Immunoglobulins (IgG, IgA, IgM, IgE) and complement components (C3, C4) in nephrotic syndrome due to minimal change and other forms of glomerulonephritis, a clue for steroid therapy?

Serum IgG, IgA, IgM, IgE, C3 and C4 were measured in 13 patients with minimal change (MC) glomerulonephritis and 10 with the nephrotic syndrome (NS) due to other forms of glomerulonephritis. The tests were repeated in all patients with MC glomerulonephritis when they went into remission. Serum IgG was reduced, IgM, IgE and C3 were raised while serum IgA was within the normal range when the patients were nephrotic. Changes in serum immunoglobulins and complement components were not specific to MC glomerulonephritis and these parameters reverted towards normal when the NS went into remission. Elevated C3 levels probably reflected increased hepatic protein synthesis since C3 correlated significantly with serum cholesterol. There was a tendency for serum IgE concentrations to positively correlate with the total dose of prednisolone required to bring the NS to remission.     

Nephrotic origin hyperlipidemia, relative reduction of vitamin E level and subsequent oxidative stress may promote atherosclerosis

BACKGROUND: The relation between nephrotic syndrome and atherosclerosis has not yet been fully clarified, although the high levels of low-density lipoprotein cholesterol usually found in this syndrome may give rise to atherosclerosis. This study was intended to test the disturbances of antioxidant/oxidant status in children with nephrotic syndrome (NS). METHODS: 8 children in the active stage (AS) of NS, 7 children during the remission stage (REM) of NS, and 14 control subjects (CTRL) were enrolled into the study. The levels of plasma total cholesterol (TC), HDL-cholesterol (HDL-chol), LDL-cholesterol (LDL-chol), triglycerides (TG), vitamin E and 7-ketocholesterol (7KCH) before and after plasma saponification were measured. RESULTS: A significant increase in the concentrations of TC, LDL-chol, vitamin E and total 7KCH in AS patients have been found. These patients had also a lower vitamin E/LDL-chol ratio. These changes have not been observed in the remission stage of nephrotic syndrome. Higher amounts of electronegatively charged-(oxidized) LDL particles as well as different oxysterols in AS patients have also been demonstrated. CONCLUSION: The study revealed significant disturbances in oxidant status during NS leading to plasma accumulation of oxidized LDL and cholesterol oxidation products that exert cytotoxicity and are known to induce atherosclerosis. We suggest that this may constitute an important link between nephrotic syndrome and atherosclerosis.     

Lovastatin therapy in nephrotic hyperlipidemia: effects on lipoprotein metabolism

The nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, and hypercholesterolemia. Hypertriglyceridemia often is present as well. In this study, the kinetics of plasma lipoproteins were investigated in four patients with nephrotic hyperlipidemia, and repeat studies were carried out in three of these patients during therapy with lovastatin. Before lovastatin therapy, the patients had an extremely delayed catabolism of very low density lipoproteins (VLDL) without evidence of overproduction of lipoproteins in this fraction. Three of four patients had elevated levels of low density lipoprotein (LDL) that were due mainly to increased production rates for LDL. In the three patients treated with lovastatin, the drug therapy lowered plasma concentrations of total cholesterol, triglycerides, VLDL-cholesterol, and LDL-cholesterol, and raised high density lipoprotein (HDL)-cholesterol. Lovastatin therapy decreased VLDL-triglycerides primarily by enhancing their catabolism, and lowered LDL-cholesterol levels mainly by reducing input rates for LDL. Overall, lovastatin appears to be an effective drug for the treatment of hyperlipidemia in the nephrotic syndrome.     

