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PubMed1987

The pathogenesis of trimethyltin chloride-induced nephrotoxicity.

In exploratory studies aimed at elucidating CNS effects due to heavy metal toxicity, signs of compromised renal function were seen in rats. The studies reported here describe the sequential steps of the development of nephrotoxicity by trimethyltin chloride (TMT) in rats. Single doses of 12.25 mg/kg TMT administered orally to 150- to 175-g Long-Evans rats elicited overt signs of toxicity including behavioral abnormalities and marked weight loss. Concurrent with the development of these signs, nephrotoxicity was manifested as functional kidney compromise and associated histopathologic evidence of tubular damage. Pathological changes in the kidneys from treated rats were hyaline droplet inclusions, attenuated brush border, basolateral vacuolization, and eosinophilic granular casts in the proximal tubule cells. These lesions were detected as early as 2 days post-treatment and progressed with time in an orderly and sequential fashion. Renal lesions between 5 and 8 days were mild to severe cortical tubular dilatation, hydropic degeneration, and diffuse hyaline droplet deposition in the lower nephron tubules. Medullary edema and exfoliation of degenerated tubular epithelial cells with cast formation followed from 8 to 11 days. The morphological changes were accompanied by marked elevation of blood urea nitrogen, parallel with polyuria at Day 2 and oliguria by Day 14. Behavioral abnormalities as well as weight loss correlated well with the time course and severity of renal dysfunction and progression of morphological changes. A second experiment compared the effects of TMT in rats of different weights. Heavier rats were more sensitive than lighter rats to the nephrotoxic effects of TMT. These effects were independent of recognizable neurotoxic effects of TMT in the hippocampus.

Animals↗
PubMed1995

Bartter's syndrome: the unsolved puzzle.

Bartter's syndrome is a congenital abnormality characterized by metabolic alkalosis [corrected], hyperreninemic hyperaldosteronism, and hypokalemia. Most patients present early in life with symptoms such as muscle weakness and polyuria, which may be attributed to potassium depletion. Despite the hyperaldosteronism, the patients tend to be normotensive, which is at least partially explained by vascular hyporesponsiveness to pressor hormones. Numerous studies have documented increased renal excretion of prostaglandins. Several different patterns of aberrant renal ion transport have been observed in patients with the syndrome, suggesting that it actually may represent a family of related but distinct tubular disorders. Therapeutic approaches to Bartter's syndrome include potassium supplementation, prostaglandin synthesis inhibitors (nonsteroidal anti-inflammatory agents), aldosterone antagonists, and converting enzyme inhibitors. During the first two decades following its initial description, Bartter's syndrome was the focus of widespread interest, based on the likelihood that its investigation might provide insight into the normal functioning of the renin-angiotensin-aldosterone and prostanoid hormone systems. During the past decade, however, little additional progress has been made in Bartter's syndrome, and its patho-physiology remains poorly understood.

Adolescent↗
PubMed1995

Toxicity of fumonisin B1 administered intraperitoneally to male Sprague-Dawley rats.

The toxicity of purified fumonisin B1 (FB1) administered ip was examined in male Sprague-Dawley rats. FB1 was injected at 7.5 or 10 mg/kg body weight/day for 4 consecutive days. This resulted in significant reductions in body weight, food consumption and faeces production. Polyuria without a compensatory increase in water consumption was observed in treated rats. Erythrocytosis, elevated haematocrits and haemoglobin levels were attributed to dehydration. Nephrotoxicity in treated rats was evident by clinical changes including elevated blood urea nitrogen and by subtle changes in kidney morphology. Histopathology and serum biochemistry also indicated that the liver was an important target organ in FB1-treated rats. A small increase in liver glutathione concentration was also evident in rats receiving 10 mg FB1/kg body weight. Effects on the immune system included reduced thymus weight, disseminated thymic necrosis and consistently elevated serum immunoglobulin M levels. Circulating phagocytic cell numbers were elevated in treated rats, probably owning to tissue damage associated with ip dosing. The liver and kidneys appear to be target organs of FB1 in Sprague-Dawley rats.

Animals↗
PubMed1984

Onset of and recovery from acute N-(3,5-dichlorophenyl)succinimide-induced nephrotoxicity in Sprague-Dawley rats.

