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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred ten episodes of renal salt retention (urinary sodium and/or chloride less than 10 mEq/L) were studied retrospectively to determine the significance of discordance of urinary sodium from chloride. In 16 episodes the urinary sodium exceeded chloride by at least 15 mEq/L. This disparity was associated with the necessity for urinary excretion of substantial quantities of poorly reabsorbed anions (penicillin, ketones, or diatrizoate), a rapidly falling serum bicarbonate level (due to resolving metabolic or developing respiratory alkalosis), or substantial renal insufficiency (serum creatinine greater than 3 mg/dL). In 14 of 110 episodes, urinary chloride exceeded urinary sodium by at least 15 mEq/L. These patients were more often oliguric and had a higher mean serum chloride than patients without this dissociation. In patients with oliguria, hyponatremia, or metabolic alkalosis, measurement of urinary sodium or chloride alone will, in a substantial number of cases, fail to detect renal salt retention. When evidence is sought for renal salt retention, both urinary sodium and chloride should be determined.
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PMID:Urinary sodium and chloride during renal salt retention. 661 92

The fall in serum albumin which occurs after operation can be modified by an intraoperative infusion of 20 g salt-poor human albumin, and the associated fall in colloid osmotic pressure is also corrected. There is a decrease in postoperative oliguria following a colloid infusion but no significant effect has been demonstrated on urinary sodium excretion. Th alteration of fluid and electrolyte metabolism after surgery does not appear to be a direct effect of lowered plasma colloid osmotic pressure. It is suggested that the effect of intraoperative albumin infusion is predominantly haemodynamic.
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PMID:Colloid osmotic pressure and serum albumin following surgery. 706 51

Despite extensive study, the pathogenesis of cirrhotic ascites and its relationship to salt and water retention and the hepatorenal syndrome remain unclear. This article reexamines the underlying disturbance in microcirculatory exchange of fluid and protein in the liver and digestive tract and specifically stresses that, in keeping with current interpretation of the Starling hypothesis, ascites appears when the driving force of elevated portal pressure overwhelms the "safety factors" of widened transmural colloid asmotic pressure gradient and accelerated regional lymph flow. In light of recent findings that enhancement of ascitic fluid returned to the bloodstream produces a natriuresis, diuresis, and amelioration of ascites, a "lymph imbalance" theory distinct from the "classic" and "overflow" theories is advanced. This theory proposes that a circulatory imbalance between the rate of fluid leaving and returning to the bloodstream (i.e., the relative rates of lymph formation and lymph absorption) is responsible for a maldistribution of extracellular fluid, which, in turn, stimulates renal salt and water retention, progression of ascites, and finally, the hepatorenal syndrome. Should compensatory factors suffice to prevent or reverse this lymph imbalance, the full cycle is not activated or, if already operating, is deactivated. Thus, portacaval shunt (by reducing the rate of lymph formation) or peritoneovenous shunt (by acting as a megalymphatic collateral to accelerate resorption as well as prevent sequestration of peritoneal fluid), both tend to restore the lymph balance and thereby suppress salt and water retention, correct functional oliguria, and ameliorate ascites.
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PMID:Lymph imbalance in the genesis and perpetuation of the ascites syndrome in hepatic cirrhosis. 738 Jan 79

Prerenal failure is traditionally accompanied by oliguria and represents the normal renal adaptation to retain salt and water and correct the prerenal state. Nonoliguria occurring in the setting of acute renal failure usually represents acute tubular necrosis (ATN) since the kidney has lost its ability to extract salt and water. We report nine cases of patients with acute renal failure occurring in the setting of impaired systemic hemodynamic states and yet who were nonoliguric without strong evidence for ATN. The common defect in these subjects with "polyuric prerenal failure" was a blunted urinary concentrating ability. Polyuria and renal failure occurring despite evidence for impaired systemic hemodynamics may not necessarily be ATN, may still be prerenal, and should be recognizable and promptly reversible if treated appropriately.
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PMID:Polyuric prerenal failure. 738 98

Fluid loading with balanced salt solution (BSS) was carried out in 200 patients with extensive soft tissue injuries from severe beatings. Urinary volume and dipstick specific gravity testing were used to monitor renal function with administration of furosemide for persistent oliguria. Acute intrinsic renal failure (AIRF) occurred in 21 patients (10.5%) and five patients died (2.5%); two of hyperkalemia, two of sepsis and one of multiple organ failure. Significantly increased rates of AIRF and death were associated with injury-admission intervals of more than 12 hours, severe metabolic acidosis, low initial hemoglobin, heavy pigmenturia, and high serum creatine kinase (CK) levels. An increased serum creatinine/BUN ratio was noted in four of the five patients who died. An average of 7.5 L fluids was needed in non-AIRF patients to achieve adequate diuresis with a mean positive fluid balance of 4.7 L. No patient without pigmenturia developed AIRF. Balanced salt solution volume diuresis supplemented with furosemide as necessary appears to be safe and effective in preventing AIRF in soft tissue injuries sustained in beatings.
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PMID:Traumatic rhabdomyolysis from severe beating--experience of volume diuresis in 200 patients. 806 19

