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PubMed1980

Effect of L-thyroxine on renal excretion of water and electrolytes in both normal and mercury-intoxicated rats.

The urine output and the change in excretion of electrolytes (sodium, potassium, calcium, chloride, inorganic phosphate) in rats following mercury-induced acute tubular lesions showed marked recovery during L-thyroxine therapy. The kidney mechanisms responsible for this effect are discussed, considering especially the observation that rats treated with L-thyroxine have a reduced urinary output, unlike other species, including man, which react with polyuria. The oliguric effect of thyroid hormone in rats is attributed to the greater length of the vasa recta and loops of Henle.

Animals↗
PubMed1980

Modification of the glomerular basement membrane in sucrose-fed and streptozotocin-diabetic rats.

Rats were fed on diets containing either sucrose or starch as the carbohydrate component (55%) for eight months. Diabetes was induced in animals of both groups by injecting streptozotocin (50 mg/kg body weight). Diabetic rats failed to gain weight, had enlarged kidneys, polyuria and elevated blood glucose levels. Starch and sucrose fed rats gained weight normally and had normal blood glucose levels. Sucrose fed rats had enlarged kidneys. Regional thickening of the glomerular basement membrane was present in sucrose-fed and diabetic rats but not in starch-fed controls. Glomerular basement membrane isolated from pooled kidney cortices from rats in the different experimental groups were analysed for amino acid, disaccharide and hexosamine content. Hydroxylysine (9 to 20%), hydroxyproline (21 to 24%), disaccharide (27%) and hexosamine (26%) were increased in membranes insolated from the three experimental groups, compared with starch-fed non-diabetic controls. An increase in low molecular weight components of the glomerular basement membrane of sucrose-fed and diabetic rats was observed using electrophoresis in sodium dodecyl sulphate. Significantly higher (p < 0.001) glucosyltransferase activity was present in kidney supernatants prepared from sucrose-fed (1050 +/- 60 nmol/2h/kidney) compared to starch-fed rats (510 +/- 40 nmol/2h/kidney). Sucrose feeding induces changes similar to those found in diabetes and the induction of diabetes made little difference over the feeding of sucrose alone.

Amino Acids↗
PubMed1976

Current determination of lithium-induced minimum sodium requirement in rats.

Lithium administration raises the minimum sodium requirement of the organism. Lithium treated-rats drink spontaneously a hypertonic sodium chloride solution and thereby protect themselves against the toxic effects of lithium. In the present paper it was studied whether the consumption of sodium chloride can be used as a quantitative measure of the sodium requirement. Rats given different amounts of lithium with food for about 2 months were given free access to water and a 0.46 M NaCl solution, and the 24-h intake of the latter was followed. It was found that the consumption of hypertonic sodium chloride increased with the lithium dosage and the serum lithium level. The consumption showed the following characteristics: (a) It was sufficient to prevent death from lithium poisoning. (b) When access to hypertonic chloride was discontinued for 48 h, the rats lost body weight; the body weight was reestablished within 1 h when the rats again had access to sodium chloride solution. (c) When sufficient amounts of sodium were given with the food, the lithium-treated rats drank no more sodium chloride solution than did the control rats. (d) When lithium administration was discontinued, the consumption of sodium chloride solution fell within 10 days to the control level. (e) The lithium-treated rats developed polyuria, but this was not the cause of the extra intake of sodium chloride. (f) The lithium-treated rats did not drink more of the hypertonic sodium chloride solution than was necessary to cover the minimum sodium requirement. The results indicate that the intake of hypertonic sodium chloride solution can, in fact, be used as a measure of the minimum sodium requirement in lithium-treated rats.

Animals↗
PubMed1983

Lithium-induced polydipsia: dependence on nigrostriatal dopamine pathway and relationship to changes in the renin-angiotensin system.

