Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A woman in her mid-forties had repeated vomiting and diarrhoea accompanied by muscle weakness soon after she started taking seven different diet pills imported from Thailand. After she had taken the pills for 8 days, respiratory depression progressed rapidly to arrest. Blood tests at the Emergency Department showed severe hypokalaemia with metabolic alkalosis. We diagnosed that she had developed pseudo-Bartter syndrome from the findings based on ionic abnormalities and high renin and aldosterone levels, and hyperplasia of the juxtaglomerular apparatus. A postmortem blood analysis indicated subtherapeutic levels of furosemide. We concluded that the patient died from pseudo-Bartter syndrome, which was triggered by chronic self-administration of furosemide and aggravated by the diet pills. This is the first pseudo-Bartter syndrome autopsy report to show histological localisation of calcification in the kidneys.
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PMID:Autopsy report on pseudo-Bartter syndrome with renal calcification induced by diuretics and diet pills. 2168 46

An 18-year-old woman with Gitelman syndrome (GS) associated with idiopathic intracranial hypertension (IIH) is described. She was obese and showed a 10 kg gain in body weight over a period of 8 months. She presented with headache, vomiting, and diplopia. She had bilateral papilledema, and right abducens palsy. CSF examination demonstrated high pressure (over 320 mmH(2)O) with normal cytochemistry. Brain MRI was normal. She showed mild alkalosis, hypokalemia, hypomagnesemia, increased plasma renin activity, and normal blood pressure. Two heterozygous mutations in the SLC12A3 gene were identified. Therefore, she was diagnosed as GS with IIH. We should keep in mind the possible occurrence of IIH in GS.
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PMID:A case of Gitelman syndrome associated with idiopathic intracranial hypertension. 2175 36

Neuroblastoma is the most common extracranial solid tumor in childhood. Its presenting signs and symptoms may be highly variable, depending on the location of the primary tumor and its local or metastatic diffusion and, rarely, with paraneoplastic syndrome such as opsoclonus-myoclonus-ataxia syndrome and gastrointestinal disturbances, due to autoantibodies or to aberrant secretion of vasoactive intestinal peptide. Herein we describe a 10-month-old child with neuroblastoma presenting with a complex clinical picture characterized by acute kidney injury manifested by renal insufficiency and signs and symptoms of tubulointerstitial damage, with polyuria, polydipsia, glucosuria, aminoaciduria and hypochloremic metabolic alkalosis, and of glomerular damage with heavy proteinuria. Imaging study documented a suprarenal mass enveloping the aorta and its abdominal and renal ramifications and bilaterally renal veins. This clinical picture shows some analogies with the hyponatremic-hypertensive syndrome concerning the renovascular disease; however, in absence of systemic arterial hypertension, the heavy proteinuria and the polyuria could be explained by sectional increased intraglomerular pressure, due to local renal blood vessels constriction. Hypochloremic metabolic alkalosis probably developed because of local production of renin, responsible of renin-angiotensin-aldosterone system activation, but above all because of chloride loss through sweating. The long lasting dehydration, due to vomiting, sweating and polyuria, caused prolonged prerenal failure evolving in proximal tubular damage manifestations.
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PMID:Neuroblastoma presenting with acute kidney injury, hyponatremic-hypertensive-like syndrome and nephrotic proteinuria in a 10-month-old child. 2194 89

Pheochromocytomas have been described to be associated with rare vascular abnormalities, most common of them being renal artery stenosis. A 45-year-old woman was admitted to our hospital with complaints of headache, sweating, anxiety, dizziness, nausea, vomiting and severe hypertension. Hypertension was confirmed to result from both excess catecholamine production and hyperreninemia of left kidney. The technical images (abdominal CT and renal arteriography) revealed the presence of a left adrenal pheochromocytoma and stenosis of the renal artery. Surgical removal of pheochromocytoma and correction of renal artery stenosis restored the postoperative plasma catecholamine, renin and blood pressure to normal. To our belief, this is the first such case report from India citing this rare association. We conclude that when the two diseases occur simultaneously, both must be diagnosed accurately and treated in a different manner. We also hereby review the existing literature.
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PMID:Pheochromocytoma with renal artery stenosis: A case-based review of literature. 2234 44