Albumin synthesis, albuminuria and hyperlipemia in nephrotic patients

Hyperlipemia is a common manifestation of the nephrotic syndrome. Serum lipid concentrations have been observed by others to be negatively correlated with serum protein concentration. Hyperlipemia has been postulated to result from a coordinate increase in the synthesis of both albumin and lipoproteins, as well as from their decreased catabolism. Simultaneous measurements of serum lipid concentration and the rate of albumin synthesis have not been previously reported. We measured the rate of albumin synthesis, urinary albumin loss, serum albumin, protein, cholesterol and triglyceride concentration in 13 nephrotic patients. Changes in the rate of albumin synthesis and in urinary albumin excretion were induced in eight patients by alteration in dietary protein intake. The resultant changes in serum triglyceride and cholesterol were analyzed by multiple regression analysis. The rate of albumin synthesis measured while patients were eating a low protein diet was 12.61 +/- 1.20 g/1.73 m2/day, well within normal limits, yet both serum triglyceride and cholesterol concentrations were markedly elevated (265 +/- 65 mg/dl and 325 +/- 44 mg/dl, respectively). Albumin synthetic rate increased to 17.60 +/- 1.25 g/1.73 m2/day when dietary protein intake was increased, while serum triglyceride and cholesterol concentrations changed little; triglyceride concentration was 306 +/- 75 mg/dl and cholesterol 376 +/- 55 mg/dl. Serum cholesterol concentration, by multiple regression analysis, was dependent only upon the renal clearance of albumin P less than 0.0001, and changes in serum cholesterol concentration was dependent only upon changes in the renal clearance of albumin, P less than 0.001. Serum cholesterol concentration was completely independent of the rate of albumin synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dyslipidemia and nephrotic syndrome: recent advances.

Patients with nephrotic syndrome (NS) have one of the most pronounced secondary changes in lipoprotein metabolism known, and the magnitude of the changes correlates with the severity of the disease. These changes are of a quantitative as well as a qualitative nature. All apolipoprotein B (apo B)-containing lipoproteins, such as very-low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and lipoprotein(a) [Lp(a)], are elevated in nephrotic syndrome. High-density lipoproteins (HDL) are reported to be unchanged or reduced. In addition to these quantitative changes, the lipoprotein composition is markedly changed, with a higher ratio of cholesterol to triglycerides in the apo B-containing lipoproteins and an increase in the proportion of cholesterol, cholesterol ester, and phospholipids compared with proteins. Also apolipoproteins show major changes, with an increase in apolipoprotein A-I, A-IV, B, C, and E. Particularly the changes in apo C-II, which is an activator of the enzyme lipoprotein lipase (LPL), and apo C-III, an inhibitor of LPL, with an increase of the C-III to C-II ratio, might contribute to the impaired lipoprotein catabolism in NS. The mechanisms for these changes in lipoprotein metabolism are discussed in this review as far as they are known. Furthermore, the tremendous elevations of Lp(a) in nephrotic syndrome and its primary and secondary causes are reviewed. Primary causes became recently apparent by a significantly higher frequency of low-molecular-weight apo(a) phenotypes in patients compared with controls. The secondary causes were shown by an increase of Lp(a) in all apo(a) isoform groups. Because Lp(a) is an LDL-like particle that is usually included in the measured or calculated LDL cholesterol fraction, the influence of the extremely high Lp(a) levels in NS on the measurement of LDL cholesterol is discussed.     

Serum vitamin A,retinyl esters and vitamin E in nephrotic syndrome

Serum vitamin A, retinyl esters and vitamin E were increased in a group of 33 patients with chronic glomerulonephritis and nephrotic syndrome without reduction of mean glomerular filtration rate. Despite hypoproteinaemia and reduced values of serum proteins with a different molecular weight, increased values of vitamin A protein carriers were found. Serum total cholesterol, LDL cholesterol, triglyceride, prebeta und beta lipoproteins were increased, HDL cholesterol was within the reference range. Direct relationships were found between serum retinyl esters and vitamin A, and between serum retinyl esters and prealbumin. Indirect relationships were detected between serum total cholesterol and total proteins, serum total cholesterol and albumin, and serum vitamin E and albumin. The increased values of vitamin A, retinyl esters as well as of its protein carriers and of vitamin E were probably a manifestation of enhanced protein and lipid synthesis in the liver as a result of albumin depletion. These results show true A and E hypervitaminosis in patients with nephrotic syndrome.     

Serum apolipoproteins A and B, lecithin: cholesterol acyl transferase activities and urinary cholesterol levels in nephrotic syndrome patients before and during steroid treatment

Serum apolipoproteins A (Apo-A) and B (Apo-B) and lecithin: cholesterol acyl transferase (LCAT) activities and 24-hour urinary cholesterol levels were estimated in 25 nephrotic children before and during steroid treatment with 4 weeks of daily prednisolone followed by another 4 weeks of alternate-day prednisolone. The patients with untreated nephrotic syndrome (NS) showed significant decrease in serum Apo-A and LCAT activities associated with significant increase in serum Apo-B and urinary cholesterol levels compared to healthy controls (n = 25). Serum Apo-A levels correlated directly and Apo-B levels inversely with the serum albumin concentrations. After a transient elevation, the serum Apo-A level returned to control range by 8 weeks of treatment accompanied by a gradual increase in serum LCAT activity and decrease in urinary cholesterol excretion. Though, the serum Apo-B level was decreased with treatment, it was still significantly high compared to the controls.     

