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Renal Calculi in Primary Hyperaldosteronism 561 Postgrad Med J: First Published As 10.1136/Pgmj.71.839.561 on 1 September 1995

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Renal Calculi in Primary Hyperaldosteronism 561 Postgrad Med J: First Published As 10.1136/Pgmj.71.839.561 on 1 September 1995 Renal calculi in primary hyperaldosteronism 561 Postgrad Med J: first published as 10.1136/pgmj.71.839.561 on 1 September 1995. Downloaded from Renal calculi in primary hyperaldosteronism Udaya M Kabadi Summary nism was established by documentation of low Increased urinary calcium (Ca"+) excre- renin (<0.2ng/ml/h) and elevated plasma tion and the presence of negative Ca++ aldosterone (42-54 ng/dl; normal 3-10 ng/dl) balance is well documented in primary on several occasions as well as the lack of hyperaldosteronism. However, renal cal- suppression following a high sodium (300 mM/ culi as a major manifestation of this day) diet for three days and further confirmed disorder has not previously been des- by abdominal computed tomography (CT) cribed. This report describes a patient scan, showing bilateral adrenal enlargement, who presented with renal calculi in arteriography with no unilateral localisation, ie, association with primary hyperaldo- tumour blush and raised aldosterone concen- steronism. We believe that primary trations in bilateral adrenal venous blood sam- hyperaldosteronism was a major patho- ples without a significant gradient between two genetic factor in the formation of renal sides, as well as a lack of suppression on oral calculi since the increased urinary excre- administration of 8 mg cyproheptadine (Merk, tion of Ca+ + and uric acid noted at onset Sharp & Dohme Inc, West Point, PA, USA), as declined following a short-term spiro- described previously.2 Intravenous pyelo- nolactone administration and remission graphy revealed bilateral multiple renal calculi. from renal calculi has persisted following Spironolactone therapy in gradually increasing initial nephrolithotomy and continued dosage with a final daily dose of300 mgpermit- spironolactone therapy, which also cor- ted withdrawal ofother antihypertensive drugs rected hypertension and hypokalemia, a and normalised serum K+ level between hallmark of this disorder. 4.2-4.6 mM/l as well as 24-h urinary excretion of Ca+ and uric acid (table). Subsequently, Keywords: renal calculi, hyperaldosteronism the patient underwent elective bilateral neph- rolithotomy in two stages in 1981 and 1982. The chemical analyses of the calculi demon- Primary hyperaldosteronism is reported to strated both calcium urate and pyrophosphate facilitate urinary calcium excretion and induce crystals. During the follow-up period of about a negative calcium balance.1 However, the 12 years, the patient reported no recurrence of occurrence of renal calculi in this disorder has renal colic, nor gross haematuria and a recent http://pmj.bmj.com/ not been reported. Herein, we describe a intravenous pyelography revealed no renal cal- patient, in whom renal calculi were present for culi. Finally, 24-h urinary Ca + and uric acid several years prior to diagnosis of primary excretion have also remained normal (table). hyperaldosteronism and continuous therapy with spironolactone (Searle, Skokie, IL, USA), Discussion following initial nephrolithotomy, prevented subsequent stone formation during the follow- Chronic mineralocorticoid administration and on September 29, 2021 by guest. Protected copyright. up period of 12 years. primary hyperaldosteronism are both known to facilitate renal Ca + excretion.1,3-5 Further- Case report more, excretion ofacidic urine due to increased tubular reabsorption ofbicarbonate induced by A 47-year-old white man presented for evalua- elevated aldosterone may also enhance urate tion of hypertension and persistent hypo- crystallisation and promote formation of urate kalemia (serum K+, <3.0mM/l) while not stones. Finally, normalisation of 24-h urinary Medical Service, VA receiving therapy with diuretics. The patient Ca+ and uric acid excretion as well as total Medical Center, related presence of hypertension for 10 years, remission from new stone formation with Phoenix, and College initially detected at the time of hospitalisation spironolactone therapy in our patient definitely ofMedicine, for of University ofArizona, management subarachnoid haemorrhage indicate primary hyperaldosteronism to be res- Tucson, Arizona, USA secondary to a rupture of an intracranial ponsible for formation of renal calculi and not UM Kabadi arteriovenous malformation. Several regimens just a coincidental occurrence. We believe that using different drugs were not optimally the use of spironolactone or other agents (eg, Correspondence to effective in blood with ACE Udaya M Kabadi, Chief, controlling pressure inhibitors) causing hypoaldosteronism Endocrine Section, Medical recordings ranging from 140/85 to 170/ may be extended also to patients with mixed Service (11 E), VA Medical 110 mmHg. He also related recurrent passage renal calculi who receive a multiple drug Center, 650 East Indian of stones and gravel in the urine with several School Road, Phoenix, AZ regimen, eg, thiazides, allopurinol, and/or 85012, USA short hospitalisations and visits to emergency alkalinising solutions. rooms over the previous 3-4 years. The diag- The author would like to thank Marcia Gregory for Accepted 15 March 1995 nosis of idiopathic primary hyperaldostero- secretarial assistance. 