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At least 685 records · Page 38Linked to original sources
PubMed1998

Neonatal Bartter syndrome: spontaneous resolution of all signs and symptoms.

This baby boy was born after a pregnancy complicated by severe polyhydramnios at a gestational age of 28 weeks. Analysis of the amniotic fluid had shown a high chloride content, but normal concentrations of sodium, potassium, and calcium. After birth he displayed extreme polyuria, severe renal sodium and chloride loss, and marked hypercalciuria. Five weeks after birth, his sodium chloride loss turned into renal potassium loss, along with a marked decrease in urine output. All these features are characteristic of the neonatal variant of Bartter syndrome. He was discharged after 11 weeks with oral supplements of sodium chloride, potassium gluconate, and 500 ml of fluid. The follow-up for a period of 6 years showed a surprising evolution: he has no hypokalemic alkalosis, no polyuria, and no hypercalciuria; growth and development are within the normal ranges and, at the time of writing, he is a healthy boy needing no medication and with no medical problems whatsoever.

Bartter Syndrome↗
PubMed2001

Amphotericin B-induced partial nephrogenic diabetes insipidus in a child.

The case of a 12-year-old boy who developed polyuria and polydipsia while on amphotericin B treatment is discussed. The clinical and laboratory features are most consistent with partial nephrogenic diabetes insipidus. Several adult patients have been reported with amphotericin B-induced nephrogenic diabetes insipidus. To the knowledge of the authors, this is the first pediatric patient described with this condition. Pharmacological doses of antidiuretic hormone in conjunction with diuretic treatment significantly reduced the polyuria and alleviated the associated symptoms. The authors propose that in amphotericin B-induced partial nephrogenic diabetes insipidus, pharmacological doses of antidiuretic hormone may offer an additional benefit to commonly used diuretic therapy.

Amphotericin B↗
PubMed2003

Nephrogenic diabetes insipidus due to hydronephrosis in a patient with a solitary kidney.

A 68-year-old man with a history of nephrectomy of the right kidney was admitted to our hospital with a 1-month history of polyuria (> 41 per day). He also exhibited hyposthenuria, which was unresponsive to treatment with exogenous vasopressin. Radiographic examination revealed partial obstruction of the left ureter and moderate hydronephrosis. The cause of the obstruction was cancer of the ureter. After drainage using a nephrostomy tube, the polyuria and hyposthenuria were gradually resolved. This is the first known case of nephrogenic diabetes insipidus due to hydronephrosis in a patient with a solitary kidney.

Aged↗
PubMed2005

Management of methylmalonic acidaemia by combined liver-kidney transplantation.

Methylmalonic acidaemia (MMA) is a rare autosomal recessive inborn error of metabolism that typically presents in infancy with recurrent episodes of metabolic acidosis, developmental delay and failure to thrive. The disease course is complicated by the development of chronic tubulointerstitial nephritis progressing to end-stage renal disease in adolescence. We describe two adolescents with cobalamin-nonresponsive MMA (mut0) who developed polyuria, chronic tubulointerstitial nephritis, dystonia but normal synthetic liver function. Both patients received combined liver-kidney transplantation (CLKT), preceded by a single pretransplant haemodialysis for clearance of methylmalonic acid. Post CLKT there was 95-97% reduction in serum and urine methylmalonic acid, leading to significant liberalization of dietary protein intake and a consequent increase in body mass index, muscle strength and energy. In addition, renal function normalized and clinical neurological status stabilized. We propose that CLKT be considered as a therapeutic option early in the course of cobalamin-nonresponsive MMA. Progressive tubulointerstitial nephritis with disabling polyuria is a confounder in patient management even in the absence of end-stage renal disease. Successful CLKT restores methylmalonyl-CoA mutase enzyme levels in the liver and kidney, improves clearance of methylmalonic acid with resultant dietary protein liberalization, and offers excellent graft and patient outcomes with improvement in quality of life.

Adolescent↗
PubMed1995

Polyhydramnios and hypercalcemia associated with congenital mesoblastic nephroma: case report and a new appraisal.

