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PubMed1991

Adrenal adenoma in a cross-bred terrier.

An adrenal tumour was diagnosed in a 12-year-old female cross-bred terrier. The dog was presented to the veterinary clinic because she had been gaining weight and had started urinating in the owners' house. Clinical findings included obesity, abdominal enlargement, thinning of the hair coat, seborrhoea sicca, and polydipsia and polyuria. The diagnosis was made by clinical pathology, endocrine function tests and abdominal radiography. Surgical removal of the neoplastic right adrenal gland resulted in resolution of the clinical signs, including regrowth of the hair coat.

Journal Article↗
PubMed1993

Canine hyperadrenocorticism.

Hyperadrenocorticism is a common endocrinopathy which results from the excessive production of cortisol by the adrenal cortex. In the majority of cases, this increased secretion of cortisol results from stimulation of the adrenal cortex by adrenocorticotrophic hormone secreted from the pituitary gland. In a smaller number of cases adrenal tumours are present. Clinical signs are variable but commonly include polydipsia and polyuria, polyphagia, obesity, a pendulous abdomen, hepatomegaly, alopecia, lethargy, weakness and anoestrus. Haematology, serum chemistry analysis and urinalysis should be performed on a dog with suspected hyperadrenocorticism. Finding a significant number of changes that are consistent with hyperadrenocorticism often allows a presumptive diagnosis to be made. Other tests can then be used to confirm the diagnosis and to help localise the cause, including liver biopsy, radiology, ultrasonography, gamma camera imaging, computed tomography, and measurement of blood and urine hormone levels. The ACTH stimulation test, low dose dexamethasone suppression test and measurement of the urine cortisol:creatinine ratio are used to assess whether hyperadrenocorticism is present. The high dose dexamethasone suppression test, measurement of plasma ACTH, corticotropin-releasing hormone stimulation test, and a modification of the urinary cortisol:creatinine ratio test are then implemented to determine the aetiology. The treatment of choice for adrenal neoplasia is surgical removal of the affected adrenal. On the other hand, pituitary hyperplasia or neoplasia may be treated either surgically, by bilateral adrenalectomy or hypophysectomy, or medically. The drug which is chosen most commonly for medical management is 1,1-dichloro-2(O-chlorophenyl)-2-(P-chlorophenyl) ethane (op'-DDD), which can be used to suppress adrenal function or to completely destroy the adrenal cortex. The antifungal agent ketoconazole also suppresses adrenal steroid synthesis and provides an alternative form of medical treatment for hyperadrenocorticoid dogs.

Journal Article↗
PubMed2006

Infectivity and persistence of an outbreak strain of Salmonella enterica serotype Typhimurium DT160 for house sparrows (Passer domesticus) in New Zealand.

AIM: To examine the infective dose, incubation period and disease progression of an isolate of Salmonella enterica serotype Typhimurium definitive type 160 (DT160) originating from a naturally-infected house sparrow (Passer domesticus) during an outbreak of the disease in New Zealand. METHODS: Thirty-six house sparrows captured from the wild and free of Salmonella spp were divided into six groups of six birds, housed individually, and inoculated orally with phosphate buffered saline (PBS) or 10(1), 10(2), 10(3), 10(5), 2 x 10(8) colony forming units (cfu) of the outbreak strain of S. Typhimurium DT160. The birds were observed for 10 days for clinical signs and/or mortality, and faecal samples were collected to determine excretion of S. Typhimurium. The birds were euthanised 11 days post-inoculation (p.i.) and a wide range of tissue samples were collected for histopathological examination, and culture and typing of Salmonella spp. Macro-restriction profiling by pulsed-field gel electrophoresis (PFGE) using XbaI was performed for the epidemiological typing of S. Typhimurium DT160 isolates. RESULTS: Mortality in house sparrows inoculated with S. Typhimurium DT160 was dose-dependent, and 2/6 birds inoculated with 10(5) cfu and all six birds inoculated with 2 x 10(8) cfu died during the study. Infected sparrows displayed few clinical signs, apart from diarrhoea and/or polyuria, fluffed plumage, and sitting on the floor of the cage. Faecal excretion of DT160 occurred briefly in two birds inoculated with 10(2) cfu and four birds inoculated with 10(3) cfu, on most days in five birds inoculated with 10(5) cfu, and continuously in six birds inoculated with 2 x 10(8) cfu. DT160 was isolated from the livers of three birds which received 10(3) cfu, five birds dosed with 10(5) cfu, and all six birds given 2 x 10(8) cfu. Following necropsy, histopathological lesions similar to those seen in the natural disease were observed in the liver or spleen of three birds which received 10(3) cfu, and all birds dosed with > or =10(5) cfu. CONCLUSION: The results indicate that an isolate of S. Typhimurium DT60 originating from house sparrows in New Zealand is pathogenic to these birds and that the response is dose dependent. The persistence and excretion of the pathogen may last for at least 10 days. This confirms that sparrows infected with DT160 could be a source of infection to humans and other in-contact animals.