The dependence of lithium-induced polydipsia (LIP) on central monoamine pathways was investigated using several pharmacological manipulations. Intracisternal administration of 6-hydroxydopamine (6-OHDA) in combination with pargyline or desipramine was used to deplete dopamine (DA), norepinephrine, or both catecholamines. Significant decreases in LIP were seen after treatments that depleted brain DA, whereas depletion of norepinephrine alone did not affect LIP. Site-specific injection of 6-OHDA into the substantia nigra or caudate nucleus, but not the nucleus accumbens or noradrenergic dorsal bundle, also caused a decrease in LIP. Depletion of serotonin by intracisternal administration of 5,7-dihydroxytryptamine also had no effect on LIP. Consistent with these findings, the DA receptor blocker haloperidol attenuated LIP. Thus, LIP appears to be dependent on intact nigrostriatal DA fibers, but not on other monoaminergic systems in the brain. Lithium also increased plasma renin activity (PRA) and angiotensin I and II immunoreactivity in plasma, though the time course of LIP onset did not directly parallel these latter changes in the renin-angiotensin axis. Neither the PRA or angiotensin II immunoreactivity in lithium-treated animals was sufficiently high to account for LIP. In addition, the 6-OHDA lesions of the caudate nucleus or substantia nigra that attenuated LIP did not affect the lithium-induced increases in PRA or in angiotensin I or II concentrations. Thus, LIP probably involves mechanisms other than just being a direct response to lithium-induced increases in PRA or angiotensin II concentration and simply may not be secondary to lithium-induced polyuria. Because of the similar pharmacological characteristics of angiotensin II and lithium-induced drinking, a role for angiotensin receptors in LIP cannot be ruled out.

Angiotensin II↗
PubMed1979

Cyclic 3',5'-adenosine monophosphate (cAMP) in a 42-month-old child with clinical evidence of multiple hormonal disturbances.

In a boy aged 42 months, small stature, retarded psychomotor development, dry skin, excessive thirst, polyuria, cryptorchidism, and rickets were signs of multihormonal disturbances. Contrary to the clinical manifestations, laboratory investigations showed normal or raised levels of hormones (hGH, insulin, T3RU, T4, TSH, PTH). The cAMP level in the plasma was low and its urinary excretion was reduced. After administration of hGH, adrenaline, T3, T4, pitressin, vitamin D3 and aminophylline there was no rise in the cAMP concentration in plasma and urine. In the light of these results it may be assumed that deficient function of the adenyl cyclase system led to development of a clinical syndrome of tissue insensitivity to multiple hormonal factors in this case.

Child, Preschool↗
PubMed1985

Congenital renal arteriovenous malformation (aneurysmal type) in childhood.

We report on a 9-year-old boy with a congenital renal arteriovenous fistula of the aneurysmal type, a form previously not observed in childhood. The clinical picture was unusual with severe arterial hypertension, excessive polyuria and decreased levels of serum sodium and chloride as main signs. Clinical and biochemical findings normalised after nephrectomy of the kidney involved.

Arteriovenous Malformations↗
PubMed1978

Chronic hypertension induced by streptozotocin in rats.

An intravenous injection of 40 or 65 mg/kg streptozotocin induced not only diabetes but also severe hypertension in rats. Whereas the hyperglycemia developed fully within a few days after the injection of streptozotocin, the hypertension progessively advanced and reached maximum level several weeks after the treatment and lasted more than 20 weeks. Twenty mg/kg streptozotocin did not induce hyperglycemia but significantly increased blood pressure several weeks after the treatment. Arrest of growth, polyuria, glycosuria, hyperlipemia and lenticular cataracts developed in the animals treated with 40 or 65 mg/kg streptozotocin, but in none of the animals treated with 20 mg/kg. In histological examinations in the 24th week after the treatment, degranulation and necrosis in the pancreatic beta-cells, and vacuolization and deposition of PAS-positive materials in the renal proximal tubules were found in the animals treated with 40 or 65 mg/kg streptozotocin.