BACKGROUND: Polyhydramnios and hypercalcemia are known complications of congenital mesoblastic nephroma. Hypercalcemia has been shown to cause polyuria. Polyuria is believed to be the probable cause for the polyhydramnios, but the exact mechanism remains unknown. To our knowledge, this is the first reported case of a relationship between hypercalcemia and polyhydramnios. CASE: A 26-year-old primigravida was diagnosed with congenital mesoblastic nephroma and polyhydramnios at 36 weeks' gestation. Neonatal hypercalcemia was detected immediately after delivery at 40 weeks' gestation. After removal of the nephroma, the calcium level normalized. CONCLUSION: Hypercalcemia may be the mechanism underlying polyhydramnios in cases of congenital mesoblastic nephroma. Calcium levels should be monitored after delivery, and prompt surgical removal of the tumor should be performed.

Adult↗
PubMed1997

Upregulation of the expression of vasopressin gene in the paraventricular and supraoptic nuclei of the lithium-induced diabetes insipidus rat.

The expression of arginine vasopressin (AVP) gene in the paraventricular (PVN) and supraoptic nuclei (SON) was investigated in rats with lithium (Li)-induced polyuria, using in situ hybridization histochemistry and radioimmunoassay. The male Wistar rats consuming a diet that contained LiCl (60 mmol/kg) for 4 weeks developed marked polyuria. The Li-treated rats produced a large volume of hypotonic urine with low ionic concentrations. Plasma sodium concentrations were found to be slightly increased in the Li-treated rats compared with those in controls. Plasma concentration of AVP and transcripts of AVP gene in the PVN and SON were significantly increased in the Li-treated rats compared with controls. These results suggest that dehydration and/or the activation of visceral afferent inputs may contribute to the elevation of plasma AVP and the upregulation of AVP gene expression in the PVN and the SON of the Li-induced diabetes insipidus rat.

Animals↗
PubMed2000

Nocturia in the adult: classification on the basis of largest voided volume and nocturnal urine production.

PURPOSE: We propose a criterion to clarify the underlying etiologies of nocturia. MATERIALS AND METHODS: Frequency-volume charts were recorded for 24 hours by 35 men and 32 women who were subjectively free of lower urinary tract symptoms and had no evidence of voiding disorders. At least 5 subjects were included in each of 5 age groups of 20 to 49, 50 to 59, 60 to 69, 70 to 79, 80 to 89 years for both genders. The charts were used to make a tentative criterion, which was validated in 39 elderly individuals with nocturnal frequency. RESULTS: Correlation and regression analyses indicated that the quotients of nocturnal urine output divided by body weight (U(N)/BW) and largest voided volume divided by body weight (V(L)/BW) were useful classification factors. Cutoffs, which were set close to worst quartiles, were 10 ml./kg. for U(N)/BW and 4 ml./kg. for V(L)/BW, respectively. Correction by body weight made the same criterion applicable irrespective of weight. Symptomatic elderly patients were classified into 3 mutually exclusive groups of nocturnal polyuria (U(N)/BW greater than 10 ml./kg.), low bladder capacity (V(L)/BW less than 4 ml./kg.) and combined nocturia. Of 20 subjects who voided 2 times a night 11 (55%) were classified as having nocturnal polyuria and 15 of 19 who voided 3 or 4 times (79%) were classified as having low bladder capacity or combined nocturia. CONCLUSIONS: The criterion provides a reasonable distinction of etiologies of nocturia, and may be usefulness in examination and treatment.

Adult↗
PubMed1982

Familial Bartter's syndrome and the effect of indomethacin in one family member.

