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PubMed2001

Evidence for further genetic heterogeneity in nephronophthisis.

BACKGROUND: A new type of nephronophthisis (NPH) has been recently identified in a large Venezuelan kindred: adolescent nephronophthisis (NPH3) causes end-stage renal disease (ESRD) at a median age of 19 years. The responsible gene (NPHP3) maps to 3q21-q22. NPH3 shares with juvenile nephronophthisis (NPH1) the same disease manifestations such as polyuria, polydipsia, and secondary enuresis. Histopathological findings consist of tubular basement membrane changes, cysts at the corticomedullary junction, and a chronic sclerosing tubulointerstitial nephropathy. The only difference is a younger age at ESRD in NPH1 (median age of 13 years) when compared with NPH3. METHODS: In order to evaluate whether there might be a fourth locus of isolated nephronophthisis, we studied eight NPH families without extrarenal disease manifestations and without linkage to the NPH1 locus (NPHP1) on chromosome 2q12-q13. ESRD was reached at ages ranging from 7 to 33 years. Individuals were haplotyped with microsatellites covering the genetic locus of NPHP3. Infantile NPH (NPH2) was excluded in all families by the clinical history and histological findings. RESULTS: In four of the examined families haplotype analysis was compatible with linkage to the NPHP3 locus. In one of these families identity by descent was observed. In contrast, in another four families linkage was excluded for NPHP3. CONCLUSION: Four NPH-families were neither linked to NPHP1 nor to NPHP3, indicating further genetic heterogeneity within the group of nephronophthisis. The finding of further genetic heterogeneity in NPH has important implications for genetic counselling.

Adaptor Proteins, Signal Transducing↗
PubMed2005

Glomerular hyperfiltration and hypertrophy in the rat hypoplastic kidney as a model of oligomeganephronic disease.

BACKGROUND: Rat male hypogonadisim (hgn/hgn) is accompanied by bilateral hypoplastic kidney (HPK). The HPK contains a reduced number of nephrons that progress to chronic renal failure. In this study, we describe the renal pathophysiology in adult HPK rats as a potential model of oligomeganephronic disease. METHODS: Urine and blood samples were collected from adult male HPK rats and phenotypically normal littermates at 70 days of age for measurements of urea-nitrogen and creatinine clearances (Cun and Ccr). Glomerular number (GN) and glomerular projective area were determined using the maceration method. Blood pressure was measured. Urinary protein and renal histology were examined. Urinary albumin concentration was determined at early postnatal ages. RESULTS: Renal weight was significantly smaller in adult HPK males than in normal males. Polyuria and polydipsia were observed in HPK rats. Ccr and Cun were low in HPK rats compared with those in normal rats. The HPK contained only 20% of the nephrons present in normal kidneys. The Cun and Ccr divided by GN (average values of single nephron Cun and Ccr) of HPK rats were about two and four times greater than normal levels, respectively. This hyperfiltration was not accompanied by systemic hypertension, but was associated with marked glomerular hypertrophy and glomerulosclerosis, which were observed mainly in the inner cortex. A considerable heterogeneity of glomerular size was found in HPK and most glomeruli of surface nephrons retained normal size and histology. A remarkable leakage of albumin into urine was found at 35 and 70 days of age. CONCLUSIONS: The HPK rat is a useful model for studying the pathophysiology of oligomeganephronic disease as well as glomerular hyperfiltration and hypertrophy induced by severe congenital reduction of nephrons.

Age Factors↗
PubMed2000

Primary hyperparathyroidism with normal serum intact parathyroid hormone levels.