Animals↗
PubMed1983

Effects of lithium on water intake and renal concentrating ability in rats with vasopressin-deficient diabetes insipidus (Brattleboro strain).

Male and female Long Evan rats and Brattleboro rats with ADH-deficient diabetes insipidus were treated with lithium administered in the diet for 12 weeks. The plasma lithium level was about 1 mmol/l in all groups. Lithium caused polydipsia and polyuria and lowering of renal concentrating ability in normal rats. In rats with ADH deficiency lithium tended to increase water intake, but did not influence spontaneous urine osmolality or maximal urine osmolality during water deprivation. The results indicate that the renal concentrating defect caused by lithium in rats can be explained by ADH-blockade as the only mechanism. However, there is circumstantial evidence that lithium in addition may stimulate thirst mechanisms by an ADH-independent action.

Animals↗
PubMed1983

Chronic recurrent demyelinating encephalomyelitis associated with hemophagocytic lymphohistiocytosis.

A man aged 31 with remittent fever, leukopenia, polyuria, and splenomegaly in addition to chronic and recurrent episodes of neurologic abnormalities was examined pathologically. A chronic type of perivenous encephalomyelitis was found in the CNS, and chronic inflammatory lesions were noticed in the infundibulo-hypophyseal system and also in the peripheral nerves. Moreover, hemophagocytic lymphohistiocytosis predominated in the reticuloendothelial system. This seemed to be the first adult case of demyelinating disease with hemophagocytic lymphohistiocytosis.

Adult↗
PubMed1989

Nephrotoxicity of 5-(N-phenylcarboxamido)-2-thiobarbituric acid in the Fischer 344 rat.

In the present investigation, administration of a single i.p. dose of the anticancer drug merbarone [5-(N-phenylcarboxamido)-2-thiobarbituric acid] produced an acute and reversible decrease in renal function in female but not male Fischer 344 rats. The renal lesion in female rats was biochemically characterized as a decrease in p-aminohippuric acid accumulation by renal slices along with polyuria, glucosuria, proteinuria, and enzymuria. These functional changes were accompanied by histopathologic changes of focal tubular necrosis that was confined to the deep cortex and outer stripe of the outer medulla. The changes in these parameters were dose-dependent and were observed at doses as low as 0.2 x MELD(10) (12 mg/kg). This low merbarone dose increased urinary glucose and protein excretion by 26- and 9-fold, respectively, in the initial 16-h urine collection in female rats. This increase was accompanied by a 2- to 15-fold increase in the excretion of N-acetyl-beta-D-glucosaminidase (NAG), gamma-glutamyl transpeptidase (gamma-GTP), and lactate dehydrogenase (LDH) activities. No significant changes in renal function were observed in male rats apart from mild enzymuria after a high dose of merbarone (36 mg/kg). The drug did not increase urea nitrogen levels in male or female rats, reflecting the focal nature of this tubular lesion. Merbarone produced small elevations in serum transaminase activities [i.e., glutamic-oxalacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT)] at doses that produced marked alterations in renal function in female rats, suggesting only mild hepatotoxicity. The present study establishes the kidney as a possible dose-limiting target organ for merbarone toxicity.

Alanine Transaminase↗
PubMed1992

Severe tubular resistance to aldosterone in a child with familial juvenile nephronophthisis.

A 9.5-year-old girl, whose early symptoms were polyuria and growth retardation, is described. During the progression of her disease, hyperkalaemia developed out of proportion to the degree of renal insufficiency. Her fractional excretion of sodium increased from 3.3% to 35%, and her fractional excretion of potassium decreased from 55% to 22%. The plasma aldosterone level and plasma renin activity (PRA) were very high--290 ng/ml and 100 ng/dl per hour, respectively (normal range for this age 2.6-20.8 ng/ml and 1.2-2.7 ng/ml per hour, respectively). In an attempt to reduce these hormone levels, an acute and sustained saline load, captopril and peritoneal dialysis were used. Only the sustained saline load normalized the PRA, and only peritoneal dialysis sufficiently suppressed the plasma aldosterone level. Successful renal transplantation normalized both plasma aldosterone and PRA. This girl presents the unusual occurrence of pseudohypoaldosteronism type I, during the course of familial juvenile nephronophthisis.

