Soluble CD40 in the serum of healthy donors, patients with chronic renal failure, haemodialysis and chronic ambulatory peritoneal dialysis (CAPD) patients.

CD40 and its ligand CD40L are key players in T cell-B cell interaction and T cell-antigen-presenting cell (APC) interaction. Inhibition of CD40-CD40L interaction leads to severe humoral and cellular immunodeficiency. In this study we examined the presence of soluble CD40 (sCD40) in the serum of haemodialysis (HD) patients, CAPD patients, chronic renal failure (CRF) patients and healthy donors in order to evaluate the possible involvement of CD40 in uraemic immunodeficiency. Soluble CD40 was detected in the serum of healthy donors (n = 41) with a mean of 0.14 +/- 0.12 ng/ml and in the urine of healthy donors with a mean of 1.80 +/- 0.74 ng/ml. Soluble CD40 was highly elevated in all patients with impaired renal function. HD patients (n = 22) had up to 100-fold elevated sCD40 levels with a mean concentration of 8.32 +/- 4.11 ng/ml, whereas CAPD patients (n = 10) had considerably lower levels of sCD40 with a mean of 3.58 +/- 2.40 ng/ml. A strong correlation between sCD40 and serum creatinine levels was noted in CRF patients (n = 66). The highly elevated levels of sCD40 may point to the involvement of CD40 and its ligand CD40L in the clinical manifestation of uraemic immunodeficiency.     

重组人脑利钠肽对急性心力衰竭早期肾损伤的疗效研究

目的 运用血清及尿液中性粒细胞明胶酶相关脂质运载蛋白（NAGL）、肾损伤因子-1（KIM-1）评估重组人脑利钠肽（rh-BNP）对住院急性心力衰竭患者早期肾损伤的临床疗效。方法 从我院2016年6月~2017年6月住院急性心力衰竭患者中选取SCr正常、血清及尿液NAGL、KIM-1同时升高者200例,随机分为rhBNP治疗组及常规治疗组,治疗组106例,常规组94例,同时治疗1周,于治疗结束时、结束后1周分别检测两组血清及尿液NGAL、KIM-1水平,并与治疗前比较。结果 治疗结束时两组血清NAG[（409.42±18.24）ng/ml vs（359.68±19.02）ng/ml]、尿液NAGL[（52.29±7.41）ng/ml vs （44.78±11.25）ng/ml]、血清KIM-1[（169.72±74.46）ng/ml vs （144.03±66.95）ng/ml]、尿液KIM-1[（7.39±2.96）ng/ml vs （6.38±3.01）ng/ml]水平均较治疗前下降,差异有统计学意义（P＜0.05）;治疗结束后1周两组血清NAGL[（343.72±16.45）ng/ml vs （321.04±17.34）ng/ml]、尿液NAGL[（30.89±7.94）ng/ml vs （21.01±8.49）ng/ml]、血清KIM-1[（133.32±64.09）ng/ml vs （109.60±45.29）ng/ml]、尿液KIM-1[（5.78±3.03）ng/ml vs （4.50±2.27）ng/ml]水平均较治疗前下降,差异有统计学意义（P＜0.05）。结论 rhBNP对于住院急性心力衰竭患者早期肾损伤有治疗价值。     

Assessment of erythropoietin levels and some iron indices in chronic renal failure and liver cirrhosis patients

This study was constructed to investigate the relationship between renal anaemia and erythropoietin (EPO) concentrations in chronic renal failure (CRF) patients and to evaluate the possible role of the liver. Serum EPO levels were measured in blood samples from 20 CRF patients on hemodialysis (HD), 20 liver cirrhosis (LC) patients, 20 patients having both CRF and LC and undergoing HD, and 20 normal control subjects. Blood cell counts, iron indices (iron, total iron-binding capacity (TIBC) and ferritin), renal function (blood urea nitrogen (BUN) and creatinine), hepatic function (ALT, AST, ALP and bilirubin) investigations were carried out for all the subjects enrolled in this study. CRF patients without LC had serum EPO concentration of 6.21 +/- 0.53 mU/ml (mean +/- SE), which was significantly higher than that in patients having both CRF and LC (4.32 +/- 0.52) (p < 0.01). Both groups showed significantly lower values than the controls (12.75 +/- 0.70) (p < 0.001). LC patients with intact kidneys had significantly higher EPO level (22.70 +/- 1.70) (p < 0.001). No correlation was found between EPO level and any of the hematologic or iron indices.     