A Japanese family in which a father, daughter and son had hypokalemia and hyperreninemia was investigated. Both father and daughter had reduced vascular sensitivity to angiotensin II; in addition, the daughter had juxtaglomerular cell hyperplasia and dwarf glomeruli. These features are consistent with Bartter's syndrome occurring in 2 successive generations in 1 family. The 12-year-old girl had growth retardation in spite of normal growth hormone secretion. No chromosomal abnormalities were found. Indomethacin administration to this patient in doses sufficient to reduce urinary prostaglandin excretion resulted in a marked improvement of polydipsia and polyuria, and an increase in serum sodium, potassium and chloride concentrations. Even though plasma aldosterone concentrations were reduced to within the normal range, serum potassium concentrations remained low, and plasma renin activity (PRA) remained elevated. Thus it is not likely that hypokalemia is induced only by aldosteronism. These results suggest that prostaglandins are the major determinant of polydipsia, polyuria and high plasma aldosterone levels and contribute to the hypokalemia observed in this patient. However, the failure of complete correction of the hypokalemia and the persistence of the raised PRA with a significant reduction of the prostaglandins suggest the possibility that additional factors are involved in the pathogenesis of Bartter's syndrome.

Adult↗
PubMed1997

[Endocrine theory of idiopathic nocturnal enuresis].

Body fluid homeostasis is maintained by the kidney. Such an accurate control in achieved via the secretion of antidiuretic hormone (ADH), the secretion of which is regulated by hypothalamic osmoreceptors. Both urine flow rate and the excretion of most electrolytes have a diurnal rhythm; they increase during daytime and decrease during nighttime. Such a rhythm seems to be absent in some subjects who suffer from bedwetting because of relative polyuria. In these cases, the polyuria is associated with a decreased nocturnal secretion of ADH and the subsequent excretion of dilated urine. A deficit in the nocturnal secretion of ADH thus appears to explain the response to desmopressin of children with a polyuric form of enuresis.

Child↗
PubMed1999

[Early hypomagnesemia, hypercalciuria and nephrocalcinosis: two cases in a family].

BACKGROUND: Hypomagnesemia-hypercalciuria and nephrocalcinosis is a rare inherited syndrome which is characterized by persistent hypomagnesemia despite supplementation, hypercalciuria, nephrocalcinosis and progressive renal failure. OBSERVATIONS: Case 1. A girl was referred at the age of 18 months because of polyuria, polydipsia and vitamin-resistant rickets. There was hypomagnesemia, hypercalciuria and mild renal insufficiency; ultrasonography showed nephrocalcinosis. For two years, she received hydrochlorothiazide and the course of the disease was marked by a significant reduction of urine output and hypercalciuria, recurrent urinary tract infections and a progression toward chronic renal failure. Case 2. The brother of this child was investigated at the age of nine months because of polyuria and polydipsia. He also had hypomagnesemia, hypercalciuria and nephrocalcinosis. Renal function was initially normal. After two years on continuous treatment with hydrochlorothiazide, hypercalciuria decreased without deterioration of renal function. No signs of rickets were noted and nephrocalcinosis remained stable. CONCLUSION: To our knowledge, these two patients are the youngest reported in the literature. The long-term deterioration of renal function is hazardous but rickets may be avoided by early administration of hydrochlorothiazide.

Calcinosis↗
PubMed1999

Hypophyseal non-Hodgkin's lymphoma presenting with diabetes insipidus: a case report.

We report the case of a 64 year old male patient with a history of ischemic heart disease who underwent surgery for an abdominal mass. The histological diagnosis was highly malignant non-Hodgkin's lymphoma. After surgery the patient was admitted to our Department and received 6 courses of chemotherapy according to the COP schedule, followed by radiotherapy to the left upper abdominal region and ipsilateral lung base. The patient achieved partial remission. One month later he began to complain of left axillary lymphadenomegaly, polydipsia and polyuria. A NMR brain scan showed a hypophyseal mass. The patient was treated with DDAVP and chemotherapy with the PRO-MACE protocol; the polyuria and lymphadenomegaly disappeared and the size of the hypophyseal mass reduced markedly. The clinical picture was, therefore, attributed to a hypophyseal localization of the non-Hodgkin's lymphoma, which is a very rare manifestation of lymphomatous spread to the central nervous system. Our case is also interesting because it shows that a favorable outcome can be obtained with chemotherapy, provided that the latter is sufficiently aggressive. This is not necessarily the case with radiotherapy which may also be followed by late and severe neurologic sequelae.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2003

Serial MR intensity changes of the posterior pituitary in patients with diabetes insipidus after transsphenoidal surgery for pituitary adenomas: report of two cases.