The time course for the onset of N-(3,5-dichlorophenyl)succinimide (NDPS)-induced nephrotoxicity was studied in male Sprague-Dawley rats. The ability of rats to recover from a single nephrotoxic dose (100 or 200 mg/kg) of NDPS also was examined. One hour following NDPS administration (200 mg/kg, i.p.), p-aminohippurate (PAH) accumulation by renal cortical slices was decreased 51%. Changes in renal morphology, proteinuria, hematuria, and diuresis were observed at 3 h. Renal damage at 6 h was similar to that seen at 24 h with tubular necrosis greater than that observed at 3 h and some lumina plugged with PAS+ material. Accumulation of both PAH and tetraethylammonium (TEA) by renal cortical slices was decreased; and proteinuria, hematuria, and polyuria were increased at 6 h and 24 h. Blood urea nitrogen (BUN) was not increased until 24 h. Renal function began to return to normal in rats receiving NDPS (100 mg/kg, i.p.) by 48 h, and functional recovery was complete by 168 h, although slight morphological changes were still evident. However, not all rats receiving NDPS (200 mg/kg, i.p.) recovered by 168 h, and some rats (3 of 7) died of renal failure between 96 h and 168 h. Widespread tubular necrosis and increased kidney weight were also present in this group at 168 h. Thus, NDPS-induced nephrotoxicity was evident by 1 h, established by 6 h and maximum between 24 h and 48 h. Recovery from NDPS-induced nephropathy was found to be dose-dependent, and incomplete in some animals at a dose of 200 mg/kg.

Animals↗
PubMed1984

A diabetes insipidus-like syndrome in the intact Yucatan miniature boar following implantation of desoxycorticosterone-acetate (DOCA).

A syndrome of polydipsia and polyuria is described in the intact adult Yucatan miniature boar following implantation of silicone rubber strips impregnated with desoxycorticosterone-acetate (DOCA). Water intake was significantly greater than control 5 days post-DOCA. Urine output was significantly greater than control 7 days post-DOCA, and urine osmolality was significantly decreased 8 days post-DOCA. Serum potassium was significantly less than control 24 hr post-DOCA, and serum sodium was consistently and significantly greater than control by 1 week post-DOCA. As suggested in the dog, the increase in water turnover following DOCA administration in the pig is initiated by an increased thirst followed by an increase in urine output.

Animals↗
PubMed1984

Fetal hypothalamic transplants: neuronal and neurovascular interrelationships.

This investigation is one of a series aimed at developing an understanding of the neuroanatomical correlates of neuronal and vascular interactions that occur between heterografts of normal fetal hypothalamic tissue transplanted into the third cerebral ventricle of adult Brattleboro rats with homozygous autosomal diabetes insipidus (DI). Rapid vascular invasion of fetal neurografts occurred within 3 days and arose from the mantle plexus of portal capillaries in the underlying host median eminence. Host vessels also invaded from the periventricular stratum and preoptic area. In the ventral regions of heterografts neurites were observed to terminate upon perivascular spaces that surrounded local capillaries. Despite the development of apparently normal neurovascular zones, none of the DI host recipients demonstrated an amelioration of polydipsia or polyuria characteristic of diabeties insipidus.

Angiography↗
PubMed1993

Streptozocin-induced diabetic rats: behavioural evidence for a model of chronic pain.

Painful diabetic neuropathy is one of the most common complications of insulin-dependent diabetes in man. Conflicting results have been obtained in experimentally diabetic animals subjected to pain stimuli. This work aimed to systematically study the response of rats made diabetic (hyperglycemia > or = 14 mM) by injection of streptozocin (STZ) (75 mg/kg, i.p.), to various pain stimuli: mechanical, thermal (warm and cold) and chemical. The time course of the scores was followed for 4 weeks simultaneously with the clinical symptoms (weight, body and skin temperature, motility) and hyperglycemia. A decrease in reaction thresholds to noxious heat stimuli (44 degrees C and 46 degrees C) and to non-painful thermal (cold: 10 degrees C, and warm: 38-42 degrees C) and mechanical stimulation (paw pressure) was observed. This can be considered as evidence for hyperalgesia and allodynia, respectively. These troubles appeared gradually and required at least 2 weeks of diabetes to reach statistical significance. Four weeks after the induction of diabetes, the scores obtained in diabetic rats injected with formalin were greater than those in normal rats, indicating hyperalgesia. Variation in sensitivity to pain occurred at the same time as arrested weight increase, fall in skin temperature, some amyotrophy measured in terms of hind-paw volume, and the usual polyuria-polydipsia syndrome. Spontaneous motor activity of the rats was lowered. This model is thus of interest as the observed reactions to noxious and non-noxious stimuli correspond to hyperalgesia and allodynia, symptoms encountered in painful diabetic neuropathy in man. Operating conditions for this model are discussed.

