摘要:

The Fc-receptor function of the mononuclear phagocyte system was examined in 30 patients affected by multisystem diseases with glomerular involvement by measuring the immune clearance of IgG-sensitized autologous red blood cells in vivo and the immune phagocytosis of monocytes in vitro. Patients studied in the phase of clinically active renal disease showed a significantly reduced Fc-receptor function by both in vivo (p < 0.001) and in vitro (p = 0.003) assays, as compared to those studied during an inactive phase. Though the nature of the defect remains uncertain, it appears to be related to the active phase of the renal disease as also confirmed by the analysis of individual cases studied longitudinally.

ISSN:0250-8095    

DOI:10.1159/000167441

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

In 72 patients with end-stage renal failure and 70 healthy subjects, the influence of blockade of opioid receptors by naloxone on secretion of prolactin, lutropin (LH), follitropin (FSH), adrenocorticotropin (ACTH), somatotropin (HGH), insulin (IRI), glucagon (IR-G), parathyroid hormone (PTH) and calcitonin (CT) was studied. Administration of naloxone stimulated luliberin-induced LH and FSH secretion quantitatively equally in patients and controls. Blockade of opioid receptors was followed by a less marked suppression of chlorpromazine-induced prolactin secretion but by a higher response of hypoglycemia-induced ACTH secretion in uremic patients than in controls. In addition, a less marked suppressive effect of naloxone was noted on hypoglycemia-induced HGH secretion in chronic renal failure as compared with controls. Blockade of opioid receptors improved significantly glucose tolerance and glucose-induced insulin secretion in uremic patients and suppressed nearly completely glucagon secretion response during the second phase of a glucose tolerance test. Finally, administration of naloxone was followed by a blunted response of Ca-induced CT secretion and suppression of PTH. Data presented in this paper suggest the existence of hyperendorphinism in end-stage renal failure.

ISSN:0250-8095    

DOI:10.1159/000167442

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

We analyzed routine serum potassium concentration measurements and conditions temporally associated with abnormalities in potassium concentration in outpatients on chronic hemodialysis (136 nondiabetics, 36 diabetics) and continuous ambulatory peritoneal dialysis (16 nondiabetics, 10 diabetics). The following potassium concentration frequencies were found: prehemodialysis, nondiabetics: normal 51.3%, severe hyperkalemia ( > 6.0 mmol/l) 10%, severe hypokalemia ( < 3.0 mmol/l) 0.3%; diabetics: normal 57.8%, severe hyperkalemia 8.7%, severe hypokalemia 0.5%. Peritoneal dialysis, nondiabetics: normal 73.7%, severe hyperkalemia 0.6%, severe hypokalemia 4.9%; diabetics: normal 72.5%, severe hyperkalemia 0.9%, severe hypokalemia 2.9%. Normokalemia and severe hypokalemia were significantly (χ2 40 mmol/l), metabolic acidosis (Tco2 30 mmol/l), was associated with a statistically higher risk of hyperkalemia

ISSN:0250-8095    

DOI:10.1159/000167443

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Of 240 adults with sickle cell anemia seen over 11 years, 12 had the nephrotic syndrome. In 9 (75%) the glomerular lesion, sickle glomerulopathy, consisted of mesangial expansion and basement membrane duplication. Six patients had type IV renal tubular acidosis. Four of the 9 Patients died within 24 months (17 ± 5; mean ± SD), while 5 survived 36 months or longer (80 ± 49); no significant differences were seen between the former and the latter in age, admission serum creatinine and C3 levels, urinary protein excretion, or the frequency of renal tubular acidosis. Chronic azotemia developed in 3 and acute renal shutdown in another 2. Of 22 patients with sickle glomerulopathy (our 9 added to 13 from the literature) 11 died within 2 years. Ten of these (91 %) had developed renal failure, compared to only 5 of the 11 (45%) who survived longer than 2 years (p < 0.05). The 5-year mortality in the general population of sickle cell anemia is 3.75%, and 75% of patients aged 15 years or older survive 18 years or longer. The nephrotic syndrome, most often caused by sickle glomerulopathy, occurs in 4% of patients with sickle cell anemia, leading to renal failure in two-thirds and death in 2 years in half the patients. The development of chronic azotemia correlates strongly with early mortality. The prognosis is much worse than that in the general population of sickle cell anem

ISSN:0250-8095    

DOI:10.1159/000167444

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

We hypothesized that intraperitoneal air might be one of the causes of peritoneal fluid eosinophilia. To test our hypothesis, we injected 100–500 ml of sterile air intraperitoneally into 5 patients receiving continuous ambulatory peritoneal dialysis (CAPD). All patients responded with a transient increase in peritoneal fluid nonerythrocyte cell count (peak counts ranging from 23 to 335 cells/mm3, mean peak count 140 ± 125) lasting 4 days (after injection of 100 ml of air) to 7 weeks (after injection of 500 ml of air). In 2 patients, the cells were predominantly monocytes(80 ± 6.5%), whereas in 3 patients, eosinophils predominated (63 ± 12%), while monocytes (30 ± 19%) also increased. Resolution of peritoneal fluid pleocytosis correlated temporally with absoption of subdiaphragmatic air. Our results suggest that intraperitoneal introduction of air into CAPD patients can induce peritoneal fluid eosinophilia and/or monocy

