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PubMed1998

Glycated plasma proteins in experimentally induced acute toxic renal failure by dichromate injection: evidence for loss with urine and decreased plasma levels.

In the rat, a single subcutaneous injection of sodium dichromate (20 mg/kg) causes acute renal injury and significant polyuria, proteinuria, and glycosuria (peaking 2-3 days after treatment, and returning to normal by day 5) without any changes in the plasma levels of protein, glucose, and glycated haemoglobin. Surprisingly, the percentage levels of glycated plasma total proteins and albumin (assayed by boronate affinity chromatography) transiently and significantly decrease during recovery from proteinuria (days 4 and 10 after treatment) and were found in the normal range of values by day 18. These changes are concomitant with a significant increase in the percentage level of glycated albumin in urine. Constancy of total plasma protein and the temporal pattern of levels of glycation suggest that changes in the percentage values of glycated proteins are secondary to a transient selective loss of glycated plasma proteins in urine.

Acute Kidney Injury↗
PubMed1998

Recovery from Marie-Bamberger's syndrome and diabetes insipidus after removal of a lung adenocarcinoma with neuroendocrine features.

A 44-year-old woman with Marie-Bamberger's syndrome and diabetes insipidus had a lung tumour with mediastinal metastases, but no signs of metastases to the hypothalamus or pituitary gland. A week after removal of the tumour, the joint pain, polyuria and polydipsia disappeared. The tumour was diagnosed histopathologically as a moderately differentiated adenocarcinoma with focal neuroendocrine cell differentiation and dispersed cells reacting with antisera against neurone-specific enolase, S-100 protein, neuropeptide Y, follicle-stimulating hormone, substance P, vasoactive polypeptide (VIP), adrenocorticotropic hormone and pancreatic polypeptide (PP) as well as to one of three tested antisera raised against antidiuretic hormone (ADH). It was suggested that Marie-Bamberger's syndrome might be caused by one of these immunoreactive substances or by a substance that shares an amino acid sequence with one of these neuroendocrine peptides. It was also suggested that the tumour might produce an ADH-like substance which might have an ADH-antagonist effect.

Adenocarcinoma↗
PubMed1996

Osmoregulation of plasma vasopressin in diabetes mellitus with sustained hyperglycemia.

We studied osmoregulation of plasma vasopressin in 5 patients with newly diagnosed diabetes mellitus. All patients showed typical symptoms of uncontrolled diabetes mellitus such as marked hyperglycemia, polyuria, and polydipsia, but did not have advanced diabetic complications. Vasopressin release was studied using 5% hypertonic saline infusion test twice: before treatment when the patient was hyperglycemic, and after treatment 1 to 2 months later when the patient was euglycemic. Plasma vasopressin was measured by a sensitive and specific radioimmunoassay. The mean basal plasma vasopressin value in the patients was significantly higher in the hyperglycemic compared with the euglycemic state (3.75 +/- 0.70 vs 1.18 +/- 0.46 pmol/l, respectively; P < 0.05). The relationship of plasma vasopressin with serum sodium, but not plasma osmolality, during hyperglycemia showed an apparent hypersecretion of vasopressin. In both cases, the sensitivity of the vasopressin response to osmotic stimuli was significantly decreased. During euglycemia, the sensitivity of vasopressin secretion to either sodium or osmolality was almost normal, although a slight rise in the osmostat was observed compared with normal subjects. Together, we found that the positive correlation of vasopressin with sodium or osmolality is maintained but significantly altered in patients with untreated diabetes mellitus. Especially noteworthy is the lowered threshold and decreased sensitivity of osmotically-induced vasopressin secretion during hyperglycemia, which may be caused by multiple factors such as diabetes-associated hypovolemia, osmogenic effects of glucose and other osmoles, depletion of the pool of vasopressin available for release, and the metabolic derangement of osmoreceptor/magnocellular neurons.

Adult↗
PubMed2003

Rare association of xanthoma disseminatum with skeletal involvement.