Animals↗
PubMed1997

Metabolism of 36Cl-ornidazole after oral application to the male rat in relation to its antifertility activity.

1. The antimycotic ornidazole (a male antifertility agent in rats) was synthesized incorporating 36Cl in the chloropropyl sidechain and its metabolism was investigated in the male rat after oral ingestion. 2. Blood levels of radioactivity were low over the first 24 h and there was no tissue accumulation of radioactivity over 48 h. 3. Most of the excreted radioactivity (20% of the ingested dose) appeared in the urine within the first 24 h. 4. Three major compounds were detected in 0-24-h urine samples and were characterized as ornidazole (13% of total radioactivity), Cl- (22%) and 3-chlorolactate (30%), the oxidation product of 3-chlorolactaldehyde. 5. No polyuria or glucosuria was observed following the oral administration of ornidazole, suggesting that any (R)-3-chlorolactate produced was insufficient to affect renal metabolism. 6. Conversion of ornidazole initially to (R, S)-alpha-chlorohydrin or ultimately to the glycolytic inhibitor (S)-3-chlorolactaldehyde could explain its antifertility action in the male rat.

Administration, Oral↗
PubMed1998

Familial juvenile nephronophthisis. An ultrasonographic follow-up of seven patients.

PURPOSE: To evaluate progressive US changes in the kidneys of patients with familial juvenile nephronophthisis (NPH), an autosomal recessive progressive kidney disease with polyuria, polydipsia, anemia and growth retardation. MATERIAL AND METHODS: The data from 29 US investigations of 5 boys and 2 girls comprised findings relating to kidney size, echogenicity of the kidney parenchyma, visualization of the corticomedullary junction, and the parameters of renal cysts. RESULTS: In the early stages of NPH, when the serum creatinine values were between 134 and 370 micromol/l, the corticomedullary differentiation was weak in 6 patients, the echogenicity of the kidney parenchyma was equal to or greater than that of the liver in 5 patients, and 6 patients had developed renal cysts. The findings became more intensive with the progression of NPH. The size of the kidneys remained normal in 4 patients. CONCLUSION: Renal US reveals characteristic changes already in the early stages of NPH and should therefore be an important part of the diagnostics of NPH because no specific diagnostic test is as yet available.

Adolescent↗
PubMed2000

Mesangial nephropathy in Sjögren's syndrome.

We describe a 36-year-old woman with Primary Sjögren's Syndrome (PSS). Purpura, corneal perforation, metabolic acidosis, decreased glomerular filtration, hypokalemia, hyposthenuria, and polyuria were present. Chronic renal insufficiency and renal tubular acidosis type I were diagnosed. Kidney biopsy revealed mesangial glomerulonephritis, interstitial nephritis, and tubular atrophy. Replacement treatment with saliva, tears, and potassium citrate was started. She was given prednisone and cyclophosphamide. This would be the first description of PSS, mesangial glomerulonephritis, and chronic renal insufficiency.

Acidosis, Renal Tubular↗
PubMed2003

The role of sleep and arousal in nocturnal enuresis.

