Cases reported "Alkalosis"

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1/184. Neutral phosphate-induced renal tubular metabolic alkalosis.

    A severely burned patient receiving neutral phosphate supplement developed renal tubular alkalosis. This phenomenon is compared with the results of experimental observations on animals, reported in the literature. The physiologic mechanism, including the possible role of parathyroid hormone, is illustrated. ( info)

2/184. Gitelman's syndrome: report of a 19-year old woman with intractable hypomagnesemia and hypokalemia, and a review of the syndrome.

    A case of refractory hypomagnesemia associated with hypokalemic alkalosis and hypocalciuria (Gitelman's syndrome) is described. The genetic mutations discovered to cause the hypokalemic alkalotic syndromes are described (the thiazide-sensitive sodium chloride co-transporter gene or TSC mutations in Gitelman's syndrome, and the sodium-potassium-chloride co-transporter gene or NKCC2 mutations in Bartter's syndrome). The molecular, electrolyte, and volume abnormalities are described, and the implications for diagnosis, therapy, and future research discussed. ( info)

3/184. Saline-resistant metabolic alkalosis, severe hypokalemia and hypertension in a 74-year-old woman.

    The case of a 74-year-old woman with past history of hypertension and cerebrovascular accident admitted with pneumonia, dehydration, hypernatremia and severe hypokalemic alkalosis is presented. After correction of the hypertonic dehydration, the hypokalemia and alkalosis persisted in spite of aggressive potassium supplementation and the patient became hypertensive. Mineralocorticoid excess was suspected and excluded after extensive endocrinological testing. The use of aldactone failed to revert the abnormalities. triamterene administration corrected the electrolytes and acid base aberrations, and dramatically improved the blood pressure control. This clinical picture is compatible with the diagnosis of Liddle's syndrome. Our patient exemplifies the unique occurrence of hypokalemic metabolic alkalosis in association with volume contraction at the start of the hospitalization and volume expansion later on her course. ( info)

4/184. Liddle's syndrome: a report in a middle-aged woman.

    A 54-year-old woman with diabetes mellitus was hospitalized with generalized edema and weakness. She was also found to have hypertension, hypokalemia and metabolic alkalosis. Detailed examination showed subnormal plasma renin activity and plasma aldosterone concentration. Adrenal CT scanning revealed no adrenal tumor. A successful treatment with amiloride established the diagnosis of Liddle's syndrome for the patient. Liddle's syndrome, a rare hereditary disease usually found in young patients, should be considered in the differential diagnosis of hypertension even in elderly individuals. ( info)

5/184. hypokalemia and metabolic alkalosis: algorithms for combined clinical problem solving.

    This article reviews an approach to patients with hypokalemia and metabolic alkalosis using the information obtained from spot urine chloride values, blood pressure determinations, and renin and aldosterone measurements in order to simplify clinical problem solving. ( info)

6/184. Marked hyperlactatemia associated with severe alkalemia in a patient with thrombotic thrombocytopenic purpura.

    This report describes a case of severe alkalemia associated with a blood lactate level greater than 13 mEq/L in a patient without evidence of hypotension or hypoxemia. The patient, who had the clinical manifestations of thrombotic thrombocytopenic purpura (TTP), developed the alkalemia from an acute respiratory alkalosis superimposed on an existing metabolic alkalosis. Profound alkalemia may impair oxygen delivery because of stronger hemoglobin-oxygen affinity, vasoconstriction, and alterations in the redox potential of cytochrome c. We suggest that the synergistic effects of a sudden, extreme alkalemia and the localized tissue hypoxia that resulted from extensive microvascular thrombi secondary to TTP caused the patient's hyperlactatemia. ( info)

7/184. syndrome of hypokalemic metabolic alkalosis and hypomagnesemia associated with gentamicin therapy: case reports.

    Nephrotoxicity, as evidenced by renal insufficiency is a well-known consequence of gentamicin therapy. We report two patients with gentamicin-induced syndrome of hypokalemic metabolic alkalosis and hypomagnesemia. Both had complete recovery of renal tubular function after cessation of antibiotic therapy. These cases emphasize the need to routinely monitor patients receiving gentamicin therapy for electrolyte abnormalities to avoid potential morbidity. ( info)

8/184. nephrocalcinosis and renal cysts associated with apparent mineralocorticoid excess syndrome.

    Apparent mineralocorticoid excess (AME) syndrome is a rare inherited disorder caused by 11beta-hydroxysteroid dehydrogenase (11-HSD 2) isozyme deficiency in the kidney. This enzyme is responsible for oxidizing cortisol to its inactive metabolite cortisone. An elevated tetrahydrocortisol (THF) and allotetrahydrocortisol (aTHF) to tetrahydrocortisone (THE) ratio in the urine is pathognomonic of AME syndrome. Clinical features include hypertension, hypokalemia, alkalosis, reduced plasma renin activity (PRA), low aldosterone levels, and occasionally nephrocalcinosis. Here we describe a 13-year-old boy who presented with severe hypertension, hypokalemia, low PRA and aldosterone levels, and elevated THF plus aTHF/THE ratio in the urine consistent with a diagnosis of AME syndrome. On ultrasound examination, he had severe nephrocalcinosis, and bilateral renal cysts. Renal cysts have not been previously reported in AME syndrome. The development of nephrocalcinosis and renal cysts may be associated with chronic long-standing hypokalemia. An early diagnosis and treatment of AME syndrome could help to prevent these sequelae, and to preserve renal function. ( info)

9/184. Approach to the patient with hypertension, unexplained hypokalemia, and metabolic alkalosis.

    We present a patient with hypertension and hypokalemia secondary to an aldosterone-producing adenoma that was renin responsive (APARR). We discussed the sequential approach to the diagnosis of the different subtypes of primary aldosteronism and confirmed the presence of an APARR. The most common cause of primary aldosteronism is an aldosteronoma; functionally, these adenomas respond poorly to angiotensin ii but show a brisk response to adrenocorticotropin hormone. They have a pattern of aldosterone level that declines in parallel with cortisol levels. Our patient had an APARR, with an increase of aldosterone in the upright posture. The unusual physiologic response, incidence, and clinical characteristics of APARR are reviewed. ( info)

10/184. Sixty-eight-year-old patient with hypokalemia.

    A 68-year-old patient with severe hypokalemia and metabolic alkalosis is described. Six years before admission he had been treated for a small cell bronchial carcinoma. We discuss the diagnostic approach of hypokalemia and the way in which we reached the diagnosis. The patient suffered from metastatic small cell carcinoma with a very high plasma adrenocorticotropic hormone concentration, possibly due to production of corticotropin-releasing hormone by the malignancy. ( info)
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