A ten-year-old boy presented with a 2.5-year history of painful shoulder and hip joints, 1.5 years of yellow-brown papules and plaques on the face, flexures and trunk, and 6 months of polyuria and polydipsia. Skin biopsy revealed histological and immunohistochemical features typical of xanthoma disseminatum. Lytic bone lesions were seen in the femur and pelvis and sclerotic changes in the humerus on X-ray. Diabetes insipidus was also diagnosed

Biopsy↗
PubMed1999

Renal function in chronically catheterized conscious diabetic rats using constant and servo-controlled infusion.

1. Infusion experiments were performed on chronically catheterized conscious rats to assess kidney function before and after the induction of diabetes mellitus with streptozotocin. 2. Two infusion regimens were used, a conventional constant-infusion protocol and a novel computer-driven, servo-controlled fluid replacement technique. The latter enables body fluid status to be maintained throughout a study occasion by servo-controlled replacement of spontaneous urinary fluid losses. 3. The chronically catheterized conscious rat infused using a servo-controlled system appears to be the optimum model for a study of diabetic renal function. The conscious preparation circumvents problems associated with anaesthesia and acute surgery. The servo-controlled infusion protocol maintains the altered fluid status of the diabetic condition. Both hyperfiltration and polyuria, characteristics of human diabetes often absent in anaesthetized and/or constantly infused diabetic rats, were seen in all conscious servo-controlled diabetic animals. 4. The new regimen enables a more accurate assessment of renal function in experimental diabetes than with previous protocols. It should prove useful in future studies, particularly those assessing the role of anti-diabetic drugs on the kidney.

Animals↗
PubMed2001

Interactions between sodium and angiotensin.

1. Increased sodium intake causes decreased formation of angiotensin (Ang) II and increased AngII causes increased Na+ retention. 2. Increased sodium intake and increased AngII causes cardiac hypertrophy, but decreased sodium intake regresses cardiac hypertrophy despite high AngII levels. Likewise, decreased Na+ and blockers of the renin-angiotensin system (RAS) in neonatal rats have similar effects on subsequent blood pressure development. 3. Cardiac hypertrophy due to renal hypertension does not regress when the RAS is blocked and rats are on a high salt intake. Likewise, sodium restriction alone does not cause regression; combination of reduced NaCl intake and RAS blockade is required. 4. High doses of perindopril and losartan in combination cause a syndrome in rats on 0.2% NaCl that leads to profound hypotension, polyuria, renal impairment and involution of the heart and death. This is reversed or prevented by a high (4%) NaCl intake, which also prevents the plasma angiotensinogen depletion that occurs with combined blockade on 0.2% NaCl intake. 5. Intake of NaCl and AngII interact at many levels. It is postulated that there is an important interaction at the cellular level that can explain the above events.

Angiotensin II↗
PubMed1998

Monosymptomatic primary enuresis: differences between patients responding or not responding to oral desmopressin.

OBJECTIVES: To evaluate the 24-h diuresis, urinary osmolality, plasma arginine vasopressin (AVP) and urinary prostaglandin E2 (PGE2) before and during desmopressin treatment in patients with monosymptomatic primary enuresis (MPE), and to investigate the possible depressor effect of desmopressin on the detrusor in such patients with urodynamically confirmed bladder instability. PATIENTS AND METHODS: Seven healthy children (control group) and 11 consecutive patients with MPE (mean age 10.4 years, range 7-15) were assessed using laboratory tests, renal and bladder ultrasonography, and video-urodynamic investigations. A 24-h inpatient assessment with a controlled water intake of 20 mL/kg per day included determinations of diuresis, urinary osmolality, AVP and PGE2 in both normal children and those with MPE. After 30 days of treatment at optimal doses of desmopressin, all children were hospitalized and re-evaluated during desmopressin treatment; all completed 3 months of treatment at optimal doses. At the end of this period, patients whose symptoms improved by > or = 80% were defined as 'responders' while those in whom they did not were defined as 'non-responders'. RESULTS: After treatment, six of the 11 patients with MPE were 'responders' and five 'non-responders'. Urodynamic evaluation showed bladder instability in seven of the 11 patients with MPE but in those with bladder dysfunction, urodynamic studies carried out during desmopressin treatment showed no changes in detrusor activity. There were significant differences in the morning values of AVP between normal children and responders (P < 0.03), and between responders and non-responders (P < 0.02); none of the non-responders had AVP levels of < 2.5 pg/mL, while none of the responders exceeded this value. At midnight, responders had the lowest mean AVP and non-responders the highest; this correlated with the highest PGE2 value in the nonresponders at 00.00-08.00 hours. Non-responders had an overnight mean PGE2 level greater than that in normal subjects or responders. CONCLUSIONS: Polyuria occurred in all patients with MPE, independently of the response to desmopressin. Responders had the lowest AVP values over the 24 h; the morning AVP levels differentiated normal subjects from enuretic patients and responders from non-responders. In patients with MPE, clinically undetected bladder instability was unrelated to the results of treatment and there were no urodynamic changes during desmopressin treatment. The differences between enuretic patients suggested a different aetiology of MPE, probably related to an increase in PGE2 concentration and an antagonistic mechanism of action of AVP or desmopressin.

