Cardiac Function in Chronic Renal Failure Before and After Hemodialysis

Cardiology ◽  
1973 ◽  
Vol 58 (2) ◽  
pp. 109-117 ◽  
Author(s):  
D. Strangfeld ◽  
K.H. Günther ◽  
Renate Bohm ◽  
Helga Günther ◽  
K. Buchali ◽  
...  
PEDIATRICS ◽  
1982 ◽  
Vol 70 (5) ◽  
pp. 742-750 ◽  
Author(s):  
Anthony C. Hsu ◽  
Sang Whay Kooh ◽  
Donald Fraser ◽  
William A. Cumming ◽  
Victor L. Fornasier

The incidence, age at onset, and progression of the biochemical, radiographic, and histologic characteristics of renal osteodystrophy were studied in 50 children in whom chronic renal failure had been recently diagnosed. During a ten-year observation period, 19 patients progressed to end-stage renal failure and radiographic signs of renal osteodystrophy developed in 15 of these (79%). Renal osteodystrophy developed in all nine patients whose chronic renal failure was diagnosed before 3 years of age and in six of the ten children with later onset of failure. The mean interval from diagnosis of renal failure to development of osteodystrophy was 1.4 years. Radiographically, growth zone lesions predominated in the younger children, whereas cortical erosions were more prevalent in the older children. Histologic examination, performed in 38 patients, showed both defective mineralization and excessive resorption and was a more sensitive diagnostic index than radiography. Noticeable deformities developed in one third of the patients with osteodystrophy, despite medical treatment including vitamin D2 therapy. Deformities were particularly frequent and Severe in patients whose renal failure developed in infancy. In all 13 patients whose growth patterns were studied before and after osteodystrophy developed, the onset of bone lesions was associated with a deterioration of growth, indicating that osteodystrophy plays a major role in causing the growth retardation commonly observed in children with chronic renal failure.


1981 ◽  
Author(s):  
M Bern ◽  
J Green

Sulfinpyrazone can reduce the incidence of thrombosis of A-V shunts in chronic renal failure. The drug is also reported to prevent acute deaths from coronary artery disease. This study was to determine mechanisms for these protective effects.Patients on chronic hemodialysis served as the study models. Six patients on dialysis three times per week for 6 or more months received sulfinpyrazone 200 mgm t.i.d. p.o. for 14 days. Blood samples were obtained before dialysis was begun before and after the 14 days of drug therapy.Results are shown as mean ± standard error of mean.AT III levels rose significantly by functional and immune assays. Functional levels (by von Kaulla technique) rose 24.5 ± 3.1 sec. to 47.3 + 5.5 sec. (P>.005) Plasma protein AT III (by radial immunodiffusion) rose 31.2 ± 2.17 mg/dl to 37.9 ± 2.1 mgm/dl. (P>.01) Platelet factor 4 (by Abbot radioimmunology assay) fell from 46.4 + 13.6 ngm/ml to 9.5 ± 1.1 ngm/ml.(P>.005) The concentration of thrombin-anti-thrombin complex (by R. Rosenberg, Harvard Medical School, Boston) rose from 4.2 ± .09 to 8.4 ± 1.0 (P>.005)Thus it appears that sulfinpyrazone elevates antithrombin concentration and function while simultaneously suppressing platelet release. These two effects may or may not be mutually dependent. The clinical efficacy of sulfinpyrazone may relate in part to the elevation of antithrombin III, probably by inhibiting its consumption, while also inhibiting platelet function.


2013 ◽  
Vol 62 (18) ◽  
pp. C170
Author(s):  
Abdulkadir Yıldız ◽  
Abdurrahman Akyuz ◽  
Murat Yuksel ◽  
Mustafa Oylumlu ◽  
Mehmet Zihni Bilik ◽  
...  

