Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Polyuria”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,009 records · Page 56Linked to original sources
PubMed1976

Renal tubular defects in recurring bilateral nephrolithiasis.

A metabolic study was performed in 28 patients with bilateral recurrent calcium-containing renal staghorn calculi and chronic pyelonephritis ("obstructive nephropathy"). Fourteen had normal GFR and 14 mild renal insufficiency. Ten normal subjects were used as controls. Under basal conditions, polyuria and negative sodium balance were commonly observed in patients with obstructive nephropathy and normal renal function. After an acute acid load (NH4Cl) an acidifying defect, i.e. high values for urine pH and reduced excretion of titratable acid and ammonium, was observed in 64% of patients with normal GFR and in 71.4% of those with renal insufficiency. During intravenous infusion with neutral sodium phosphate, the urine pH changed little but the rate of excretion of titratable acid increased in direct proportion to that of urinary phosphate in both groups of patients. These results, associated with the finding of normal blood pH in almost all patients, lead to the conclusion that an incomplete Type 1 or "distal" renal tubular acidosis is a frequent complication of obstructive nephropathy secondary to bilateral nephrolithiasis. The anatomical abnormalities of renal tubules and collecting ducts and the superimposed interstitial nephritis might be the pathogenetic factors responsible for the acidifying defect and for the impairment in sodium and water conservation.

Acidosis, Renal Tubular↗
PubMed1998

Central diabetes insipidus with spontaneous remission. A case report.

We report a case of central diabetes insipidus with spontaneous remission 8 months after clinical beginning of the disease. A 20 years-old man developed polydipsia and polyuria in October 1994. A water deprivation study showed a defect in the urine concentrating function, which was corrected by vasopressine. A Magnetic Resonance imaging of the skull revealed a thickening of the pituitary stalk. His condition was well controlled by nasal DDAVP administration and 6 months later patient reduced spontaneously medication dose without clinical worsening. 8 months after clinical beginning, patient has become completely free from the need for medication to control clinical symptoms and urine concentrating function, as demonstrated by a re-evaluation study with water deprivation. A control Magnetic Resonance showed the regression of stalk enlargement. The clinical and radiological features of this case are discussed.

Adult↗
PubMed1998

[Polyuropolydipsic syndromes].

PROGNOSIS: Intracellular dehydration is the major risk in case of a polyuropolydipsic syndrome. Excepting osmotic polyuria, prognosis depends on a possibly progressive functional anomaly of the hypothalamopituitary axis. PATHOPHYSIOLOGY: Polyuropolydipsia occurs when antidiuretic hormone (ADH) secretion is absent (central diabetes insipidis), the kidney does not respond to ADH (nephrogenic diabetes insipidus) or in case of physiological inhibition of ADH secretion (primary polydipsia). EXPLORATION: Dynamic explorations are associated with radioimmunoassay of ADH. They are particularly useful in case of atypical diabetes insipidus and include the water restriction test and a study of the sensitivity to exogenous ADH (dDAVP). The results orient the etiologic diagnosis and allow an evaluation of the fluid intake required as a function of the maximal concentrating capacity of the kidneys. TREATMENT OF CENTRAL DIABETES INSIPIDUS: Treatment is based on ADH analogs (dDAVP). The aim is to obtain a constant antidiuretic effect without hyponatremia or escape. In case of partial central diabetes insipidus, a non-hormone treatment using compounds which increase vasopressin release or its effect on the kidney can be proposed.

Diagnosis, Differential↗
PubMed2005

Nephronophthisis: a variant.

The case report describes a young boy with renal, retinal, hepatic and cerebellar involvement in a rare syndrome. He had polyuria, deranged renal functions and cystic lesions in kidneys, which led to the diagnosis of nephronophthisis (NPH). Extra-renal involvement with night blindness, truncal ataxia, mental retardation and hepatosplenomegaly. Thus, every patient with NPH should be carefully examined for extra-renal involvement.

Abnormalities, Multiple↗
PubMed1980

Acute lymphoblastic leukemia. Association with vasopressin-responsive diabetes insipidus.

