1/45. syndrome of inappropriate antidiuretic hormone secretion associated with lisinopril.OBJECTIVE: To describe a case of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) associated with lisinopril therapy. CASE SUMMARY: A 76-year-old white woman who was being treated with lisinopril and metoprolol for hypertension presented with headaches accompanied by nausea and a tingling sensation in her arms. Her serum sodium was 109 mEq/L, with a serum osmolality of 225 mOsm/kg, urine osmolality of 414 mOsm/kg, and spot urine sodium of 122 mEq/L. diclofenac 75 mg qd for osteoarthritic pain and lisinopril 10 mg qd for hypertension was begun in 1990. lisinopril was increased to 20 mg qd in August 1994 and to 20 mg bid pm in August 1996 for increasing blood pressure; metoprolol 50 mg qd was added in July 1996. A diagnosis of SIADH was postulated and further evaluation was undertaken to exclude thyroid and adrenal causes. After lisinopril was discontinued and the patient restricted to 1000 mL/d of fluid, serum sodium gradually corrected to 143 mEq/L. The patient was discharged taking metoprolol alone for her hypertension; serum sodium has remained > or =138 mEq/L through April 1999, 32 months after discharge, despite daily use of diclofenac. DISCUSSION: Angiotensin-converting enzyme (ACE) inhibitors in antihypertensive doses may block conversion of angiotensin I to angiotensin ii in the peripheral circulation, but not in the brain. Increased circulating angiotensin I enters the brain and is converted to angiotensin ii, which may stimulate thirst and release of antidiuretic hormone from the hypothalamus, eventually leading to hyponatremia. CONCLUSIONS: SIADH should be considered a rare, but possible, complication of therapy with lisinopril and other ACE inhibitors.- - - - - - - - - - ranking = 1keywords = hypertension (Clic here for more details about this article) |
2/45. hypertension-hyponatremia syndrome in neonates: case report and review of literature.hypertension hyponatremia syndrome occurred in a 32-week male neonate following septicemic shock on Day 9. The systolic blood pressure rose from 60 to 85 mmHg as the serum sodium dropped from 136 to 121 mmol/L associated with natriuresis, polyuria, and dehydration. Convulsions occurred at a systolic blood pressure of 102 mmHg. Investigations for hypertension revealed hyper-reninemia without cardio/renovascular or neuroendocrine abnormalities. Salt supplementation and antihypertensive therapy with captopril led to resolution of natriuresis and hyponatremia. review of literature revealed associated renovascular pathology in all neonatal cases of the syndrome reported so far. Renal ischemia from possible renal microthrombi may have been the triggering event in our case. Decline in renin levels during follow-up favors this hypothesis.- - - - - - - - - - ranking = 7.9483044807677keywords = renovascular, hypertension (Clic here for more details about this article) |
3/45. Hyponatremic hypertensive syndrome.We report on a 4-year-old girl with hyponatremic-hypertensive syndrome (HHS), a rare entity in childhood. The girl was referred to us from a local hospital with a history of recurrent fever, vomiting, and seizures. On admission she was markedly dehydrated. Initial investigations revealed severe hyponatremia (serum Na 120 mmol/l), hypochloremia (serum Cl 68 mmol/l), and mild hypokalemia (serum K 3.3 mmol/l), while serum calcium and magnesium were normal. serum urea was 5 mmol/l and serum creatinine was 62 mumol/l. Despite hyponatremic dehydration, her urine output was high (2050 ml/24 h), as was her urinary sodium (168 mmol/24 h). She had massive transient proteinuria (maximal 1642 mg/24 h) while being severely hypertensive (blood pressure 210/160 mmHg). Further investigations revealed right kidney scarring, hyper-reflexive bladder dysfunction, massive brain infarcts, and myocardial left ventricular hypertrophy. Renal arteries were normal on arteriography. blood pressure control resulted in normalization of serum and urinary electrolytes and decrease of proteinuria. hyponatremia and transient massive proteinuria in this patient seem to be caused by high-pressure-forced diuresis due to malignant renoparenchymal hypertension.- - - - - - - - - - ranking = 0.33333333333333keywords = hypertension (Clic here for more details about this article) |
4/45. Central and extrapontine myelinolysis in a patient in spite of a careful correction of hyponatremia.We report the case of a 54-year-old alcoholic female patient who was hospitalized for neurologic alterations along with a severe hyponatremia (plasma Na : 97 mEq/l). She suffered from potomania and was given, a few days before admission, a thiazide diuretic for hypertension. A careful correction of plasma Na levels was initiated over a 48-hour period (rate of correction < 10 mEq/l/24h) in order to avoid brain demyelination. After a 2-day period of clinical improvement, her neurologic condition started to deteriorate. By the 5th day of admission, she became tetraplegic, presented pseudobulbar palsy, ataxia, strabism, extrapyramidal stiffness and clouding of consciousness. Scintigraphic and MRI investigations demonstrated pontine and extrapontine lesions associated with Gayet-wernicke encephalopathy. After correction of ionic disorders (hyponatremia, hypokaliemia) and vitamin B (thiamine) deficiency, the patient almost completely recovered without notable disabilities. This case illustrates that profound hyponatremia, in a paradigm of slow onset, can be compatible with life. It also demonstrates that demyelinating lesions, usually considered as a consequence of a too fast correction of hyponatremia, may occur despite the strict observance of recent guidelines. There is increasing evidence to suggest that pontine swelling and dysfunction may sometimes occur in alcoholic patients even in absence of disturbance in plasma Na levels. It is therefore of importance, while managing a hyponatremic alcoholic patient, to identify additional risk factors (hypokaliemia, hypophosphoremia, seizure-induced hypoxemia, malnutrition with vitamin b deficiency) for brain demyelination and to correct them appropriately.- - - - - - - - - - ranking = 0.33333333333333keywords = hypertension (Clic here for more details about this article) |
