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)

Body water and electrolyte contents have been measured by means of muscle biopsy analysis in 11 patients with untreated acute renal failure and in one patient during the diuretic recovery phase of his illness. Patients with acute oliguric renal failure show two main types of imbalance. One group shows evidence of a reduction in extracellular sodium and chloride with normal intracellular water and electrolytes. These findings are thought to be due to a combination of excess urinary salt loss during the development of oliguric renal failure, and inadequate replacement of extrarenal electrolyte losses. A second group shows overhydration of both extra- and intracellular phases, associated with an excess of sodium and chloride. The intracellular potassium concentration is reduced, owing to the intracellular water excess. The patient studied during the diuretic recovery phase of acute renal failure showed a marked loss of sodium and chloride, which emphasizes the necessity to replace urinary electrolyte losses at this stage of the illness. It is often extremely difficult to assess fluid and electrolyte balance in patients presenting with acute renal failure, and muscle biopsy analysis or isotope dilution studies may be required before accurate replacement therapy is possible.
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PMID:Body water and electrolyte composition in acute renal failure. 557 38

Enalapril is a long-acting, sulphydryl-free, ACE inhibitor whose humoral and hypotensive effects are maximal at 4-8 h and remain detectable at 24 h after a single dose. Serum profiles after chronic dosing of enalapril show little accumulation of the active diacid metabolite, enalaprilat. Comparison between the observed and predicted steady-state urinary recoveries of enalaprilat yields an effective accumulation half-life of approximately 11 h. In normotensive subjects, enalapril increases renal blood flow whilst leaving glomerular filtration unchanged irrespective of the state of sodium balance. Similarly under conditions of salt loading and salt depletion, a biphasic saluretic response is seen which parallels the excretory maxima for unchanged enalapril (1-2 h) and enalaprilat (4-8 h) suggesting direct interference by the drug moieties with tubular NaCl reabsorption. During the period of maximal enalapril action, uricosuria and phosphaturia are seen, supporting a direct action of enalaprilat on proximal tubular handling of these anions. Detailed documentation of the chronic metabolic effects of enalapril remains incomplete. A small rise in plasma potassium concentrations can occur but overt hyperkalaemia is unlikely in the absence of gross renal failure. Continued dosing is associated with a fall in plasma uric acid concentrations; plasma prolactin concentrations remain unaltered.
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PMID:Kinetic and metabolic aspects of enalapril action. 610 Aug 75

Haemofiltration was used in 12 children with terminal chronic renal failure. This method is an alternative for short-term treatment of renal failure by haemodialysis and can be combined with the single-needle-technique. It was also used in a 2 years old girl with acute renal failure. The main advantages of haemofiltration versus haemodialysis are a more rapid removal of fluid in the presence of stable blood pressure readings and a good tolerance by the patient. The primary indication for haemofiltration is hypervolaemia. The high water and salt losses during the procedure have to be exactly calculated and substituted. According to our current experience the volume needed for substitution of filtrate by fluid to be infused i.v. has to be in the range of 50% of body weight.
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PMID:[Haemofiltration in children. First experiences (author's transl)]. 611 Jan 76

Glaphenine, a nonsteroid analgesic compound, administered by gastric gavage in rats (800 mg/kg), induced nonoliguric reversible acute renal failure (ARF). Intratubular deposits were found in medullary collecting ducts. Intratubular hydrostatic pressure (Pt) increased from 11.7 +/- 0.7 to 30.0 +/- 0.9 mmHg. Renal failure was almost completely prevented by concomitant high water and solute diuresis, achieved by furosemide infusion in Wistar rats and by high salt intake in Brattleboro rats with diabetes insipidus. In the latter protected animals, Pt was only slightly elevated (17.0 +/- 0.5 mmHg). Urinary excretion of prostaglandin E2 (PGE2) dropped dramatically after glaphenine administration in Wistar rats; the fall was slight in Brattleboro rats in which PGE2 excretion was normally low. We conclude that tubular obstruction plays a prominent role in glaphenine-induced ARF in the rat. High water and solute diuresis prevented tubular obstruction. Reduced renal PGE2 synthesis is probably not involved in the pathophysiology of this ARF model, inasmuch as Brattleboro rats on a high salt intake were protected despite low basal urinary excretion of PGE2.
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PMID:Glaphenine-induced acute renal failure in the rat: a new experimental model. 612 34

The effects of clonidine on renal hemodynamics and renal function make it a particularly useful antihypertensive agent. During treatment of hypertensive patients with clonidine, renal blood flow and glomerular filtration rate are well maintained, and renin secretion is reduced. Early in therapy, a slight tendency to retain salt and water may be seen as blood pressure is lowered. This effect on salt and water excretion is usually transient and may be avoided if a diuretic is used concomitantly. No deterioration of renal function was noted in patients with primary hypertension who were treated with clonidine for periods from 6 months to at least 5 years. The drug is effective in patients with renal hypertension with or without renal failure and well tolerated. Clonidine is also effective in hypertensive patients undergoing chronic hemodialysis, but doses may have to be reduced because the drug is excreted chiefly by the kidney.
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PMID:Clonidine and the kidney. 615 36