A rare case of acute lymphoblastic leukemia presenting with vasopressin-responsive diabetes insipidus (DI) is reported. The patient presented with polydypsia and polyuria of 9 L/day. Findings from special investigations of the CNS, including brain scan, computerized tomographic scan, EEG, and lumbar puncture were within normal limits. The patient's condition improved substantially after receiving vasopressin injections and later chlorpropamide. The incidence and underlying mechanism of this rare complication of acute leukemia are reviewed, and the response of DI to chlorpropamide is discussed briefly. In this patient it is presumed that the DI was caused by leukemic infiltration of the supraopticohypophyseal tract, posterior pituitary, or hypothalamus.

Adult↗
PubMed1999

Efficacy of indapamide in central diabetes insipidus.

BACKGROUND: Central diabetes insipidus (CDI) results from deficient vasopressin (antidiuretic hormone) secretion and causes polydipsia and polyuria. Desmopressin, a synthetic analog of vasopressin, is the drug of choice in the treatment of CDI, but in mild cases, there are alternative drugs that can be used, including chlorpropamide, carbamazepine, and thiazides. METHODS: In this study, we investigated the efficacy of treatment with indapamide, which is an antihypertensive diuretic oral agent, in 20 consecutive patients with CDI. The diagnosis of CDI was established by water-deprivation and vasopressin tests. Before the study, serum and urinary osmolality, daily urinary volume, and serum electrolyte levels were measured in all 20 patients. Indapamide (2.5 mg/d) was administered for 10 days, and then the investigations were performed again; for purposes of comparison, 250 mg/d of chlorpropamide was also administered to 11 of the 20 patients who had been given indapamide. RESULTS: Indapamide revealed a 40.56% +/- 9.70% (mean +/- SD) (range, 19.6%-55.0%) reduction in 24-hour urinary volume and an increase in urinary osmolality, as well as a decrease in serum osmolality, and was as effective as chlorpropamide (P<.05) in the treatment of CDI. CONCLUSION: Because of its low cost and lack of significant adverse effects, indapamide may be a suitable, easy-to-use alternative oral agent for some patients with CDI.

Adolescent↗
PubMed2007

Cerebral salt-wasting syndrome in a patient with neuroleptic malignant syndrome.

BACKGROUND: Hyponatremia associated with neuroleptic malignant syndrome has thus far been described as a syndrome of inappropriate secretion of antidiuretic hormone. OBJECTIVES: To ascertain and describe the role of cerebral salt-wasting syndrome as the cause of hyponatremia in a patient with neuroleptic malignant syndrome. PATIENT: A psychotic patient being treated with olanzapine presenting with sopor, muscle rigidity, polyuria, tachycardia, pyrexia, and severe hyponatremia. METHODS: Serial serological examinations of plasma tonicity (sodium level and osmolality), brain natriuretic peptide, and antidiuretic hormone were performed, and sodium excretion and urine osmolality were determined from 24-hour urine collection. In addition, markers for rhabdomyolysis were monitored. RESULTS: The patient shows clear symptoms of cerebral salt-wasting syndrome in association with neuroleptic malignant syndrome, characterized by severe hyponatremia, volume depletion, and elevated brain natriuretic peptide but normal antidiuretic hormone levels. Cerebral salt-wasting syndrome improved under dantrolene sodium treatment and concomitant fluid and sodium replacement. CONCLUSION: Hyponatremia in patients with neuroleptic malignant syndrome might more likely reflect cerebral salt-wasting syndrome than a syndrome of inappropriate secretion of antidiuretic hormone as an additional aspect of autonomic dysregulation caused by antidopaminergic drugs.

Creatine Kinase↗
PubMed1980

Renal tubular acidosis and sensorineural deafness: an autosomal recessive syndrome.

This is the first known reported case of autosomal recessive syndrome of renal tubular acidosis and sensorineural deafness in the otorhinolaryngological literature. Ten cases in six families have been reported in the pediatric literature. Most cases manifested at birth or soon after with vomiting, dehydration, polydipsia, polyuria, hyposthenuria, and failure to thrive. Renal tubular acidosis is a clinical syndrome of disordered acidification out of proportion to the impairment of glomerular filtration, and is associated with alkaline urine. Sensorineural deafness is variable and, in most cases, present in early childhood.

Acidosis, Renal Tubular↗
PubMed1980

Renal venous thrombosis in neonates. Initial and follow-up abnormalities.