Serum immunoreactive trypsin concentration after a Lundh meal. Its value in the diagnosis of pancreatic disease.

The changes in serum trypsin concentration have been measured in 47 subjects for up to 2 hours after a Lundh meal. In 18 healthy controls, mean fasting trypsin concentration was 285 +/- 125 ng/ml (mean +/- 2 SD). The maximum increase after the Lundh meal (the trypsin response ratio) was 6.7 +/- 7.5%. Six patients with chronic renal failure had elevated fasting serum trypsin concentrations (range 460-1100 ng/ml) but trypsin response ratios fell within the control range. Of five patients with relapsing pancreatitis, two had raised and three normal or low fasting trypsins. After stimulation two had elevated trypsin response ratios; one of the two had evidence of main duct obstruction. Eleven out of 12 patients with chronic pancreatitis (with or without insufficiency) had low fasting trypsin concentrations (range 0-120 ng/ml) Seven of the 12 also had raised trypsin response ratios. In six patients with cancer of the pancreas, fasting trypsin was low in three, normal in two, and raised in one. Both patients with a normal fasting level had a raised trypsin response ratio. The combination of a single estimation of fasting serum trypsin concentration followed by serial measurements after a Lundh meal provides a useful screening test for chronic pancreatic disease.     

Serum vitamin E levels in patients with chronic renal failure

27 patients with chronic renal failure, 21 patients on chronic intermittent dialysis treatment and 27 healthy controls were tested for serum level of vitamin E estimated spectrophotometrically. Both patient groups had significant higher mean values (12.1 +/- 1.2 and 7.2 +/- 0.8 micrograms/ml respectively) in comparison with normal controls 4.6 +/- 0.7 micrograms/ml). No correlation was found to serum creatinine, hematologic values, protein and lipoprotein concentration, nor to mode and duration of treatment regimes. Vitamin E was not extracted from blood throughout dialysis. Under normal conditions of conservative or dialysis treatment of chronic renal failure patients vitamin E seems not to be a factor concerning uremic symptoms and there is no need for supplementation.     

Study on changes of serum vitamin K1 level and K dependent coagulation factors in patients with coumarin derivatives (warfarin) therapy]

Serum level of vitamin K1 (= phylloquinone, hereinafter K1) and K dependent blood coagulation factors were determined by HPLC in normal subject, liver cirrhosis, hepatocellular carcinoma, acute hepatitis, chronic hepatitis, chronic renal failure with hemodialysis and patients under warfarin therapy. Normal range of serum K1 concentration was decided on 0.20-2.30 (0.87 +/- 0.53, n = 96) ng/ml. Serum K1 level showed no significant differences among normal subject, various diseases and warfarin therapy. Correlation between serum K1 level and F-VII (r = 0.879, p less than 0.001) or protein C activity (r = 0.839, p less than 0.01) was found in patients whose thrombotest was 20% and less. However serum K1 level didn't correlate with any K dependent coagulation factors in patients if thrombotest was over 20%.     

Serum profiles of C-C chemokines in acute myocardial infarction: possible implication in postinfarction left ventricular remodeling.

