Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve patients with cirrhosis, refractory ascites, and varying degrees of renal failure (creatinine clearance, 5 to 44 ml/min) were studied before and up to 2 weeks following peritoneovenous shunt. Creatinine clearance increased 60% or more in seven patients (group I) and 22% or less in five patients (group II). There were no significant differences in maximum urine output or sodium excretion between groups (group I, 4,272 ml/14 hr, 372 mEq/24 hr; group II, 3,722 ml/24 hr, 255 mEq/24 hr). Aldosterone and renin concentrations were higher in group I and showed a greater decrease after shunting. Renin substrate levels also were higher in group I and rose following shunt insertion, while group II remained low. Ascitic fluid was found to contain renin substrate in concentrations of approximately 25% to 50% of plasma concentrations. Patients with the greatest increase in creatinine clearance showed the largest rise in substrate concentration and fall in renin and aldosterone secretion, suggesting a dynamic relationship between these factors. That a diuresis could occur without significant change in these parameters in five of 12 patients suggests independent control mechanisms for renal salt and water excretion and glomerular filtration in the ascitic patient.
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PMID:Improved renal function and inhibition of renin and aldosterone secretion following peritoneovenous (LeVeen) shunt. 66 20

A prospective analysis of the value of urinary diagnostic indices in ascertaining the cause of acute renal failure was undertaken. Our results show that in the setting of acute oliguria a diagnosis of potentially reversible prerenal azotemia is likely with urine osmolality greater than 500 mosm/kg H2O, urine sodium concentration less than 20 meq/litre, urine/plasma urea nitrogen ratio greater than 8, and urine/plasma creatinine ratio greater than 40. Conversely, a urine osmolality less than 350 mosm/kg, urine sodium concentration greater than 40 meq/liter, urine/plasma urea nitrogen ratio less than 3, and urine/plasma creatinine ratio less than 20 suggest acute tubular necrosis. A significant number of oliguric patients will not have urinary indices that fall within these guidelines. In this setting, urine sodium concentration divided by the urine-to-plasma creatinine ratio (the renal failure index) and the fractional excretion of filtered sodium provide a reliable means of differentiating reversible prerenal azotemia from acute tubular necrosis.
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PMID:Urinary diagnostic indices in acute renal failure: a prospective study. 66 84

In rats with renal failure produced by excision of one kidney and infarction of large portions of the other kidney, given a low calcium, high phosphorus diet for 2-3 weeks, GFR was reduced by 80 percent, the fractional excretion of sodium increased from 7 to 23 percent, that of bicarbonate from 16 to 23 percent and that of water from 4 to 13 percent. Single nephron GFR in the remaining nephrons was nearly doubled and end-proximal TF/P(In) was depressed from 2.3 to 1.8, and proximal TF/P(HCO3) from 0.52 to 0.35, the latter figure corresponding to an increase of absolute proximal HCO(3) reabsorption from 1.7 to 3.5 nEq/min or from 2.8 to 3.2 Eq/L of single nephron glomerular filtrate. Acute parathyroidectomy had no influence on the fall of GFR or the rise of SNGFR in the remaining nephrons and failed to cause any significant changes in proximal tubular bicarbonate reabsorption. Parathyroidectomy, on the other hand, practically prevented the rise of the fractional excretion of sodium and of water and inverted the rise of the fractional excretion of bicarbonate to a fall. The data are interpreted to indicate that secondary hyperparathyroidism in renal failure impairs distal nephron bicarbonate and sodium reabsorption and, thus, contributes to the maintenance of sodium balance, but could possibly aggravate acidosis.
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PMID:A micropuncture study of HCO3 reabsorption by the hypertrophied proximal tubule. 73 50