Five neonates with renal venous thrombosis (RVT) were studied at the onset of the disease, and four have been followed up for from 24 to 32 months after the time of diagnosis. Reduced glomerular filtration (two of four cases) on follow-up occurred only in infants with bilateral abnormalities as shown by results of physical examination, urography, renal scan, and angiography. Results of contrast studies showed the similarity between resolved RVT and certain congenital renal abnormalities. Renal tubular defects (polyuria, acidosis, hyperkalemia) constituted the primary clinical abnormalities in one of the two infants with renal insufficiency. Although the prognosis of RVT after medical management has improved, the ultimate outcome is unknown; the possibility of unsuspected neonatal RVT should be considered during investigation of children with unilaterally or bilaterally small kidneys.

Child, Preschool↗
PubMed1987

Lack of effect of lithium carbonate in patients with glycogenosis Ib.

Lithium carbonate has been observed to induce neutrophilia in psychiatric patients and has been used in a number of childhood neutropenic disorders. We tried lithium carbonate in three children with glycogenosis Ib to see if the drug would alleviate the neutropenic complications of the disorder. Mean absolute neutrophil counts rose in one patient but not in the other two. Despite high-dosage schedules, serum lithium levels were highly erratic. Two patients developed potentially severe side effects, including polyuria, diarrhea, and altered mental status. One patient developed pneumonia despite a neutrophil count rise in response to therapy. Lithium carbonate is not useful in patients with glycogenosis Ib.

Adolescent↗
PubMed1991

Epidemic nephropathy in children.

Epidemic nephropathy, a form of hemorrhagic fever with renal syndrome, caused by the Puumala serotype of hantaviruses and occurring endemically in northern Scandinavia, was studied in 13 children. The clinical symptoms and signs were somewhat different from those reported in adults; none of our patients had hemorrhagic manifestations despite low thrombocyte counts. The most common presenting symptoms were fever, abdominal pain, and renal tenderness with oliguria followed by polyuria. The predominant laboratory findings were proteinuria and/or hematuria and elevated serum creatinine levels. Thrombocytopenia was a constant finding in the children in whom thrombocyte count was obtained. Most children had a decreased serum sodium concentration during the oliguric phase of the disease. All the children recovered, with no long-term renal disease. Epidemic nephropathy is an important alternative for differential diagnosis in children with findings suggesting nephritis, especially in endemic areas. An awareness and knowledge of this syndrome and an ability to diagnose it by means of a specific antibody measurement will probably improve our understanding of its epidemiologic features in children.

Alanine Transaminase↗
PubMed1977

Nephropathia epidemica. The Scandinavian form of hemorrhagic fever with renal syndrome.

We report epidemiologic, clinical, laboratory, and biopsy findings in 14 cases of nephropathia epidemica. The patients were between 19 and 49 years of age. The onset of the disease was characterized by high fever, nausea, headache, backache, abdominal pain, proteinuria, oliguria, hematuria, and uremia. The symptoms subsided rapidly during the polyuria phase, which followed the oliguria stage. Because of renal failure, hemodialysis was required in eight cases. Edema of eyelids, conjunctival injection and hemorrhages, transitory myopia, and acute glaucoma were the most common eye abnormalities. Renal biopsy specimens showed glomerular changes, with mild swelling of the epithelial cells of Bowman's capsule, thickening of the basement membrane of glomerular capillaries, glomerular adhesions, inflammatory cell infiltration, leukocytoclasis and hemorrhages in the interstitium, and eosinophilic hyaline degeneration and vacuolization of the epithelial cells of the proximal tubuli.

Acute Disease↗
PubMed1998

Diabetes insipidus and blindness caused by a suprasellar tumor: Pieter Pauw's observations from the 16th century.

Tumors in the suprasellar region may cause both visual and endocrinologic symptoms. This association, well known to modern physicians, was established during the 19th century. However, we have identified a 16th-century autopsy report, written by the Dutch professor of anatomy Pieter Pauw (1564-1617), which describes an 18-year-old girl who developed marked polyuria and subsequently became totally blind from a cystic tumor compressing the optic chiasm. Based on prevailing theories on the nature of diabetes, Pauw attributed the disease to the kidneys. Undoubtedly, however, his lucid report is the earliest known account of diabetes insipidus caused by an arachnoid cyst, the Rathke cleft cyst, or craniopharyngioma in the region of the pouch of Rathke. The description also gives insights into the role of anatomic dissections in late 16th-century northern Europe.