Antenatal Bartter syndrome (ABS) is a rare autosomal recessive renal tubular disorder. The defective chloride transport in the loop of Henle leads to fetal polyuria resulting in severe hydramnios and premature delivery. Early onset, unexplained maternal polyhydramnios often challenges the treating obstetrician. Increasing polyhydramnios without apparent fetal or placental abnormalities should lead to the suspicion of this entity. Biochemical analysis of amniotic fluid is suggested as elevated chloride level is usually diagnostic. Awareness, early recognition, maternal treatment with indomethacin, and amniocentesis allow the pregnancy to continue. Affected neonates are usually born premature, have postnatal polyuria, vomiting, failure to thrive, hypercalciuria, and subsequently nephrocalcinosis. Hypokalemia, metabolic alkalosis, secondary hyperaldosteronism and hyperreninaemia are other characteristic features. Volume depletion due to excessive salt and water loss on long term stimulates renin-angiotensin-aldosterone system resulting in juxtaglomerular hyperplasia. Clinical features and electrolyte abnormalities may also depend on the subtype of the syndrome. Prenatal diagnosis and timely indomethacin administration prevent electrolyte imbalance, restitute normal growth, and improve activity. In this paper, authors present classification, pathophysiology, clinical manifestations, laboratory findings, complications, and prognosis of ABS.
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PMID:Antenatal bartter syndrome: a review. 2251 85

A 3-year-old girl presented to the emergency department with seizures, low-grade fever and vomiting. She had tachycardia and a slow capillary refill. Blood pressure could not be measured. Because of suspected sepsis and/or meningo-encephalitis, broad spectrum antibiotics and antiviral medication were given together, along with volume expansion and anticonvulsive therapy. A few hours later, after a second seizure, the blood pressure was extremely high (156/116 mm Hg). The girl was treated with anticonvulsants and intravenous antihypertensive agents. MRI of the brain showed signs of posterior reversible encephalopathy syndrome. Cultures of blood and cerebrospinal fluid remained sterile. Further investigation into the cause of the malignant hypertension revealed hypokalemia, metabolic alkalosis and extremely high plasma renin activity, caused by a rare renal abnormality: bilateral renal segmental hypoplasia or Ask-Upmark kidneys.
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PMID:A 3-year old girl with seizures, hypokalemia and metabolic alkalosis. 2279 82

Inherited classic Bartter syndrome (cBS) is an autosomal recessive renal tubular disorder resulting from inactivating mutations in the asolateral chloride channel (C1C-Kb) and usually presents in early infancy or childhood with mild to moderate hypokalemia. Profound hypokalemic paralysis in patients with cBS is extremely rare, especially in middle age. A 45-year-old Chinese female patient was referred for evaluation of chronic severe hypokalemia despite regular K+ supplementation (1 mmol/kg/d). She had had two episodes of muscle paralysis due to severe hypokalemia (K+ 1.9 - 2.1 mmol/l) in the past 3 years. She denied vomiting, diarrhea, or the use of laxatives or diuretics. Her blood pressure was normal. Biochemical studies showed hypokalemia (K+ 2.5 mmol/l) with renal potassium wasting, metabolic alkalosis (HCO3- 32 mmol/l), normomagnesemia (Mg2+ 0.8 mmol/l), hypercalciuria (calcium to creatinine ratio 0.5 mmol/mmol; normal < 0.22 mmol/mol), high plasma renin activity, but normal plasma aldosterone concentration. Abdominal sonography revealed neither renal stones nor nephrocalcinosis. Acquired causes of cBS such as autoimmune disease and drugs were all excluded. Molecular analysis of the CLCNKB gene, encoding ClC-Kb, and SLC12A3, encoding the thiazide-sensitive sodium chloride cotransporter (NCC), revealed compound heterozygous mutations in CLCNKB (L335P and G470E) inherited from her parents; her SLC12A3 was normal. These two mutations were not identified in 100 healthy subjects. Her plasma K+ concentration rose to 3 - 3.5 mmol/l after the addition of spironolactone. Inherited cBS may present with hypokalemic paralysis and should be considered in adult patients with hypokalemia and metabolic alkalosis.
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PMID:Hypokalemic paralysis in a middle-aged female with classic Bartter syndrome. 2285 65

