Hypokalaemia and hypertension early after kidney transplantation.

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 185u95 mmHg and serum creatinine was 6.0 mgudl. Urinary microscopy was unremarkable. Proteinuria was 570 mgu24 h. Renal ultrasonography showed normal-sized kidneys with a lack of corticomedullary 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 endstage 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 mgudl and 3.05 mEqul, respectively. The patient had no diarrhoea. He was not taking diuretics. Blood pressure at home and at the outpatient clinic averaged 150u90 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 mEqul, respectively. Hypokalaemia persisted despite oral supplementationwith potassium (40 mEqo.d.) and magnesium (1.5 g o.d.) (Table 1). Metabolic alkalosis appeared progressively. Blood and urinary cortisol were 487 nM (Nl 260–540) and 144 mgu24 h (Nl -90), respectively.