To evaluate the features of primary hyperparathyroidism (HPT) with normal serum intact parathyroid hormone (iPTH) levels, we studied 271 consecutive patients undergoing surgery for primary HPT. In 20 patients, serum iPTH levels were within the normal range (10-65 ng/l). In their records, the most common clinical features were fatigue (n=13), polyuria (n=6), renal stone (n=5), and hypertension (n=5). Mean serum calcium and phosphorus were 2.78 and 0.85 mmol/l, respectively: 14 had serum phosphorus within the normal range. Mean serum iPTH was 48.5 ng/l, and was <45 ng/l in nine patients. Cervical ultrasound demonstrated a parathyroid adenoma in nine, and was normal in four. Tc sestamibi parathyroid scintigraphy always demonstrated an adenoma (9/9). In eight patients, normal iPTH values delayed diagnosis. Physicians should be aware of the possibility of HPT in patients with hypercalcaemia, even when serum phosphorus and iPTH levels are within the normal limits. Particularly, HPT cannot be excluded when serum iPTH levels are below the upper part of the normal range. In such cases, cervical imaging, which has the same sensitivity as in other HPT, should be undertaken. These explorations are useful, because many patients are symptomatic and can take advantage of surgery.

Adenoma↗
PubMed1991

Atrial natriuretic peptide and catecholamines in obstructive sleep apnea syndrome.

Nocturnal polyuria with repeated micturitions during the night is a clinically evident feature of obstructive sleep apnea syndrome (OSAS). These effects are reversed by continuous positive airway pressure (CPAP). There is some evidence that atrial natriuretic peptide (ANP) and catecholaminergic activity may be implicated in the pathogenesis of these symptoms. We studied these biochemical parameters in six patients with severe OSAS during two nights: the first (basal) in their normal conditions and the second during CPAP treatment. CPAP treatment reversed apnea episodes in all our patients. A significant (p less than 0.035) reduction of nocturnal urine volume (from 902 +/- 297 to 447 +/- 130 ml; mean +/- SD), sodium excretion (from 150 +/- 33 to 89 +/- 35 mEq/12 h), noradrenaline excretion (from 95 +/- 101 to 52 +/- 16 micrograms/g creatinine), noradrenaline plasma concentrations (from 325 +/- 96 to 259 +/- 75 pg/ml), ANP plasma concentrations (from 35 +/- 20 to 19 +/- 5 pg/ml) was observed during the night under CPAP application. These data suggest that in OSAS patients the high ANP plasma concentration is responsible for the observed elevated diuresis and sodium excretion. These effects are rapidly reversible, as they are reversed during the first CPAP treated night.

Adult↗
PubMed2002

Nephrotoxicity of chlorofluoroacetic acid in rats.

Dichloroacetic acid (DCA), chlorofluoroacetic acid (CFA), and difluoroacetic acid (DFA) are inhibitors of pyruvate dehydrogenase kinase. DCA is used for the clinical management of congenital lactic acidosis. Glutathione transferase zeta (GSTZ1-1) catalyzes the biotransformation of DCA and CFA, and DCA is a mechanism-based inactivator of GSTZ1-1. In rodents, DCA causes multiorgan toxicities and is hepatocarcinogenic. The toxic effects of CFA, which is an excellent substrate but a poor inactivator of GSTZ1-1, have not been investigated. The objective of this study was to investigate the nephrotoxicity of CFA. Rats given a single dose of 1.5 mmol/kg CFA became anuric and died within 24 h. Urinalysis and light microscopic analysis showed that rats given 0.6-1.2 mmol/kg CFA developed polyuria, glycosuria, and renal proximal tubular damage. Electron microscopic analysis indicated a role for apoptosis in CFA-induced cell death. The nephrotoxicity of CFA was associated with a dose-dependent increase in inorganic fluoride excretion. Treatment of rats with DCA for 5 days to inactivate GSTZ1-1 failed to prevent metabolism of CFA to fluoride and did not block CFA-induced renal damage. A role for GSTZ1-1-catalyzed release of fluoride from CFA is proposed but a role for other enzymes cannot be excluded. DFA, which is not metabolized to fluoride by GSTZ1-1, was given to rats as a control and was also nephrotoxic: rats given 1.2 mmol DFA/kg/day for 5 days had normal urine volumes but showed proximal and distal tubular damage; fluoride excretion was not elevated. The mechanism of DFA-induced nephrotoxicity is not known but appears to differ from that of CFA.

Acetates↗
PubMed2005

Autophagy is a prosurvival mechanism in cells expressing an autosomal dominant familial neurohypophyseal diabetes insipidus mutant vasopressin transgene.

Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is a progressive, inherited neurodegenerative disorder that presents as polydipsia and polyuria as a consequence of a loss of secretion of the antidiuretic hormone vasopressin (VP) from posterior pituitary nerve terminals. VP gene mutations cause adFNDI. Rats expressing an adFNDI VP transgene (Cys67stop) show a neuronal pathology characterized by autophagic structures in the cell body. adFNDI has thus been added to the list of protein aggregation diseases, along with Alzheimer's, Parkinson's and Huntington's, which are associated with autophagy, a bulk process that delivers regions of cytosol to lysosomes for degradation. However, the role of autophagy in these diseases is unclear. To address the relationships between mutant protein accumulation, autophagy, cell survival, and cell death, we have developed a novel and tractable in vitro system. We have constructed adenoviral vectors (Ads) that express structural genes encoding either the Cys67stop mutant protein (Ad-VCAT-Cys67stop) or an epitope-tagged wild-type VP precursor (Ad-VCAT). After infection of mouse neuroblastoma Neuro2a cells, Ad-VCAT encoded material enters neurite processes and accumulates in terminals, while the Cys67stop protein is confined to enlarged vesicles in the cell body. Similar to the intracellular derangements seen in the Cys67stop rats, these structures are of ER origin, and colocalize with markers of autophagy. Neither Ad-VCAT-Cys67stop nor Ad-VCAT expression affected cell viability. However, inhibition of autophagy or lysosomal protein degradation, while having no effect on Ad-VCAT-expressing cells, significantly increased apoptotic cell death following Ad-VCAT-Cys67stop expression. These data suggest that activation of autophagy by the stress of the expression of an adFNDI mutant protein is a prosurvival mechanism.

Acridine Orange↗
PubMed2005

Autophagy-dependent cell survival and cell death in an autosomal dominant familial neurohypophyseal diabetes insipidus in vitro model.

Mutations in the human gene encoding the antidiuretic hormone vasopressin (VP) cause autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI), a rare inherited disorder that presents as polydipsia and polyuria as a consequence of a loss of secretion of VP from posterior pituitary nerve terminals. Work from our laboratories has shown that adFNDI, like other neurodegenerative diseases such as Alzheimer's, Parkinson's and Huntington's, is associated with autophagy. We have recently shown that the activation of autophagy in mouse neuroblastoma Neuro2a cells after adenoviral vector-mediated delivery of an adFNDI mutant VP transgene (Cys67stop) is a cell survival mechanism; its inhibition induces apoptosis. We now show that expression of Cys67stop sensitizes Neuro2a cells to the lethal effects of dopamine. This mode of cell death exhibits features typically associated with classical apoptosis. Yet inhibition of autophagy reversed these effects and rescued cell viability. We propose that autophagy-mediated cell death is a "two-hit" process: Following the cellular stress of the accumulation of a misfolded mutant protein, autophagy is prosurvival. However, a second insult triggers an autophagy-dependent apoptosis.

Adenoviridae↗
PubMed1995

Mixed-lineage acute myeloid leukemia associated with a suprasellar dysgerminoma.

An association between primary mediastinal germ cell tumors and hematologic malignancies has been recognized since 1985. We present a patient with a suprasellar germ cell tumor and an associated leukemia. A 20-year-old black female presented in December 1987 with a 6-month history of headaches and weight loss, confusion, polyuria, and polydipsia. Evaluation revealed hypernatremia, normal neurologic examination except poor recall, and an enhancing inhomogeneous suprasellar mass on cranial computed tomography. Biopsy of the mass diagnosed a dysgerminoma, which was treated with craniospinal radiation. In February 1988, the patient developed pancytopenia, which resolved with discontinuation of cimetidine and phenytoin. She did well until June 1988 when she presented with skin lesions over the trunk and extremities. Skin biopsy revealed a leukemic infiltration. She was admitted with a WBC 1,500/microliter (without blasts), Hb 11.6 g/dl, PLT 210,000 microliter. Bone marrow biopsy revealed hypercellularity with 50% blasts, demonstrating mixed-lineage acute myeloblastic leukemia (myelomonocytic-M4; megakaryoblastic-M7). The patient was induced with a standard Ara-C/daunorubicin regimen. Two weeks postinduction, she became septic and expired. An autopsy demonstrated leukemic involvement of the spleen, liver, bone marrow, and skin, without residual dysgerminoma. This represents the first reported case of suprasellar dysgerminoma associated with a mixed-lineage leukemia not related to chemotherapy.