Anatomy↗
PubMed1997

Diabetes insipidus associated with Langerhans cell histiocytosis: is it reversible?

Fourteen of 58 (24%) children with Langerhans cell hisiocytosis (LCH) currently attending the Hospital for Sick Children (London) developed thirst and polyuria during the course of their disease. Three had single-system disease confined to bone, and 11 had multisystem disease. The median age at presentation of LCH was 2 years 0 months, and polyuria/polydipsia developed at a median age of 3 years 9 months (range 1 month before diagnosis of LCH to 4 years after diagnosis). Each child had a water deprivation test with measurement of urinary arginine vasopressin (AVP) to document diabetes insipidus. The doses of 1-desamino-8-D arginine vasopressin (DDAVP) required to control symptoms were compared at diagnosis and at a mean follow-up of 7 years 8 months. Local and systemic treatment was recorded. Ten of 14 children were shown to have "complete" diabetes insipidus, whilest the other four had "partial" diabetes insipidus. Seven children were treated with irradiation. with or without systemic chemotherapy, six with systemic chemotherapy only, and one with DDAVP replacement only. No child, including two with partial diabetes insipidus irradiated within 4 weeks of the onset of symptoms, lost symptoms of polyuria/polydypsia and none was able to discontinue DDAVP replacement. One child treated with Etoposide showed a temporary rise in urinary AVP level to within the normal range but still needed DDAVP to control her symptoms. The mean doses of DDAVP at onset of diabetes insipidus and at follow-up were 9.3 micrograms and 18 micrograms daily, respectively. We conclude that the most appropriate treatment for reversing diabetes insipidus complicating Langerhans cell histiocytosis is yet to be determined. Precise documentation of posterior pituitary dysfunction, including measurement of urinary AVP levels, is essential if the effects of new forms of treatment are to be assessed accurately.

Child↗
PubMed1997

Diabetes insipidus secondary to Langerhans' cell histiocytosis: is radiation therapy indicated?

Langerhans' cell histiocytosis (LCH) is a proliferative disease of Langerhans' cells that has multiple clinical manifestations including diabetes insipidus (DI). This study reviews the effectiveness of hypothalamic-pituitary radiation therapy (HPRT) as a treatment of LCH-induced DI in the modern era. A retrospective review was done of 116 pediatric patients with LCH seen from 1975 to 1992. Seventeen of the 116 patients (15%) were diagnosed with complete or partial diabetes insipidus. Diagnosis was made either by water deprivation test or on clinical grounds. Fourteen patients received hypothalamic-pituitary irradiation as treatment for DI. The median interval from the onset of DI symptoms (polyuria and polydipsia) to treatment was 30 days. The median interval from the onset of diagnosis to treatment was 4 days. With a mean follow-up of 7.3 years (range, 2.4-14.3), only two patients had a complete response to therapy, as defined as no need for antidiuretic hormone (ADH) replacement therapy. No patient had a partial response, defined as a decrease in the dose of ADH replacement. Of the two responders, neither had a complete ADH deficiency, suggesting "early" disease. In addition, both received RT within 3 days. We feel that the standard treatment of RT to all patients with LCH-induced DI is no longer justified. Our series has shown no benefit in treating patients with a long history of DI. Rather, an improved rationale would be rapid initiation of hypothalamic-pituitary irradiation in patients with new symptoms of DI and an abnormal water deprivation test.

Adolescent↗
PubMed1997

Spontaneous regression of primary intracranial germinoma. A case report.

