Review of the Diagnostic Evaluation of Normal Anion Gap Metabolic Acidosis

Berend, Kenrick

doi:10.1159/000479279

Cited by 24 publications

(54 citation statements)

References 43 publications

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“…It can occur in patients with a normal or only mildly decreased glomerular filtration rate (GFR), as well as those with chronic kidney disease (CKD) [ 7 , 8 ]. RTA is a cause of hyperchloremic normal anion gap acidosis, in which the loss of serum HCO 3 – leads to retention of Cl – so that the anion gap remains normal [ 9 ].…”

Section: Classification Of Rtamentioning

confidence: 99%

“…Extrarenal metabolic acidosis is associated with elevated levels of H + and urinary NH 4 + excretion [ 7 ]. Severe or chronic diarrhea commonly causes hyperchloremic metabolic acidosis through the loss of large amounts of gastrointestinal HCO 3 – , particularly as HCO 3 – concentrations are usually higher in diarrheal fluid than in plasma [ 8 , 9 ]. The reduction in plasma volume triggers an increase in kidney NaCl reabsorption which, in combination with HCO 3 – losses, leads to normal anion gap metabolic acidosis [ 7 ].…”

Section: Clinical Management Of Rtamentioning

confidence: 99%

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Renal Tubular Acidosis and Management Strategies: A Narrative Review

2020

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Renal tubular acidosis (RTA) occurs when the kidneys are unable to maintain normal acid−base homeostasis because of tubular defects in acid excretion or bicarbonate ion reabsorption. Using illustrative clinical cases, this review describes the main types of RTA observed in clinical practice and provides an overview of their diagnosis and treatment. The three major forms of RTA are distal RTA (type 1; characterized by impaired acid excretion), proximal RTA (type 2; caused by defects in reabsorption of filtered bicarbonate), and hyperkalemic RTA (type 4; caused by abnormal excretion of acid and potassium in the collecting duct). Type 3 RTA is a rare form of the disease with features of both distal and proximal RTA. Accurate diagnosis of RTA plays an important role in optimal patient management. The diagnosis of distal versus proximal RTA involves assessment of urinary acid and bicarbonate secretion, while in hyperkalemic RTA, selective aldosterone deficiency or resistance to its effects is confirmed after exclusion of other causes of hyperkalemia. Treatment options include alkali therapy in patients with distal or proximal RTA and lowering of serum potassium concentrations through dietary modification and potential new pharmacotherapies in patients with hyperkalemic RTA including newer potassium binders.

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Section: Classification Of Rtamentioning

confidence: 99%

Section: Clinical Management Of Rtamentioning

confidence: 99%

Renal Tubular Acidosis and Management Strategies: A Narrative Review

2020

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“…The findings of chronic hyperkalemia, low-normal serum bicarbonate and urine PH <5.5 is very suggestive of RTA type 4 as the tonic effect of cortisol makes hyponatremia rare. Moreover, the absence of thirst prevents antidiuretic hormone (ADH) stimulation [8]. Withdrawal of precipitants is often enough in managing these patients.…”

Section: Discussionmentioning

confidence: 99%

Intradialysis Cardiac Arrest in a 40 year old Woman with Diabetic Nephropathy Precipitated by Hyperkalemia Induced by Type 4 Renal Tubular Acidosis.

Nwinne

Adedeji

2022

IJHS

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Purpose: We present a rare case of intra-dialytic cardiac arrest secondary to renal tubular acidosis precipitated by severe hyperkalemia. Renal tubular acidosis (RTA) type 4 results from defective distal tubular (DT) response to aldosterone and could lead to hyperkalemia and metabolic acidosis, conditions which in their severe forms, can precipitate cardiac arrest. Methodology: Here, we present the management of intra-dialysis cardiac arrest precipitated by severe hyperkalemia. Results: Patient was an 18 year old female, diabetic who had 3 episodes of intra-dialysis cardiac arrest requiring cardiac defibrillation. She was dyspneic, drowsy, pale, had flapping tremor and a tunneled internal jugular catheter insitu. Her pulse was 124/min, blood pressure was 166/98 mmHg and the third heart sounds was heard. Urinalysis showed 3 (+++) of protein. Arterial blood gases (ABGs) revealed hyperkalemia (7.0mmol/l), hypobicarbonatemia (12mmol/l), blood PH (7.2) and blood glucose (249mmol). Serum creatinine was 947umol/l and tall tented T waves were seen on electrocardiogram. Unique contribution to theory, practice and policy: With a carefully prescribed dialysis, meal and drug regimen, intra-dialysis cardiac arrest can be prevented, and well managed when it occurs.

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“…The increases in potassium and chloride were expected; however, the increase in potassium was less than that of chloride, which led to an increase in anion gap. The anion gap measurement is an important diagnostic tool, introduced by Gamble (1936), that measures the main cations and anions in the blood (Berend, 2017). It is known that a mechanism to buffer an increase in potassium in the ECF is the intracellular internalization of potassium.…”

Section: Discussionmentioning

confidence: 99%

Electrocardiographic changes in the acute hyperkalaemia produced by intragastric KCl load in rats

Fazan

Colombari

Menani

et al. 2021

Experimental Physiology

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A variety of animal models have been proposed to study hyperkalaemia, but most of them have meaningful limitations when the goal is to study the effect of potassium overload on healthy kidneys. In this study, we aimed to introduce a new approach for induction of hyperkalaemia in a reliable and reproducible animal model. We used intragastric administration of potassium chloride [KCl 2.3 M, 10 ml/(kg body weight)] to male Holtzman rats (300-350 g) to induce hyperkalaemia. The results showed that this potassium load can temporarily overwhelm the renal and extrarenal handling of this ion, causing an acute and severe hyperkalaemia that can be useful to study the effect of potassium imbalance in a variety of scenarios. Severe hyperkalaemia (>8 meqiv/l) and very profound ECG alterations, characterized by lengthening waves and intervals, were seen as early as 30 min after intragastric administration of KCl in rats. In addition, a transient increase in arterial blood pressure and time-dependent bradycardia were also seen after the KCl administration. No metabolic acidosis was present in the animals, and the potassium ion did not increase proportionally to chloride ion in the blood, leading to an increased anion gap. In conclusion, the results suggest that intragastric KCl loading is a reliable model to promote rapid and severe hyperkalaemia that can be used for further research on this topic.

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Review of the Diagnostic Evaluation of Normal Anion Gap Metabolic Acidosis

Cited by 24 publications

References 43 publications

Renal Tubular Acidosis and Management Strategies: A Narrative Review

Renal Tubular Acidosis and Management Strategies: A Narrative Review

Intradialysis Cardiac Arrest in a 40 year old Woman with Diabetic Nephropathy Precipitated by Hyperkalemia Induced by Type 4 Renal Tubular Acidosis.

Electrocardiographic changes in the acute hyperkalaemia produced by intragastric KCl load in rats

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