Adult↗
PubMed1985

Diabetes insipidus from metastatic oat cell carcinoma: recovery after brain irradiation.

A hypothalamic metastasis was demonstrated by computed tomography in a 71-year-old patient, with previously unknown small cell lung cancer, who presented with diabetes insipidus and biological signs of hypothyroidism and hypogonadism. Brain irradiation resulted in resolution of polyuria, elevation of thyroid hormones, improvement of pituitary responsiveness to hypothalamic releasing hormones, and complete disappearance of contrast-enhanced suprasellar metastasis.

Aged↗
PubMed1990

Plasma prohormone atrial natriuretic peptides 1-98 and 31-67 increase with supraventricular and ventricular arrhythmias.

Recently two peptides consisting of amino acids (AA) 1-30 and 31-67 of the N-terminus of the 126 AA prohormone of atrial natriuretic factor (pro ANF) as well as atrial natriuretic factor (ANF, AA 99-126; C-terminus) were found to have vasodilatory and natriuretic properties. These peptides as well as ANF circulate in man as part of the N-terminus of the prohormone. To determine if the polyuria, associated with both ventricular and supraventricular arrhythmias, is associated with increased circulating concentrations of the N-terminus and C-terminus of the ANF prohormone, 20 individuals with spontaneous arrhythmias, including ten persons with atrial fibrillation, six with paroxysmal supraventricular tachycardia, and four with ventricular tachycardia, were evaluated before and after conversion to sinus rhythm. In all 20 patients, the circulating concentrations of the whole N-terminus (ie, AA 1-98), the midportion of the N-terminus (pro ANF 31-67) that circulates as a distinct 3900 molecular weight peptide after being proteolytically cleaved from the N-terminus, and the C-terminus were significantly higher (p less than 0.001) than their concentration in 54 persons with sinus rhythm. With conversion to sinus rhythm, the plasma C-terminus concentration of these 20 arrhythmia patients decreased to the level of persons with sinus rhythm within 30 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Schizophrenia and fatal self-induced water intoxication with appropriately-diluted urine.

A 31-year-old woman with untreated chronic schizophrenia developed extreme polydipsia which rapidly led to coma and death due to cerebral edema. Hyponatremia (120 mEq/liter) and serum hypo-osmolality (260 mOsm/kg) were associated with marked polyuria (up to 1850 ml/hour) and appropriately low urinary osmolality (90 mOsm/kg) which responded to treatment. This case and few qualifying previous reports which are reviewed support the possibility that pure self-induced water intoxication with no major contribution of inadequate release of antidiuretic hormone may occur, and that extreme polydipsia can sometimes overwhelm normal renal diluting capacity in psychotic patients.

Adult↗
PubMed1977

Renal decapsulation in the prevention of post-ischemic oliguria.

The delayed onset of anuria/oliguria in acute tubular necrosis has been theorized to represent a complicating compartment syndrome, i.e., parenchymal swelling within an unyielding capsule. To test this proposition, 12 monkeys had suprarenal aortic cross-clamping, followed by unilateral renal decapsulation to create an experimental as well as a control kidney unit in the same animal. Histologic examination uniformly confirmed tubular necrosis at death or sacrifice. Subsequent split renal function studies (creatinine, urea, and free water clearances) indicated significantly greater maintenance of renal function by the decapsulated kidney than by its paired control. Clinical evaluation in 21 hemorrhagic shock patients, with the capsule of one kidney stripped, revealed on follow-up that 15 developed a renal failure consistent with acute tubular necrosis. Although three patients with polyuric failure died before split studies could be run and two others have been too recent for computer analysis to have been completed, nine of the remaining ten had significantly greater renal plasma flows (194 versus 121 ml/min M(2), p < .01) and significantly greater urine flows (.99 versus .18 ml/min M(2), p < .01) on the decapsulated side than on the control, as determined by differential renal scans. No significant difference in these same lateralized renal functions was noted in the tenth patient with renal failure and in the six survivors without renal failure. Renal decapsulation as prophylaxis reduced the anticipated incidence of oliguria/anuria from an expected 75% to 7% (p < .01) in these 21 shock patients. Such data suggest that delayed renal ischemia, possibly based on a compartment syndrome, may be the cause for a progression of acute tubular necrosis from polyuria to oliguria and then to anuria.