AIM: To review what is known about the role of sleep and arousal mechanisms in the pathogenesis of nocturnal enuresis. METHODS: A review of the literature was carried out. RESULTS: The sleep of enuretic children, although polysomnographically quite normal, is exceedingly "deep"; that is enuretic children have high arousal thresholds. Apart from some overlap between enuresis and the (other) classic parasomnias, the sleep of enuretic children is no more problematic than that of the general population. Recently, the exciting possibility has arisen that the low arousability of enuretic children may be linked to the autonomous nervous system and to disturbances in the upper pons. CONCLUSIONS: Enuresis is not just a nocturnal problem but a disorder of sleep. The high arousal threshold is one of three major pathogenetic factors in enuresis-nocturnal polyuria and detrusor hyperactivity being the other two.

Autonomic Nervous System↗
PubMed2006

Infantile polyarteritis nodosa presenting as hyponatraemic hypertensive syndrome.

UNLABELLED: The association of arterial hypertension with hyponatraemic dehydration, known as hyponatraemic hypertensive syndrome (HHS), is a rare and serious hypertensive complication. Here, we describe a 17-mo-old girl who presented with severe hyponatraemic dehydration, hypokalaemia, polyuria, and nephrotic-range proteinuria associated with malignant arterial hypertension and systemic inflammatory disease. Diagnosis of classic polyarteritis nodosa (c-PAN) was made on the basis of renal arteriography demonstrating small arterial aneurysms in association with non-aneurismal changes such as arterial cut-off, arterial tapering stenosis and nephrogram perfusion defect. A decrease of blood pressure by antihypertensive treatment resulted in the normalization of HHS abnormalities. However, c-PAN became well controlled only after 4 mo of immunosuppressive therapy. CONCLUSION: The main interest of this case was the uncommon presentation of systemic polyarteritis nodosa in a very young child. Renal ischaemia from intrarenal vessel disease may have been the trigger event for HHS in our case. Management of PAN-associated severe arterial hypertension is based on immunosuppressive and antihypertensive treatment.

Female↗
PubMed1996

Respiratory distress, weakness, and electrolyte abnormalities.

A 56-year old man was admitted to the hospital with malaise, weakness, and fatigue. He was short of breath and had bilateral foot edema. Even though he had been very active a month earlier, he could no longer climb stairs. For the last two weeks, he had had a cough producing green sputum, a "tight feeling" in his chest, polyuria, and polydipsia. He had not had radiating chest pain, palpitations, leg pain or erythema, hemoptysis, diaphoresis, flushing, fever, chills, nausea, vomiting, diarrhea, or a loud snore.

Adrenocorticotropic Hormone↗
PubMed1998

A woman with sudden paralysis.

A 37-year-old Hispanic woman complained of having awakened with a tingling sensation, followed by sudden weakness, in both legs. A month earlier, she had experienced heart palpitations but had not had chest pain or dyspnea. She had lost 10 lb in the last two months despite an increased appetite and no polyuria, polydipsia, vomiting, or diarrhea.

Adult↗
PubMed1976

Hydrostatic pressure treatment for carcinoma of the bladder. A clinical and urodynamic evaluation of the effect on bladder hemorrhage and fibrosis in irradiated patients.

Hydrostatic pressure treatment as described by Helmstein was given to 12 patients with hematuria secondary at irradiation for carcinoma of the bladder. The bladder function was evaluated on the basis of urodynamic examinations before and after the treatment. The study includes examination of the effect on the renal function. In 6 patients, hemostasis was obtained for a period averaging 10 months. No serious complications occurred. Following irradiation, the patients showed a characteristic micturition pattern with a small bladder capacity and a marked increase in pressure during the filling phase. The micturition took place partly by use of the abdominal musculature; the detrusor pressure was falling during the whole voiding time. The voiding was almost complete, and the flow values were slightly reduced. The hydrostatic pressure treatment resulted in no demonstrable changes in this micturition pattern. Evaluated from the creatinine clearance, the renal function was unchanged after the treatment, and neither polyuria nor an increased excretion of sodium was demonstrated during the first hours after the treatment. We conclude that before major surgery is decided on, hydrostatic pressure treatment should be given to patients with hemorrhage following irradiation for carcinoma of the bladder. No improvement can be expected in patients where the often pronounced pollakiuria is due to fibrosis of the bladder secondary to irradiation.