1991 ◽  
Vol 37 (12) ◽  
pp. 2153-2154 ◽  
Author(s):  
Ljerka Lukinac ◽  
Zvonko Kusic ◽  
Petar Kes

Abstract Concentrations of thyroid-related hormones in serum of patients with chronic renal failure are known to be abnormal (1, 2). In our study on thyroid-function testing of patients undergoing hemodialysis, we determined, in addition to concentrations of free and total triiodothyronine, free and total thyroxin, “reverse” triiodothyronine, and thyroxin-binding globulin, the titers of thyroglobulin and microsomal autoantibodies (TGA and TMA, respectively). The study was provoked by the appearance of an uncommon agglutination pattern in the control wells of some samples from patients with chronic renal failure during the standard procedures of detecting TGA and TMA with hemagglutination methods (Thymune-T and Thymune-M assays from Welcome, London, U.K.). For these samples we were not certain whether positive titers for TGA and (or) TMA represented false-positive or true-positive values. Therefore, we assayed the absorbed serum samples and samples after addition of excess nonspecific immunoglobulin. Furthermore, we wanted to determine the difference in TGA and TMA titers of serum samples before and after hemodialysis.


1994 ◽  
Vol 40 (8) ◽  
pp. 1544-1548 ◽  
Author(s):  
N C France ◽  
P T Holland ◽  
M R Wallace

Abstract We tested the possibility that the buffering agents in dialysis bath fluid might contribute to increased endogenous oxalate production in dialyzed patients. Using stable isotope dilution mass spectrometry, we obtained oxalate production rates and pool sizes directly for 10 patients in chronic renal failure, 5 of whom were undergoing continuous ambulatory peritoneal dialysis (lactate-buffered fluid). All peritoneal dialysis patients had either increased oxalate production rates or expanded oxalate pools when compared with undialyzed patients in renal failure. From a further four patients receiving maintenance hemodialysis we took blood samples immediately before and after three consecutive dialysis sessions in which the bath-fluid buffering agent (bicarbonate or acetate) was alternated; we analyzed these samples for oxalate and key precursors by capillary gas chromatography. Plasma glycine and serine concentrations remained within the physiological range. Glycolate and oxalate concentrations decreased, but the oxalate remained above normal after dialysis. All changes were independent of the bath-fluid buffering agent. We suggest that dialysis might stimulate the formation of oxalate by removing product inhibition of a late catabolic step.


1988 ◽  
Vol 35 (6) ◽  
pp. 865-876 ◽  
Author(s):  
SHINICHI SAKURAI ◽  
YOSHIHITO HARA ◽  
SHIRO MIURA ◽  
MICHIYUKI URABE ◽  
KENICHI INOUE ◽  
...  

Open Medicine ◽  
2007 ◽  
Vol 2 (2) ◽  
pp. 154-158 ◽  
Author(s):  
Jacek Rysz ◽  
Eugeniusz Kocur ◽  
Robert Błaszczak ◽  
Robert Stolarek

AbstractChronic renal failure (CRF) is a complex clinical entity caused by progressive destruction of functional renal parenchyma in the course of various pathological processes resulting in complete failure of renal function and subsequent metabolic, acid base and electrolyte as well as immune disorders. Renal transplantation (RT) is one of the renal replacement therapy options in the terminal stage of chronic renal failure. The replacement of the failing organ with one from a healthy donor may be complicated with immune host response. This study was designed to investigate the changes in serum concentration of integrins CD11a/CD18, CD11b/CD18, CD69 on the surface of human polymorphonuclear leukocytes (PMNL) after the RT within two six-month periods. The study included 25 RT patients (mean 5.4±2.7 yrs after the transplantation, 10 females and 15 males) treated with immune suppressive therapy including cyclosporine A, azathioprine and prednisolone. The expression was assessed with monoclonal antibodies by means of flow cytometry. Also, the expression of CD69 was determined before and after phytohemaglutinine (PHA) stimulation. There was no significant alternation in serum concentration of CD11a/CD18, CD11b/CD18 and CD69 at baseline, six months and twelve months later. The expression of integrins was not altered in renal transplantation patients in the current study setting.


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