1 Department of Nephrology and 2 Department of Renal Transplantation Cliniques universitaires Saint-Luc Université Catholique de Louvain Brussels, Belgium
Case
A 48-year-old Caucasian male underwent a cadaveric renal transplantation in November 2000 after 15 months of haemodialysis. He was treated by nifedipine (30 mg o.d.) and nisoldipine (20 mg o.d.) for arterial hypertension evidenced more than 20 years before. No laboratory investigation was performed until May 1999, when he was admitted for chest pain. Blood pressure was 185/95 mmHg and serum creatinine was 6.0 mg/dl. Urinary microscopy was unremarkable. Proteinuria was 570 mg/24 h. Renal ultrasonography showed normal-sized kidneys with a lack of cortico-medullary distinction. Renal biopsy showed aspecific interstitial fibrosis and tubular atrophy. A diagnosis of nephroangiosclerosis complicating long-lasting primary arterial hypertension was considered. Coronarography showed a 75% stenosis on a diagonal artery, not requiring revascularization. The treatment was changed to atenolol (50 mg o.d.) and furosemide (160 mg o.d.). Renal function progressively deteriorated, and haemodialysis was started in August 1999. At the time of transplantation, the homolateral native kidney was removed (a routine procedure in our centre) and histological examination showed end-stage kidney disease. Delayed graft function required four haemodialysis sessions. The results of a laboratory examination obtained 4 days after the last haemodialysis session (day 12) are provided in Table 1. The patient was discharged on day 17 (Table 1
). Serum creatinine and potassium were 2.1 mg/dl and 3.05 mEq/l, respectively. The patient had no diarrhoea. He was not taking diuretics. Blood pressure at home and at the outpatient clinic averaged 150/90 mmHg. Maintenance therapy included tacrolimus 5 mg b.i.d., mycophenolate mofetil 500 mg b.i.d., prednisolone 10 mg o.d., dipyridamole 200 mg b.i.d., valaciclovir 1 g t.i.d. and citalopram 20 mg o.d. Urinary sodium, potassium and chloride excretion were 77, 27 and 86 mEq/l, respectively. Hypokalaemia persisted despite oral supplementation with potassium (40 mEq o.d.) and magnesium (1.5 g o.d.) (Table 1
). Metabolic alkalosis appeared progressively. Blood and urinary cortisol were 487 nM (Nl 260540) and 144 µg/24 h (Nl <90), respectively.
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Questions
How do you explain hypokalaemia?
What kind of complementary tests would you recommend to confirm your diagnosis?
Answer to the quiz on preceding page
A stepwise diagnostic approach of hypokalaemia is summarized in Figure 1 [1]. In this patient, an extra-renal K+ loss was easily ruled out by the absence of diarrhoea and the elevated amount of urinary K+ excretion. At that point, the level of blood pressure would be the next diagnostic clue in most patients. However, this step is less discriminating in renal transplant recipients, given the high prevalence of systemic hypertension in such patients [2].
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We have thus to consider the causes of hypokalaemia associated with hypertension (Figure 1). As indicated above, blood and urine cortisol were normal, which excluded hypercorticism. Rather, the association of hypokalaemia, inappropriate kaliuresis, and a long-lasting history of mild hypertension evokes a diagnosis of hyperaldosteronism. Complementary laboratory investigations included serum aldosterone level and plasma renin activity (PRA). PRA was very low (<0.2 ng/ml/h (Nl <5)), while serum aldosterone concentration (PAC) was high (2.3 nM (Nl <0.4)). These results are highly suggestive of primary hyperaldosteronism. The various causes of pseudohyperaldosteronism (Liddle's syndrome, abuse of liquorice, apparent mineralocorticoid excess, deoxycorticosterone excess) can be excluded by the high aldosterone level. The next step is thus to perform MRI or CT scans of the adrenals. Abdominal MRI showed a left adrenal mass of 4.5x3x1.5 cm (Figure 2a
). Adrenal vein catheterism confirmed excessive aldosterone production by the left adrenal gland (Figure 2b
). Spironolactone treatment (100 mg o.d.) readily corrected electrolytic disorders (Table 1
). Left adrenalectomy showed an adrenal adenoma with two areas of hyperplasia. Spironolactone treatment was withdrawn with a persistently normal ionogram at day 175 (Table 1
).
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Finally, the nephroangiosclerosis diagnosed in this patient may have been related to long-lasting primary hyperaldosteronism.
Notes
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Email: m.tintillier{at}ibelgique.com
References