BACKGROUND: Testicular seminomas are well known to regress spontaneously at a higher incidence than other tumors. To date, there have been no reports of spontaneous regression of an intracranial germinoma, although these tumors are histologically identical to testicular seminomas. METHODS: The authors present a patient with a primary intracranial germinoma that regressed spontaneously. RESULTS: A 21-year-old man was admitted to the study facility with acute onset of headache and vomiting. He had a 3-year history of polydipsia and polyuria. Computed tomography (CT) demonstrated a large tumor in the third ventricle, accompanied by hydrocephalus. He underwent ventriculoperitoneal shunt placement on the second day of hospitalization. A CT scan obtained on the fifth postoperative day demonstrated a remarkable decrease in tumor size. Because serial magnetic resonance imaging (MRI) demonstrated a gradual decrease in tumor size, tumor resection was not performed at that time. The patient was discharged and followed with MRI. The tumor continued to regress for more than 2 months. The patient was readmitted due to tumor regrowth, confirmed by MRI 4 months after the initial admission, despite the absence of symptom exacerbation. Two weeks later, the suprasellar portion of the tumor was resected through a right frontotemporal craniotomy. The histopathologic diagnosis was a germinoma. No concurrent tumors were found on whole body examination. The residual tumor gradually regressed after conventional radiation therapy and there has been neither tumor recurrence nor metastasis to date. CONCLUSIONS: Although the precise cause of the transient partial regression is unknown, this case indicates that, like their testicular counterparts, intracranial germinomas may on occasion spontaneously regress.

Adult↗
PubMed1999

Evaluation of the etiology of nocturia in men: the nocturia and nocturnal bladder capacity indices.

To determine and quantify the cause of nocturia in men, we describe and evaluate the relative contribution of two complementary indices of nocturia: the nocturia index (Ni), a measure of nocturnal urine overproduction, and the nocturnal bladder capacity index (NBCi), reflective of nocturnal bladder capacity. The records of 100 consecutive men with lower urinary tract symptoms (LUTS), having undergone video-urodynamic studies (VUDS), were prospectively studied. Evaluation included American Urological Association symptom score (AUASS), micturition diary (day, night, and 24-hr voided volume), and VUDS. Voiding diary analysis was carried out as previously described by us, determining the Ni, NBCi, and nocturnal polyuria index (NPi) (nocturnal urine volume/24-hr urine volume). In the case of AUASS question #7 (degree of nocturia), the odds of having a severe AUA question #7 response was found to be 4.09 times higher for patients with NBCi > 2.0 compared with patients whose NBCi was </= 2.0 using logistic regression analysis. In comparing patients with severe nocturia and low NBCi with those having mild nocturia and low NBCi, Ni performed in a fashion superior to NPi in identifying relative nocturnal urine overproduction as the suspected explanation for their nocturia (Ni = 3.42 vs. 1.42, P = 0.0002 cf. Npi = 0.44 vs. 0.27, P = 0.018, Mann-Whitney test, respectively). We suggest a discriminating threshold of NBCi > 2 as highly significant in defining diminished NBC as a factor in the etiology of nocturia. In addition, we propose Ni of 1.5 as a threshold greater than which nocturia may be attributed to nocturnal urine overproduction in excess of maximum bladder capacity. Together, these indices describe in quantitative fashion the relative contributions of nocturnal urine overproduction and diminished NBC in identifying the etiology of nocturia in male patients. Neurourol. Urodynam. 18:559-565, 1999.

Aged↗
PubMed2001

Clinical and genetic characterization of an autosomal dominant nephropathy.

Autosomal dominant familial nephropathies with adult onset, no macroscopic cysts, and progressive deterioration include medullary cystic disease (ADMCKD) as well as other less specific entities. We studied a kindred of Jewish ancestry in which 15 members (both male and female) have suffered from chronic renal failure. The first evidence of renal involvement was observed between 18 and 38 years. It included hypertension followed by progressive renal insufficiency. No polyuria, anemia, gout, hematuria, nor proteinuria were seen. An average of 4.5 years elapsed from diagnosis to end-stage renal disease. Renal pathology at early stages of the disease showed extensive tubulointerstitial fibrosis and global glomerulosclerosis. Linkage analysis was performed at the two known loci of ADMCKD, on Chromosomes 1 and 16. Linkage to the chromosome 16 locus was excluded. However, linkage to the chromosome 1q21 locus of ADMCKD was established with a maximum two-point LOD score of 3.82 to D1S394. The disease interval could be narrowed to about 9 cM/7.4 Mb between D1S1156 and D1S2635. Multiple-point linkage analysis revealed a maximum LOD of 4.21, with a broad peak from markers D1S2858 and D1S2624. This report establishes linkage between a familial nephropathy characterized by hypertension and progressive renal failure to the locus described for ADMCKD, a disease classically associated with macroscopic corticomedullary cysts, salt-losing tubulointerstitial nephropathy, and anemia. This finding broadens the clinical spectrum of ADMCKD positioned on chromosome 1q21 locus.

Adult↗