Renal tubular acidosis type IV in hyperkalaemic patients – a fairy tale or reality?
Article first published online: 10 APR 2013
© 2012 Blackwell Publishing Ltd
Volume 78, Issue 5, pages 706–711, May 2013
How to Cite
Haas, C. S., Pohlenz, I., Lindner, U., Muck, P. M., Arand, J., Suefke, S. and Lehnert, H. (2013), Renal tubular acidosis type IV in hyperkalaemic patients – a fairy tale or reality?. Clinical Endocrinology, 78: 706–711. doi: 10.1111/j.1365-2265.2012.04446.x
- Issue published online: 10 APR 2013
- Article first published online: 10 APR 2013
- Accepted manuscript online: 14 AUG 2012 10:00AM EST
- Manuscript Accepted: 21 APR 2012
- Manuscript Revised: 18 APR 2012
- Manuscript Revised: 15 FEB 2012
- Manuscript Received: 2 FEB 2012
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.
A single-centre retrospective study.
Patients admitted to a University Hospital over 12 months.
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.
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.
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.