This is the first report describing magnetic resonance (MR) intensity changes of the posterior pituitary gland in the patients suffering from the classical "triphasic" diabetes insipidus (DI) after transsphenoidal surgery for pituitary adenomas. A 21-year-old female and a 54-year-old female were admitted to our hospital with the diagnosis of Cushing's disease and acromegaly due to pituitary microadenomas, respectively. No evidence of DI was found, and T1-weighted MR images exhibited "bright spot" corresponding to the posterior pituitary in both cases. Both experienced the classical "triphasic" pattern of water metabolism disturbance after successful transsphenoidal resection of pituitary adenomas, that is, polyuria-oliguria-polyuria. The MR signal hyperintensity in posterior pituitary was detected during the first polyuric phase, but the hyperintensity disappeared during the second polyuric phase. In addition, "bright spot" was restored along with the recovery from DI in the chronic phase. These findings of serial MR images supported that the first DI phase of the classical triphasic course of water metabolism disturbance was caused by secretional dysfunction of stored vasopressin from the posterior gland, whereas the second DI phase was due to impairment in the functional integrity producing vasopressin-containing granules after depletion of vasopressin in the oliguric phase.

Adenoma↗
PubMed2000

TGF-beta1-induced glomerular disorder is associated with impaired concentrating ability mimicking primary glomerular disease with renal failure in man.

Transforming growth factor-beta1 (TGF-beta1) may play a major role in the pathogenesis of glomerulopathy and end-stage renal disease (ESRD). The aim of this study was to explore the functional consequences of localized overproduction of TGF-beta1 in relation to glomerular ultrastructure and the composition of the extracellular matrix (ECM) in the inner medulla. We used a transgenic mouse with overexpression of TGF-beta1 targeted to the juxtaglomerular apparatus (JGA) by the Ren-1c promoter. The kidney function was evaluated using urine production and metabolite excretion over a 24-hour period, glomerular filtration rate (GFR), and concentrating ability. The glomerular structure was analyzed in terms of volume, ie, the volume of the mesangium per glomerulus (Vv[mes/glom]) and the volume of the matrix per glomerulus (Vv[matrix/glom]), ECM per glomerulus, the area of the filtration surface, and the thickness of the peripheral basement membrane (PBM). Immunohistochemistry or in situ hybridization was used to examine the expression of aquaporin 2 (AQP2), plasminogen activator inhibitor-1 (PAI-1), and the composition of the ECM in the inner medulla. The mice exhibited polyuria, reduced concentrating ability, decreased GFR, and albuminuria paralleled by increased glomerular volume, with increased volume of ECM, decreased filtration surface, and thickening of the PBM being detectable between 1 and 2 months of age. The deposition of glomerular ECM was accompanied by increased levels of PAI-1. As estimated by excretion of Clara cell protein-1 (CC16) and lysozyme, tubular damage occurred only in older mice. Collagen Type I was deposited in the inner medulla in the presence of normal AQP2-expression in the collecting ducts. This study reached the following conclusions: (a) TGF-beta1 reduces the GFR and the glomerular filtration surface, (b) TGF-beta1 induces albuminuria in association with widening of the PBM, (c) expansion of the mesangial volume seems to precede the widening of the PBM, (d) TGF-beta1-induced accumulation of glomerular ECM is partly explained by increased PAI-1 expression, (e) Decreased concentrating ability and polyuria caused by accumulation of ECM in the inner medulla may be an early marker of glomerular diseases associated with increased expression of TGF-beta1 in man.

Aldosterone↗
PubMed2004

The Fanconi-Bickel syndrome: a case of neonatal onset.

