POLYTETRAFLUOROETHYLENE (PTFE) GRAFTS FOR HAEMODIALYSIS IN CHRONIC RENAL FAILURE: ASSESSMENT OF DURABILITY AND FUNCTION AT THREE YEARS

1981 ◽  
Vol 51 (6) ◽  
pp. 562-567 ◽  
Author(s):  
ADAM RAPAPORT ◽  
GEORGE P. NOON ◽  
CHARLES H. MCCOLLUM
2001 ◽  
Vol 16 (8) ◽  
pp. 1607-1614 ◽  
Author(s):  
Céline Veau ◽  
Christine Leroy ◽  
Hélène Banide ◽  
Daniel Auchère ◽  
Sylviane Tardivel ◽  
...  

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.


2008 ◽  
Vol 149 (17) ◽  
pp. 789-794 ◽  
Author(s):  
Endre Balázs ◽  
Andrea Ruszwurm ◽  
Miklós Székely ◽  
István Wittmann ◽  
Judit Nagy

Age-related changes in renal morphology and function cannot be regarded physiological. The number of glomeruli falls, sclerotic glomeruli and aglomerular arterioles develop. Besides tubular atrophy interstitial fibrosis is often seen, and the age-related vascular changes strongly affect the kidneys. Renal blood flow and GFR decrease, without concomitant changes in se-creatinine. Disorders of tubular transport manifest mainly in salt- and water-excretion and lead to hyposthenuria. The pathogenesis of these age-related changes is not fully understood. Nevertheless, such changes impair the excretory functions and the pharmacokinetics of drugs. In real chronic renal failure other functions (erythropoietin production, vitamin-D, Ca and P metabolism) are also impaired. Due to more frequent occurrence of systemic diseases (diabetes, hypertension, etc.) in the elderly, real chronic renal failure is also more common, and various forms of acute renal failure develop more easily.


2009 ◽  
Vol 296 (5) ◽  
pp. F1166-F1178 ◽  
Author(s):  
Ben Fogelgren ◽  
Shiming Yang ◽  
Ian C. Sharp ◽  
Odaro J. Huckstep ◽  
Wenbin Ma ◽  
...  

The Br/+ mutant mouse displays decreased embryological expression of the homeobox transcription factor Six2, resulting in hertitable renal hypoplasia. The purpose of this study was to characterize the renal physiological consequences of embryonic haploinsuffiency of Six2 by analyzing renal morphology and function in the adult Br heterozygous mutant. Adult Br/+ kidneys weighed 50% less than those from wild-type mice and displayed glomerulopathy. Stereological analysis of renal glomeruli showed that Br/+ kidneys had an average of 88% fewer glomeruli than +/+ kidneys, whereas individual glomeruli in Br/+ mice maintained an average volume increase of 180% compared with normal nephrons. Immunostaining revealed increased levels of endothelin-1 (ET-1), endothelin receptors A (ETA) and B (ETB), and Na-K-ATPase were present in the dilated renal tubules of mutant mice. Physiological features of chronic renal failure (CRF) including elevated mean arterial pressure, increased plasma creatinine, and dilute urine excretion were measured in Br/+ mutant mice. Electron microscopy of the Br/+ glomeruli revealed pathological alterations such as hypercellularity, extracellular matrix accumulation, and a thick irregular glomerular basement membrane. These results indicate that adult Br/+ mice suffer from CRF associated with reduced nephron number and renal hypoplasia, as well as glomerulopathy. Defects are associated with embryological deficiencies of Six2, suggesting that proper levels of this protein during nephrogenesis are critical for normal glomerular development and adult renal function.


This chapter provides an overview of renal problems seen in patients who live with HIV. It outlines the causes of renal dysfunction, including acute and chronic renal failure. Assessment of a patient presenting with renal failure is discussed. The direct effect of HIV on the kidney is discussed. The effect of drugs on the kidneys and the need to modify drug doses are discussed.


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