Water intoxication is a life-threatening disorder accompanied by brain function impairment due to severe dilutional hyponatremia. We treated a 22-year-old man without psychotic illness who had been put in a detention facility. He drank 6 liters of water over a 3-hour period at the facility as a game's penalty, and he showed progressive psychiatric and neurological signs including restlessness, peculiar behavior and convulsions. On his admission, 15 h after the discontinuation of the water drinking, he was in a coma, showing intermittent convulsions and remarkable hyponatremia (120 mmol/l). Because his laboratory tests showed hypertonic urine and normal sodium excretion, the diagnosis of secondary development of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was strongly suggested and later confirmed by the suppression of the renin-aldosterone system and the inappropriately elevated secretion of ADH. Saline infusion and an initial administration of furosemide in addition to dexamethasone as treatments for the patient's brain edema successfully improved his laboratory data and clinical signs by the 3rd hospital day, and he was returned to the facility without physical or psychiatric abnormalities on the 6th day. The secondary SIADH might have been due to the prolonged emesis, recurrent convulsions and rapid elevation of intracranial pressure.
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PMID:A case of water intoxication with prolonged hyponatremia caused by excessive water drinking and secondary SIADH. 2457 Jun 85

Resistant hypertension is a common and refractory complication of hemodialysis (HD) patients and is associated with a higher risk of cardiovascular morbidity and mortality. Here we present a case of resistant hypertension treated successfully by nocturnal HD. A 63-year-old female with end-stage kidney disease was hospitalized for severe headache, objective vertigo and persistent vomiting for 1 month on February 6, 2012. She had been on intermittent HD for 3 months, and her blood pressure maintained 200-240/100-130 mm Hg even after using 7 kinds of antihypertensive drugs including olmesartan, benazepril, nitrendipine, arotinolol, terazosin, clonidine and torasemide. A CT of the abdomen revealed a mild hyperplasia of the left adrenal gland (fig. 1). However, plasma renin, angiotensin and aldosterone were all within the normal range. Nocturnal extended HD was initiated with a blood flow rate of 150 ml/min and a dialysis time of 7 h. After 3 months of nocturnal HD, all symptoms were relieved and her systolic blood pressure started to decrease by 10-20 mm Hg. Six months later, the predialysis blood pressure was decreased to 140-160/90-100 mm Hg and the antihypertensive drugs were reduced to 4 kinds. Meanwhile, the blood biochemical parameters including hemoglobin, serum calcium, phosphate and parathyroid hormone were all controlled well during 2 years of treatment. This case indicates that nocturnal extended HD is probably a promising and effective choice for resistant hypertension in HD patients.
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PMID:Improvement of resistant hypertension by nocturnal hemodialysis in a patient with end-stage kidney disease. 2587 95

A 54-year-old woman presented with a history of nausea, vomiting, diarrhea, and recurrent episodes of severe hypokalemia requiring hospitalization. Imaging revealed a pancreatic mass with liver metastases, histologically confirmed to be a neuroendocrine tumor. Elevated active renin and aldosterone levels were identified, and the patient was treated with 4 induction cycles of Lu-DOTATATE, which resolved the diarrhea, nausea, and hypokalemia, and normalized the renin and aldosterone levels. After 3 additional maintenance Lu-DOTATATE treatments, the pancreatic tumor had decreased in size, was deemed operable, and was resected. She remains on maintenance Lu-DOTATATE therapy with progression-free survival of 45 months thus far.
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PMID:Resolution of Hyperreninemia, Secondary Hyperaldosteronism, and Hypokalemia With 177Lu-DOTATATE Induction and Maintenance Peptide Receptor Radionuclide Therapy in a Patient With Pancreatic Neuroendocrine Tumor. 2635 64


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