C-C chemokines are essential factors in the recruitment and activation of leukocytes from the circulation into inflamed tissue and may play a role in ischemia-induced myocardial injury and left ventricular remodeling after acute myocardial infarction (AMI). We investigated the kinetics of three major C-C chemokines, macrophage chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1 alpha (MIP-1 alpha), and regulated on activation normally T cell expressed and secreted (RANTES), in the sera of AMI patients and correlated the findings with the severity of the disease. Serum levels of C-C chemokines were determined in 35 AMI patients by ELISA assays serially during the first week of hospitalization and 1 month after hospital admission. Patients (n = 18) with uncomplicated AMI (Killip class I) were classified as group A, patients (n = 17) with AMI complicated by heart failure manifestations (Killip classes II and III) were classified as group B, and 15 age-matched and sex-matched volunteers were used as healthy controls. A sustained increase in serum C-C chemokines was observed in both AMI groups during the 7-day hospitalization period. Peaks of these inflammatory factors were significantly higher in group B than in group A (MCP-1, 295 +/- 11 vs. 203 +/- 9 pg/ml, p < 0.01; MIP-1 alpha, 30 +/- 1 vs. 24 +/- 2 pg/ml, p < 0.05; RANTES, 32 +/- 2 vs. 16 +/- 1 ng/ml, p < 0.01) and healthy controls (MCP-1, 125 +/- 7 pg/ml, p < 0.001; MIP-1 alpha, 14 +/- 1 pg/ml, p < 0.001; RANTES, 12 +/- 1 ng/ml, p < 0.001). In group B, significant correlations were found between the peak of MCP-1 and the peak of C-reactive protein levels (r = 0.55, p < 0.02) as well as wedge pressure (r = 0.40, p < 0.05). In the same group, the peak of MIP-1 alpha levels was also significantly correlated with the peak of serum creatine kinase-myocardial band (MB) (r = 0.51, p < 0.04) and left ventricular ejection fraction (LVEF) (r = -0.45, p < 0.05). After 1 month, AMI patients (n = 14) with severe left ventricular dysfunction (LVEF < or = 35%) exhibited significantly higher levels of C-C chemokines (all p < 0.05) than the other AMI patients (n = 21) (LVEF > 35%). A significant correlation was found between MIP-1 alpha levels and left ventricular end-diastolic diameter (r = 0.47, p < 0.03) in this patient population. In conclusion, we have detected a significant elevation of major C-C chemokines during the course of AMI, with the highest levels in patients with AMI complicated by heart failure manifestations and severe left ventricular dysfunction. The elevation of these chemotactic inflammatory factors may actively contribute to the pathophysiology of the disease and the subsequent left ventricular remodeling.     

Detection of a soluble form of the complement membrane attack complex inhibitor CD59 in plasma after acute myocardial infarction

Activation of the complement system has been documented in both experimental and clinical studies of acute myocardial infarction (AMI). Our earlier immunohistochemical studies have shown that the deposition of the membrane attack complex (MAC) of complement is associated with the loss of protectin (CD59), a glycosyl-phosphatidylinositol (GPI)-anchored sarcolemmal regulator of MAC, from the human and rat infarcted myocardium. In this study we detected, using an enzyme immunoassay (EIA), CD59 in the plasma of AMI patients at a concentration of 23.0+/-8.4 ng/ml (mean +/- SD; n = 17) at 4 h and 27.3+/-11.8 ng/ml (n = 24) at 24 h after AMI. Both values were significantly higher than in healthy controls (7.8+/-6.4 ng/ml; n = 20; P<0.001). The amount of CD59 correlated with the level of soluble terminal complement complexes (SC5b-9; r = 0.84; P<0.01) in the plasmas of AMI patients. Our results suggest that myocardial damage leads to release of CD59 from the sarcolemmal cell membranes during AMI.     

Serum levels of IL-1, IL-6 and tumour necrosis factors in patients undergoing coronary artery bypass grafts or cholecystectomy.