Aged↗
PubMed2003

Transient gestational diabetes insipidus: report of two cases and review of pathophysiology and treatment.

Gestational diabetes insipidus is a rare disorder characterized by polyuria and polydipsia due to the inability of the kidneys to concentrate urine. We report two cases of transient gestational diabetes insipidus in which patients responded to intranasal DDAVP (1-deamino-8-D-arginine vasopressin) with greater than 50% increase in urine osmolality and marked reduction in urine output. Intranasal DDAVP was discontinued after their discharge and both patients maintained normal urine output and appropriate urine osmolality. In determining whether diabetes insipidus is present in a patient who is polyuric and hypernatremic, a urine osmolality below that of the plasma suggests the presence of diabetes insipidus. Understanding of the pathophysiology may soon lead to improved methods of prevention, diagnosis and treatment.

Adult↗
PubMed2001

Effect of chronic treatment with losartan on streptozotocin induced diabetic nephropathy.

Angiotensin converting enzyme (ACE) inhibitors produce a number of beneficial effects in a condition where diabetes - mellitus and hypertension co-exist. The present investigation was undertaken to study the effect of chronic treatment with losartan (2mg/kg, p.o.) on streptozotocin (STZ)-induced (45mg/kg, single dose, tail vein) diabetic nephropathy in rats. Treatment of rats with STZ produced a significant loss of body weight, polyuria. polydipsia, hypoinsulinemia, hyperglycemia and increase in blood pressure. There was a significant increase in blood glucose levels in STZ-diabetic rats. Serum cholesterol, creatinine, urea and blood urea nitrogen (BUN) levels were found to be increased significantly in the STZ group diabetic rats. Treatment with losartan significantly prevented the raise in cholesterol, creatinine, urea and blood urea nitrogen levels. Creatinine clearance was significantly less in STZ-diabetic rats as compared to control animals and treatment with losartan significantly increased creatinine clearence. Our data suggest a beneficial effect of losartan in STZ-induced nephropathy in rats.

Animals↗
PubMed2001

Early administration of PDTC in adriamycin nephropathy: effect on proteinuria, cortical tubulointerstitial injury, and NF-kappaB activation.

The persistence of NF-kappaB independent inflammatory signals in the cortical tubulointerstitium may explain the incomplete suppression of interstitial monocyte accumulation by the antioxidant NF-kappaB inhibitor, pyrrolidine dithiocarbamate (PDTC), in nephrotic rats with established Adriamycin nephropathy (AN). Because PDTC is known to have anti-proteinuric effects, in this study we investigated whether earlier commencement, during the pre-nephrotic phase of AN, would be more effective in reducing interstitial monocyte accumulation. Male Wistar rats with AN received either vehicle or PDTC (50 mg/kg bd i.p.i.) from d7 until d30 (n = 8 per group). On d30, PDTC reduced renal cortical lipid peroxidation (43%), wet kidney weight and tubulointerstitial injury in AN, but did not decrease proteinuria. Accordingly, inhibition of interstitial ED-1 accumulation remained incomplete (52%). Interestingly, the early administration of PDTC in AN, induced polyuria and renal cortical NF-kappaB DNA-binding activity was reduced by only 35%. These results suggest that: (i) the combination of an anti-proteinuric agent with PDTC may be required to completely suppress interstitial monocyte cell accumulation in AN and, (ii) the timing and duration of PDTC therapy are an important determinant of its efficacy to reduce NF-kappaB activation, in vivo.

Animals↗
PubMed2003

Study of serum and tissues angiotensin converting enzyme (ACE) activity in rat with gentamicin induced renal toxicity.