Aldosterone↗
PubMed1989

Infantile chronic tubulo-interstitial nephritis with cortical microcysts: variant of nephronophthisis or new disease entity?

Over a 15-year period we observed seven children (four girls, three boys) who presented within the first months of life with severe renal failure and acidosis, associated with hypertension in five patients and polyuria in four. In addition, one patient had a severe cholestatic liver disease. In two families, a similarly affected sibling had died previously. Four patients were referred with the clinical diagnosis of polycystic kidney disease because of moderate enlargement of kidneys, but renal imaging (intravenous pyelography and ultrasonography) did not confirm this diagnosis. A renal biopsy, performed in all patients, showed similar features characterized by a diffuse chronic tubulo-interstitial nephritis (TIN) and particularly by the presence of microcystic dilatation of proximal tubules and Bowman's space. Liver pathology was normal in two patients, including one with hepatomegaly. However, in the patient with cholestasis there was inflammatory portal fibrosis with mild duct proliferation. Progression of the renal disease was extremely rapid and all patients reached end-stage renal failure (ESRF) before the age of 2 years (11-22 months). Two children had successful renal transplants. Although this chronic TIN shares some features with nephronophthisis, we suggest that it represents a distinct entity both on clinical and morphological grounds. The specific clinical features of this disease are its early onset and rapid progression to ESRF. Pathologically, it differs from nephronophthisis by the absence of medullary cysts and thickened tubular basement membranes and by the presence of cortical microcysts.

Child, Preschool↗
PubMed1988

Growth from birth to adulthood in a patient with the neonatal form of Bartter syndrome.

Growth from birth to the age of 19 years was studied in a patient with the neonatal form of Bartter syndrome. The initial modes of therapy (extra fluid, potassium supplements and triamterene) resulted in satisfactory but not optimal growth. Treatment with spironolactone together with potassium led to impressive catch-up growth. When the patient reached the age of 9 years, indomethacin therapy was started, which resulted in a second growth acceleration and was also accompanied by a significant reduction of both polyuria and hypercalciuria. Puberty developed normally, menarche occurred at 12 years 4 months and a normal adult height of 162 cm was reached at the age of 14 years. Treatment with prostaglandin synthetase inhibitors seems to be the best therapy for children with the neonatal form of Bartter syndrome.

Adolescent↗
PubMed1995

Concealed administration of frusemide simulating Bartter syndrome in a 4.5-year-old boy.

A 4.5-year-old boy was admitted to three different hospitals because of a tendency towards dehydration and polyuria, along with normal blood pressure, hypochloraemia, hypokalaemia, metabolic alkalosis and an impaired urinary concentrating ability. A renal biopsy failed to reveal juxtaglomerular hyperplasia. The clinical and laboratory findings failed to improve despite supplementation with potassium chloride and treatment with indomethacin. The urine was found to contain frusemide. The parents denied any drug administration to the boy. The child is now doing well more than 1 year after separation from his mother. Since ingestion of diuretic cannot be differentiated from true Bartter syndrome by blood and urinary electrolyte measurements alone, a diuretic screen is warranted in children with findings consistent with Bartter syndrome.

Bartter Syndrome↗
PubMed1988

Investigation of the dilated urinary tract.

