Hyperkalemia is a common electrolyte disorder in chronic kidney disease (CKD): it carries cardiovascular risks and may have serious consequences if not adequately controlled.

The use of standard therapies and osmotic resins (calcium and sodium polystyrene sulfonate) has an uncertain efficacy for chronic treatment.1 In recent years, new tools have also become available: patiromer and zirconium cyclosilicate. The latter, when compared to placebo, has demonstrated a significant and sustained reduction in potassium levels at 48 h in patients with stage 3-4 CKD.2

Here we present the case of the use of zirconium cyclosilicate by an uncommon means of administration with good results.

The case is a 45-year-old woman with a personal history of arterial hypertension, aortic insufficiency and CKD due to interstitial nephropathy that required nephrectomy at the age of 18 years due to chronic pyelonephritis. She had a renal transplant from a living related donor (her sister) with baseline renal function of 22 ml/min GFR.

She was taken to the emergency room due to an abrupt loss of consciousness and fever. In the previous days she had little food ingestion and reported dysuria and mechanical chest pain.

Complementary tests: negative urine culture, normal cardiac function and analytical tests revealed plasma creatinine (sCr) of 3.2 mg/dl and K+ of 4.2 mEq/l. Benzodiazepine intoxication was ruled out. Lumbar puncture was performed with positive PCR for HSV. Cranial CT showed right herpetic meningoencephalitis and multiple foci of intraparenchymal hemorrhagic necrosis with mass effect.

The patient's neurological status deteriorated, requiring admission to ICU. During her stay in ICU she presented worsening renal function with peak Crp of up to 4 mg/dl and hyperkalemia of 7 mEq/l secondary to tissue release and in the context of exacerbated CKD (Table 1). We initiated intravenous calcium gluconate, calcium polystyrene sulfonate (CPS) in enemas and by nasogastric tube, 1/6 M intravenous bicarbonate and intravenous furosemide, without improvement. There were important problems for the use of CPS by nasogastric tube due to obstruction, making administration impossible.

Hemodialysis was ruled out due to the findings of these acute brain lesions and the risk of increasing cerebral edema. In view of the poor prognosis, the use of continuous techniques was ruled out.

We decided to initiate treatment via nasogastric tube with sodium cyclosilicate and zirconium 5 g up to 2 sachets every 8 h (for 2 days and subsequently 1 sachet every 24 h). From the second day, we achieved and maintained control of K+ (4.7 mEq/l), without administration complications.

Finally, and after the use of antivirals, the patient evolved favorably, leaving the coma state and recovering basal renal function, as well as stabilizing her condition.

Hyperkalemia is a common problem in patients with CKD. Its incidence is variable (1.4–10% in hospitalized patients) and causes high morbidity and mortality with high healthcare costs.3

Treatment is complex and limited to a small number of therapies, with so far limited efficacy, delayed onset of action and intolerance due to gastrointestinal symptoms.

CPS has been the only K+ chelator available for the management of hyperkalemia for more than 50 years. Its use presents adverse effects such as gastrointestinal alterations (nausea and diarrhea up to mucosal damage and intestinal necrosis, hypernatremia, hypocalcemia and hypomagnesemia).4

The emergence of new, better tolerated and effective drugs offers good options for the treatment of hyperkalemia.

The new drugs are nonabsorbable polymers that bind potassium in the gastrointestinal tract and facilitate the elimination of fecal potassium. Zirconium cyclosilicate has a faster onset, from 1 to 6 h.4,8

These agents are an important advance in our arsenal for the treatment of hyperkalemia, as they are more selective for potassium ion, exhibit an improved adverse event profile, and have a more consistent potassium-lowering effect. The efficacy of both has been documented in clinical trials, while clinical data for CPS are limited.7

Sodium zirconium cyclosilicate has established efficacy and safety in clinical trials. In studies of patients with chronic hyperkalemia, zirconium cyclosilicate 3 times daily significantly reduced serum K+ concentrations within 48 h, and a dose of 5 or 10 g once daily effectively maintained normal potassium levels for 14 to 28 days.5–8

There has been some concern due to the sodium content of a 10 g dose (approximately 1000 mg), which produces edema and/or hypertension4; in our case there were no adverse effects associated with the drug.

In our case, faced with a complex scenario and an unusual administration route,9 we obtained a very good response with sodium cyclosilicate and zirconium, also allowing the reintroduction of iSRAA treatment, reinforcing the importance of individualization and the need, on many occasions, to change recommended dosages to adapt to each of our patients.