Administration, Oral↗
PubMed2002

Reduction in nocturnal functional bladder capacity is a common factor in the pathogenesis of refractory nocturnal enuresis.

OBJECTIVE: To evaluate the diurnal and nocturnal bladder reservoir function in patients with refractory primary nocturnal enuresis (PNE). PATIENTS AND METHODS: Ninety-five children (68 boys, 27 girls, mean age 9.3 years) with significant PNE (>/=3 wet nights/week) that was refractory to treatment with desmopressin +/- an enuretic alarm were assessed using detailed recording of voiding frequency and urinary volume both day and night, natural filling cystometry during the day and continuous cystometry with simultaneous electroencephalogram monitoring during sleep at night. RESULTS: Patients could be broadly categorized into two groups. Group A comprised those with normal daytime urodynamics and functional bladder capacity (FBC) on detailed frequency-volume recording, but who developed marked detrusor instability associated with a significant reduction in nocturnal FBC and small-volume voiding only after sleep at night (33 patients, 35%); and group B, those with abnormal daytime urodynamics and with reduced FBC and small-volume voiding both day and night, but who somehow managed to mask their bladder symptoms during the day (62 patients, 65%). There was no evidence of nocturnal polyuria in either group and the ratios of day : night urinary output volumes for type A and type B patients were 1.48 and 1.99, respectively. CONCLUSION: A reduction in nocturnal FBC, either occurring only after sleep at night in association with the appearance of detrusor instability in patients with normal daytime urodynamics and FBC, or as a manifestation of occult voiding dysfunction or bladder outlet obstruction that affects the bladder reservoir function both day and night, appears to be a common factor and probably the main cause for a mismatch between nocturnal urine output and bladder storage capacity in patients with severe bed-wetting that was refractory to treatment.

Adolescent↗
PubMed1999

Migraine associated with panic attacks.

Migraine headache and panic disorder are two conditions that have a number of underlying physiological and psychological abnormalities in common. The temporal relationship between the occurrence of migraine headache and panic attacks could be different, however. According to our observations, some migraine subjects develop panic attacks with the typical symptoms (palpitation, dyspnea, anxiety/fear, shiver, sweating, polyuria) on the "peak" of their attacks. This variant of migraine without aura was conditionally defined as "panic migraine". Here we describe two patients suffering from migraine without aura in whom migraine was associated with the typical panic attack. It is suggested that a pronounced autonomic dysregulation along with marked psychological abnormalities could be responsible for the constellation of migraine and panic symptoms during one episode. Taking into account the previously obtained results, it is concluded that compared to "pure" migraine, "migraine associated with panic attacks" is characterized by a severe course, marked autonomic and emotional disturbances during pain-free intervals, seriously impaired quality of life, and requires a specific therapeutic approach.

Adult↗
PubMed2001

Renal phenotype of low kallikrein rats.