Adolescent↗
PubMed1983

Acute renal failure associated with increased intra-abdominal pressure.

Anuric renal failure developed in four patients in association with increased intra-abdominal pressure from postoperative hemorrhage. Polyuria and resolution of the renal failure occurred in each patient in response to operative decompression of the abdomen. Renal failure secondary to increased intra-abdominal pressure has been previously produced experimentally in dogs by the intraperitoneal installation of graded amounts of saline. This is the first report of this type of renal failure in clinical practice.

Abdomen↗
PubMed1995

Clinical manifestations of primary hyperparathyroidism before and after parathyroidectomy. A case-control study.

BACKGROUND: There has been an National Institutes of Health consensus meeting concerning the management of patients with "asymptomatic" primary hyperparathyroidism, yet there is no clear definition of this condition. The authors, therefore, documented the clinical manifestations and frequencies of these manifestations in unselected patients with primary hyperparathyroidism and determined whether these clinical manifestations resolved after parathyroidectomy. METHOD: The authors studied 152 unselected consecutive patients with primary hyperparathyroidism and 132 control patients with nontoxic thyroid disorders who were treated by parathyroidectomy or thyroidectomy, respectively, between January 1986 and June 1991. All patients received a questionnaire during their initial office visits and the same questionnaire again after their operations. Patients were also questioned about their perception of the success of the operation. Eighty percent of the parathyroid patients and 70.5% of the thyroid patients completed the questionnaires, and the mean follow-up time was 20 months. RESULTS: Only 7 (4.6%) patients with primary hyperparathyroidism had no symptoms, and 26 (17.1%) had no associated conditions despite 74.3% of these patients having serum calcium levels less than 12 mg/dL. Symptoms including fatigue, exhaustion, weakness, polydipsia, polyuria, nocturia, joint pain, bone pain, constipation, depression, anorexia, nausea, heartburn, and associated conditions, including nephrolithiasis, and hematuria occurred more often in patients with primary hyperparathyroidism than in the thyroid control patients (p < 0.05). After parathyroidectomy, only eight (5.3%) patients failed to have any improvement in symptoms or associated conditions. Fifty-seven percent of the parathyroid patients versus 30% of the thyroid patients felt better overall after the operation, strength subjectively improved in 29% of parathyroid patients versus 13% in thyroid patients; thirty-seven percent of the parathyroid patients versus 13% of the thyroid patients claimed they were less depressed. CONCLUSION: When examined thoroughly, few patients with primary hyperparathyroidism were asymptomatic or without associated conditions, and most patients experienced subjective improvement after successful parathyroidectomy.

Adolescent↗
PubMed1997

Upregulation of neuronal NOS mRNA in the PVN and SON of inherited diabetes insipidus rats.

We investigated the expression of neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) of rats with inherited diabetes insipidus (DI), using in situ hybridization histochemistry. The DI rats showed hypo-osmotic polyuria and polydipsia with arginine vasopressin (AVP) deficiency. The expression of nNOS gene in the PVN and SON in homozygous (di/di) rats was significantly increased in comparison to normal Wistar and heterozygous (di/+) rats. nNOS gene-expressing cells were distributed throughout the PVN and SON, including the divisions of AVP and oxytocin gene expressing cells in di/di rats. These results suggest that the expression of nNOS gene is upregulated in the magnocellular neurons in the PVN and SON of inherited DI rats.