Plasma levels of biologically active IL-1, tumour necrosis factor (TNF) and IL-6 were measured before, during and after coronary artery bypass graftings (CABG) (n = 9) and cholecystectomy (CHO, n = 9), and in normal controls (nine healthy volunteers). Mean pre-operative IL-1 concentration in four of the nine CABG patients was 0.452 + 0.03 ng/ml, significantly (P less than 0.001) higher than that of the other five (0.045 +/- 0.009 ng/ml), CHO patients (0.035 +/- 0.005 ng/ml) and controls (0.029 +/- 0.008 ng/ml). Three of the four patients with high pre-operative IL-1 had functional capacity IV, while the other five had functional capacity IIa or IIb. Slight IL-1 elevation after anaesthesia, followed by reduction after initiation of bypass, elevation on completion of surgery and reduction to basal levels after 7 days was found in patients undergoing CABG. Mean basal TNF levels of CABG and CHO patients did not differ, but were higher than those of controls (2.85 +/- 0.5 ng/ml for CABG, 2.05 +/- 0.06 ng/ml for CHO, 0.72 +/- 0.07 ng/ml for normals, P less than 0.001). A unique kinetics of release during CABG was observed also for TNF. Mean pre-operative IL-6 levels were normal (50 +/- 3 ng/ml for CABG, 50 +/- 0.5 ng/ml for CHO and 65 +/- 10 ng/ml for controls). Gradual elevation to a mean peak of 725 +/- 100 ng/ml on completion of CABG was observed as compared with 275 +/- 50 ng/ml in CHO (P less than 0.01). On the seventh post-operative day mean IL-6 levels returned to normal. Two patients with post-operative low-grade fever (38 degrees C) had high, late cytokine levels. One of these two patients had leucocytosis, sterile discharge from the operative wound and was diagnosed as suffering from the Dressler syndrome. In this study elevated cytokine values and unique kinetics of release into the serum were found in patients undergoing CABG.     

Serum amylase and isoamylase in chronic renal failure

In 37 patients with chronic renal failure (CRF) serum amylase was higher than in 33 normal subjects (483 U/L +/- SD 185 versus 267 +/- SD 66 U/L, p less than 0.05); while the percentage of pancreatic isoenzymes was within normal limits in 34 patients and only slightly increased in 3. Seventeen of the patients were on conservative treatment, 10 on hemodialysis and 10 on continuous ambulatory peritoneal dialysis; no significant differences in serum amylase levels were detected between these subgroups. No correlation was found between serum BUN or creatinine and serum amylase but a positive correlation was found between these enzyme levels and duration of CRF (p less than 0.05) in the patients on conservative treatment.     

Serum lipoprotein (a) levels in chronic renal failure and liver cirrhosis patients. Relationship with atherosclerosis

This study was carried out to investigate the relationship between lipoprotein (a) levels and the development of atherosclerosis in chronic renal failure (CRF) patients with the possible role of the liver. Serum Lp (a) levels were measured in samples from 20 CRF patients on hemodialysis (HD), 20 liver cirrhosis (LC) patients, 20 patients having both CRF and LC and undergoing HD, and 20 normal control subjects. Renal function (blood urea nitrogen (BUN) and creatinine), hepatic function (transaminases (ALT and AST), alkaline phosphatase (ALP) and total bilirubin) investigations and serum cholesterol were carried out for all the subjects enrolled in this study. Serum Lp (a) concentration in CRF patients without LC was 87.25 +/- 6.17 mg/dl, which was significantly higher than all the investigated groups (P < 0.001). Lp (a) concentration in patients with both CRF and LC was 24.65 +/- 1.98 mg/dl, which was not significantly different from the controls, but was significantly higher than that in the subjects with LC only (P < 0.001) where the latter group had significantly low Lp (a) values (11.1 +/- 0.99) relative to all the other groups (P < 0.001). Lp (a) correlated positively with cholesterol in all groups except the LC subjects, but did not correlate with age, or renal function in both CRF groups.     

Interleukin-6 production by tumor necrosis factor and lipopolysaccharide-stimulated rat renal cells

