Omeprazole-induced and pantoprazole-induced asymptomatic hyponatremia: a case report.

BACKGROUND: Hyponatremia is the most common electrolyte disorder. Thiazides, antidepressants, antipsychotic drugs, and antiepileptic drugs are well-known causes of hyponatremia. Proton pump inhibitor use is a rare cause of hyponatremia and, when reported, it is due to one specific proton pump inhibitor, mostly omeprazole. CASE PRESENTATION: A 67-year-old Caucasian male was referred to our out-patient clinic because of hyponatremia (127 mmol/L) found at routine laboratory examination. He had consulted his general practitioner because of abdominal pains. No other symptoms were present. At physical examination, he appeared euvolemic and had no abdominal tenderness. Besides omeprazole for reflux esophagitis he used no medication. Additional laboratory results included: serum osmolarity 274 mOsmol/kg, urinary osmolarity 570 mOsmol/kg, and urinary sodium 35 mmol/L. Other causes of hyponatremia were excluded and we diagnosed hyponatremia due to the syndrome of inappropriate antidiuretic hormone secretion secondary to use of omeprazole. Omeprazole was replaced by ranitidine after which his serum sodium levels normalized to 135 mmol/L. During follow-up, because of persistent reflux complaints despite ranitidine use, ranitidine was switched to another proton pump inhibitor: pantoprazole. After this intervention, his serum sodium level declined again to 133 mmol/L. We concluded that both omeprazole and pantoprazole induced syndrome of inappropriate antidiuretic hormone secretion in this patient. CONCLUSION: Hyponatremia is worrisome and awareness of medication-induced hyponatremia, especially due to proton pump inhibitors, is needed. In our case, sequential hyponatremia occurred with two different proton pump inhibitors, suggesting a class effect. Therefore, when syndrome of inappropriate antidiuretic hormone secretion due to a proton pump inhibitor is diagnosed, preferably no other medication from the same class is prescribed. When after consideration another proton pump inhibitor is prescribed, serum sodium concentrations should be monitored.

Early identification of risk factors for refractory secondary hyperparathyroidism in patients with long-term renal replacement therapy.

BACKGROUND: Secondary hyperparathyroidism can complicate renal replacement therapy (RRT) in patients with end-stage renal disease. Current medical therapies often result in hypercalcaemia and fail to correct hyperparathyroidism, but might be more effective at an early stage of disease. The aim of this study was to identify prognostic factors at the start and during the first year of RRT for refractory secondary hyperparathyroidism needing parathyroidectomy (PTx) during long-term follow-up. METHODS: A total of 202 consecutive patients starting RRT between August 1988 and August 1996 at our centre with at least 1 year of follow-up were included. Biochemical and treatment data at the start and during the first year of RRT were collected. Univariate and multivariate analyses were used to identify risk factors for PTx during follow-up. RESULTS: Thirty-three patients (16%) needed PTx after 52+/-23 months of RRT. Need for PTx was not different between patients undergoing haemodialysis and peritoneal dialysis, but was associated with parameters reflecting calcium and phosphate control at start and after 1 year of RRT. In a Cox multivariate model, serum parathyroid hormone [relative risk (RR): 1.02 per pmol/l; P<0.001], phosphate (RR: 1.107 per 0.1 mmol/l; P = 0.002) and alkaline phosphatase (RR: 1.004 per U/l; P = 0.049) after 1 year of RRT were independently associated with increased risk for PTx. CONCLUSIONS: Failure of control of calcium-phosphate metabolism at the start of and early during RRT is strongly associated with PTx during long-term follow-up. Given the high prevalence of insufficient phosphate control, patients may benefit from aggressive correction of serum phosphate in the pre-dialysis and early dialysis period.