at 5 min, and 386.3 +/- 73.8, 243.4 +/- 86.6 and 220.0 +/- 31.4 pg/ml at 15 min, respectively. The ACTH increments in SHR at 15 min after administration of 0.1 microgram of CRF were higher (p less than 0.02) than those in WKY. However, ACTH increments in SHR after administration of 10 micrograms of CRF were lower than those in WKY at 5 min (p less than 0.05) and 15 min. These data suggest that the plasma ACTH responses to various doses of CRF represent a dose-unrelated plateau response in SHR. The plasma levels of corticosterone after administration of various doses of CRF did not change significantly and there were no significant differences between the two strains. The results of these experiments suggest that SHR have an abnormal response of the pituitary-adrenocortical axis to CRF, and the abnormal response may be attributable to desensitization of the pituitary to CRF.

The T-colony-forming capacity was examined in 13 normal subjects and 8 patients with biopsy-proven focal glomerular sclerosis (FGS). Fifteen patients with chronic mesangial proliferative glomerulone-phritis (CGN) without renal insufficiency were studied as a disease control. The two main assays used were the counting of T colonies formed by the patients’ lymphocytes, and the measurement of T-colony-forming activity in conditioned medium from cultures of patients’ lymphocytes. The levels of T-colony-forming cells (TCFC) and T-colony-stimulating factor (TCSF) were decreased in patients with FGS compared with those in normal controls and lower in FGS patients with the nephrotic syndrome (NS) than in those without NS. In contrast, these parameters in CGN patients with or without NS did not differ from normal subjects. TCSF activity for TCFC in both normal individuals and FGS patients was removed from media conditioned by phytohemagglutinin (PHA)-stimulated peripheral blood lymphocytes (PHA-LCM) with interleukin-2 (IL-2) receptor bearing cultured T cells. These in vitro findings suggest that IL-2 is the essential factor contained in PHA-LCM. Thus, depressed TCFC in FGS ptients with NS may result in part from impaired generation of TCSF by lymphocytes.