Chronic nephron loss is compensated by functional adaptations which preserve electrolyte homeostasis. The response to volume expansion and diuretics was tested in dogs. Three phase recollection micropuncture studies were performed to assess the response of the remnant kidney in various stages of renal failure to furosemide administration (10 mg/Kg) and graded volume expansion (3 percent and 10 percent body weight). After the diuretic maneuvers, mean fractional excretion of sodium, potassium and water rose progressively in normal dogs (Stage I), with a greater increase in the remnant kidneys in the presence (Stage II) and absence (Stage III) of the contralateral kidney. Proximal and distal TF/P (Inulin) ratios were depressed after 3 percent volume expansion. However, proximal TF/P (Inulin) was not further lowered after 10 percent volume expansion and furosemide administration, while distal TF/P (Inulin) ratios were progressively depressed. The distal TF/P (Inulin) ratios in Stage III were significantly lower than in Stage II under analogous conditions. Our results suggest that the adaptive increase in the response of sodium transport by the remnant kidney to the diuretic maneuvers occurs in the loop of Henle, both in the azotemic and the non-azotemic stage. Adaptation of potassium excretion, as revealed by distal micropuncture, took place in the azotemic Stage III. Chronic functional adaptation for electrolyte transport occurs even before azotemia in the distal nephron and includes the proximal tubule with azotemia.
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PMID:Chronic reduction in renal mass: micropuncture studies of response to volume expansion and furosemide. 73 51

In patients with chronic renal failure due to glomerulonephritis, pyelonephritis or polycystic kidneys the urinary clearance of free chloramphenicol (C(CHL)) was depressed proportionally to GFR (C(In)). The ordinate intercept of the regression line of C(CHL) on C(In), however, consistently was positive (+3 to +5 ml/min). The fractional excretion of chloramphenicol in renal failure increased from its normal value of 50 percent as an exponential function of the decrease of GFR, and as a linear function of the fractional excretion of water or of sodium. Dietary sodium restriction had no influence on C(CHL) in the patients, while water diuresis, in normal subjects, enhanced the urinary excretion of chloramphenicol. The data suggest that chloramphenicol is reabsorbed by back-diffusion and that increases of the rate of flow of urine and tubular fluid prevent back-diffusion.
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PMID:The effects of functional adaptation of residual nephrons on the urinary excretion of drugs. 73 57

Pharmacokinetic studies were conducted in 8 patients with disseminated neoplasms refractory to conventional chemotherapy, who received gallium nitrate at doses of 300 to 600 mg/m2 intravenously in a phase I clinical trial. Gallium concentrations in biological fluids were determined colorimetrically. In patients with normal renal function, gallium showed a biphasic plasma disappearance with an initial half-life (t1/2) of 0.5 to 1.8 hr (mean 1.0) and a terminal t1/2 of 10.5 to 50.4 hr (mean 25.1). Gallium was distributed in total body water and often localized in some body compartment as evidenced by a volume of distribution ranging from 0.25 to 2.53 L/kg (mean 1.19). The total drug clearance from the plasma was 0.13 to 1.00 ml/kg/min (mean 0.65) in patients with normal renal function. Cumulative urinary excretion of gallium was 15% to 72% (mean 35%) of the administered dose in 24 hr (it fell to 23% in 8 days in a patient with acute oliguric renal failure). Gallium kinetics are altered in patients with acute renal dysfunction and in patients who have received multiple doses of gallium or other metal chemotherapy.
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PMID:Kinetics of gallium nitrate, a new anticancer agent. 75 46

The functional renal failure accompanying advanced liver disease is characterized by azotemia, a urine of very low sodium concentration and systemic hypotension with decreased renal perfusion and high renal vascular resistance. Patients with this disorder have a markedly reduced ability to excrete free water and develop hyponatremia, ascites and edema. It is postulated that this renal dysfunction is due to hepatic failure to make renin substrate. Renin released from the kidney is thus unable to exert its pressor effect. The resultant hypotension and renal hypoperfusion continue to stimulate excessive synthesis and release of renin. It is postulated that the overdriven renal renin system increases renovascular resistance at the level of the glomerular arterioles. This causes decreased renal blood flow and decreased glomerular filtration rate leading to salt and water retention and azotemia. Since no renin substrate is available for human infusion, this hypothesis could be tested either by infusion of angiotensin II to restore systemic blood pressure and renal perfusion or by beta adrenergic blockade with propranolol to attempt to decrease the intrarenal effects of renin, restore glomerular blood flow and filtration and thus return of renal function.
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PMID:Hepatorenal syndrome: a disease mediated by the intrarenal action of renin. 77 56