5/45. Transient pseudohypoaldosteronism with hyponatremia-hyperkalemia in infant urinary tract infection.PURPOSE: We describe an uncircumcised male infant and a female neonate treated for infant urinary tract infection who had multiple hormonal and electrolyte abnormalities consistent with the diagnosis of transient pseudohypoaldosteronism. MATERIALS AND methods: We retrospectively reviewed these 2 cases. RESULTS: In each case successful treatment of infant urinary tract infection was accompanied by the resolution of all hormonal and electrolyte abnormalities, including hyperaldosteronemia, hyperreninemia, hyponatremia and hyperkalemia. CONCLUSIONS: Because of future renal scarring, decreased renal function and possible hypertension, appropriate hormonal studies should be performed in infants with infant urinary tract infection who also have hyponatremia and hyperkalemia.- - - - - - - - - - ranking = 0.33333333333333keywords = hypertension (Clic here for more details about this article) |
6/45. Hyponatremic-hypertensive syndrome associated with renovascular hypertension: a case report.Renovascular hypertension occasionally manifests clinically as electrolyte disorders and albuminuria in addition to elevated blood pressure. A 49-year-old man who had renovascular hypertension also had severe hypokalemia, hyponatremia, polyuria and polydipsia that were treated by an angiotensin-converting enzyme inhibitor and resection of an atrophic kidney with a compromised blood supply. This is a case of hyponatremic-hypertensive syndrome related to renovascular hypertension and occurring as an additional abnormality.- - - - - - - - - - ranking = 25.178246775637keywords = renovascular, hypertension (Clic here for more details about this article) |
7/45. Osmotic demyelination syndrome after correction of chronic hyponatremia with normal saline.Rapid correction of severe chronic hyponatremia with hypertonic saline has been known to cause osmotic demyelination syndrome (ODS). Less recognized are the dangers of rapid correction with normal saline. A 60-year-old woman on thiazide diuretics for hypertension presented with profound hyponatremia (94 mmol/L) and hypokalemia (1.9 mmol/L) associated with volume depletion. Normal saline (2 L/day) and (KCl 40 mmol/day) were given for 5 days. serum Na concentration rose to 106 mmol/L within 18 hours. With improvement of her hyponatremia, she became more alert although the hypokalemia persisted. However, she developed progressive obtundation, quadriplegia, and respiratory failure 6 days later. magnetic resonance imaging of the brain clearly showed typical features of pontine and extrapontine myelinolysis. We suggest that the aggressive KCl supplement would have been the first-line therapy for this patient presenting with chronic hyponatremia and hypokalemia associated with volume depletion.- - - - - - - - - - ranking = 0.33333333333333keywords = hypertension (Clic here for more details about this article) |
8/45. Neonatal ascites and hyponatraemia following umbilical venous catheterization.The complications associated with umbilical venous catheterization in neonates range from pericardial effusion, portal hypertension, and peritoneal perforation with ascites, to Wharton's jelly embolism. The case of a term neonate who developed ascites and severe hyponatraemia (serum sodium 119 mmol/L) most probably following peritoneal perforation by an umbilical venous catheter is reported. The presenting feature was convulsions associated with dilutional hyponatraemia, probably following absorption of a large quantity of ascitic fluid across the peritoneum. Conservative management was associated with gradual recovery over 24 h. The case highlights that, irrespective of the route, excessive administration of salt-free fluids can lead to dilutional hyponatraemia with adverse consequences. The present case illustrates the importance of confirming intravascular positioning of umbilical catheters by ensuring free flow of blood on aspiration, to prevent/detect inadvertent peritoneal perforation. Ideally, echocardiographic confirmation of optimal intravascular placement of such catheters is preferred as radiographic confirmation is reported to be unreliable.- - - - - - - - - - ranking = 0.33333333333333keywords = hypertension (Clic here for more details about this article) |
9/45. Hyponatraemic hypertensive syndrome in two extremely low birthweight infants.Two cases of hyponatraemic hypertensive syndrome occurring in extremely low birthweight infants are presented. Both infants experienced unilateral renal ischaemia resulting in hyponatraemia and hypertension. A proposed pathophysiological mechanism, namely unilateral renal ischaemia leading to a pressure-natriuresis in the contralateral kidney, is presented. This is associated with an increase in plasma renin and aldosterone, with a paradoxical increase in urinary sodium loss. Immature renal tubular function and relative aldosterone resistance could place the extremely low birthweight infant at increased risk for the condition. The paucity of reports suggests that the condition might be under-recognized.- - - - - - - - - - ranking = 0.33333333333333keywords = hypertension (Clic here for more details about this article) |
10/45. Diuretic induced hyponatraemia in the elderly.diuretics are an important cause of symptomatic hyponatraemia in the elderly. The hyponatraemia is often associated with hypokalaemia which may play a role in the aetiology. Diuretic induced hyponatraemia must be considered in the differential diagnosis of elderly patients presenting with altered sensorium or seizures. This is especially important in those known to be hypertensives since diuretics are frequently used to treat hypertension in the elderly.- - - - - - - - - - ranking = 0.33333333333333keywords = hypertension (Clic here for more details about this article) |
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