PURPOSE: In this research ACE activity (as a marker of epithelial injury) was studied in rats with gentamicin induced renal toxicity. METHODS: Male Sprague-Dawley rats were sacrificed 1, 3, 5, and 7 days after gentamicin injection, 100 mg/kg/day for 1, 3, 5, and 7 consecutive days. ACE activity was measured in serum, kidney and lung. These data were compared with normal saline-treated rats. Histological scoring of renal cortical pathology was performed on days 1, 3, 5, and 7. RESULTS: Treatment of rats with gentamicin resulted in renal damage evidenced by proteinuria, polyuria, and decreased creatinine clearance. The damage to the kidney proximal tubule was evident by (a) the histological analysis at light microscopy and (b) the augmentation in the urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG). Kidney ACE activity decreased while lung and serum ACE activity didn't change until day 7. Lung ACE activity increased significantly on day 7. Kidney and serum ACE activity increased too. Blood pressure increased significantly on day 7. This corresponded well with the lung ACE activity increment. CONCLUSION: These data suggest that kidney ACE activity decreased significantly just one day after gentamicin administration and prior to kidney NAG decrease.

Acute Kidney Injury↗
PubMed1998

Multidrug resistance protein 1 protects the oropharyngeal mucosal layer and the testicular tubules against drug-induced damage.

The multidrug resistance protein 1 (MRP1) gene encodes a transporter protein that helps to protect cells against xenobiotics. Elevated levels of MRP1 in tumor cells can result in active extrusion of a wide range of (anticancer) drugs with different cellular targets, a phenomenon called multidrug resistance (MDR). To explore the protective function of the mouse mrp1 protein during drug treatment, we investigated the toxicity caused by the anticancer drug etoposide-phosphate (ETOPOPHOS) in mice lacking the mrp1 gene (mrp1(-/-) mice). We show here that the lack of mrp1 protein results in increased etoposide-induced damage to the mucosa of the oropharyngeal cavity and to the seminiferous tubules of the testis. The high concentrations of mrp1 that we find in the basal layers of the oropharyngeal mucosa and in the basal membrane of the Sertoli cells in the testis apparently protect wild-type mice against this tissue damage. We also find drug-induced polyuria in mrp1(-/-) mice, which correlates with the presence of mrp1 protein in the urinary collecting tubules, the major site of kidney water reabsorption. Our results indicate that specific inhibitors of MRP1 used to reverse MDR, in combination with carcinostatic drugs transported by MRP1, might lead to drug-induced mucositis, (temporary) infertility, and diabetes insipidus.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1998

Novel molecular variants of the Na-K-2Cl cotransporter gene are responsible for antenatal Bartter syndrome.

Antenatal Bartter syndrome is a variant of inherited renal-tubular disorders associated with hypokalemic alkalosis. This disorder typically presents as a life-threatening condition beginning in utero, with marked fetal polyuria that leads to polyhydramnios and premature delivery. Another hallmark of this variant is a marked hypercalciuria and, as a secondary consequence, the development of nephrocalcinosis and osteopenia. We have analyzed 15 probands belonging to 13 families and have performed SSCP analysis of the coding sequence and the exon-intron boundaries of the NKCC2 gene; and we report 14 novel mutations in patients with antenatal Bartter syndrome, as well as the identification of three isoforms of human NKCC2 that arise from alternative splicing.

Amino Acid Sequence↗
PubMed2002

Reduced nephrotoxicity of conventional amphotericin B therapy after minimal nephroprotective measures: animal experiments and clinical study.

Amphotericin B (AmB)-treated rats develop severe polyuria, polydypsia, impairment of renal concentrating ability, and morphologic signs of tubular damage. However, renal insufficiency develops quickly only in animals in which water intake is restricted to the median volume drunk by rats of the control group. Therefore, vigorous hydration seems crucial for prevention of AmB-induced nephrotoxicity. In a clinical study, 61 patients with hematologic malignancies receiving AmB therapy were massively hydrated to ensure urine output of > or =4000 mL/day. Urine sodium, potassium, and magnesium were also measured, and all losses were supplemented (potassium as a 7.45% solution via central venous catheter). AmB-treated patients developed signs of renal tubular damage (increased fractional excretion of sodium and potassium) and required large amounts of ion supplementation. The serum ion concentration and creatinine clearance remained stable. No clinically significant renal damage developed to force premature cessation of AmB treatment.

Acetylglucosaminidase↗