562 Kabadi Table 24-h urinary excretion of calcium (Ca++) and uric acid prior to (pre Rx), and during therapy (post Rx) with spironolactone at 2 Summary points months and again at 12 years in a patient with primary hyperal- Postgrad Med J: first published as 10.1136/pgmj.71.839.561 on 1 September 1995. Downloaded from dosteronism and renal calculi. are as mean ± * renal calculi may occur in primary Figures given SEM of hyperaldosteronism four values at each time point * raised urinary excretion of calcium and uric acid may occur in primary Calcium (mM/day) Uric acid (mM/day) hyperaldosteronism * spironolacatone therapy reduces urinary pre Rx 104.5 3.7 5.10 0.13 excretion ofcalcium and uric acid, and helps post Rx (2 months) 55.5 + 2.0 3.18 0.10 recurrent renal calculi in post Rx (12 years) 54.30 + 2.31 3.25 + 0.08 prevent primary normal value 62.5-75.0 3.87-4.16 hyperaldosteronism 1 Resnick LM, Largh JH. Calcium metabolism and para- 4 Massry S, Coburn JW, Chapman LW, Kleenman CR. The thyroid function in primary aldosteronism. Am J Med 1985; effect of long-term desoxycorticosterone acetate administra- 78: 385-90. tion on the renal excretion of calcium and magnesium. J Lab 2 Gross MD, Grekin RJ, Gniadek TC, Villareal J. Suppression Clin Med 1968; 71: 212-9. of aldosterone by cyproheptadine in idiopathic aldo- 5 Wright GL, Rankin GD. Concentrations of ionic and total steronism. N Engl J Med 1981; 305: 181-5. calcium in plasma of four models of hypertension. Am J 3 Luft R, Sjogren B. Some aspects of the metabolic effect of Physiol 1982; 243: H365-70. desoxycorticosterone acetate. Metabolism 1953; 2: 313-21. Giant cell carcinoma of the lung Shiekh Aejaz Aziz, Mushtaq Ahmad, Azra Shah, Gul Mohammad Bhat, Ajaz Lone, Khursheed Ahmad. Haira Bano Summary Abdominal ultrasonography was normal. A 50-year-old non-smoking, hypertensive Computed tomography (CT) scan of the chest female, presenting with superior vena showed a homogenous mass of soft-tissue den- caval compression, was found to have sity in the anterior and middle mediastinum, giant cell carcinoma of the lung. She impressing on the arch of aorta and causing received intensive combination chemo- displacement and occlusion of the superior therapy. However she died in the follow- vena cava. There was compression of the right ing 36 hours, as a consequence of refrac- upper lobe bronchus with extension into the tory hypotension. chest wall and pleural effusion on the right side http://pmj.bmj.com/ (figure). A clinical diagnosis of bronchogenic Keywords: giant cell carcinoma, superior vena caval carcinoma (T4N2MO-IIIB) was made. She obstruction was put on decompressive treatment and a Trucut biopsy was done, which subsequently revealed features suggestive of giant cell car- Giant cell carcinoma is a rare, distinctive lethal cinoma of the lung. She was put on combina- variant of large cell cancer of the lung.' The tion chemotherapy consisting of intravenous on September 29, 2021 by guest. Protected copyright. Departments of tumour is quite extensive at diagnosis and cyclophosphamide 750 mg/m2, adriamycin Medical Oncology & survival for more than one year is exceptional.2 50 mg/m2 and cisplatin 100 mg/m2 on day 1; the Pathology, Sher-i-Kashmir Case report Institute ofMedical Sciences, Srinagar, India A 50-year-old, non-smoking, hypertensive SA Aziz woman was admitted to our hospital on 19 M Ahmad October 1994, with a non-productive cough A Shah and breathlessness of one month duration. GM Bhat Clinical examination revealed features sugges- A Lone tive of superior vena caval compression, with K Ahmad partial collapse of the right upper lobe of lung. H Bano Her blood pressure was 150/100 mmHg (on Correspondence to calcium channel blockers); the rest of her Dr Shiekh Aejaz Aziz, cardiovascular and other systemic examination Consultant, Department of was Fundus occuli were Medical Oncology, non-contributory. Sher-i-Kashmir Institute of normal. Her investigations showed a normal Medical Sciences, Post Bag haemogram and biochemical parameters. Elec- No 27, Soura, Srinagar 190 was normal. Chest Figure CT scan of the chest showing a homogenous 011, India trocardiogram (ECG) X-ray mass of soft density in the anterior and middle medias- revealed a mass shadow in the right upper and tinum with impression on arch of aorta, displacement Accepted 15 March 1995 middle zone with mediastinal invasion. and occlusion ofsuperior vena cava with pleural effusion.
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