Dilatation of the urinary tract does not necessarily imply obstruction, and other factors may be operative: maldevelopment, infection, reflux, and polyuria. Obstruction of the urinary tract in intra-uterine life is associated with renal dysplasia: the original obstructive lesion may be transient but the consequent dysplasia and dilatation may be permanent. Routine antenatal ultrasound identifies a new population of infants with urinary tract dilatation, many of whom remain asymptomatic and would not otherwise have come to medical attention: the natural history and appropriate schedules of investigation and management of this group are still being evaluated. Anatomical imaging by ultrasound establishes the presence and extent of dilatation. Micturating cystourethrography, intravenous urography and antegrade pyelography establish the site but not the functional significance of an obstructive lesion. Isotope renal scanning with 99mTc-DTPA may identify an acutely obstructed kidney with a decrease renal uptake, prolonged parenchymal transit time, and delayed clearance of the isotope from the renal pelvis after furosemide. However, such analyses often give equivocal results in infants with poor renal function and markedly dilated urinary tracts. Obstructive uropathy should be seen as a disturbance of the normal pressure-flow relationships in the urinary tract, and be defined and investigated as such. Antegrade perfusion with renal pelvic pressure measurements has technical pitfalls, but is the definitive method of establishing upper tract obstruction. Videocystourethrography is the established method of investigating the lower urinary tract in older children but needs further development to be applicable to infants.

Child↗
PubMed1985

The concentration of dopamine, 5-hydroxytryptamine, and some of their acid metabolites in the brain of genetically diabetic rats.

This is a report of the concentrations of DA, DOPAC, HVA, 5-HT, and 5-HIAA in the brain of spontaneously diabetic male Wistar rats. These rats showed a marked increase in blood and urine glucose, polydipsia, polyuria, and weight loss that had an onset 11-23 days earlier. Controls were litter mates with no hyperglycemia, glucosuria or weight reduction. The spontaneously diabetic rats showed a significant reduction of DOPAC in the striatum, and DOPAC, HVA, and 5HIAA in the olfactory tubercles (to 69, 61, 62, and 65% of their respective controls). No changes were found in the concentrations of DA or 5-HT. Thus the spontaneously diabetic rats showed a marked reduction in striatal and mesolimbic DA and mesolimbic 5-HT metabolism. This reduction in metabolism could be the consequence of a reduction in the formation of DA and 5-HT.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Erythrocyte count and hemoglobin levels in diabetic women.

Fasting blood glucose, erythrocyte counts hemoglobin levels of 131 Libyan diabetic women of Tripoli , Libya were determined. The respective mean values were 223 +/- 7 mg X dl-1, 4.97 +/- 0.034 X 10(6) X mm-3 and 14.4 +/- 0.127 g X dl-1. Sixty-five percent of these diabetic women were obese. The highest percent of diabetics belong to the age group 46-55 years. The increase in prevalence of diabetes correlates with an increase in obesity. A significant positive correlation was found between body surface area and fasting blood glucose levels (r = 0.65; P less than 0.001). Elevated levels of erythrocyte count and hemoglobin were present in these diabetic patients. Significant correlations were found between body surface area and erythrocyte count, as well as between fasting blood glucose levels and erythrocyte count, indicating the effect of obesity and diabetes on erythrocyte numbers. A significant correlation was found between fasting blood glucose levels and hemoglobin (r = 0.35; P less than 0.001). The elevated levels of hemoglobin present in these patients may be the result of haemoconcentration due to polyuria, which is always present in poorly controlled diabetic patients. The results suggest a close relationship between diabetes and obesity. Regulation of body weight/surface area is an important factor in the control of diabetes. The elevated levels of erythrocyte count and hemoglobin reflect poor control of blood glucose levels in these diabetic patients.

Adolescent↗
PubMed1993

Wolfram syndrome: a clinical study of two cases.

Two unrelated patients with two different images of Wolfram (or 'DIDMOAD') syndrome are presented: a 19-year old woman suffering from all the important features of this syndrome, and a 38-year old man showing two major characteristics but several minor abnormalities. This syndrome should be considered in young diabetic patients with unexplained visual loss or with polyuria and polydipsia in the presence of adequate blood sugar control. An early diagnosis is important to prevent unnecessary diagnostic investigations.

Adult↗