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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By measuring in vitro the effect of deproteinized plasma on canine kidney Na+K+-ATPase activity, evidence was sought for the presence of a circulating inhibitor of the enzyme in 31 patients with end-stage renal failure, 10 patients treated with digoxin, and 22 patients with untreated essential hypertension. In the renal failure group, mean Na+K+-ATPase activity with plasma samples taken just before a regular haemodialysis was 88% of that obtained with plasma from a normotensive control group (P less than 0.001). In digoxin-treated patients, the result was 94% of that obtained in control subjects (P less than 0.005). There was no significant difference in mean Na+K+-ATPase activity with plasma, between the hypertensive and control groups, or between age- and sex-matched subsets of these groups. The hypertensive group did not differ significantly from the control group in plasma renin activity or erythrocyte Na+ concentration. It was concluded that a circulating digitalis-like sodium-pump inhibitor was readily detectable in volume-expanded renal failure, but not in normal-renin essential hypertension.
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PMID:Measurement of circulating sodium-pump inhibitory activity in uraemia and essential hypertension. 244 Oct 15

The present study was carried out to examine the effect of potassium depletion in rat kidneys subjected to a temporary ischemic event produced by clamping of left renal artery. The postischemic kidneys of rats on a normal diet with adequate potassium intake showed an increase in H2O, Na and K excretion, with no change in inulin clearance whereas significant differences were found in potassium-deprived rats. Potassium depletion was brought about by dietary K deprivation for 10 days. K-depleted rats (serum K = 2.5 +/- 0.1 mEq/l) had a decrease in inulin clearance of the postischemic kidney from 1.01 +/- 0.10 to 0.43 +/- 0.05 ml/min (p less than 0.01), and a greater increase in fractional excretion of H2O, Na and K when compared to normal rats. The postischemic kidney from both normal and hypokalemic rats showed a decrease in Na-K-ATPase of the inner stripe of the outer medulla. These data indicate that short-term ischemia produces polyuria, increases natriuresis and kaliuresis, associated, at least in part, with a decrease in Na-K-ATPase in the inner stripe of the outer medulla (probably the thick ascending limb of Henle) and that K depletion potentiates ischemic renal failure.
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PMID:Effect of potassium depletion on ischemic renal failure. 253 74

Gentamicin nephrotoxicity increases renal cortex calcium and sodium and decreases renal cortex Na-K-ATPase activity. Human acute renal failure is accompanied by an increase in parathyroid hormone (PTH), a hormone that stimulates calcium uptake by tissues, and by a decrease in thyroid hormone, a hormone that increases renal cortex Na-K-ATPase activity. This study evaluated the role of extracellular calcium, PTH, and thyroxine in the pathogenesis of gentamicin nephrotoxicity. Chronically parathyroidectomized hypocalcemic rats (PTXG) given gentamicin (30 mg/kg s.c. twice daily for 8 days) were not protected from renal failure when compared with intact rats given gentamicin (NG), serum creatinine being 4.4 +/- 1.0 and 3.7 +/- 0.7 mg/dl, respectively, compared with normals (N), 1.2 +/- 0.1 mg/dl. Rats given thyroxine (10 micrograms/100 g body wt for 10 days) before and during gentamicin (PTXT4G) had a serum creatinine not significantly different from normals, 2.1 +/- 0.4 mg/dl. Plasma T4 was reduced in PTXG, NG, and PTXT4G compared with N, but the value for PTXT4G was significantly higher than for either PTXG or NG. Renal cortex Na-K-ATPase activity (mumol Pi X mg prot-1 X h-1) was lower in PTXG (2.3 +/- 0.2) and NG (2.4 +/- 0.5) compared with N (3.7 +/- 0.1), but activity was not reduced in PTXT4G (3.2 +/- 0.2) Thyroxine was protective also against gentamicin nephrotoxicity in intact rats. Clearance and excretion studies indicated that this protection did not result from an increase in glomerular filtration rate, filtered load of calcium, or urinary calcium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of thyroxine but not parathyroidectomy on gentamicin nephrotoxicity. 257 82

Endogenous digoxin-like immunoreactive factors (DLIF) are factors in plasma that interact with anti-digoxin antibodies. In this report we propose specific empirical criteria that must be satisfied by any group of endogenous compounds purported to account for DLIF activity in human plasma. These criteria include immunoreactive potency relative to existing physiologic concentrations as well as the biochemical and protein binding properties of these compounds. Recent studies have identified several congeners of fatty acids and phospholipids, hydrocortisone, and dehydroepiandrosterone-sulfate as compounds likely to account for DLIF activity in plasma. Using the above criteria we demonstrate that the highest reported plasma concentrations of these compounds combined account for less than 25% of DLIF reported in healthy adult subjects, less than 11% in newborns, less than 27% in pregnant women, and less than 39% in patients with renal failure. Human serum albumin at a concentration of 40 g/l completely abolished any detectable interaction of these compounds with both anti-digoxin antibodies or canine kidney Na/K-ATPase. The immunoreactive and physical properties of these compounds are also not consistent with those reported for DLIF. We conclude that these compounds do not account for the plasma DLIF concentrations measured in human subjects nor are they likely to play a role as specific endogenous regulators of Na/K-ATPase.
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PMID:Criteria for identifying endogenous compounds as digoxin-like immunoreactive factors in humans. 284 42