Effects of HMG-CoA reductase inhibition on hepatic expression of key cholesterol-regulatory enzymes and receptors in nephrotic syndrome

BACKGROUND: Hypercholesterolemia is one of the major manifestations of nephrotic syndrome. We have previously shown that nephrotic hypercholesterolemia is associated with and, in part, due to dysregulation of hepatic HMG-CoA reductase, acyl-CoA:cholesterol acyltransferase (ACAT) and cholesterol 7alpha-hydroxylase, as well as lecithin:cholesterol acyltransferase (LCAT), low-density lipoprotein (LDL) receptor and high-density lipoprotein (HDL) receptor deficiencies. This study was carried out to discern the effect of inhibition of HMG-CoA reductase on expression of the key enzymes and receptors involved in cholesterol metabolism in the liver. METHODS: Rats with puromycin-induced nephrotic syndrome were treated with either a statin (rosuvastatin 20 mg/kg/day) or placebo for 2 weeks. Placebo-treated normal rats served as controls. Gene expression, protein abundance and/or activities of relevant receptors and enzymes were quantified. RESULTS: The untreated nephrotic rats showed heavy proteinuria, hypoalbuminemia, hypercholesterolemia, elevated total cholesterol:HDL cholesterol ratio and normal creatinine clearance. This was associated with severe reductions in hepatic LDL receptor, hepatic HDL receptor and plasma LCAT concentration, marked upregulation of hepatic ACAT, and unchanged cholesterol 7alpha-hydroxylase (rate-limiting step in cholesterol catabolism). Statin administration for 2 weeks ameliorated hepatic LDL receptor and HDL receptor deficiencies and significantly lowered plasma cholesterol, LDL cholesterol, total cholesterol:HDL cholesterol ratio and proteinuria. CONCLUSIONS: HMG-CoA reductase inhibition improved hepatic LDL and HDL receptor deficiencies, and ameliorated the associated hyperlipidemia in the nephrotic rats.     

Albumin metabolism in the nephrotic syndrome: the effect of dietary protein intake

The nephrotic syndrome is characterized by increased urinary excretion of albumin and other serum proteins, accompanied by hypoproteinemia and edema formation. Nephrotic patients have lower serum albumin concentrations than do patients undergoing continuous ambulatory peritoneal dialysis when albumin and protein losses are the same in both groups, suggesting that nephrotic patients may not maximally adapt to loss of protein. The fractional rate of albumin catabolism is increased in nephrotic patients, possibly as a result of increased albumin catabolism by the kidney, but the absolute albumin catabolic rate is decreased in nephrotic patients. The rate of albumin synthesis may be increased, but not sufficiently to maintain normal serum albumin concentration or albumin pools. Augmentation of dietary protein in nephrotic rats directly stimulates albumin synthesis by increasing albumin mRNA content in the liver, but also causes an increase in glomerular permeability to macromolecules so that much if not all of the excess albumin synthesized is lost in the urine. When dietary protein is restricted, the rate of albumin synthesis is not increased either in nephrotic patients or in rats, despite severe hypoalbuminemia. Although dietary protein supplementation may lead to positive nitrogen balance, dietary protein supplementation alone does not cause an increase in serum albumin concentration or body albumin pools, and may instead cause further albumin pool depletion because of changes induced in glomerular permselectivity. The use of angiotensin-converting enzyme inhibitors may blunt the increased albuminuria caused by dietary protein supplementation and allow albumin stores to be increased.     

Low-density lipoprotein apheresis in a pediatric patient with refractory nephrotic syndrome due to focal segmental glomerulosclerosis

Focal segmental glomerulosclerosis (FSGS) often leads to refractory nephrotic syndrome (NS). A high level of low-density lipoprotein (LDL) is a risk factor for the progression of NS. An 8-year-old girl presented with severe proteinuria refractory to steroid therapy. She was diagnosed with non-IgA diffuse mesangial proliferative glomerulonephritis. Oral prednisolone, methylprednisolone (mPL) pulse therapy, and cyclosporine and cyclophosphamide therapy failed to achieve remission. Follow-up renal biopsy revealed FSGS. Her serum level of LDL was high, and LDL-apheresis (LDL-A) was performed five times, followed by mPL pulse therapy. Urinary protein decreased from 2–4 g·day⁻ to 0.5–1.0 g·day⁻. LDL-A may be beneficial in the treatment of multidrug-resistant FSGS.     