Six patients in whom "essential hypertension" led to nephrosclerosis and kidney failure received kidney transplants from normotensive donors. After an average follow-up of 4.5 years, all were normotensive and had evidence of reversal of hypertensive damage to the heart and retinal vessels. These six patients, all of whom were black, and six control subjects matched for age, sex, and race were admitted to the General Clinical Research Center for 11 days for observation of their blood pressure and their responses to salt deprivation and salt loading. Mean arterial pressure (+/- S.E.M.) among the patients who had previously had essential hypertension was similar to that of the normal controls (92 +/- 1.9 vs. 94 +/- 3.9; P not significant), and both groups had similar responses to salt deprivation and salt loading. Thus, essential hypertension in human beings is shown to be similar to the hypertension seen in spontaneously hypertensive rats in that both can be corrected by transplantation of a kidney from a normotensive donor. This observation supports the concept of the primary of the kidney in causing essential hypertension.
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PMID:Remission of essential hypertension after renal transplantation. 635 30

This paper is a study of 117 patients with endstage renal failure, treated by continuous ambulatory peritoneal dialysis (CAPD) over periods of 1-56 months. The study has shown CAPD to be an effective form of dialysis with a number of advantages over intermittent peritoneal dialysis and hemodialysis (better control of salt and water status, hypertension and anemia, steady state biochemistry and greater ease of self-dialysis). Peritoneal clearance and ultrafiltration have remained adequate in all but a few patients. Hypoproteinemia, poor nutrition, obesity and abdominal herniae have been problems in a small percentage of patients. Hyperlipidemia has developed in half the patients but improved with diet. Peritonitis remains the major barrier to the more widespread use of CAPD, although its incidence can be considerably reduced by use of better connectors, bacterial filters and choice of patients.
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PMID:Continuous ambulatory peritoneal dialysis (CAPD): an established treatment for endstage renal failure. 636 Jan 16

Papillary necrosis, a common cause of renal failure, is a life-threatening pathophysiologic event which may have a multiplicity of mechanisms. The primary functional lesions are salt wastage, impairment of urinary concentrating ability, polyuria, and imbalances of potassium, calcium and phosphate homeostasis; urinary acidification is completely normal. Papillary necrosis is associated with a profound decrease in juxtamedullary nephron glomerular filtration rate, in addition to damage to the papillary collecting duct. 2-Bromoethylamine hydrobromide (BEA) has proved to be a useful tool in elucidating the generation of this important clinical syndrome.
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PMID:Pathophysiology of drug-induced papillary necrosis. 639 14

52 children with renal allograft received captopril during 56 periods of treatment. High blood pressure (BP) was due to renal artery stenosis in 22 patients, to diffuse vascular lesions (mainly due to chronic rejection) in 13, to high-dose corticosteroid treatment in the early phase in 11, and to various or unknown causes in 10 patients. In the last 3 groups (including 34 cases) captopril use did not induce any marked drawback. In the absence of overload, a good control of BP was obtained with a mean dosage of 2.2 mg/kg (0.7----5 mg/kg). A mild, transient renal failure (RF) was observed in 6 patients, who were given diuretics without any need. The 22 patients with renal artery stenosis received captopril during 26 periods of treatment. The mean dosage was 1.6 mg/kg (0.3-4.4). The result was excellent in 12 cases (normal BP without any RF), less good in 8 cases (moderate RF +/- borderline BP) and poor (acute RF) in 6. Sodium depletion, due to diuretics in 9, was present in all 14 cases with RF and in 10 of them captopril could be continued or reintroduced without any reappearance of RF after the correction of salt depletion. We conclude that sodium depletion is the main cause of renal failure in transplanted patients receiving captopril and that avoidance of diuretics largely diminishes the risk of RF.
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PMID:[Captopril treatment of arterial hypertension in children after renal transplantation]. 644 43

In most normal subjects, the fractional excretion of sodium is usually less than 1 percent but may be raised with an increase in salt intake. In acutely azotemic patients, a low fractional excretion of sodium usually indicates a prerenal process that is responsive to volume repletion. However, such a low fractional excretion of sodium also can be seen with azotemia due to hepatic or cardiac failure, as well as acute glomerulonephritis, pigment nephropathy, contrast nephrotoxicity, polyuric renal failure associated with burns, acute obstruction, renal transplant rejection, and occasionally non-oliguric acute renal failure, none of which is a volume-responsive process. A fractional excretion greater than 1 percent in acutely azotemic patients usually indicates intrinsic renal injury, but is consistent with volume depletion in patients receiving diuretics or in some patients with chronic renal insufficiency. Similarly, a low quotient in acute renal parenchymal injury is usually interpreted to indicate widespread tubular integrity, but is consistent with several different pathophysiologic processes. The fractional excretion of sodium must be interpreted in light of the specific clinical setting and other laboratory data to be useful in patient management.
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PMID:Interpreting the fractional excretion of sodium. 648 45


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