A male newborn infant was recognized having Fanconi-Bickel syndrome (FBS) in the neonatal period. The presenting clinical findings were hyperglycemia and polyuria detected during an episode of acute enteritis. Physical examination was normal, biochemical analyses were suggestive of FBS: glycosuria, proteinuria, phosphaturia, generalized aminoaciduria, and increased levels of urinary beta 2-microglobulin, serum glucose and serum alkaline phosphatase. The molecular genetic analysis showed homozygosity for mutations within the gene of the glucose transporter 2 (Glut 2), 1213 C>T. The patient demonstrated improved clinical and metabolic status following institution of diet with frequent small meals and galactose-free-milk as well as pharmacological treatment with phosphate and vitamin alpha-OH-D3. In conclusion, infants showing hyperglycemia and polyuria may be considered having FBS also in the neonatal period. Early institution of adequate caloric intake and replacement of electrolytes and vitamin D may avoid or reduce metabolic complications.

Age of Onset↗
PubMed1992

Effect of induced supraventricular tachycardias on changes in urine output and plasma hormone levels in man.

1. A symptomatic diuresis, polyuria, sometimes accompanies paroxysmal tachycardias in man. A study was undertaken in patients with inducible supraventricular tachycardia, irrespective of the symptom of polyuria, to measure simultaneous changes in urine output and plasma hormone levels during the arrhythmia. 2. During 14 episodes of induced tachycardia in 10 patients, there was a significant increase in mean urine flow, which was independent of the state of patient hydration. During a mean tachycardia duration of 30 +/- 3 min, the mean group urine flow increased from 3.2 +/- 2.3 ml/min to 7.6 +/- 3.7 ml/min (P less than 0.001). This was characterized by a consistent increase in free water excretion and a variable increase in sodium excretion. 3. The plasma atrial natriuretic peptide level (five patients) significantly increased from 7.6 +/- 4.6 pg/ml to 34.6 +/- 21.7 pg/ml (P less than 0.02) during the arrhythmia. There was no significant change in the plasma arginine-vasopressin level and a non-significant reduction in plasma renin activity. 4. This study has shown that induced supraventricular tachycardias in man are accompanied by a significant diuresis. The mechanisms responsible remain unknown, but do not appear to involve the plasma arginine-vasopressin level alone.

Adult↗
PubMed1998

The efficacy of DDAVP is related to the circadian rhythm of urine output in patients with persisting nocturnal enuresis.

OBJECTIVE: Desmopressin may be a useful treatment in some, but not all, patients with nocturnal enuresis. We have evaluated a relation between nocturnal urine output in patients with primary monosymptomatic nocturnal enuresis and the treatment response to synthetic vasopressin. DESIGN: Adolescent or adult enuretics and normal subjects were enrolled in the study and admitted to hospital for a 24 hour investigation of the diurnal variation in urine output, plasma vasopressin (AVP) and plasma atrial natriuretic peptide (ANP). The enuretics were characterized prior to investigation as either 1-desamino-8-D-arginine vasopressin (DDAVP) responders or non-responders. During admission the fluid intake was restricted to 25 ml/kg per day. PATIENTS: Twenty-four patients (15-37 years) with primary monosymptomatic nocturnal enuresis and 9 normal subjects (24-31 years). MEASUREMENTS: Circulating levels of AVP, ANP, plasma electrolytes and plasma osmolality were measured (1400, 2000, 2300, 0200, 0500 and 0800 hours) together with urine volume, urine osmolality and urine electrolytes during daytime and nighttime. Tubular reabsorptive capacity for water, osmoles and creatinine were assessed as well as urinary and fractional excretion rates of sodium and potassium. RESULTS: Controls and DDAVP non-responders had a significant decrease in urine output at night concomitant with a significant plasma AVP amplitude in peak/nadir values although both groups lacked a significant nocturnal increase in AVP. In contrast, in DDAVP responders there was no circadian variation in urine output and thus a nocturnal polyuria together with no oscillation in plasma AVP. The DDAVP responding group had a nocturnal urine production significantly larger than the two other groups. However, the mean 24 hour AVP levels were similar in all groups. The excessive urine production at night in DDAVP responders was accompanied by nocturnal natriuresis due to an increased fractional excretion of sodium. In contrast, nocturnal antidiuresis in controls and DDAVP non-responding enuretics coincided with diminished sodium excretion. Average ANP levels were elevated in both enuretic groups compared to normals, whereas a circadian variation was detected only in the latter. CONCLUSION: It is concluded that DDAVP responsiveness is linked to the nocturnal urine production and that no pathophysiological role can be ascribed to AVP or ANP in DDAVP refractory adolescent and adult enuretics. Moreover, it is suggested that an abnormal tubular handling of sodium may contribute to the nocturnal polyuria seen in DDAVP responders.