Hyperlipidemia in childhood nephrotic syndrome

Hyperlipidemia is an important characteristic of nephrotic syndrome (NS). Elevation of plasma total cholesterol, or more specifically low-density lipoprotein cholesterol, is the major lipid abnormality in NS, although hypertriglyceridemia may develop as the disorder progresses. The pathophysiology of nephrotic hyperlipidemia is complex. The prevailing view is that both hepatic synthesis of lipids and of apolipoproteins is increased, and that the clearance of chylomicrons and very low-density lipoproteins is reduced. The precise contribution of increased lipogenesis and decreased lipid catabolism to hyperlipidemia, and their relationship to urinary protein loss, hypoalbuminemia and reduced serum oncotic pressure remain controversial. There are two potential risks of elevated plasma lipids: atherosclerosis and progression of glomerular injury. Although neither of these complications has been proved with certainty, there is growing evidence that both may be long-term consequences of NS. Therefore, the diagnosis and treatment of lipid abnormalities, important aspects of the management of nephrotic children, is summarized here to provide pediatric nephrologists with an informed choice.     

Beneficial effects of ACTH on the serum lipoprotein profile and glomerular function in patients with membranous nephropathy.

BACKGROUND: Previous studies have shown that short-term treatment with adrenocorticotrophic hormone (ACTH) has a strong and rapid lipid-lowering effect. In this long-term study of nephrotic patients with idiopathic membranous nephropathy, the influence of ACTH on the serum lipoprotein profile and glomerular function as well as the dose-effect relationship was investigated. METHODS: Fourteen patients received ACTH intramuscularly at increasing doses during 56 days. Serum concentrations of lipids, lipoproteins, and apolipoproteins as well as variables of glomerular function were analyzed, and the side-effects were recorded. ACTH treatment, in the estimated optimal dosage, was then continued in five patients with severe steroid-resistant nephrotic syndrome. In these five patients, the total treatment period was 12 months, and the follow-up time after discontinuing treatment was 18 months. RESULTS: Taking both the statistically significant therapeutic effects and the modest side-effects into consideration, the optimal dosage of ACTH was estimated to be 1 mg twice per week. At that dose, reductions by 30 to 60% in the serum concentrations of cholesterol, triglycerides, apolipoprotein B, and lipoprotein(a) were observed, whereas the serum concentrations of high-density lipoprotein cholesterol and apolipoprotein AI rose by 30 to 40%. In addition, the urinary albumin excretion decreased by 90%, and the glomerular filtration rate increased by 25%. Deterioration was observed in all cases when ACTH was discontinued after a treatment duration of 56 days. However, the five patients in whom ACTH therapy was resumed were still in remission 18 months after discontinuance of treatment. CONCLUSIONS: In nephrotic patients with idiopathic membranous nephropathy, treatment with ACTH 1 mg twice per week was associated with significant long-term improvements in serum lipoprotein pattern and glomerular function.     

Histopathological and immunological studies in spontaneous remission of nephrotic syndrome after intercurrent measles infection

Two cases of childhood nephrotic syndrom (NS) were diagnosed in September 1981 and February 1982, respectively. The patients were first cousins. There was no other family history of renal disease. Five months after onset of nephrosis in 1 patient and 1 month after onset of nephrosis in the other both had an intercurrent measles infection and the NS rapidly went into spontaneous remission. However, relapses occurred 3 and 7 months later. At that time both patients were started on steriod treatment and obtained remission. Unfortunately, both relapsed again 14 months later. Kidney biopsies were performed, the pathologic findings demonstrated that both were mild mesangial proliferative glomerulonephritis. The mononuclear cell subsets and lymphoproliferative responses were studied during the acute measles infection, 4 weeks later, in remission and relapse of NS. The mononuclear cell subsets and lymphoproliferative response in medium containing autologous serum with complement were decreased during the acute measles infection. Both patients had an increase of OKT8 cells and Leu-7 cells in relapse and a decrease in remission. Taken together, natural measles infection caused a prolonged depression of cell-mediated immunity, T cell subset and induced a temporary remission of steroid-sensitive NS.     