BACKGROUND: Renal kallikrein has been linked with inheritance of arterial hypertension and with sensitivity to drug nephrotoxicity. Identification of a cause--effect relationship between low kallikrein and intermediate phenotypes has been hampered by the lack of adequate animal models. METHODS: Kallikrein was measured in tissues obtained from rats inbred for low urinary kallikrein excretion (LKR) and wild-type controls. Blood pressure and indices of myocardial contractility were recorded via an intraventricular cannula connected to a transducer. The functional relevance of endogenous angiotensin II (Ang II) in LKR was explored by determining the effect of Ang II subtype 1 (AT(1)) receptor blockade on glomerular filtration rate, renal blood flow, and urinary sodium excretion. In addition, sensitivity to gentamycin-induced nephrotoxicity was evaluated. RESULTS: Kallikrein activity was reduced by 60% in the kidney of LKR (P < 0.01), whereas it was increased in the heart (P < 0.05) and was unaltered in the pancreas, liver, and salivary glands. Heart rate and myocardial contractility were reduced, and the mean blood pressure (MBP) was increased in LKR as compared with controls (P < 0.05). LKR exhibited polydipsia, polyuria, glomerular hyperfiltration, and reduced fractional sodium excretion under basal conditions and impaired renal vasodilation in response to volume expansion. These functional alterations were significantly attenuated by AT(1) receptor blockade. Gentamycin reduced the glomerular filtration rate in LKR, but not in controls. CONCLUSIONS: In LKR, unopposed activity of Ang II appears to be responsible for increased glomerular hydrostatic pressure and augmented tubular reabsorption. Balance between the kallikrein-kinin and renin-angiotensin systems is essential for normal renal function.

Angiotensin Receptor Antagonists↗
PubMed2003

Reverse pharmacological effect of loop diuretics and altered rBSC1 expression in rats with lithium nephropathy.

BACKGROUND: Renal urinary concentration is associated with enhanced expression of rBSC1, a rat sodium cotransporter, in the thick ascending limb of Henle. Increased expression of rBSC1 was reported recently in nephrogenic diabetes insipidus induced by lithium chloride (Li nephropathy). However, the pathophysiological implication of altered rBSC1 expression has not yet been investigated. METHODS: Li nephropathy was induced in rats by an oral administration of 40 mmol lithium/kg dry food. In rats with reduced urinary osmolality to less than 300 mOsm/kg H2O, we examined the expression of rBSC1 mRNA and protein, plasma arginine vasopressin (AVP) and RNA expression of kidney-specific water channel, aquaporin-2 (AQP2), of collecting ducts. Rats with Li nephropathy were treated with furosemide (3 mg/kg body weight), which blocks the activity of rBSC1, and changes in urine concentration, plasma AVP, medullary accumulation of Li ions, and apical AQP2 expression were determined. RESULTS: Rats with Li nephropathy showed increased rBSC1 RNA and protein expression and reduced AQP2 RNA. In these rats, furosemide, which induces dilution of urine and polyuria in normal rats, resulted in a progressive and significant rise in urine osmolality from 167 +/- 11 (mean +/- SD) at baseline to 450 +/- 45 mOsm/kg H2O at three hours after administration, and significant oliguria. In the same rats, plasma AVP decreased significantly from 5.7 to 3.0 pg/mL. In addition, recovery of apical AQP2 expression was noted in a proportion of epithelial cells of the collecting ducts. Although Li+ in the renal medulla was slightly lower in rats with Li nephropathy treated with furosemide, statistical significance was not achieved. CONCLUSIONS: Our results suggest that dehydration or high plasma AVP results in an enhanced rBSC1 expression in Li nephropathy, and that rBSC1 expression is closely associated with the adverse effects of Li ions on collecting duct function.

Animals↗
PubMed2003

Increased endothelin-1 expression in the kidney in hypercalcemic rats.