Animals↗
PubMed1985

Vasopressin neuron survival in neonatal Brattleboro rats; critical factors in graft development and innervation of the host brain.

Previously it was found that grafts of supraoptic plus paraventricular areas from 19-day-old foetal normal rats survived in the third ventricle of the brain of 4- to 6-day-old, vasopressin-deficient Brattleboro pups, but could not alleviate their polyuria. In the present series, factors important in graft development were analysed. Again using day-19 fetuses as donors, anterohypothalamus grafts as well as grafts placed near a crushed median eminence survived relatively poorly, but showed the presence of vasopressin neurons immunocytochemically one month post-grafting. Homotopic grafting in the supraoptic nucleus, however, even failed to show surviving vasopressin neurons. Graft survival was improved by the use of donor tissue of fetuses younger than day 19. Parvocellular vasopressin cells were frequently seen, organized into clusters resembling the normal suprachiasmatic nucleus. However, magnocellular neurons, as normally seen in supraoptic and paraventricular nuclei, only survived grafting when taken between days 11 and 15 of fetal age. It was concluded that only immature vasopressin neurons survived grafting under the condition employed. Magnocellular neurons had a limited fiber outgrowth into the host brain and median eminence. Most large neurons only stained with non-specific neurophysin antiserum, not with specific vasopressin-associated neurophysin antiserum. Thin fibers of the parvocellular vasopressin neurons provided only occasional and sparse innervation of the host median eminence and lateral septum (one case), but several examples of massive fiber bundles running dorsally from graft into host brain were observed. These fibers terminated in the thalamic periventricular area, a nucleus that is normally innervated by the vasopressin neurons of the suprachiasmatic nucleus. The failure of the grafts to provide adequate vasopressinergic innervation of the host median eminence probably explains why none of the nearly 200 Brattleboro neonates operated upon showed any sign of relief of their diabetes insipidus. It suggests, however, that the present procedures might be useful in restoring central vasopressinergic functions in the developing Brattleboro rat.

Aging↗
PubMed1994

Streptococcus bovis infections in pigeons: virulence of different serotypes.

In a first experiment, the relative virulence for pigeons of 5 strains of S. bovis was assessed by experimental inoculations. Two S. bovis serotype 1 strains, one serotype 2 strain and two serotype 3 strains were examined. One of the serotype 1 strains and the serotype 2 strain were isolated from pigeons that died from septicaemia. The other strains were isolated from cloaca samples of healthy pigeons. For each strain, 10-20 pigeons were intravenously inoculated with 1 x 10(9) CFU. Morbidity after infection with the serotype 1 and 2 strains varied between 75% and 90%. Disease signs included inability to fly, lameness, emaciation, production of slimy, green droppings, polyuria and sudden death. In groups of pigeons inoculated with the serotype 3 strains, morbidity was 0% and 6%, respectively. Results demonstrate that serotype 3 strains are less virulent for pigeons than serotype 1 and 2 strains. In a second experiment, bacteriological and histological examinations were performed on organs of pigeons serially killed between 1 and 10 days after experimental inoculation with an S. bovis serotype 3 strain of low virulence. Results were compared with results of studies carried out with a highly virulent serotype 1 strain. Notwithstanding bacterial spread and replication in various organs of inoculated pigeons, clinical disease was not observed and histological lesions were scarce and of limited extent.

Animals↗
PubMed1989

Nephrotoxicity of aminoglycoside antibiotics.

Aminoglycoside antibiotics cause transient, usually nonoliguric, renal failure in up to 10-30% of patients treated with these drugs, and are the cause of the largest proportion of drug-induced acute nephrotoxicities. The toxic mechanism includes (i) uptake of the drug by proximal tubular cells, where it is first sequestered within lysosomes and (ii) development of a lysosomal phospholipidosis, which is rapidly associated with cell necrosis and various alterations to subcellular structure and function. Tubular necrosis is often accompanied by (and probably triggers) tubular regeneration and peritubular proliferation. The means whereby such tubular alterations eventually cause a decline in glomerular filtration and hypo-osmotic polyuria has not been established. Various in-vitro and acellular models have been designed to assess and screen for the nephrotoxic potential of aminoglycosides; of these, methods based on the analysis of aminoglycoside-phospholipid interactions appear to be the most meaningful. A number of patient- and drug-related risk factors have been identified, and their avoidance could significantly reduce the risk of nephrotoxic reactions. Because the uptake of aminoglycosides by the kidney is saturable, administration of daily doses of these drugs as one or two injections, rather than as multiple injections or by continuous infusion, may also decrease the risk for toxicity.