Relationship between serum albumin concentration and tubular reabsorption of glucose in renal disease

Micropuncture studies in rats and dogs have provided evidence for a cause-and-effect relationship between peritubular protein concentration and proximal tubular reabsorption (PTR). If this effect is obtained in man, hypoalbuminemia in nephrotic syndrome should lead to a fall in PTR. Sodium excretion, however, is very low in nephrotic patients; but this sodium retention may be due to distal over-reabsorption. Glucose may be used as a marker of PTR. Because of the linkage between glucose and sodium, glucose reabsorption is expected to be suppressed when PTR of sodium is suppressed. Glucose titration studies were performed in 21 patients with chronic glomerulonephritis without renal failure divided in three groups: I (six patients) with serum albumin greater than 3 g/100 ml; II (five patients) with serum albumin of 2 to 3 g/100 ml; and III (10 patients with edema and nephrotic syndrome) with serum albumin less than 2 g/100 ml. The minimum threshold for glucose decreased in nephrotic patients (group III), and its fall was related directly to hypoalbuminemia. The splay of titration curve was markedly increased in group III when compared to the titration curves of patients without nephrotic syndrome (groups I and II). The splay point was 0.78 in group I, 0.52 in group II, and 0.37 in group III. These data provide evidence that glucose reabsorption is decreased in nephrotic syndrome and are consistent with a fall in PTR in nephrotic syndrome.     

A special, supplemented 'vegan' diet for nephrotic patients.

High dietary protein intake, in the past recommended for nephrotic syndrome, does not improve hypoproteinemia and may accelerate progressive renal damage. In contrast, low-protein diets reduce proteinuria and preserve renal function in experimental renal models of nephrotic syndrome. In this study, 20 steroid-resistant, nephrotic patients were treated with a pure vegetarian, low-protein diet, supplemented with essential amino acids and ketoanalogues (supplemented vegan diet, SVD) for 4.6 +/- 3.1 months. Before the study, these patients followed an unrestricted protein, low-sodium diet (LSD). Proteinuria, daily urea nitrogen excretion and creatinine clearance decreased significantly on SVD. A similar lowering effect of SVD was observed on serum total cholesterol. Seven of the 20 patients changed from LSD to SVD and vice-versa on 3 occasions, and in all cases, we found an increase of proteinuria during the LSD period. Serum albumin, HDL cholesterol, triglycerides and anthropometric measurements did not change on SVD. Our data suggest that SVD exerts a favorable effect on proteinuria and hypercholesterolemia in nephrotic patients, without inducing clinical or laboratory signs of malnutrition.     

Altered expression of B lymphocyte surface immunoglobulins in minimal change nephrotic syndrome and focal glomerulosclerosis

In 20 patients with nephrotic syndrome (10 minimal change glomerulonephritis, MCN; 10 focal glomerulosclerosis, FGS) the peripheral blood lymphocytes showed a statistically significant increase in IgG-bearing cells (SIgG-C) in comparison with 30 patients with other histological types of primary glomerulonephritis with and without nephrotic syndrome (14 and 16, respectively). In the same MCN and FGS patients the serum IgG levels were slightly decreased. Furthermore, 5 cases of MCN in sustained remission for 1 year after steroid therapy showed normalization of the SIgG-C and the serum IgG levels. The possible significance of these phenomena in the pathogenesis of the hypo-IgG-globulinemia in MCN and FGS is discussed.     

Lipoprotein(a)- and low-density lipoprotein-derived cholesterol in nephrotic syndrome: Impact on lipid-lowering therapy?

