Reducing urine

Oliguria Reduced urine output usually defined as less than 400 mL in 24 hours or less than 0.5 mL/kg/hour. 

In mice, extirpation of the VNO has many behavioral effects. It reduces aggression in male mice (Bean, 1982 Wysocki etal, 1986), reduces urine marking and aggressive behavior in sexually naive male mice (Maruniak etal, 1986) lowers marking to some extent also in sexually experienced males (Labov and... 

A second unusual action of this class of diuretics is their utility in treating nephrogenic diabetes insipidus. Patients who have an adequate supply of ADH but whose kidneys fail to respond to ADH excrete large volumes of very dilute urine, not unlike those who have an ADH deficiency. The thiazides reduce glomerular filtration modestly and decrease positive free water formation (Ch2o), that is, production of dilute urine. These actions combine to cause patients with nephrogenic diabetes insipidus to excrete a somewhat reduced urine volume with increased osmolality. 

Kidney They directly depress the tubular reabsorption of sodium, reduce urine flow and increase ADH release. 

Diabetes insipidus They reduce urine volume in both pituitary and renal diabetes insipidus. They are especially valuable for the latter in which ADH is ineffective. 

Antidiuretic agents reduce urine volume and are used in the treatment of diabetes insipidus. They are classified as in table 4.7.2. 

Tricyclics may also pose a threat to vision by causing dry eyes, blurred vision, and even vision loss when narrow-angle glaucoma is present. Also, tricyclics may result in dry mouth that can lead to dental cavities, reduced urine output, and constipation. Although not fully understood, weight gain is also an effect. Whether a result of the drug or of the illness, sexual drive is decreased. 

In vivo, i.v. administration of 1 to rats dose-dependently inhibited AVP-induced increases in blood pressure with an /Z)50 of 13 pg/kg. Administration of 1 also significantly increased urine volume (ED of 28 pg/kg)18 and reduced urine osmolality in a dose-dependent manner.16 Compound 1 proved orally active in rats, dose-dependently inhibiting AVP-induced increases in diastolic blood pressure and providing dose-dependent diuretic effects that were sustained for 8-10 h after a 3-mg/kg dose.19 Similar results were obtained in dog pharmacodynamic studies.20 Notably, daily dosing of rats with 1 (1 or 3 mg/kg for 1 week) resulted in sustained increases in urine volume without sodium excretion, with no evidence of tachyphylaxis.21... 

The inherent limitations of the Jaffe method for determination of creatinine have been discussed in section Assessment of Renal Injury by Serum Chemistry . Factors which result in reduced excretion of creatinine without acute tubular injury (e.g., chronic renal disease in aged animals with pronounced loss of nephron mass, prerenal reduction of GFR) will also result in reduced urine creatinine and falsely elevated enzyme activity when normalized to creatinine (Price 1982, Plummer et al. 1986, Casadevall et al. 1995). 

Two studies in rats have potential implications for humans. In rats with mild to severe lithium-induced nephropathy, urine TV-acetyl-p-D-glucosaminidase was an early indicator of renal insufficiency (369). Both 6Li and 7Li caused reduced urine concentrating ability and increased urine volume and renal tubular lesions, but 6Li was more nephrotoxic (370). The authors suggested that eliminating 6Li from pharmaceutical products might reduce nephrotoxicity (although 6Li accounts for only about 7% of the lithium in such products). 

Nephrogenic diabetes insipidus secondary to lithium led to severe dehydration in two patients who required intravenous rehydration followed by a thiazide diuretic to reduce urine volume (382). One patient had persistent polyuria (6.7 1/day) 57 months after stopping lithium (296). 

A 17-year-old who took olanzapine 75 mg and praze-pam 7.5 mg in a suicide attempt developed polyuria (5400 ml/24 hours), reduced urine osmolality (166 mos-mol/kg H20), normal plasma osmolality, and an increasing serum sodium concentration, consistent with a diagnosis of diabetes insipidus (259). 

Nephrogenic diabetes insipidus, paradoxically, may respond to diuretics which, by contracting vascular volume, increase salt and water reabsorption in the proximal tubule, and thus reduce urine volume. 

Renal failure In about 50% of patients with acute hver failure, renal insufficiency develops. This can be expressed in three forms (7.) prerenal kidney failure due to hypovolaemia, (2.) acute tubular necrosis, mainly secondary as a result of circulatory hypotension with cylindruria, a higher concentration of sodimn in the urine (50—70 mmol/1) and a reduced urine creatinine/ser m creatinine quotient (<20) or urine urea/serrrm urea quotient (<3), or (3.) hepatorenal syndrome. (41) (s. tab. 17.3)... 

