Captopril-Induced Metabolic Acidosis with Hyperkalemia

Sakemi, Takanobu; Ohchi, Nobuaki; Sanai, Toru; Rikitake, Osamu; Maeda, Toshiro

doi:10.1159/000167591

Cited by 11 publications

(8 citation statements)

References 11 publications

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“…Urine analysis and clinical findings led us to suspect hypoaldosteronism: this boy had hyperchloremic metabolic acidosis with high urinary excretion of Na + accompanied by very low excretion of K + suggesting aldosterone deficiency or resistance [6]. He did not have the hyperkalaemia that is often described in these cases [3]. Moreover, it has been mentioned in the literature that hypoaldosteronism alone does not necessarily lead to hyperkalaemia: in order for hyperkalaemia to appear, some additional impairment of potassium secretion is essential [7].…”

Section: Discussionmentioning

confidence: 94%

“…There is already some evidence in the literature that ACE inhibitor can induce hypoaldosteronism in adult patients [3]: there have been reports that in the presence of impaired renal function or of a stimulated renin-angiotensin system (RAS) [3], ACE inhibitors lower aldosterone levels acting on angiotensin II, leading to insufficient re-uptake of sodium and excessive retention of H + , with resulting metabolic acidosis [4].…”

Section: Discussionmentioning

confidence: 99%

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ACE-inhibitors-induced metabolic acidosis in a child with nephrotic syndrome

Bruno

Pennesi

Marchetti

2003

Pediatric Nephrology

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

ACE-inhibitors-induced metabolic acidosis in a child with nephrotic syndrome

Bruno

Pennesi

Marchetti

2003

Pediatric Nephrology

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“…There is also an effect of lowmolecular-weight heparin on K + levels [77,78]. ACE inhibitors and AT2RA can cause hyperkalemia and acidosis, particularly in patients with advanced renal insufficiency [79][80][81]. The risk of hyperkalemia is increased by simultaneous administration of ACE inhibitors and heparin [82].…”

Section: Inhibition Of the Aldosterone Axis (Angiotensin Inhibition Amentioning

confidence: 99%

Drug-induced acid-base disorders

et al. 2014

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The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal antiinflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g

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“…Although hyperkalemia from ACEI is uncommon in patients with normal renal functions, reports of fatal hyperkalemia from ACEI exist in the literature [11][12][13][14]. It is likely that patients with CRF, who have diabetes and congestive heart failure, are at higher risk of hyperkalemia from ACEI due to preexisting defects in potassium hemostasis.…”

Section: Introductionmentioning

confidence: 99%

Predictors of the Development of Hyperkalemia in Patients Using Angiotensin-Converting Enzyme Inhibitors

Ahuja¹,

et al. 2000

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Background/Aims: Angiotensin-converting enzyme inhibitors (ACEI) are the antihypertensives of choice in patients with chronic renal failure (CRF). ACEI by decreasing the synthesis of aldosterone, the main regulator of serum potassium, predispose to the development of hyperkalemia. Although hyperkalemia with administration of ACEI is uncommon in patients with a normal renal function, a preexisting abnormality in potassium hemostasis, as seen in patients with chronic renal failure, may increase the risk of hyperkalemia. Method: To determine the predictors of development of hyperkalemia (K >5.1 mEq/l) in patients on ACEI, we retrospectively reviewed medical records of 119 patients followed in our renal clinic. Results: The mean age of the patients was 56 ± (SD) 13 (range 20–84) years. Sixty-three percent were males, and 37% were females. Sixty-seven percent had a history of diabetes. Eighty five percent of the patients had CRF [creatinine clearance (CrCl) <80 ml/min]. The baseline serum Cr was 2.3 ± 1.2 (range 0.6–6.9) mg/dl, and the CrCl was 50 ± 27.5 ml/min. Of the 119 patients 46 (38.6%) developed hyperkalemia (mean K 5.68 ± 0.3, range 5.2–6.7 mEq/l). Ninety-six percent of the patients who developed hyperkalemia had CRF, and 84% were diabetics. Pearson product-moment correlation revealed a significant positive correlation of hyperkalemia with Cr and a negative correlation of hyperkalemia with CrCl and HCO₃ (Cr: r = 0.42, p < 0.0001; CrCl: r = –0.34, p < 0.0001; HCO₃: r = –0.41, p < 0.0001). Multivariate logistic regression analysis revealed diabetes and serum creatinine to be the main predictors of hyperkalemia. In 31 patients hyperkalemia resolved either with a low-potassium (2 g/day) diet or with diet and a decrease in the dose of ACEI. In 15 patients ACEI had to be discontinued due to persistent hyperkalemia. Conclusions: We conclude that hyperkalemia is common in patients with CRF on ACEI. The majority of the patients who develop hyperkalemia on ACEI have CRF and diabetes. A large number of patients with CRF require discontinuation of ACEI due to hyperkalemia and are deprived of their renoprotective effects.

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Captopril-Induced Metabolic Acidosis with Hyperkalemia

Cited by 11 publications

References 11 publications

ACE-inhibitors-induced metabolic acidosis in a child with nephrotic syndrome

ACE-inhibitors-induced metabolic acidosis in a child with nephrotic syndrome

Drug-induced acid-base disorders

Predictors of the Development of Hyperkalemia in Patients Using Angiotensin-Converting Enzyme Inhibitors

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