Saudi Journal of Kidney Diseases and Transplantation

CASE REPORT
Year
: 2009  |  Volume : 20  |  Issue : 2  |  Page : 285--287

Hypokalemic paralysis due to primary hyperaldosteronism simulating gitelman's syndrome


Timucin Kasifoglu1, Aysen Akalin2, Dondu Uskudar Cansu1, Cengiz Korkmaz1,  
1 Divisions of Rheumatology, Department of Internal Medicine, Eskisehir Osmangazi University Medical Faculty, Eskisehir, Turkey
2 Divisions of Endocrinology, Department of Internal Medicine, Eskisehir Osmangazi University Medical Faculty, Eskisehir, Turkey

Correspondence Address:
Timucin Kasifoglu
Visnelik M. Oncag Sitesi E Blok Daire 13, Eskisehir
Turkey

Abstract

Some diseases, such as Gitelman俟Q製 syndrome, Bartter俟Q製 syndrome, and primary hyperaldosteronism (Conn俟Q製 syndrome), may bear some similar clinical and laboratory findings. Their treatment modalities being different from one another, the need for a scrupulous diagnostic evaluation arises as far as clinical practice is concerned. In this report, we present a patient with Conn俟Q製 syndrome who was initially considered to have Gitelman俟Q製 syndrome due to displaying a few overlapping features of both diseases. We also give an account of the hardships encountered during the diagnostic evaluation.



How to cite this article:
Kasifoglu T, Akalin A, Cansu DU, Korkmaz C. Hypokalemic paralysis due to primary hyperaldosteronism simulating gitelman's syndrome.Saudi J Kidney Dis Transpl 2009;20:285-287


How to cite this URL:
Kasifoglu T, Akalin A, Cansu DU, Korkmaz C. Hypokalemic paralysis due to primary hyperaldosteronism simulating gitelman's syndrome. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2019 Jul 17 ];20:285-287
Available from: http://www.sjkdt.org/text.asp?2009/20/2/285/45581


Full Text

 Introduction



Acute muscular weakness is a common com計laint in the emergency departments resulting from several causes. [1],[2] Paralysis is usually li衫ited to skeletal muscles. Involvement of res計iratory muscles or cardiac arrhythmia due to hypokalemia can result in life-threatening con貞equences. After improving hypokalemic para衍ysis by potassium replacement, all patients must be examined to detect the underlying aetiology. Although hypocalcemia, hypomag要esemia and metabolic alkalosis with hypokalemia can be seen in Gitelman's syndrome, vitamin D deficiency associated with a disease苞ausing hypokalemia can manifest with similar laboratory findings. Therefore, a meticulous diagnostic approach to these patients is very important in clinical practice. In this case re計ort, we present a patient who diagnosed as having hypokalemic paralysis attributable to Conn's syndrome associated with vitamin D deficiency. We also discuss some diagnostic hardships in evaluating her laboratory results.

 Case Report



A 50-year-old woman was admitted to the emergency department with a sudden onset of progressive paralysis involving four extre衫ities. She denied having nausea, vomiting, diarrhoea or the use of drugs, including diuretics and licorice. Her family history was un訃emarkable. One year ago she had preented to the hospital with muscle weakness and myal茆ias. Laboratory workup at that time revealed potassium level of 2.1 mEq/L (normal 3.5-5.5) but the cause of hypokalemia was not inves負igated in detail. During her current presen負ation blood pressure was 130/80 mmHg, she was afebrile with no respiratory distress. She had symmetric flaccid paralysis with areflexia in all extremities. Her muscle strength was 1/5 in the proximal muscle groups. Her laboratory tests revealed the following values: severe hypokalemia (1.51 mEq/L), metabolic alkalosis (pH 7.52), creatine kinase (CK) 6330 IU/L (16190), lactic dehydrogenase (LDH) 886 IU/L (240-480), aspartate aminotransferase (AST) 192 IU/L (7-39), alanine aminotransferase (ALT) 101 IU/L (2-40), calcium 7.3 mg/dL (8.510.5), phosphorus 2.1 mg/dL (2.7-4.5), magne貞ium 0.57 mmol/L (0.85-1.15). 25(OH) vitamin D level was 7 IU/L (> 25). Urinary potassium excretion was 70 mEq/day. Transtubular pota貞sium gradient was 5.2. Parathormone (PTH) level was 178 ng/mL (15-65). Normal or ne茆ative tests included sodium chloride, blood urea nitrogen, creatinine, glucose, total pro負ein, albumin, thyroid function studies, and liver. Intravenous administration of potassium chloride (KCL) at the rate of 10 mmol/h prog訃essively improved her muscle strength with concomitant increase in her potassium levels. Muscle biopsy and electroneuromyography were performed one week after resolution of hypokalemia. Metabolic alkalosis, hypocalce衫ia and hypomagnesemia with hypokalemia prompted us to suspect of Gitelman's syn苓rome. However, because this syndrome mostly appears in younger ages, a few other possible factors, such as mineralocorticoid excess syn苓rome, were taken into consideration.