A 73-year-old white man took levofloxacin for a lower urinary tract infection for 3 days and developed palpable purpura and erythematous skin lesions over the lower limbs and trunk, with a markedly reduced urine output. Serum creatinine was 560 pmol/l (6.4 mg/dl). Levofloxacin was withdrawn, and prednisone, furose-mide, and intravenous fluids were given. The patient recovered fully over the next 4 weeks. 

Acute opioid poisoning involves marked CNS depression, with drowsiness, loss of consciousness, and coma. Other prominent features are a reduced respiratory rate, hypotension, and sjmmetrical pinpoint pupils (unless the patient has been hjrpoxic for some time, in which case the pupils can be dilated). Reduced urine output, hypothermia, flaccid skeletal muscles, and pulmonary edema can also be present. Convulsions have occurred in children. 

Clinically, the animals do not show signs until 24-48 or more hours after ingestion of the bait. The affected animals are depressed, have reduced urine production, and the urine is of low specific gravity. Severely poisoned animals have hematemesis, azotemia, and cardiac arrhythmias. Animals with renal impairment are more susceptible to cholecalciferol poisoning than those with normal renal function. Cholecalciferol poisoning requires protracted treatment, which may require as long as 3 weeks in severe intoxications. Appropriate treatment consists of fluid therapy to assist the kidneys in removing the excess calcium, corticosteroids to minimize inflammation, and calcitonin to enhance calcium resorption into the bone. Pamidronate disodium is the new antidote for this poison. 

Signs Not likely present May present with fluid retention, anemia, dyspnea, reduced urine output... 

The best approach to the treatment of hyperlipidemia in patients with nephrotic syndrome is to induce remission of the disease (see Chap. 47), or at least to reduce urine protein excretion by aggressive treatment of concurrent hypertension and/or administration of ACEIs or ARBs. Several trials have assessed the effect of L-carnitine supplementation on abnormal lipid metabolism in dialysis patients, but results have been contradictory. ... 

Signs of hypernatremia may include postural hypotension, diminished skin turgor, and reduced urine output. 

Nephrotoxins or ischemic disorders can initiate acute renal failure. Shock, hemorrhage, septicemia, or vasodilation due to hypertensive medication can precipitate ischemic acute renal failure. Systemic reactions to certain drugs and nephrotoxins such as aminoglycoside antibiotics and heavy metals lead to acute renal failure. The extent of retention of creatinine and urea in blood is directly related to the severity of acute renal failure. This condition is not readily reversible and, as such, should be distinguished from reversible phenomena such as prerenal or postrenal azotemia, in which there is also an increase in levels of plasma urea and creatinine (13). In volume-depleted states, for example, diarrhea, the kidney is hypoprefused. This results in increased back diffusion of urea into the circulation from the tubular fluid because of the reduced urine flow. In addition to an increase in urea levels in circulation, there is also a slow increase in creatinine levels. Plasma urea and creatinine levels can be restored to normal within 24 hours by appropriate fluid and electrolyte replacement in prerenal azotemia. In condi-... 

The prostate is both a blessing and a curse. This small walnut-shaped organ surrounds the urethra (the tube through which urine passes) and is situated at the base of the bladder. It is the source of seminal fluid and is thus intimately involved in maintenance of sexual performance and libido. But to many men over the age of 40 (and to just about all over the age of 70), it is a source of annoyance and discomfort. With advancing age, the prostate grows and begins to constrict the urethra, reducing urine flow - a condition known as prostatic hyperplasia. 

The vitamin has also been routinely prescribed in cases of threatened abortion, thyroxidosis, achlorhydia, diarrhoea, prickly heat, rheumatic fever, rheumatic arthritis, and in cases of spinal injury to reduce urine acidity. The physiological basis of these therapeutic applications is not entirely clear except in the cases of achlorhydia and diarrhoea where there is a risk of anaemia caused by a reduction in the intestinal absorption of non-haem iron which is enhanced by vitamin C. 

Kidney damage with oliguria (reduced urine production). Anuria is often the result of tubular necrosis. 

Nephrotoxic effects can range from mild to severe cell necrosis, and changes in functionality can also range from minor alterations of tubular function (e.g., glucosuria) to severe renal failure with reduced urine output (decreased—oliguria or absent— anuria) and electrolyte imbalance. Renal tubular damage can lead to the loss of cells of the nephron into the tubule (e.g., tubular epithelial cells that subsequently appear in the urine) the loss of renal function can have an impact on major organs such as the heart and liver. 

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