1/18. 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.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
2/18. 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.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
3/18. Extreme metabolic alkalosis treated with normal bicarbonate hemodialysis.Metabolic alkalosis (MA), defined as a primary increment in plasma bicarbonate concentration, is a common complication in hospitalized patients and is associated with high morbidity and mortality in severe cases. One of the major routes of compensation for MA (ie, the secretion of an alkaline urine) is lost in renal failure patients. We report three cases involving four episodes of extreme MA with an arterial pH value greater than 7.60, serum bicarbonate concentration greater than 55 mmol/L, and stupor or seizure. Profound vomiting or massive gastric drainage combined with concurrent oliguric renal failure was the underlying mechanism for severe MA. Hydration and normal central venous pressure failed to improve the MA. The extreme MA was reversed quickly and safely by conventional hemodialysis with normal bicarbonate dialysate of 25 to 28 mmol/L. To our knowledge, this is the first reported successful use of normal bicarbonate dialysate in the treatment of severe MA. We also found that either H(2) blockers or proton-pump inhibitors have a prophylactic effect on the formation of MA.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
4/18. Severe hypomagnesaemia-induced hypocalcaemia in a patient with Gitelman's syndrome.Gitelman's syndrome (GS) is characterized by hyperreninaemic hyperaldosteronism, hypokalaemia, metabolic alkalosis, hypomagnesaemia and hypocalciuria and is due to a defect of the Na-Cl cotransporter at the distal tubule, which may appear in a sporadic or in a familial form. It is an autosomal recessive disorder associated with normal or reduced blood pressure. We report a case of severe hypomagnesaemia-induced hypocalcaemia in a 39-year-old Caucasian woman with GS. The patient had impaired parathormone (PTH) responsiveness to peripheral stimuli, as proved by the marked PTH increase and normalization of plasma calcium levels after acute and chronic administration of magnesium salts. Secondary normotensive hyperreninaemic hyperaldosteronism with hypokalaemia and metabolic alkalosis was also present. Normal plasma renin activity (PRA) and aldosterone levels were restored by administration of an inhibitor of prostaglandin synthesis. The electrolyte imbalance was successfully corrected with chronic treatment with magnesium and potassium salts. Genetic analysis identified a compound heterozygous mutation in the Na-Cl cotransporter gene (NCCT), confirming the diagnosis of GS. The striking feature of this case of GS was impaired PTH responsiveness to peripheral stimuli determined by hypomagnesaemia and the resulting severe hypocalcaemia, which had not previously been described in this syndrome.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
5/18. Electrocardiographic QT prolongation and sudden death in renal hypokalemic alkalosis.A 3-year-old boy was found to have a mixed tubulopathy with hypokalemia (1.9 mmol/l), alkalosis (blood pH 7.51, plasma carbon dioxide pressure 46 mm Hg, plasma bicarbonate 35.7 mmol/l) and hypophosphatemia (1.21 mmol/l). An electrocardiogram disclosed a prolonged heart rate corrected QT interval of 490 ms. The boy was put on potassium chloride, phosphate and nonsteroidal anti-inflammatory agents. With this treatment plasma phosphate normalized and plasma potassium increased up to 3.0-3.3 mmol/l. Three years later the child, who did not have history of gastroesophageal reflux or epileptic convulsions, suddenly died during sleep. The cause of death could not be determined through gross examination of the body. The history of hypokalemia, the QT-prolongation, the sudden death and the failure to assess the cause of death through gross examination of the body suggest that death was caused by an arrhythmia secondary to hypokalemia.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
6/18. liddle syndrome in a newborn infant.A 10-week-old female infant developed hypertension. The elevated blood pressure was associated with metabolic alkalosis and urinary chloride wastage. The family history was unremarkable. Her urinalysis, blood urea nitrogen (BUN), and serum creatinine concentrations were all normal. A renal ultrasound was normal. A technetium-99m diethylenetriaminopentoacetic acid (DTPA) renal scan with captopril showed normal blood flow bilaterally. The head ultrasound and echocardiogram were normal. Blood epinephrine, norepinephrine, catecholamines, thyroxine, and steroid levels were also normal. Treatment with various combinations of labetalol, hydralazine, captopril, methyldopa, nifedipine, and spironolactone, all at high doses, failed to control the elevated blood pressure. serum aldosterone level and peripheral plasma renin activity were low. The lack of therapeutic response to spironolactone, with a good response to amiloride and recurrence of hypertension and metabolic alkalosis after amiloride cessation that was subsequently treated with amiloride, established the diagnosis of liddle syndrome. To our knowledge, this is the youngest patient with liddle syndrome that has been reported in the literature.- - - - - - - - - - ranking = 2keywords = pressure (Clic here for more details about this article) |