Acute mountain sickness (AMS) affects, to varying degrees, all travelers to high altitudes (elevations greater than 5280 feet). In a small percentage of patients, AMS can lead to high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE). Symptoms of AMS range from a combination of headache, insomnia, anorexia, nausea, and dizziness, to more serious manifestations, such as vomiting, dyspnea, muscle weakness, oliguria, peripheral edema, and retinal hemorrhage. Although the primary cause of these symptoms is related to the reduced oxygen content and humidity of the ambient air at high altitudes, the physiologic pathway relating hypoxemia to AMS and its sequelae remains unclear. Tips on self-diagnosis and symptom recognition are critical elements to be included in educating patients who are contemplating a trip to high altitudes. Preventive strategies include allowing 2 days of acclimatization before engaging in strenuous exercise at high altitudes, avoiding alcohol, and increasing fluid intake. Conditioning exercise for patients older than 35 years is also recommended before departure. A high-carbohydrate, low-fat, low-salt diet can also aid in preventing the onset of AMS. Acetazolamide (125 mg two or three times daily, or once at bedtime) has also been shown to reduce susceptibility to AMS and the incidence of HAPE and HACE. Although effective in treating cerebral symptoms of AMS, dexamethasone is not routinely recommended as a prophylactic agent for AMS.
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PMID:A trek to the top: a review of acute mountain sickness. 855 56

The sequence in which the various therapies discussed above are instituted can be viewed as a continuum that parallels the severity of the underlying cirrhotic state (Figure 6). In the earliest stages of the disease urinary sodium excretion is plentiful and negative salt balance can be achieved by simply lowering dietary sodium intake. As the disease advances neurohumoral effectors become more activated initially resulting in more intense renal salt retention and later in a progressive decline in renal function. Eventually, the filtered load of sodium becomes completely reabsorbed by the tubule and the final urine becomes virtually devoid of salt. If some component of the filtered load reaches the collecting duct or beyond, spironolactone will be effective in increasing urinary sodium excretion. Once sodium reabsorption is complete, proximal to the collecting duct, then thiazides and later loop diuretics will have to be added to spironolactone to increase urinary sodium excretion. Eventually, the filtered load is completely reabsorbed proximal to the thick ascending limb of Henle. At this point the patient is resistant to the effects of diuretics and requires more invasive procedures such as repetitive large volume paracentesis to remain in salt balance. In the terminal stages of the disease the glomerular filtration rate falls to such a degree that oliguria, azotemia, and eventually uremia are present and the patient is clinically diagnosed with hepatorenal syndrome. Vasoconstrictive input focused on the kidney is severe and irreversible. Renal failure is functional in nature; however, restoration of near normal renal function can be obtained following a liver transplant.
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PMID:Pathogenesis of ascites and renal salt retention in cirrhosis. 1036 77

Ovarian hyperstimulation syndrome is a complication of the ovulation stimulation, most commonly by gonadotrophins. It frequently occurs in patients included in in vitro fertilization program. The exact mechanism of development of this syndrome has not been elucidated yet. The basic pathogenic mechanism of development of this syndrome is vasodilation of the ovarian blood vessels. Dilated ovarian blood vessels become permeable. Permeability of dilated ovarian blood vessels is more increased by released ovarian mediators. Due to increased permeability of the blood vessels, there is leakage of the intravascular fluid into the extravascular areas resulting in hypovolemia, edema and ascites. Hypovolemia leads to renal perfusion decrease. Increased salt and water reabsorption occurs in the renal tubules so oliguria develops. Decreased arterial blood volume results in stimulation of the renin-angiotensin-aldosterone system, the sympathetic nervous system as well as the antidiuretic hormone. The activation of the sympathetic nervous system via beta adrenergic receptors stimulates renin release and aldosterone secretion. Renin stimulates release of angiotensin I which transforms into angiotensin II. Angiotensin II increases the pressure and stimulates aldosterone secretion. In patients with this syndrome, there is an elevated plasma endothelin and natriuretic peptide level. Endothelin is an important vasoconstrictor. It increases secretion of renin, aldosterone, catecholamines, antidiuretic hormone, and atrial natriuretic peptide, and enhances the vasoconstrictive effect of norepinephrine and angiotensin II. The platelet number increase together with the elevated factor of blood coagulation and hyperviscosity in a severe form of this syndrome may result in development of intravascular thrombosis. The treatment consists of maintenance of circulatory function, i.e. the increase of effective arterial blood volume by applying the plasma volume expanders.
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PMID:[The significance of the ovarian arteriolar vasodilatation in pathogenesis of the ovarian hyperstimulation syndrome]. 1700 17

Bath salts are substance of abuse that are becoming more common and are difficult to recognize due to negative toxicology screening. Acute kidney injury due to bath salt use has not previously been described. We present the case of a previously healthy male who developed acute kidney injury and dialysis dependence after bath salt ingestion and insufflation. This was self-reported with negative toxicology screening. Clinical course was marked by severe hyperthermia, hyperkalemia, rhabdomyolysis, disseminated intravascular coagulation, oliguria, and sepsis. We discuss signs and symptoms, differential diagnoses, potential mechanisms of injury, management, and review of the literature related to bath salt toxicity.
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PMID:Bath salts: a newly recognized cause of acute kidney injury. 2455 35

Cerebral salt wasting syndrome is a hyponatremic and hypovolemic condition caused by intracranial disorders, such as head injury, subarachnoid hemorrhage, brain tumor, and brain operations. We report a case of a 5-year-old girl that had cerebral salt wasting syndrome with marked polyuria who showed transient oliguria during general anesthesia. The patient had undergone an operation for traumatic intracranial hemorrhage three months prior and has had marked polyuria and hyponatremia since then. After induction of anesthesia for cranioplasty, the patient had oliguria during surgery and then resumed polyuria in the post-operative period.
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PMID:Transient Oliguria during Anesthesia in Cerebral Salt Wasting Syndrome. 2792 87


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