Aminoglycosides↗
PubMedDate not supplied

Basal encephaloceles with morning glory syndrome, and progressive hormonal and visual disturbances: case report and review of the literature.

We report an 11-year-old girl with progressive hypopituitarism and visual loss of the right eye caused by trans-sphenoidal and sphenoethmoidal encephaloceles associated with morning glory syndrome. She was first seen at the age of 8 years, because of polydipsia and polyuria, and examination at that time revealed pituitary dwarfism and morning glory syndrome with visual disturbance of the right eye. Hormonal examinations revealed deficiency of growth hormone (GH) and anti-diuretic hormone (ADH). MR image showed trans-sphenoidal and sphenoethmoidal encephaloceles. At the age of 9 years, she was found at another institution to be blind in the right eye. Our examination of the patient at the age of 11 years revealed no change of the findings for the encephaloceles or optic system. Hormonal examination disclosed deficiencies of all hormones except for thyrotropin (TSH). This patient showed progressive hormonal and optic disturbances during the follow-up period. The natural course is still unclear, but our review of reported cases of trans-sphenoidal encephalocele with hormonal disturbance revealed that the most frequent findings were GH and ADH disturbance (over 60%), most patients (77.8%) showed progression of hormonal disturbance, and 40% of those with optic dysfunction showed progression. A patient with basal encephalocele with hormonal and / or optic disturbances requires careful long-term follow up.

Blindness↗
PubMed1987

Concentrations of luteinizing hormone, follicle stimulating hormone and prolactin following transection of the pituitary stalk in ovariectomized ewes.

Two experiments (Spring and Fall) were conducted in ovariectomized ewes to determine changes in pituitary hormone secretion immediately after pituitary stalk-transection. Ewes underwent either pituitary stalk-transection (SS), sham-transection (SH) or administration of anesthesia only (AO). Stalk-transected, but not sham-operated or anesthetized ewes had polyuria and polydipsia for 7 to 14 days after surgery. Concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin were measured in peripheral blood samples collected every 10 minutes for a six-hour period. Results were comparable for each season. During the six hours following surgery or removal from anesthesia, concentrations of LH declined in all ewes, but more slowly in SS ewes. No differences in patterns or mean concentrations of FSH were observed. Immediately after surgery, concentrations of prolactin were elevated, then declined in SH and SS ewes. The decrease was greater in SH than SS ewes. Data are consonant with the view that hypothalamic inhibition as well as LHRH stimulation regulate gonadotropin release by the pituitary.

Animals↗
PubMed1990

Polydipsia and hyponatremia in psychiatric patients: challenge to creative nursing care.

Among patients with psychiatric disorders, especially schizophrenia, a pattern of extreme polydipsia and polyuria sometimes emerges, usually without readily identifiable medical causes. Hyponatremia may develop and progress to water intoxication, with symptoms including restlessness, confusion, seizures, or even death. We review the clinical features and pathophysiology of this syndrome and discuss nursing roles in identifying and managing patients with polydipsia and hyponatremia. While the causes of polydipsia and hyponatremia are unclear, relevant factors seem to include a possible dysfunction in central nervous system (CNS) thirst and osmoregulatory centers, the inappropriate secretion of or sensitivity to antidiuretic hormone (ADH), and psychoactive drugs. Management techniques for affected patients concentrate on careful observation, fluid restriction, and the minimization of possible exacerbating factors such as high neuroleptic dosage and cigarette consumption.

Humans↗
PubMedDate not supplied

Unusual case of Klüver-Bucy syndrome in a Chinese boy.

Following an encephalopathic illness, a 13-year-old Chinese boy had a partial form of Klüver-Bucy syndrome with emotional disturbance, recent memory loss, hypersexuality, and polyphagia. Other unusual features included narcolepsy, polydipsia, and polyuria. Virologic studies failed to incriminate the etiologic agent, including herpes simplex virus. Brain biopsy of the frontal lobe demonstrated Alzheimer type II astrocytosis.

Adolescent↗
PubMedDate not supplied

Assessment of the acute acrylonitrile-induced neurotoxicity in rats.