BACKGROUND: Although hypercalcemia causes diuresis and natriuresis, the molecular mechanisms of these effects are not well established. Recently, the important role of the calcium-sensing receptor (CaR) in hypercalcemia-induced polyuria was reported. Endothelin-1 (ET-1) that is locally produced in the nephron has been suggested to have the natriuretic and/or diuretic effects in the kidney. Therefore, we hypothesized that ET-1 expression could be increased through the activation of CaR in the kidney in hypercalcemia. METHODS: Rats were made hypercalcemic by dihydrotachysterol (DHT) treatment. The urinary concentration of ET-1 and the mRNA expression of ET-1 in the kidney were determined. Immunohistochemistry was performed to determine types of the cells that produce ET-1. CaR and ET-1 promoter luciferase constructs were co-expressed in COS-7 cells and the ET-1 promoter activity following the addition of extracellular calcium was measured by the luciferase assay. RESULTS: In hypercalcemic rat, urinary ET-1 excretion was increased by twofold, and ET-1 mRNA expression was increased in the kidney cortex by threefold. In cortical collecting duct (CCD), both principal cells and intercalated cells synthesized ET-1. In cells that express CaR, ET-1 promoter was activated in a dose-dependent manner by extracellular calcium over the range of 0.5 to 3.0 mmol/L. CONCLUSIONS: First, activation of CaR increases ET-1 transcription in a dose-dependent manner. Second, hypercalcemia increases ET-1 production in the kidney cortex. These data suggest the possibility that CaR might play an important role in hypercalcemia-induced increase in ET-1 production.

Animals↗
PubMed2000

Overcorrection of hyponatremia: where do we go wrong?

Predicted sodium concentrations [Na(+)] based on traditional calculations for the correction of hyponatremia often do not match treated [Na(+)], for various reasons. In many situations, hyponatremia is corrected at unexpectedly rapid rates. The authors present an analysis of two cases of overly rapid correction of hyponatremia despite apparently appropriate management based on initial evaluations. The mistakes involved are discussed and simple calculations demonstrated to prove that the overcorrections did not occur at random. Overcorrection in one case involved miscommunications between the emergency room and admitting physicians regarding the amount of saline and potassium already administered to the patient. Unexpected hypoosmotic polyuria was responsible for overcorrection in the other case. Overcorrection of hyponatremia may be preventable in many cases. In general, overcorrection of hyponatremia is caused by either "too much salt (Na(+) + K(+)) gained" or "too much water lost." Recognizing common pitfalls will enable physicians to avoid overcorrection and its attendant risk of fatal osmotic demyelinating syndrome (ODS).

Adult↗
PubMed2002

Infantile cystinosis presenting as chronic constipation.

An infant presented with persistent constipation as the first clinical symptom of cystinosis before evidence of renal Fanconi's syndrome. The history of muscle weakness, failure to thrive, polydipsia, and polyuria prompted subsequent clinical and laboratory evaluations, leading to the correct diagnosis of cystinosis. Primary and persistent constipation as an initial manifestation of cystinosis has not been reported previously. Although rare, cystinosis should be considered in the differential diagnosis of constipation if other suggestive signs or symptoms are present.

Chronic Disease↗
PubMed2002

Nephrogenic diabetes insipidus associated with hemochromatosis.

Although hemochromatosis is one of the most common genetic disorders in humans, the clinical information on iron-induced renal impairment is limited. We describe the clinical features of nephrogenic diabetes insipidus (NDI) observed in a case of hemochromatosis. A 57-year-old diabetic man was admitted to the hospital with a 6-month history of persistent polyuria, which had been sustained after glycemic optimization with insulin therapy and resulted in hepatic coma. Despite sufficient basal excretion of arginine vasopressin, impaired urinary concentrating capacity was observed, which could not be corrected by supraphysiologic doses of exogenous arginine vasopressin. Histochemical investigations showed widely distributed iron deposition in hepatocytes and moderately increased iron deposits in the tubular epithelium of distal urinary tubules and collecting ducts, suggesting that iron deposition resulting from hemochromatosis leads to NDI. This may be the first case report of NDI associated with hemochromatosis in humans. More attention should be paid to latent NDI as another complication of hemochromatosis.

Diabetes Insipidus, Nephrogenic↗
PubMed2006

Nephrogenic diabetes insipidus.

