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Biomedical subjects

E Matthys

Publications and source records attributed to E Matthys.

27 records · Page 2Linked to original sources
PubMed1986

Influence of progressive salt restriction on urinary bicarbonate wasting in uremic acidosis.

In steady state, the acidosis in the majority of 17 uremic patients was characterized by a persistent bicarbonaturia (FEHCO3 ranging between 0% and 17.65%). An NH4Cl loading test in 17 patients revealed two distinct groups: group A (n = 11) with complete disappearance of the urinary bicarbonate loss and a mean UpH of 5.39 +/- 0.10 at a PHCO3 level of 13.3 +/- 0.5 mEq/L; and group B (n = 6) with urinary acidification disturbances with a persistent FEHCO3 ranging between 1.06% and 3.15% and a mean UpH of 6.53 +/- 0.06 at a PHCO3 level of 13.5 +/- 0.7 mEq/L. Between the two groups, there were no differences in CCr, plasma Na, K, Cl, Ca, PO4, PCO2, and aldosterone levels. Calculation of the THCO3/TNa reabsorption ratio over a wide range of PHCO3 levels revealed no differences between the two groups. The mean levels of circulating PTH were significantly higher in group B compared with group A (40.1 +/- 10.8 mU/dL v 19.3 +/- 4.4 mU/dL; P less than .05), and the spontaneous steady-state FENa was more pronounced in group B than in group A (12.1% +/- 1.5% v 4.9% +/- 0.7%; P less than .05). Four patients from group B with a well-documented salt-losing nephropathy (FENa ranging from 10.20% to 15.10%) were submitted to a progressive dietary salt restriction over several weeks. At this stage, the four patients no longer had bicarbonaturia, and the urinary pH decreased to levels between 5.15 and 5.65 during NH4Cl-induced acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗
PubMed1986

Effect of premercurial resetting of intrarenal vascular resistance on HgCl2-induced acute renal failure.

The role of renal hemodynamics in the first hours of HgCl2-induced acute renal failure was examined by studying the influence of resetting the total renal vascular resistance (RT) within the limits of autoregulation before and after the mercury administration. Intravenous HgCl2 alone (3 mg/kg) caused an early fall of glomerular filtration rate (GFR) from 69 +/- 3 to 38 +/- 4 ml/min/100 gm kidney weight (KW) and of renal blood flow (RBF) from 535 +/- 42 to 276 +/- 27 ml/min/100 gm KW, 3 hours after HgCl2 (P less than 0.01). In a second series, the RT was decreased by clamping the aorta before and after HgCl2 so that the mean renal perfusion pressure (MRPP) was lowered to a mean of 87 +/- 5 mm Hg). This maneuver did not prevent the fall in GFR (from 81 +/- 5 to 36 +/- 6 ml/min/100 gm KW) or in RBF (from 510 +/- 79 to 197 +/- 20 ml/min/100 gm KW) after HgCl2 (P less than 0.01). In a third group, the RT was increased by a rise of MRPP to 158 +/- 8 mm Hg by bilateral carotid clamping. Subsequently, 3 hours after HgCl2, the GFR decreased not significantly from 72 +/- 6 to 61 +/- 7 ml/min/100 gm KW, and RBF increased from 405 +/- 66 to 431 +/- 71 ml/min/100 gm KW. Three hours of continued carotid clamping alone caused a rise of GFR from 64 +/- 7 to 83 +/- 7 ml/min/100 gm KW (P less than 0.05) and of RBF from 425 +/- 16 to 581 +/- 28 ml/min/100 gm KW (P less than 0.01). Autoregulation of RBF was studied in a control period and after 3 hours of carotid clamping and found to be lost during prolonged carotid clamping. The autoregulatory capacity remained intact after HgCl2 alone. The renal vasoconstrictive response to norepinephrine was not affected 3 hours after carotid clamping. It is concluded that the fall of GFR and RBF after HgCl2 can be prevented by prolonged carotid clamping. This is related to a loss of the capacity to maintain renal vasoconstriction after carotid clamping because of a concomitant loss of autoregulation of RBF and points at least in part to a pathogenetic role of changes in renal hemodynamics in the first hours after HgCl2. The tubular effects of HgCl2 were, however, maintained, despite the protection of GFR.

Acute Kidney Injury↗
PubMed1984

Lipid alterations induced by renal ischemia: pathogenic factor in membrane damage.

Lipids of the renal cortex and outer stripe of outer medulla were analyzed in rats during ischemia and 2 hr after blood reflow. After 15 min of ischemia, there were marked elevations of free fatty acids (FFA) and diacylglycerol (DG), increasing further at 60 min. Percentile increases were greater for polyunsaturated FFA. These elevations were accompanied by alterations in phospholipids (PL): Elevations of lysophosphatidylcholine (LPC) at 15 min, phosphatidic acid at 15 and 60 min, and declines of phosphatidylcholine and phosphatidylinositol at 60 min. Triacylglycerol (TG) showed only modest decline, at 60 min, and in insufficient degree to account for increments in FFA and DG. Two hours after 15 min of ischemia, LPC returned to control levels and other PL were normal except phosphatidylinositol which was decreased, and phosphatidic acid, which remained elevated. FFA and DG approached or reached control values. Two hours after 60 min of ischemia, LPC, FFA, DGs and phosphatidic acid remained elevated; phosphatidylcholine and phosphatidylinositol remained decreased. Histological injury was seen 2 and 24 hr after blood reflow only in kidneys injured by 60 min of ischemia. Thus, irreversible ischemic damage correlates with persistent abnormalities of phosphatidylcholine metabolism and persistent elevations of FFA, LPC, and DG. It is not known whether lipids break down at normal or accelerated rates during ischemia. In this context, accumulation of lipid breakdown products in ischemic cells may be due to failure of their reutilization, or disposal. Similarly, depletion of phospholipids during ischemia may be due to the inability of cells to reconstitute the lipid following degradation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Alterations in vascular function and morphology in acute ischemic renal failure.

Left renal arteries of rats were clamped for 40 min, and the kidneys were studied 48 hr and 7 days following restoration of blood flow. At 48 hr, there was severe oliguria or anuria. Renal blood flow (RBF) was in the normal range, but there was a loss of RBF autoregulation between 95 to 120 mm of mercury in seven out of nine rats. Morphologically, arcuate and interlobular arteries and afferent arterioles showed focal, segmental necrosis of smooth muscle cells and diapedesis of red blood cells across their walls. At 7 days, renal function was still severely depressed. RBF showed a slight decrease that did not reach statistical significance, and RBF autoregulatory capacity was lost in 8 out of 11 rats. Morphologically, vascular lesions were characterized at this stage by marked thickening and fibrosis of the tunica adventitia of the interlobular arteries and afferent arterioles. Structural vascular alterations may impair smooth muscle contractile function and thus interfere with RBF autoregulatory function in this model of acute renal failure.

Acute Kidney Injury↗
PubMed1979

Sonically guided renal biopsy.

The results of 91 sonically guided renal biopsies are reported. In the 53 cases where renal size and function allowed other localization techniques, renal tissue was obtained in 100 percent and glomeruli in 88.6 percent. In 38 cases no other techniques could have been used because of poor renal function (serum creatinine greater than or equal to 4.0 mg/dl) and/or decreased renal size (less than or equal to 10 cm); in these biopsies renal tissue was obtained in 86.8 percent and glomeruli in 73.7 percent.

Biopsy, Needle↗