Acrylonitrile (VCN) is an aliphatic nitrile which is used extensively in manufacturing of synthetic fibers, plastics, and rubber. Although the neurotoxicity of VCN is recognized, no thorough characterization of this effect has been reported. Current studies were designed to quantitatively characterize the acute phase of VCN-induced cholinomimetic neurotoxicity, and to determine the effects of dose, route of administration, and atropine on such toxicity. Administration of a single gavage or subcutaneous doses of 20, 40, or 80 mg VCN/kg to male Sprague-Dawley rats causes two distinctive phases of acute neurotoxic effects. Signs observed in the early phase had a rapid onset, and were cholinomimetic in nature. They included salivation, lacrimation, chromodacryorrhea, polyuria, miosis, vasodilatation in face, ears and extremities, increased gastric secretion, and diarrhea. A late phase developed hours after VCN dosing, and the toxic signs included depression, convulsions, and respiratory failure followed by death at high doses. These results revealed that the cholinomimetic toxicity induced by VCN was dose related regardless of the route of administration. In another study, rats were pretreated with atropine (1 mg/kg, IP) prior to VCN (40 mg/kg) in order to investigate the role of the cholinergic system. Atropine protected rats against VCN-induced cholinomimetic neurotoxicity, suggesting possible involvement of the cholinergic system. Finally, this work provides essential basic information for studying the biochemical, pharmacological, and neurological basis of VCN-induced neurotoxicity in the rat.

Acrylonitrile↗
PubMed1995

Treatment of polydipsia and hyponatremia in psychiatric patients. Can clozapine be a new option?

Polydipsia occurs frequently in chronic schizophrenic patients, some of whom develop intermittent hyponatremia. Most therapeutic efforts have tried to control the hyponatremia. Four schizophrenic patients, followed for more than one year, showed improvement on clozapine. Case 1 was an outpatient without history of hyponatremia who improved from polydipsia and psychosis. The last three were inpatients with polydipsia, intermittent hyponatremia, and psychosis who showed minimal improvement of psychosis but significant decrease in polydipsia and water intoxication. Case 2 relapsed to polydipsia when clozapine was discontinued on two occasions. Case 3 demonstrated polyuria during 39% of days before clozapine and in 0% of days after two weeks of clozapine. In case 4, most baseline sodium levels were abnormal, but all became normal after clozapine. A time-series analysis for intervention effects showed a significant effect of clozapine (p = .017). The limited information provided by these case reports suggest the need for controlled studies of the clozapine effect on polydipsic patients.

Adult↗
PubMed1988

Renal prostaglandins in postobstructive diuresis. Comparative study of unilateral and bilateral obstruction in conscious dogs.

An experimental model in conscious dogs was developed to investigate the role of prostaglandins (PG) in the obstructed kidney. Renal veins were separately catheterized. Urine flow was shunted to the skin by surgically implanted polyurethane loop ureterostomy so as to allow atraumatic manipulation with maintained continuous flow to the bladder between experiments. One week or more after surgery, renal function parameters as well as renal vein and urinary PGE2 and PGF2 alpha, and renal vein renin were studied during and after unilateral (UUO) and bilateral (BUO) ureteral obstruction. The release of ureteral obstruction produced a constant and marked elevation in urinary PGE2 and PGF2 alpha, two times higher after BUO than after UUO. A close correlation exists between PGE2 and sodium excretion in UUO and BUO. Increasing polyuria was observed only after chronic BUO. In BUO, renal vein renin concentration was augmented after 2 hours but was suppressed after 24 hours of BUO. Renal vein PG concentration was also elevated after chronic UUO and BUO but was in the normal range immediately prior to release of obstruction. The data obtained with the current experimental dog model indicate that the release of ureteral obstruction induces a striking increase in renal PGE2 and PGF2 alpha production which may mediate at least partly the phenomenon of postobstructive diuresis.

Animals↗
PubMed1993

Neurosarcoidosis presenting as secondary amenorrhea in a teenager.

Sarcoidosis is a systemic inflammatory disease of unknown etiology characterized by non-caseating epithelioid cell granulomata. The lungs and reticulo-endothelial system are typically involved, and virtually any organ system may be affected. Sarcoidosis involving the central nervous system is relatively uncommon, estimated to occur in approximately 5% of patients with sarcoidosis in the United States, while the incidence throughout the world may be as high as 15%. Hypothalamic dysfunction is the most common manifestation of central nervous system parenchymatous disease in neurosarcoidosis. Polyuria and polydipsia are the most frequently occurring symptoms in patients with sarcoidosis who have dysfunction of the pituitary and hypothalamus. We describe a patient with secondary amenorrhea resulting from neurosarcoidosis involving the pituitary and hypothalamus.

Adolescent↗