BACKGROUND: Patients with nephrotic syndrome have the highest lipoprotein(a) [Lp(a)] concentrations known. Lp(a) is an low-density lipoprotein (LDL)-like particle consisting of 45% cholesterol. The usual methods to determine LDL cholesterol do not distinguish between cholesterol derived from LDL and Lp(a) and are thus the net result of cholesterol levels from both lipoproteins. High Lp(a) concentrations therefore significantly contribute to the measured or calculated LDL cholesterol levels. Since statins have no influence on Lp(a) levels, it can be expected that the LDL cholesterol-lowering effect of statins may be diminished in patients who have a pronounced elevation of Lp(a) levels accompanied by only moderate elevations of LDL cholesterol. METHODS: We investigated 207 patients with nondiabetic nephrotic syndrome in whom Lp(a) concentrations were strikingly elevated when compared to 274 controls (60.4 +/- 85.4 mg/dL vs. 20.0 +/- 32.8 mg/dL, P < 0.0001). RESULTS: According to National Kidney Foundation Dialysis Outcomes Quality Initiative (K/DOQI) Clinical Practice Guidelines for Managing Dyslipidemias, almost 95% of these patients are candidates for a therapeutic intervention to lower LDL cholesterol. LDL cholesterol levels corrected for Lp(a)-derived cholesterol, however, were 27 mg/dL lower than uncorrected concentrations (compared to only 9 mg/dL in controls). If Lp(a)-corrected levels instead of total LDL cholesterol levels were used, 25.7% of patients with low-molecular-weight (LMW) apolipoprotein(a) [apo(a)] isoforms were classified no longer to be in need of LDL cholesterol-lowering therapeutic intervention compared to only 2.3% of patients with high-molecular-weight (HMW) apo(a) phenotypes (P < 0.00001). This ("pseudo") pharmacogenetic effect results in incorrect determination of LDL cholesterol. CONCLUSION: Our observation has an impact on the indication for, and assessment of efficacy of intervention. This potential artifact should be investigated in ongoing large trials in renal patients as well as in nonrenal African American subjects who have on average markedly higher Lp(a) levels. In nonrenal Caucasian subjects with much lower Lp(a) concentrations, this issue will be less relevant.     

Urinary annexin V in children with nephrotic syndrome: a new prognostic marker?

Annexin V has a molecular weight of 32–35 kDa and has been reported to possess anticoagulant activity, inhibition of phospholipase A₂, regulation of membrane transport, proliferation and signal transduction. It is reported that urinary annexin V concentration may be an indicator of apoptosis and acute renal injury related to the urinary protein level. The aim of this study was to define the role of urinary annexin V excretion and serum annexin V concentrations as new prognostic tools and follow-up criteria in children with steroid-sensitive (SSNS) and steroid-resistant nephrotic syndrome (SRNS). Annexin V concentrations were measured in serum and 24-h urine samples in 23 SSNS patients in both relapse and remission periods of each patient and in 22 SRNS patients and 22 healthy controls. Total protein, albumin, blood urea nitrogen (BUN), creatinine, total cholesterol concentrations, and 24-h urinary excretion of protein and creatinine were also measured in each patient. In the SRNS group, median 24-h urinary annexin V levels were significantly higher than for all other groups (5,048.8 ng/g creatinine vs. 2,839.5 ng/g creatinine in SSNS relapse group; 2,500.0 ng/g creatinine in SSNS remission group, and 2,018.3 ng/g creatinine in healthy control group). No significant correlation was found between urinary protein excretion and 24-h urinary annexin V levels in all subjects. Twenty-four-hour urinary annexin V excretion may be a predictor in children with SRNS, and it may be a prognostic marker in children with NS.     

Impaired cell-mediated immunity in focal glomerular sclerosis

Cell-mediated immunity (CMI) was evaluated in 8 patients with focal glomerular sclerosis (FGS), 50 patients suffering from chronic mesangial proliferative glomerulonephritis without renal insufficiency and 24 healthy controls. The following parameters were measured: delayed skin reactivity to purified protein derivative, circulating lymphocytes, lymphocyte cell-surface markers (neuraminidase-treated sheep erythrocyte and erythrocyte-antibody-complement rosettes) and functional markers (mitogenic responses to concanavalin A and phytohemagglutinin). The FGS patients with nephrotic syndrome (NS) had a significant depression in CMI, characterized by decreased responses of the lymphocytes to both concanavalin A and phytohemagglutinin, impaired delayed hypersensitivity to purified protein derivative and a decreased proportion of T lymphocytes as compared with normal subjects. In contrast, the levels of all CMI parameters studied in FGS patients in remission and in patients with chronic glomerulonephritis with or without NS did not differ from normal subjects. Thus, the majority of FGS patients with NS demonstrated an impaired response in a CMI assay system. The possible significance of these phenomena in the pathophysiology of FGS is discussed.     

Serum lipid changes after estrogen therapy in prostatic carcinoma

A study of serum lipid fraction changes in 15 estrogen-treated patients with carcinoma of the prostate is conducted. Estrogen therapy is known to be associated with cardiovascular complications. Certain serum lipid fraction changes, particularly elevated low-density lipoprotein (LDL) and decreased high-density lipoprotein (HDL), are known to increase the risk of cardiovascular diseases. In our study, decrease in total cholesterol, increase in triglycerides, decreased LDL, and LDL/HDL ratio in combination with elevated HDL fraction suggest that the lipid changes are not the mediators of above complications.