How does hyperkalemia impair ammoniagenesis

History of diarrhea suggests stool bicarbonate loss urine anion gap should be negative. See below. Often seen with accompanying hyperkalemia. Carbonic anhydrase inhibitors: Prevents proximal resorption of bicarbonate. Accompanying hypokalemia and high urine pH. History of diabetes, chronic kidney disease and interstitial nephritis can be associated with type 4 RTA.

Calculate the urinary anion gap. In normal subjects, without metabolic acidosis, the urinary anion gap is positive. In metabolic acidosis, an increased amount of ammonium is excreted as ammonium chloride.

As the ammonium concentration increases, so too does the chloride concentration and the urine anion gap decreases and becomes negative in patients with intact ammonia production. Thus, in patients with metabolic acidosis due to diarrhea or proximal type 2 RTA where ammonia production is normal , one will usually find a negative urine anion gap. The urine anion gap will remain positive in patients with non anion gap metabolic acidosis and diminished ammonium excretion such as in those with distal type 1 RTA, hypoaldosteronism type 4 RTA , and chronic kidney disease.

Check the urine pH. Recall that in distal type 1 RTA, urinary acidification is impaired and urine pH in metabolic acidosis is greater than 5. Check the serum potassium concentration. Hyperkalemia suggests type 4 RTA, which is most common however the voltage defect form of distal type 1 RTA is also possible. Check for other tubular defects which could suggest Fanconi Syndrome. A fast clinical clue is a positive urine dipstick for glucose in a patient without hyperglycemia.

Clinical clues: nephrolithiasis, nephrocalcinosis, confirm medications NSAIDs, amiloride, ifosfamide. It is critical to gather an accurate medication list including over-the-counter medications and history of chemotherapy. When interpreting the laboratory findings, it is important to know if the patient is on treatment for the RTA currently. Renal tubular acidosis is essentially a laboratory diagnosis. When present in the pediatric patient, symptoms and signs tend to be more severe, including growth defects.

In adults, there are few clinical signs or symptoms that would point to a diagnosis of RTA. Basic metabolic panel with calculation of the anion gap hyperchloremic non anion gap metabolic acidosis. More specialized tests with nephrology consultation could include: fractional K excretion, fractional HCO3 excretion, hour urine collection for creatinine, calcium, and citrate. Treatment will result in bicarbonaturia and high urine pH.

Accompanying resorptive defects Fanconi syndrome may occur with phosphaturia, glucosuria, aminoaciduria, uricosuria. Associated clinical clues: nephrocalcinosis, nephrolithiasis particularly calcium phosphate stones , hypercalcemia, hypocitraturia.

Response to treatment: depends on the etiology. Withdraw any causative medications. Fludrocortisone can be effective in hyporeninemic hypoaldosteronism. The key principles are treatment of the acidosis with alkali therapy and management of potassium derangement:. Fludrocortisone for primary adrenal insufficiency and for hyporeninemic hypoaldosteronism may require concurrent loop diuretic to avoid volume overload.

Shayakul, C, Alper, SL. Soriano, JF. Reddy, P. Int J Clin Pract. All rights reserved. No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC.

Delpire Laboratory. Mechanism of Hyperkalemia-Induced Metabolic Acidosis. Abstract Hyperkalemia in association with metabolic acidosis that are out of proportion to changes in glomerular filtration rate defines type 4 renal tubular acidosis RTA , the most common RTA observed, but the molecular mechanisms underlying the associated metabolic acidosis are incompletely understood.

ACE-inhibitors and Angiotensin-2 receptor blockers These first-line heart failure drugs are probably responsible for a massive proportion of unrecognised type 4 RTA. As these block the actions of angiotensin-2, the release of aldosterone is also inhibited. Weirdly, heparin can block the angiotensin-2 receptors — specifically in the aldosterone-secreting zona glomerulosa. It seems that with prolonged heparin use the zona glomerulosa can actually atrophy.

This, in spite of the many causes, is reasonably simple. If the patient has been intoxicated with a drug which it is feasible to cease, one expends little intellectual energy in ceasing that drug. Burk, Carol D. Schwarz, Christoph, et al.

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