In Europe, about 1% of the women using oral contraceptives develop hypertension. Predisposing factors seem to be age, hypertension problems in past pregnancies, family history of hypertension, personal histories of kidney disorders, diabetes mellitus or adipositas, or diastolic pressure over 80 mm Hg. An overactive renin-angiotensin-aldosterone system may be an important factor in the etiology of this type of hypertension. Oterh possible factors are: reduced excretion of angiotensin 2, increased sensitivity of the arterioles to substances such as angiotensin 2 and noradrenaline, direct effect of ethinyl estradiol and mestranol on the sodium and water system, cardiovascular changes, disorders in the adrenergic system (e.g., catecholamine metabolism). Blood pressure should be checked before beginning any treatment with oral contraceptives and every 3 months after that. For the purpose of differential diagnosis angiotensin 2 in the plasma and catecholanin and its by-products should be checked (24-hour urine samples). In cases of serious hypertension hormone therapy should be discontinued at once. Primary aldosteronism and renal artery stenosis must be excluded in the differential diagnosis, for although these hypertensive disorders exhibit similar biochemical changes, they should be treated by surgical intervention. Usually hypertension is reversible after cessation of therapy with contraceptive steroids. However, some cases of irreversible hypertention, kidney failure, and malignant nephrosclerosis have been described. Hypertensive somen who wish to use oral contraceptives may, under medical supervision try a modified hormonal contraceptive (minipill without estrogen) or sequential or lower dosages.
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PMID:[Clinical aspects of hypertension under contraceptive steroids]. 79 66

In a previously nephrectomized patient with a well functioning renal allograft, acute renal failure with massive polyuria and hypertension developed. Relief of a periureteric obstruction resulted in rapid correction of all three. Pathogenesis of hypotonic polyuria is thought to be a defect in the collecting duct permeability to water, stimulating nephrogenic diabetes insipidus. Normal urinary dilution and acidification suggest intact function of the ascending loop of Henle and distal convoluted tubules. The quick reversal of polyuria and renal failure after obtaining relief of the obstruction suggest that both the decrease in the glomerular filtration rate and tubular dysfunctions are due to functional changes in the nephron rather than to organic damage, a possibility also borne out by the findings in a renal biopsy specimen showing normal glomeruli and intact tubular epithelial cells. Ureteric obstruction should be considered in any patient with renal failure and polyuria; it may be a correctable cause of hypertension.
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PMID:Obstructive polyuric renal failure following renal transplantation. 79 85

Digitoxin concentration, measured by radio-immunoassay, was significantly lower in 51 patients in chronic renal failure (23.2 +/- 7.8 mug/l) than in 29 patients in heart failure (26.5 +/- 7.3 mug/l), although both groups were on the same maintenance dose of 0.1 mg daily. Despite a normal serum albumin concentration, digitoxin protein binding was less in uraemic patients than in those with normal renal function. Renal failure did not affect intestinal digitoxin absorption. In patients in chronic renal failure elimination half-time was significantly shorter (5.7 +/- 0.9 days) than in healthy controls (7.6 +/- 1.6 days). There was no significant difference in the excretion of water-soluble ("cardioinactive") digitoxin metabolites in urine between patients in chronic renal and those in heart failure. In patients with normal renal function, of dichloromethane-soluble (cardioactive) metabolites only digitoxin could be demonstrated by thin-layer chromatography. The results indicate that patients in chronic renal failure can safely be given the same dose as those with normal renal function, without danger of over- or underdosage.
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PMID:[Pharmacokinetics of digitoxin in chronic renal failure (author's transl)]. 83 89


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