Interleukin-6 (IL-6) is produced by various cell types, including monocytes, fibroblasts, and endothelial cells. IL-6 has also been detected in the urine of normal and renal transplant patients. Thus, the possible production of this cytokine by glomeruli and mesangial cells was investigated. Rat glomeruli were obtained by serial sieving of cortical homogenates of blood-free kidneys. Mesangial cells were obtained from the glomeruli and cultured under standard methods in RPMI 1640 medium containing 15% fetal calf serum. Glomeruli or confluent monolayers cells were then incubated in RPMI 1640 for 18 hr, in the presence or not of tumor necrosis factor-alpha (TNF alpha), lipopolysaccharide (LPS), or platelet-activating factor (PAF). IL-6 activity was measured using the IL-6-dependent cell line subclone (B 9-9) and expressed with respect to a standard curve established with recombinant IL-6. Glomeruli generate IL-6 upon TNF alpha (100 ng/ml) and LPS (1 microgram/ml), 11,500 +/- 3000 and 22,000 +/- 7500 U/ml, respectively. Nonstimulated mesangial cells produced 50 +/- 5 U/ml (mean +/- SEM, n = 4) of IL-6. TNF alpha (1 ng/ml) and LPS (1 microgram/ml) induced the production of 800 +/- 90 and 40,000 +/- 5000 U/ml, respectively (n = 4). In contrast, PAF (0.1 nM-1 microM) did not increase IL-6 production from glomeruli or mesangial cells. These results demonstrate that renal cells spontaneously generate minimal amounts of IL-6 and that this production is significantly increased by TNF alpha or LPS. A synergy between LPS and TNF alpha was induced in glomerular cells with 10 ng/ml of TNF alpha and graded concentrations of LPS. Thus, the production of IL-6 by glomerular cells and its modulation by other cytokines or endotoxins may play a role in the local immunological processes leading to immune glomerular diseases.     

Urinary indoxyl sulfate is a clinical factor that affects the progression of renal failure

We recently demonstrated that indoxyl sulfate is a stimulating factor for the progression of chronic renal failure (CRF). In this study we determined whether the urine or serum levels of indoxyl sulfate are related to the progression rate of CRF in undialyzed uremic patients. Fifty-five CRF patients with a serum creatinine of >2 mg/dl who had not been treated with an oral sorbent (AST-120) were randomly enrolled in the study. We measured the serum and urine levels of indoxyl sulfate, and estimated the recent progression rate of CRF as the slope of the reciprocal serum creatinine versus time (1/S-Cr-time) plot. The mean urinary amount of indoxyl sulfate in the patients was 60 mg/day. Those with indoxyl sulfate urine levels of >60 mg/day had a significantly faster progression rate of CRF than those with <60 mg/day. Especially, those patients with indoxyl sulfate urine levels of >90 mg/day had the highest CRF progression rate and those with indoxyl sulfate urine levels of <30 mg/day had the slowest CRF progression rate. Urinary indoxyl sulfate had a significantly negative correlation with the slope of the 1/S-Cr-time plot. However, the serum level of indoxyl sulfate or the ratio of serum indoxyl sulfate to creatinine was not significantly correlated with the slope of the 1/S-Cr-time plot. In conclusion, high urine levels of indoxyl sulfate are related with a rapid progression of CRF in undialyzed uremic patients. Thus, urinary indoxyl sulfate is one of the clinical factors that affect CRF progression.     

Blood Serum Levels of IL-2, IL-6, IL-8, TNF-α and IL-1β in Patients on Maintenance Hemodialysis

Cytokines are essential mediators of immune response and inflammatory reactions. Patients with chronic renal failure (CRF) commonly present with abnormalities of immune function related with impaired kidney function and the accumulation of uremic toxins in addition to bioincompatibility of dialyzer membranes. During a hemodialysis (HD) session, cytokines are released mainly by monocytes activated by endotoxin-type compounds in dialyzer fluid, complement factors and direct contact with dialyzer membrane. The study included 15 CRF patients, aged 36.4±2.9 years, on regular HD maintenance therapy for mean 68±10 months and 15 healthy controls. It was designed to assess serum levels of a panel of inflammatory cytokines: IL-1β, IL-2, IL-6, IL-8 and TNF-αin CRF patients on regular maintenance HD before, 20, 60 and 240 minutes of a single HD session in parallel with C-reactive protein (CRP) as an additional parameter. CRP concentration was increased in HD patients when compared with healthy controls. The concentrations of IL-1, IL-6, IL-8 and TNF-αwere increased, whereas the serum level of IL-2 was not altered during a single HD session.     