Nephrogenic diabetes insipidus (NDI), which can be inherited or acquired, is characterized by an inability to concentrate urine despite normal or elevated plasma concentrations of the antidiuretic hormone arginine vasopressin (AVP). Polyuria, with hyposthenuria, and polydipsia are the cardinal clinical manifestations of the disease. About 90% of patients with congenital NDI are males with X-linked recessive NDI (OMIM 304800) who have mutations in the arginine-vasopressin receptor 2 (AVPR2) gene that codes for the vasopressin V2 receptor. In about 10% of the families studied, congenital NDI has an autosomal recessive or autosomal dominant mode of inheritance (OMIM 222000 and 125800). In these families, mutations have been identified in the aquaporin-2 gene (AQP2) (OMIM 107777), which codes for the vasopressin-sensitive water channel. Most missense AVPR2 mutations lead to receptors that are trapped intracellularly; a few mutant receptors reach the cell surface but are unable to bind AVP or to properly trigger an intracellular cyclic adenosine monophosphate signal. Similarly, most AQP2 mutant proteins are also misrouted. Prior knowledge of AVPR2 or AQP2 mutations in NDI families and perinatal mutation testing is of direct clinical value because early diagnosis and treatment can avert the physical and mental retardation associated with repeated episodes of dehydration.

Aquaporin 2↗
PubMed2005

A case of lymphocytic hypophysitis with masked diabetes insipidus unveiled by glucocorticoid replacement.

Lymphocytic hypophysitis may involve the pituitary gland and various hormonal abnormalities. A 72-year-old man presented with euvolemic hyponatremia caused by glucocorticoid deficiency. After glucocorticoid replacement, hypernatremia in the presence of dilute urine was found. Central diabetes insipidus (DI) was confirmed later by a significant increase in urine osmolality after vasopressin administration. Brain magnetic resonance imaging showed a pituitary mass and loss of hyperintense signal in the posterior pituitary gland on T1-weighted imaging. The patient underwent a transsphenoidal adenectomy, and pathological examination of dissected tissues showed a typical finding of lymphocytic hypophysitis. Two months after surgery, the patient's central DI had resolved sufficiently that 1-desamino-8- d -arginine vasopressin therapy was discontinued without polyuria. However, he was kept on glucocorticoid and levothyroxine therapy. In conclusion, lymphocytic hypophysitis may feature a concealed central DI caused by glucocorticoid deficiency-associated hyponatremia.

Aged↗
PubMed2003

Treatment of malignancy-associated hypercalcemia and cachexia with humanized anti-parathyroid hormone-related protein antibody.

Parathyroid hormone-related protein (PTHrP) plays a central role in humoral hypercalcemia of malignancy (HHM), which is one of the most frequent paraneoplastic syndromes. PTHrP produced by the tumor acts through a common PTH/PTHrP receptor to promote bone resorption, inhibit calcium excretion from the kidney, and induce hypercalcemia. Patients with HHM often develop cachexia associated with typical symptoms such as anorexia, malaise, nausea, constipation, polyuria, polydipsia, and confusion. The etiology of the cachexia is not fully understood but is thought to be caused by hypercalcemia and various cytokines such as interleukin-6, tumor necrosis factor-alpha, leukemia inhibitory factor, and others. In this study, we investigated the role of PTHrP in hypercalcemia and cachexia in HHM by using humanized anti-PTHrP antibody. A mouse monoclonal antibody that binds to PTHrP amino acid sequence 1-34 and inhibits PTHrP function has been humanized to create a specific and potent agent for the treatment of patients with HHM. The mouse monoclonal antibody has been shown to have antihypercalcemic activity against nude mice bearing human tumors. Because a mouse antibody is highly immunogenic in human patients, the complementarity-determining regions from the mouse antibody were grafted into a human antibody. The resulting humanized antibody specifically recognizes PTHrP(1-34) and neutralizes PTHrP functions in vitro and in vivo. The humanized anti-PTHrP antibody was administered intravenously to HHM model animals bearing tumors such as LC-6 human lung carcinoma. These animals showed symptoms similar to those of patients with HHM (eg, hypercalcemia and cachexia). The humanized anti-PTHrP antibody-treated animals responded with normalization of blood ionized calcium level through an improvement of bone metabolism and calcium excretion. Moreover, the treated animals also showed an improvement in body weight, ultromotivity, metabolic alkalosis, food consumption, water intake, serum phosphorus, and renal function. Consequently, the humanized antibody-treated animals experienced complete resolution of hypercalcemia and cachexia. These results suggest that the humanized antibody would be an effective and beneficial agent for patients with HHM, and that PTHrP is a major pathogenetic factor of hypercalcemia and cachexia in patients with HHM.

Animals↗