Animals↗
PubMed1987

Ultralow doses of vasopressin in the management of diabetes insipidus.

Management of postoperative diabetes insipidus (DI) frequently requires intermittent treatment with multiple subcutaneous injections of pituitrin or vasopressin, in doses averaging 20 IU/24 h. Use of a syringe pump for a continuous infusion of ultralow doses of pituitrin produced uniform, constant, and sustained reduction of urinary output, thus facilitating regular fluid replacement. Twelve patients with postoperative DI received iv pituitrin at a dose of 1.6 +/- 0.26 mIU/kg X h (1 to 2 IU/24 h). The antidiuretic effect began at the third hour of treatment, peaked by the sixth hour (diuresis of 37 ml/h, specific gravity of 1.018 +/- 0.002), and was sustained throughout infusion. Polyuria recurred 3 h after the infusion was discontinued; this rapid reversibility is highly advantageous when excessive fluid intake causes overhydration. Pressor effects were not observed during the treatment period.

Adolescent↗
PubMed1992

Diabetes insipidus.

OBJECTIVES: To review the pathophysiology, diagnosis, and treatment of the syndromes of diabetes insipidus with an emphasis on those situations likely to be encountered in the critical care setting. DATA SOURCES: Extensive clinical experience and relevant publications from the English literature identified via MEDLINE search, citation in reviews, publications of original data, and endocrine texts. STUDY SELECTION AND DATA EXTRACTION: Landmark papers pertaining to all aspects of diabetes insipidus were selected. Reviews, primary articles, and case reports pertaining to diabetes insipidus in the critical care setting were identified and selected according to their content of clinically useful information. DATA SYNTHESIS AND CONCLUSIONS: Diabetes insipidus may result from impaired synthesis and release of vasopressin from the hypothalamic-pituitary unit (neurogenic) or renal insensitivity to circulating vasopressin (nephrogenic). A number of interventions, diseases, and drugs commonly encountered in the critical care setting may result in the development or exacerbation of diabetes insipidus. The diagnosis of diabetes insipidus requires the exclusion of other causes of polyuria and a systematic demonstration of the response of homeostatic mechanisms to controlled dehydration. The treatment of diabetes insipidus depends on many factors, including the clinical setting, degree and pathophysiologic classification, ability of the patient to compensate for free water losses, and expected duration of the abnormality. Underlying disorders should be treated appropriately whenever possible.

Blood Volume↗
PubMed1987

Chronic treatment with L-5-hydroxytryptophan prevents the development of DOCA-salt-induced hypertension in rats.

Chronic subcutaneous (s.c.) infusion (osmotic minipump) of L-5-hydroxytryptophan (L-5-HTP, 4.2 to 12.6 mg/day) to uninephrectomized, deoxycorticosterone acetate-salt-treated (DOCA) rats (1.36 mg/kg per day via s.c. silastic implants) reduced their exaggerated intake of isotonic saline significantly (12.6 mg/day), prevented the elevation of blood pressure (4.2 to 12.6 mg/day), prevented cardiac hypertrophy (12.6 mg/day), and provided modest protection against reduction of urinary concentrating ability, characteristic of DOCA-treated rats during a 24-h dehydration. The exaggerated dipsogenic response of DOCA-treated rats to administration of angiotensin II (AII, 50 and 100 micrograms/kg, s.c.) was also reduced by treatment with L-5-HTP (4.2 and 8.4 mg/day). The specific binding of AII to its receptors in membranes from the diencephalon of the brain was increased significantly above control level by chronic treatment with DOCA, but was returned to control level by concomitant treatment with L-5-HTP. Daily urinary excretion of dopamine, increased by treatment with DOCA, was unaffected by treatment with L-5-HTP (6.3 mg/day). Daily urinary excretion of epinephrine was increased by treatment with L-5-HTP (6.3 and 12.6 mg/day). These results suggest that chronic administration of L-5-HTP provides significant protection against the development of DOCA-induced hypertension, polydipsia, polyuria, and cardiac hypertrophy in rats. The mechanism by which L-5-HTP protects is unclear and remains to be established.

5-Hydroxytryptophan↗