Osteocalcin in chronic hemodialysis patients as an additional parameter in the diagnosis of advanced secondary hyperparathyroidism

Osteocalcin (OC), also called Bone Gla Protein (BGP), is a bone matrix protein of 5800 MW synthesized by osteoblasts. Since OC is mainly metabolized in the kidney, its blood concentration is altered in renal failure. The relationship between OC and the calcium-phosphorus regulating hormones (parathyroid hormone, calcitonin) and the biochemical parameters of bone metabolism (serum calcium, serum phosphorus and serum alkaline phosphatase) was studied in 30 patients on chronic hemodialysis (mean age: 51 years; mean duration of dialysis treatment: 39 months). OC levels were significantly elevated in all patients on chronic hemodialysis (34.7 +/- 31.5 ng/ml) when compared to healthy subjects (6.25 +/- 1.39 ng/ml, p less than 0.001). In 2 patients the OC levels were excessively high (127.54 ng/ml; 148.02 ng/ml), which was associated with severe renal osteodystrophy due to secondary hyperparathyroidism. When divided into 2 groups in the patients with secondary hyperparathyroidism the mean OC value was markedly elevated (50.5 +/- 12.7 ng/ml) compared to the patients without secondary hyperparathyroidism (24.1 +/- 2.8 ng/ml) (p less than 0.05). 70 per cent of the patients on chronic hemodialysis with OC levels greater than 30 ng/ml showed moderate to severe scintigraphic findings of bone disease. In neither of the 2 groups could a correlation between OC and serum alkaline phosphatase be demonstrated. The results indicate, that OC levels could be useful additional parameter in hemodialyzed patients with secondary hyperparathyroidism and OC levels could reflect bone formation in these patients.     

The clinical significance of serum and urinary neopterin levels in several renal diseases

Neopterin is a pyrazino-pyrimidine compound, and is known to be a marker associated with cell-mediated immunity in various diseases. We hypothesized that the levels of serum and urine neopterin would be elevated in renal disease, and would correlate with certain clinical parameters. We evaluated serum and urinary neopterin levels in patients with several renal diseases, including nephrotic syndrome (NS, n=19), chronic renal failure (CRF, n=8), end stage renal disease (ESRD, n=64) and controls (n=22). Serum neopterin was elevated in patients with CRF and ESRD, as compared to controls. Urinary neopterin levels were also found to be elevated in patients with CRF and ESRD, as compared to controls. Serum neopterin levels showed significant positive correlation with age, serum BUN and creatinine levels, and inverse correlation with WBC, hemoglobin, hematocrit, serum albumin and total iron binding capacity. Urine neopterin levels exhibited positive correlation with age and serum creatinine levels, and inverse correlation with WBC, hemoglobin, hematocrit, BUN and serum albumin. In conclusion, increased serum and urinary neopterin levels were found in some patients with renal disease and were correlated with certain clinical parameters.     

A one step sandwich enzyme immunoassay for gamma-carboxylated osteocalcin using monoclonal antibodies

A highly sensitive, simple and reliable one-step sandwich enzyme immunoassay (EIA) for the gamma-carboxylated form of osteocalcin (Gla-OC) has been developed using a monoclonal antibody. The minimum amount of Gla-OC detected by this EIA was approximately 0.2 ng/ml when a 10 microliter aliquot of the sample was used. The serum Gla-OC level in 30 healthy subjects was 3.6 +/- 2.19 ng/ml (mean +/- SD). A significant increase was seen in patients with chronic renal failure (20.3 +/- 4.60 ng/ml), atherosclerosis (8.3 +/- 4.94 ng/ml) and osteoporosis (10.1 +/- 4.60 ng/ml). The correlation between the values obtained by the sandwich EIA and competitive RIA methods was given by the linear regression equation, y = 2.896 + 0.759 chi, for which the correlation coefficient (r) was 0.815 (n = 58). This newly developed Gla-OC specific EIA may be useful for the diagnosis of metabolic bone disease and ectopic calcification.     

