Renal tubular acidosis type IV in hyperkalaemic patients--a fairy tale or reality?

OBJECTIVE: Hyperkalaemia is a common feature in hospitalized patients and often attributed to drugs antagonizing the renin-angiotensin-aldosterone system (RAAS) and/or acute kidney injury (AKI), despite significantly preserved glomerular filtration rate (GFR). The objective of this study was to determine the prevalence and role of renal tubular acidosis type IV (RTA IV) in the development of significant hyperkalaemia. DESIGN: A single-centre retrospective study. PATIENTS: Patients admitted to a University Hospital over 12 months. MEASUREMENTS: Patients with a potassium value > 6·0 mm were identified. Clinical and laboratory data were revisited, and patients with a normal anion gap metabolic acidosis were evaluated for the existence of RTA IV. RESULTS: A total of 57 patients having significant hyperkalaemia (>6·0 mm) were identified. Twelve patients had end-stage renal disease, while 21 patients had solely AKI or progressive chronic renal failure. RTA IV was present in 24 patients (42%), of whom 71% had pre-existing renal insufficiency because of diabetic nephropathy or tubulointerstitial nephritis. All hyperkalaemic patients with urinary/serum electrolytes suggestive of RTA IV had evidence of AKI, but creatinine levels were significantly lower (P < 0·05), while the number of drugs antagonizing the RAAS was comparable. CONCLUSION: We demonstrated that RTA IV (i) is very common in patients with hyperkalaemia; (ii) should always be suspected in hyperkalaemic patients with only moderately impaired GFR; and (iii) may result in significant hyperkalaemia in the presence of both AKI and drugs antagonizing the RAAS.

Beating the odds--surviving extreme hyperkalemia.

Severe hyperkalemia (>7 mmol/L) is a medical emergency because of possible fatal arrhythmias. We here report the case of a 58-year-old woman surviving extreme hyperkalemia (>10 mmol/L). The patient with a history of congestive heart failure, a DDD pacemaker and mild chronic renal insufficiency was admitted with progressive weakness and sudden onset of hypotension and bradycardia in the absence of any pacemaker action. Laboratory tests revealed an extreme serum potassium level of 10.1 mmol/L, with a slightly elevated serum creatinine of 149 µmol/L. Treatment with norepinephrine, sodium bicarbonate, and insulin improved both the hemodynamic situation and the serum potassium with subsequent regaining pacemaker actions even before additional hemodialysis normalized the potassium level. A thorough investigation demonstrated that several mechanisms contributed to the extreme potassium level: urinalysis and a low transtubular potassium gradient in the presence of metabolic acidosis with normal anion gap pointed to preexisting interstitial nephritis, with renal tubular acidosis type IV as the predisposing factor, whereas several drugs and acute impairment of renal function contributed to the dangerous situation. Despite the odds for fatal outcome, the patient recovered completely, and long-term management was initiated to prevent recurrent hyperkalemia.

[Resistant hypertension despite nine different antihypertensive drugs?]. / Therapierefraktärer Hypertonus unter 9-facher antihypertensiver Medikation?

BACKGROUND: Treatment-resistant hypertension is a common problem in an outpatient setting and often results in hospital admission. Non-identified secondary hypertension, hypertensive nephrosclerosis and non-compliance are major reasons for treatment resistance. CASE REPORT: A 75-year old woman was admitted to the emergency room because of a hypertensive crisis with alleged treatment-resistant hypertension and progressive headache. Two months ago, renal artery stenosis had been ruled out and a diagnosis of hypertensive cardiomyopathy was established. On admission, the patient had a blood pressure of 210/100 mmHg despite an antihypertensive treatment with nine different drugs. Further investigations ruled out secondary hypertension due to an endocrine cause but were consistent with hypertensive nephrosclerosis. With a supervised drug intake the blood pressure was rather normal to hypotensive, resulting in the need for significant reduction of the antihypertensive medication. The apparent discrepancies were discussed in detail with the patient who finally admitted a previous inconsistent intake of the antihypertensive drugs. Following thorough training and education on the purpose of continued antihypertensive therapy, the patient could be discharged with a normotensive blood pressure profile. CONCLUSIONS: Therapy of treatment-resistant hypertension should always consider non-compliance and secondary hypertension as possible reason.