ISSN:0250-8095    

DOI:10.1159/000167445

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

During hemodialysis with cuprophan membranes, the complement system as well as leukocytes become activated. In order to clarify the role of dialyzer geometry, the effect of hollow-fiber versus flat-sheet dialyzers and of different surface areas on C3a generation and leukocyte degranulation was investigated. Plasma levels of leukocyte elastase in complex with α1-proteinase inhibitor were significantly increased after 1 h (+55%) and 3 h (+62%) of hemodialysis with flat-sheet dialyzers as compared to hollow-fiber devices. In addition, plasma levels of lactoferrin, released from the specific granules of leukocytes during activation, were significantly higher (+ 42 %) 3 h after the onset of dialysis treatment with flat-sheet than with hollow-fiber dialyzers. With respect to surface area, larger dialyzers tended to cause more release of leukocyte elastase as compared to dialyzers with smaller surface areas, irrespectively of the configuration of the dialyzer used. On the other hand, activation of the complement system, as measured by the generation of C3a-desarg, did not differ with both types of configurations. The same held true for leukopenia, which was almost identical for hollow-fiber and flat-sheet dialyzers. From these findings two lines of evidence emerge: First, not only the type of membrane material used in a dialyzer may influence its biocompatibility, but the geometry of the extracorporeal device also determines the degree of compatibility. Hence, the extent of leukocyte activation correlated with both configuration of the dialyzer and surface area of the membrane. Second, the fact that both types of configurations activated the complement system to virtually the same extent favors a more mechanical route of leukocyte activation and demonstrates that leukocytes do not necessarily need the involvement of the complement system to become activated

ISSN:0250-8095    

DOI:10.1159/000167446

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

Previous studies suggested that increased blood levels of, or increased tissue sensitivity to, glucocorticoids may contribute to catabolism in acute uremia. To examine this possibility we determined urea nitrogen (urea-N) appearance, plasma levels of Nl-methylhistidine and the activity of the alkaline myofibrillar proteinase in acutely uremic rats with and without treatment with RU 38486, a selective antiglucocorticoid. Forty-eight hours after bilateral nephrectomy, the rats had markedly elevated serum levels of urea-N, creatinine, potassium and phosphorus. In uremic rats receiving RU 38486, comparable levels of serum creatinine were found, but the serum levels of urea-N (221 ± 4 vs. 259 ± 5 mg/dl) and phosphorus (6.5 ± 0.3 vs. 8.5 ± 0.4 mmol/l) were significantly decreased as compared to uremic animals without RU 38486. In comparison to sham-operated rats, urea-N appearance (net urea production) was increased by 56% 48 h after bilateral nephrectomy. This increment was almost completely reversed in uremic animals receiving the antiglucocorticoid. In untreated uremic rats, plasma levels of Ntethylhistidine were 10.3 ± 0.9 μg/dl, whereas the administration of RU 38486 caused a significant decline in the levels of this amino acid (7.6 ± 0.5 μg/dl). This reduction in N’-methylhistidine was associated with a concomitant decrease of myofibrillar proteinase activity in muscle tissue homogenates. Compared to sham-operated animals, this proteinase activity was increased by 30% in uremic rats, but was normal in those given RU 38486. Taken together, these data support the view that in acute uremia accelerated ureagenesis occurs, while enhanced muscle protein breakdown, owing to an increment in myofibrillar proteinase activity, provides the necessary amino acid precursors. Furthermore, the activity of this proteinase, and therefore the rate of muscle protein breakdown, strongly depend on the presence or absence of glucocorticoids

ISSN:0250-8095    

DOI:10.1159/000167447

出版商:S. Karger AG    

年代:1987

数据来源: Karger

ISSN:0250-8095    

DOI:10.1159/000167448

出版商:S. Karger AG    

年代:1987

数据来源: Karger

ISSN:0250-8095    

DOI:10.1159/000167449

出版商:S. Karger AG    

年代:1987

数据来源: Karger

摘要:

A 21-year-old heroin addict with right-sided staphylococcal endocarditis developed skin purpura, abdominal pain, bloody diarrhea, proteinuria and microscopic hematuria. Skin biopsy showed leukocytoclastic vasculitis with IgA deposits in dermal vessels and renal biopsy disclosed proliferative glomerulonephritis with granular mesangial IgA and fibrinogen deposition. These features are typical of Henoch-Schönlein purpura. Symptoms abated spontaneously. Since the syndrome appeared during cloxacillin therapy, both this drug or the infectious disease itself could have triggered the immune response. Henoch-Schönlein purpura is a distinct clinical entity that can complicate the course of staphylococcal endocarditi

ISSN:0250-8095    

DOI:10.1159/000167450

出版商:S. Karger AG    

年代:1987

数据来源: Karger