Serum angiotensin-converting enzyme levels in patients with chronic renal failure

Disagreement concerning serum angiotensin-converting enzyme (ACE) levels in patients with chronic renal failure has been observed in recent reports. Because ACE is considered as a useful tool for the diagnosis and management of sarcoidosis, and because chronic renal failure may be associated with sarcoidosis, the present work was designed to reinvestigate the possible changes of serum angiotensin-converting enzyme activity in a series of 36 non-hemodialysed consecutive patients with chronic non-sarcoid renal failure. Enzyme activity was significantly lower (p less than 0.004) in the patients (15.8 +/- 5.0 units/ml, mean value +/- 1 SD) than in 47 healthy controls (20.2 +/- 7.6 units/ml, mean value +/- 1 SD). Serum angiotensin-converting enzyme and creatinine clearance values were significantly correlated in these patients (p less than 0.0002). These results indicate that, in non-hemodialysed patients with chronic renal failure, serum angiotensin-converting enzyme levels may not be useful in establishing the diagnosis of sarcoidosis.     

Small gastrin (G-17) serum levels after stimulation with food during conservative treatment of patients with chronic renal insufficiency

The physiological release mechanism for gastrin is complex, including both mechanical and chemical stimuli. Distention of the antrum is the main mechanical stimulus, and proteins and their degradation products constitute the most potent chemical stimuli. The aim of the present study was to examine the little gastrin (G-17) response to a test meal and to study the relationship between the G-17 concentration and gastric acid secretion in patients with various degrees of chronic renal failure (CRF). In 14 CRF patients under conservative treatment and 12 healthy control subjects, fasting and stimulated G-17 concentrations, as well as basal (BAO), maximal (MAO) and peak acid secretion (PAO) were measured. Mean fasting serum G-17 in CRF patients was 7.8 +/- 0.8 pmol/L, significantly higher (p less than 0.001) than in control subjects (5.9 +/- 1 pmol/L). However, the range of basal G-17 concentrations in both groups of subjects was not different from the normal values (4.2 +/- 11.3 pmol/L). The serum G-17 response to the food stimulation was significantly higher (p less than 0.001) in the control subjects than in the CRF patients. In normal subjects, the increment in the serum G-17 concentration rose to a peak at 30 min, but in the CRF patients the peak increment occurred at 60 min, and the response was more prolonged. There was a little difference in meal-stimulated serum G-17 concentrations in patients with various degrees of renal functional impairment. Basal acid output (BAO) was significantly higher (p less than 0.001) in the control subjects (2.62 +/- 0.51 mmol/h) than in the CRF patients (1.68 +/- 0.4 mmol/h). No significant difference in both the maximal acid output (MAO) and peak acid output (PAO) was found between the groups of CRF patients and control subjects. There was no relationship between G-17 concentrations and the gastric acid output in the CRF patients. From the results of the present study it is concluded that the human kidney is unimportant in the catabolism of G-17 but that the renal failure seems to decrease the rate of the peripheral extraction of gastrin by other tissues. The raised basal and meal-stimulated G-17 concentrations sometimes seen in CRF patients are associated with decreased rather than increased gastric acid secretions.     

Correlation between the renal C1q deposition and serum anti-C1q antibody: a potential role of anti-C1q antibody in lupus nephritis

The anti-C1q antibody has been shown to be associated with lupus patients with renal involvement. We conducted a study to determine the relationship between the serum anti-C1q titer and the renal deposition of C1q. The serum anti-C1q was measured in 26 healthy controls and 47 systemic lupus erythematosus (SLE) patients who were divided into 2 groups as non-nephritis and nephritis SLE. We analyzed the relationship between the anti-C1q titers and SLE, renal C1q staining and the WHO classification for lupus nephritis. The result revealed that the serum anti-C1q was present in 50.8% of the SLE patients, that its levels in those with renal involvement were significantly higher than in the normal control group (61.540 +/- 87.720 U/ml vs 15.750 +/- 2.530 U/ml, p = 0.005). Besides, the serum anti-C1q levels were higher in the patients with lupus nephritis with C1q deposition in the kidney tissue (66.038 +/- 91.141 U/ml vs 16.652 +/- 3.097 U/ml, p < 0.01). There seems to be evidence supporting that the autoantibody anti-C1q might play a pathogenic role in lupus nephritis.