Adolescent↗
PubMed1999

Renal prostanoids: physiological relevance in healthy salt-depleted women.

The effective role played by prostanoids in the control of renal function has been investigated in healthy women with salt depletion. Salt depletion (SD2 group, n = 6) was induced by low sodium chloride dietary intake (< or = 60 mmol per day) and combined treatment with natriuretic and potassium-sparing drugs. At the end of the depletive treatment, the cumulative sodium deficit was 513 +/- 56 mmol. The renal function and urinary excretions of prostaglandin (PG) E2, 6-keto-PGF1 alpha (6KPGF) and thromboxane (Tx) B2 were evaluated during hypotonic polyuria. The basal values of plasma sodium and potassium concentrations, plasma renin activity (PRA) and urinary aldosterone excretion were determined before the induction of hypotonic polyuria. Paired studies were performed in the absence (control) and presence of indomethacin both in the SD2 group and in a previously studied group (N2, n = 6) of healthy women in normal sodium and potassium balance. Women in normal balance received 100 mg i.m. of indomethacin, salt-depleted women received only 50 mg (because 100 mg of the drug produced a prolonged anuria). In the SD2 vs. N2 group in the absence of treatment the following significant differences were found: (a) higher basal values of PRA and urinary aldosterone excretion; (b) higher urinary excretions of 6KPGF and TxB2 but not of PGE2; (c) lower values of urinary flow rate, creatinine clearance, absolute and fractional excretions of sodium and chloride, plasma osmolality and plasma electrolyte concentrations. The effects of the indomethacin have been assessed as percentage variations by using paired data for each experimental group. In the SD2 vs. N2 group the reduction in urinary excretions of 6KPGF, TxB2 and potassium as well as in creatinine clearance were not significantly different. On the other hand, the following were significantly different: (a) the lower reduction in PGE2 excretion; (b) the higher reduction in urinary flow rate and in CH2O; (c) the reductions in absolute and fractional excretions of sodium and chloride, and the increase in plasma potassium concentration, significant in the SD2 group but not in the N2 group. The data suggest that: (1) when stimulated by salt depletion the renal biosynthetic pathways of PGI2 and TxA2 showed greater sensitivity to indomethacin inhibition; (2) the effects of the neurohormonal systems activated by salt depletion were either modulated or mediated by renal prostanoids.

Adult↗
PubMed2002

Aquaporin gene delivery to kidney.

BACKGROUND: Several aquaporin- (AQP) type water channels are expressed in kidney tubules and microvessels, including AQP1 in proximal tubule, thin descending limb of Henle and vasa recta, AQP2 in collecting duct apical membrane, and AQP3 and AQP4 in collecting duct basolateral membrane. Mice deficient in these aquaporins have distinct phenotypic abnormalities. AQP1 null mice are polyuria and unable to generate a concentrated urine after water deprivation. AQP2-T126M mutant mice and AQP3 null mice manifest nephrogenic diabetes insipidus (NDI) with severe polyuria, whereas AQP4 null mice have only a mild defect in maximal urinary concentrating ability. We reasoned that these mice could serve as useful models for gene replacement because of their predictable and unambiguous phenotypes. METHODS: In an initial feasibility study, an adenovirus directing the expression of AQP1 was introduced into AQP1 null mice by intravenous infusion. RESULTS: At 1 week after adenovirus infusion, AQP1 was seen in many proximal tubules and microvessels. Compared with untreated null mice, the treated mice were able to partially concentrate their urine and lost less weight after water deprivation. However, AQP1 transgene expression and functional correction were lost over 3-5 weeks. CONCLUSION: Although there remain many technical problems to overcome, aquaporin gene replacement has potential applications in hereditary and acquired NDI, and in the transient modulation of renal fluid conservation.

Adenoviridae↗