7/18. Hypokalemic metabolic alkalosis--three case reports.The two most common forms of inherited normotensive hypokalemic metabolic alkalosis are Bartter's and Gitelman's syndromes. Bartter's syndrome typically present with normal or increased calcium excretion. Hypomagnesemia occurs in only one third of affected individuals. In contrast, hypomagnesemia and hypocalciuria are considered hallmarks of Gitelman's syndrome. In most patients, the symptom of muscle weakness and polyuria occur early in life, which may be attributed to potassium depletion. Despite hyperaldosteronism, the patients tend to be normotensive, which is at least explained by vascular hyperresponsiveness to prostaglandins. Therapeutic approaches to Bartter's and Gitelman's syndromes include potassium supplementation, prostaglandin synthesis inhibitors (nonsteroid anti-inflammatory agents), aldosterone antagonists and converting enzyme inhibitors. Three patients with hypokalemia, normal blood pressure, metabolic alkalosis, hyperreninemia and hyperaldosteronism are described. Two patients had Bartter's syndrome and one patients had Gitelman's syndrome.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
8/18. Severe hypotension during hemofiltration in an uremic patient with metabolic alkalosis.We describe a case of medication induced metabolic alkalosis in a maintenance dialysis patient who developed severe hypotension while undergoing a lactate hemofiltration procedure. A 73-year-old man with ESRD due to renovascular disease was used to ingesting up to 30 grams per day of a non-prescription medication (Effervescent granulare 250 grams, CRASTAN, Pisa italy) consisting of sodium bicarbonate, citric acid, glucose and lemon flavor. For technical problem lactate hemofiltration was performed and thirty minutes after dialysis was started a severe symptomatic hypotension occurred (blood pressure 65/35 mmHg). Lactate hemofiltration was suspended and one-hour later standard bicarbonate dialysis was performed without any clinical problem. The different mechanisms in acidosis buffering occurring in lactate and bicarbonate hemofiltration were discussed.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
9/18. Renal sodium handling study in an atypical case of Bartter's syndrome associated with mitochondriopathy and sensorineural blindness.Bartter's syndrome is a disorder that has been linked to mutations in one of three ion transporter proteins: NKCC2 (type I), ROMK (type II) and CCLNKB (type III), which affects a final common pathway that participates in ion transport by thick ascending limb cells. We present an atypical case of mitochondriopathy combined with tubule functional disturbances compatible with Bartter's syndrome and definitive sensorineural blindness. Our patient had a peculiar clinical presentation with signs of salt and volume depletion, low blood pressure and secondary hyperaldosteronism, associated with hypokalemic metabolic alkalosis, hypocalcemia and severe hypomagnesemia, uncommon in genetic forms of Bartter's syndrome. The enhanced absolute and fractional sodium excretion in our patient compared to volunteers was accompanied by increased post-proximal sodium rejection, suggesting a striking ion transport dysfunction in these nephron segments. These findings lead to the Bartter's syndrome diagnosis, accompanied by a suppose mitochondrial tick ascending loop of henle epithelium dysfunction that may reflect the high energy supplied by mitochondria electron transport chain, required for this nephron segment to maintain normal ion transport.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
10/18. Hypokalemic alkalosis, hyperreninemia, aldosteronism, normal blood pressure and normal juxtaglomerular apparatus--a new syndrome of renal alkalosis.An infant with hypokalemic alkalosis, hyperreninemia, aldosteronism, normal blood pressure and normal juxtaglomerular apparatus (JGA) is described. This infant, along with other similar patients reported in the literature, represents a new syndrome of renal alkalosis, clinically and chemically similar to Bartter's syndrome, but without hyperplasia of the JGA.- - - - - - - - - - ranking = 5keywords = pressure (Clic here for more details about this article) |
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