The aldosterone level was 395 pg/mL (20240), renin activity was 0.2 ng/mL per hour in supine position (0.2-3.4) and aldosterone/renin ratio was 197.5 ( [3] clay ingestion, [4] diuretic use, [5] Bartter's or Gitelman's syndrome. [6],[7]

Because concurrent presence of vitamin D deficiency and Conn's syndrome may simulate Gitelman's syndrome in consideration of hypo虺alemia, hypocalcemia, hypomagnesemia and metabolic alkalosis, we do not rule out the possibility that we could have diagnosed our patient as having Gitelman's syndrome if we had not conducted an intensive study into the aetiology of hypokalemia and other laboratory findings. In Gitelman's syndrome an autoso衫al recessive disorder, the diagnosis is usually made by late childhood or even adulthood cramps, severe fatigue, polyuria and nocturia symptoms. [8] In our patient, other electrolyte abnormalities with hypokalemia prompted us to suspect Gitelman's syndrome. However, a patient with Gitelman's syndrome is supposed to have high levels of plasma renin. [9] As to our patients, she had low levels of renin. Hypo虺alemia in a patient with myopathy should lead a physician to suspect Bartter's and Gitelman's syndromes, as well as primary hyperaldostero要ism. Bartter's syndrome is a disorder charac負erized by hypokalemia, metabolic alkalosis, hyperreninemic hyperaldosteronism secondary to extra cellular fluid volume contraction and juxtaglomerular apparatus hyperplasia. Since Gitelman's syndrome has some common cli要ical and laboratory findings with those of Bartter's syndrome, Gitelman's syndrome is accepted as a variant of Bartter's syndrome. However, hypocalciuria, hypocalcemia, and hypomagnesemia are seen in Gitelman's syn苓rome but not in Bartter's syndrome. Our pa負ient had hypocalcemia, hypomagnesemia and metabolic alkalosis. These laboratory findings complied with those of Gitelman's syndrome. However, hypocalcemia can also be seen in Conn's syndrome due to severe hypokalemia. In Conn's syndrome, hypomagnesemia may be suspected when hypokalemia is severe. [10] Chronic hypomagnesemia leads to intracellular magnesium deficiency and this, in turn, im計airs secretion of PTH and also decreases res計onse to PTH. Thus, in severe hypomagne貞emia, PTH levels are undetectable or inappro計riately low despite the stimulus of hypocal苞emia. However, in our case, PTH levels were high despite low levels of magnesium. We, therefore, concluded that hypocalcemia could be due to factors other than hypomagnesemia. A low calcium and low phosphorus implied that our patient may have vitamin D defi苞iency. Because vitamin D deficiency leads to secondary hyperparathyroidism, which affects renal tubule phosphate transport, causes renal phosphate wasting and hypophosphatemia. [11] A very low level of 25(OH) vitamin D confirmed vitamin D deficiency in our case. However, we considered this could be a sheer coincidence and not necessarily related with Conn's syn苓rome.

Hypokalemic myopathy due to an adrenal adenoma producing mineralocorticoid is repor負ed rarely. [12] The treatment of choice is surgical excision of aldosterone-producing tumour. Mineralocorticoid excess can be easily recog要ised by using ratio of plasma aldosterone level (ng/dL) to renin level (ng/mL/h), which is an indicator of increased aldosterone and sup計ressed renin levels. The ratio above 20 is usually suggestive of a functional adenoma causing mineralocorticoid exces. [13] Ultrasono茆raphy and CT scan sometimes fail to show the adrenal lesions smaller than 1 cm.

 Conclusion



In conclusion, Conn's syndrome and Gitel衫an's syndrome should be considered in a differential diagnosis of patients with hypokalemic paralysis due to occasional overlapping laboratory findings. We also concluded that a correct interpretation of laboratory tests could be instrumental in excluding other reasons of hypokalemic myopathy.

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