Renal Tubular Acidosis Type IV in Hyperkalemic Patients
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.
Hyperkalaemia (>5·5 mm) is a common observation in patients admitted to a hospital with an reported incidence between 1 and 3·3%. Hyperkalaemia in the presence of concomitant renal insufficiency is often attributed solely to impaired renal function, even if glomerular filtration rate (GFR) is only moderately reduced. Although renal tubular acidosis type IV (RTA IV) is thought to be a frequent disorder associated with hyperkalaemia, the diagnosis is often overlooked in clinical practice. RTA IV is defined as an acidification defect in the distal renal tubule as a result of real or functional hypoaldosteronism and is associated with hyperkalaemia and hyperchloraemic metabolic acidosis with normal anion gap. The tentative diagnosis of RTA IV is easy to establish, and aldosterone function can be evaluated using the transtubular potassium gradient (TTKG). Additional determination of renin and aldosterone may be helpful to confirm the diagnosis or to establish the underlying cause. Tubulointerstitial disease and diabetic nephropathy have been proposed to be the prevailing conditions observed in patients with RTA IV, usually associated with hyporeninaemic hypoaldosteronism. Typically, RTA IV is present in patients with only mild-to-moderately impaired GFR. The extent to which acute kidney injury (AKI) plays a role in the development of hyperkalaemia remains unclear though. Similarly, it has not been investigated in detail whether renal impairment or administration of nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs) and aldosterone antagonists (AAs) are a precondition for the development of significant hyperkalaemia. The objective of this retrospective study was (i) to determine the prevalence and role of RTA IV in the development of significant hyperkalaemia; (ii) to evaluate the contribution of pre-existing cardiac failure, renal insufficiency and AKI in hyperkalaemic conditions; and (iii) to define the contribution of drugs that antagonize the renin-angiotensin-aldosterone system (RAAS).
Abstract and Introduction
Abstract
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.
Introduction
Hyperkalaemia (>5·5 mm) is a common observation in patients admitted to a hospital with an reported incidence between 1 and 3·3%. Hyperkalaemia in the presence of concomitant renal insufficiency is often attributed solely to impaired renal function, even if glomerular filtration rate (GFR) is only moderately reduced. Although renal tubular acidosis type IV (RTA IV) is thought to be a frequent disorder associated with hyperkalaemia, the diagnosis is often overlooked in clinical practice. RTA IV is defined as an acidification defect in the distal renal tubule as a result of real or functional hypoaldosteronism and is associated with hyperkalaemia and hyperchloraemic metabolic acidosis with normal anion gap. The tentative diagnosis of RTA IV is easy to establish, and aldosterone function can be evaluated using the transtubular potassium gradient (TTKG). Additional determination of renin and aldosterone may be helpful to confirm the diagnosis or to establish the underlying cause. Tubulointerstitial disease and diabetic nephropathy have been proposed to be the prevailing conditions observed in patients with RTA IV, usually associated with hyporeninaemic hypoaldosteronism. Typically, RTA IV is present in patients with only mild-to-moderately impaired GFR. The extent to which acute kidney injury (AKI) plays a role in the development of hyperkalaemia remains unclear though. Similarly, it has not been investigated in detail whether renal impairment or administration of nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs) and aldosterone antagonists (AAs) are a precondition for the development of significant hyperkalaemia. The objective of this retrospective study was (i) to determine the prevalence and role of RTA IV in the development of significant hyperkalaemia; (ii) to evaluate the contribution of pre-existing cardiac failure, renal insufficiency and AKI in hyperkalaemic conditions; and (iii) to define the contribution of drugs that antagonize the renin-angiotensin-aldosterone system (RAAS).
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