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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 2  |  Page : 285-287
Hypokalemic paralysis due to primary hyperaldosteronism simulating gitelman's syndrome

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

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Some diseases, such as Gitelman's syndrome, Bartter's syndrome, and primary hyperaldosteronism (Conn's 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's syndrome who was initially considered to have Gitelman's syndrome due to displaying a few overlapping features of both diseases. We also give an account of the hardships encountered during the diagnostic evaluation.

Keywords: Hypokalemia, Myopathy, Gitelman′s syndrome

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;20:285-7

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 2023 Feb 4];20:285-7. Available from: https://www.sjkdt.org/text.asp?2009/20/2/285/45581

   Introduction Top

Acute muscular weakness is a common com­plaint in the emergency departments resulting from several causes. [1],[2] Paralysis is usually li­mited to skeletal muscles. Involvement of res­piratory muscles or cardiac arrhythmia due to hypokalemia can result in life-threatening con­sequences. After improving hypokalemic para­lysis by potassium replacement, all patients must be examined to detect the underlying aetiology. Although hypocalcemia, hypomag­nesemia and metabolic alkalosis with hypokalemia can be seen in Gitelman's syndrome, vitamin D deficiency associated with a disease­causing hypokalemia can manifest with similar laboratory findings. Therefore, a meticulous diagnostic approach to these patients is very important in clinical practice. In this case re­port, 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 Top

A 50-year-old woman was admitted to the emergency department with a sudden onset of progressive paralysis involving four extre­mities. She denied having nausea, vomiting, diarrhoea or the use of drugs, including diuretics and licorice. Her family history was un­remarkable. One year ago she had preented to the hospital with muscle weakness and myal­gias. 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 inves­tigated in detail. During her current presen­tation 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), magne­sium 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 pota­ssium gradient was 5.2. Parathormone (PTH) level was 178 ng/mL (15-65). Normal or ne­gative tests included sodium chloride, blood urea nitrogen, creatinine, glucose, total pro­tein, albumin, thyroid function studies, and liver. Intravenous administration of potassium chloride (KCL) at the rate of 10 mmol/h prog­ressively 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, hypocalce­mia and hypomagnesemia with hypokalemia prompted us to suspect of Gitelman's syn­drome. However, because this syndrome mostly appears in younger ages, a few other possible factors, such as mineralocorticoid excess syn­drome, 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 (< 10). Abdominal ultrasound was unremarkable but dynamic suprarenal CT scan showed a 20 × 30 mm hypo dense mass in the left suprarenal area. After adrenalec­tomy, the pathology confirmed an aldosterone producing adenoma. The patient has been in a normokalemic state without KCL supplemen­tation and her last muscle strength is 5/5 in all extremities. Serum calcium and magnesium le­vels remained in normal ranges with calcitriol and vitamin D supplementation.

   Discussion Top

Acute hypokalemic paralysis, a clinical syn­drome characterized by acute muscular weak­ness and low serum potassium levels, is a rare but treatable cause of acute myopathy. Among the reasons reported for development of hypo­kalemic myopathy are liquorice intake, [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 hypo­kalemia, 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 autoso­mal 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. Hypo­kalemia in a patient with myopathy should lead a physician to suspect Bartter's and Gitelman's syndromes, as well as primary hyperaldostero­nism. Bartter's syndrome is a disorder charac­terized by hypokalemia, metabolic alkalosis, hyperreninemic hyperaldosteronism secondary to extra cellular fluid volume contraction and juxtaglomerular apparatus hyperplasia. Since Gitelman's syndrome has some common cli­nical 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 syn­drome but not in Bartter's syndrome. Our pa­tient 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, im­pairs secretion of PTH and also decreases res­ponse to PTH. Thus, in severe hypomagne­semia, PTH levels are undetectable or inappro­priately low despite the stimulus of hypocal­cemia. 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 defi­ciency. 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 syn­drome.

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

   Conclusion Top

In conclusion, Conn's syndrome and Gitel­man'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.

   References Top

1.Ahlawat SK, Sachdev A. Hypokalaemic para­lysis. Postgrad Med J 1999;75:193-7.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Lin YF, Lin SH, Tsai WS, Davids MR, Halperin ML. Severe hypokalaemia in a Chinese male. Q J Med 2002;95:695-704.  Back to cited text no. 2    
3.van den Bosch AE, van der Klooster JM, Zuidgeest DM, Ouwendijk RJ, Dees A. Severe hypokalaemic paralysis and rhabdomyolysis due to ingestion of liquorice. Neth J Med 2005;63: 146-8.  Back to cited text no. 3    
4.Severance HW Jr, Holt T, Patrone NA, Chapman L. Profound muscle weakness and hypokalemia due to clay ingestion. South Med J 1988;81: 272-4.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Ozgur B, Kursat S. Hypokalemic rhabdomyo­lysis aggravated by diuretics complicating Conn's syndrome without acute renal failure. Clin Nephrol 2002;57:89-91.  Back to cited text no. 5    
6.Virdi VS, Poddar B, Parmar VR. Hypokalemic respiratory paralysis in Bartter's syndrome. Indian J Pediatr 2002;69:527-8.  Back to cited text no. 6  [PUBMED]  
7.Saiki S, Yoshioka A, Saiki M, Yamaya Y, Hirose G. A case of Gitelman's syndrome presenting with the hypokalemic periodic paralysis. Rinsho Shinkeigaku 2002;42:317-9.  Back to cited text no. 7  [PUBMED]  
8.Stein JH. The pathogenetic spectrum of Bartter's syndrome. Kidney Int 1985;28:85.  Back to cited text no. 8  [PUBMED]  
9.Bringhurst Fr, Demay MB, Kronenberg HM. Endocrine hypertension. In: Larsen R, Kronenberg HM, Melmed S, Polonsky KS, eds. Williams textbook of Endocrinology. Philadelphia: Saunders 2003;579-85.  Back to cited text no. 9    
10.Potts, JT. Diseases of the parathyroid gland and other hyper- and hypocalcemic disorders. In: Braunwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL, eds. Harrison's Principles of Internal medicine. Mc Grow Hill 1994;2151-83.  Back to cited text no. 10    
11.Bringhurst Fr, Demay MB, Kronenberg HM. Hormones and disorders of mineral metabolism. In: Larsen R, Kronenberg HM, Melmed S, Polonsky KS, eds. Williams textbook of Endo­crinology. Philadelphia,: Saunders 2003;1303-71.  Back to cited text no. 11    
12.Kasifoglu T, Korkmaz C, Pasaoglu O. Conn's syndrome (primary hyperaldosteronism) simulating polymyositis. Rheumatol Int 2005;25:133-4.  Back to cited text no. 12    
13.Kaplan NM. Clinical hypertension. 7th edn. Williams and Wilkins Baltimore: 1998;365-82.  Back to cited text no. 13    

Correspondence Address:
Timucin Kasifoglu
Visnelik M. Oncag Sitesi E Blok Daire 13, Eskisehir
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Source of Support: None, Conflict of Interest: None

PMID: 19237821

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