Studies in rats have shown that fecal potassium excretion and colonic mucosa Na-K-ATPase activity are elevated during dietary potassium loading and in chronic renal insufficiency. We studied Na-K-ATPase activity in human rectal mucosa in normal subjects as well as in patients with chronic renal insufficiency (creatinine clearance 2 to 72 mL/min). In normals, Na-K-ATPase activity was 4.34 +/- 0.83 mumol P/mg protein. After 2 weeks on a potassium intake of 300 mmol/d the mean activity did not differ significantly from the control value (2.49 +/- 1.30). In none of the patients with renal failure was Na-K-ATPase activity beyond the range found in the normal subjects, irrespective of serum potassium; the mean activity was 3.50 +/- 0.85. Like others, however, we found a two-fold increase in Na-K-ATPase activity in potassium loaded rats. Possible explanations for these differences are discussed.
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PMID:Sodium potassium ATPase activity in human rectal mucosa with and without renal insufficiency. 298 40

The catalytic activities of Na+-K+-ATPase and succinate dehydrogenase, marker enzymes for active salt reabsorptive capacity of renal basolateral plasma membranes and for respiratory capacity of mitochondrial cristae membranes, were studied in the maintenance phase of human acute post-transplant renal failure. Biopsies of 4 kidney-allografts taken at transplantation operation and additionally at different post-transplantation periods, either with good function or in various stages of dysfunction, were compared with the unaffected part of a human kidney nephrectomized due to hypernephroma. In single nephron segments, Na+-K+-ATPase activity was determined after microdissection by microfluorometry, and succinate dehydrogenase activity was determined by a microphotometric procedure in stained cryosections. In intraoperative and postoperative biopsies of a well-functioning allograft, both Na+-K+-ATPase and succinate dehydrogenase activities did not differ from those of normal renal tissue. In contrast, the catalytic activities were found to be decreased in the distal tubules of 2 anuric allografts when compared with their intraoperative controls. In addition, succinate dehydrogenase activity was reduced in distal tubules of a recovering allograft. Catalytic activities appeared to be unaffected in glomeruli, proximal tubules, and collecting ducts. It is suggested that the predominant distal tubular alterations with regard to these parameters are a consequence of increased distal tubular vulnerability due to circulatory and metabolic conditions.
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PMID:Altered distribution pattern of Na+-K+-ATPase and succinate dehydrogenase activities along the nephron in human acute post-transplant renal failure. 298 8

Human urine contains a small molecular weight natriuretic substance and similar material isolated from the kidney inhibits Na/K ATPase. Such action on smooth muscle in blood vessels would cause contraction. Human urinary natriuretic material caused contraction of the smooth muscle in the rat anococcygeus muscle and this activity correlated with its natriuretic activity. Known vasoactive substances could not explain the activity of the natriuretic factor when tested on the anococcygeus muscle. The best correlation with blood pressure of the patient was with the log of the ratio of natriuretic activity divided by the kallikrein excretion. A normotensive woman with severe renal failure had very high kallikrein excretion as well as increased natriuretic activity and her data fitted the same correlation as the hypertensives' data.
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PMID:Natriuretic and smooth muscle responses to human urinary natriuretic hormone in rats: relation to blood pressure and kallikrein excretion in patients. 299 Jul 72

The specific activity of mucosal Na-K-ATPase in segments of the small intestine and colon was examined after bilateral nephrectomies (BN), bilateral upper ureteral ligations (BUUL) and bilateral lower ureteral ligations (BLUL). Animals were studied 22-26 h after these respective operations. Bilateral nephrectomies and bilateral upper ureteral ligations resulted in an increase of the specific activity of the enzyme throughout the mucosa of the intestinal tract. Bilateral lower ureteral ligations induced no significant change in the specific activity of Na-K-ATPase in the intestinal mucosa. There were no differences in the degree of renal failure. Marked aldosteronemia was observed in the BN and the BUUL rats but not in the BLUL rats. These data suggest that the increase in the intestinal Na-K-ATPase activity in the BN and the BUUL rats may be related to the elevation of serum aldosterone as a regulator of the body potassium.
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PMID:The intestinal profile of Na-K-ATPase in three rat models of acute renal failure. 299 17

Endocochlear Potential (EP) was measured in male Wistar rats under control conditions and renal failure produced by means of bilateral nephrectomy. Results show a statistically significant (p less than 0.01) decrease in EP measured in animals with renal failure. This finding is in accordance with the decrease in Na-K ATPase activity found in the cochlea and other structures in human and experimental kidney insufficiency.
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PMID:[The endocochlear potential in experimental renal insufficiency]. 300 91

Digitalis-like factors were assayed by radioimmunoassay of digoxin in 6 bile samples obtained from patients at autopsy and in plasma from three patients with combined hepatic and acute renal failure. None of the patients received digoxin. Digitalis like factor values in bile samples were 23 to 85 nmol digoxin equivalents/1. Bile salt concentrations ranged from 38-104 mmol/l in the bile and 28-184 mumol/l in the plasma of these subjects. Bile, plasma digitalis like factor extracts and bile salt standards (0.1-3 mM) showed concentration dependent displacement of [125I]-digoxin from digoxin antibody, inhibition of hog brain Na,K-ATPase and displacement of [3H]-ouabain from Na,K-ATPase. The concentration-displacement curves suggest that bile salts could account for 50-79% of the total digitalis like factors in the six bile samples and 2-7% in the plasma of the three patients. High performance liquid chromatographic fractionation of a bile sample showed digitalis like factor peaks co-eluating with standards of tauro- and glycocholate, tauro- and glycochenodeoxycholate and tauro- and glycodeoxycholate. These bile salt peaks accounted for 78% of the total digitalis like factors in all high performance liquid chromatographic peaks in bile, but only 7% of the total digitalis like factor activity in all high performance liquid chromatographic peaks in an extract of plasma from one of the patients with hepatic and renal failure. The bile salts appear to be examples of endogenous digitalis like compounds which do not act by simple competitive ligand binding to antidigoxin antibody and Na,K-ATPase. They make an important contribution to digitalis like factor activity in bile, but not in plasma.
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PMID:Bile salts as endogenous digitalis like factors. 301 98


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