Hyperammonemia associated with distal renal tubular acidosis or urinary tract infection: a systematic review

Clericetti, Caterina M.; Milani, Gregorio P.; Lava, Sebastiano A. G.; Bianchetti, Mario G.; Simonetti, Giacomo D.; Giannini, Olivier

doi:10.1007/s00467-017-3829-7

Cited by 20 publications

(13 citation statements)

References 48 publications

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“…This would be consistent with her neurological recovery and resolving lactataemia with the use of laxatives. However, recent publications have suggested a link between RTA and hyperammonemia where altered distal renal tubular acidification may cause hyperammonemia 12 13…”

Section: Discussionmentioning

confidence: 99%

Impaired consciousness, hypokalaemia and renal tubular acidosis in sustained Nurofen Plus abuse

Hasan

Armstrong

et al. 2019

BMJ Case Rep

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Ibuprofen-induced renal tubular acidosis is a rare but important diagnosis which should be considered in patients presenting with hypokalaemia and metabolic acidosis. This case report details the case of a 33-year-old woman presenting with reduced conscious state, metabolic acidosis and profound hypokalaemia without an obvious cause. With correction of the patient’s electrolyte and acid-base disturbance, her conscious state improved allowing disclosure of her use of Nurofen Plus for its euphoric opiate effects. The diagnosis of renal tubular acidosis had been considered and subsequent disclosure of excessive chronic ingestion of ibuprofen suggested this to be the underlying cause. The striking feature of our patient was the insidious development of the problem and delayed accurate drug history. An important safety message arising from our case is the composite risk of dependence on the opiate component of over the counter analgesics, such as Nurofen Plus, and adverse events related to the ibuprofen component.

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Section: Discussionmentioning

confidence: 99%

Impaired consciousness, hypokalaemia and renal tubular acidosis in sustained Nurofen Plus abuse

Hasan

Armstrong

et al. 2019

BMJ Case Rep

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“… 2 , 7 - 9 , 20 - 22 NH 3 is then transported through the portal circulation to hepatocytes where 90% is converted to urea through the urea cycle (UC) and the remainder is converted to glutamine (Gln) via glutamine synthetase (GS). 1 , 7 , 9 , 10 , 16 , 20 , 21 , 23 - 25 This enzyme serves an identical function in non-hepatic tissues such as the brain and skeletal muscle. 2 , 7 - 9 , 22 Gln can then be used for energy production in the gut or be excreted in the urine.…”

Section: Pathophysiologymentioning

confidence: 99%

“… 1 , 7 , 9 , 10 , 16 , 20 , 21 , 23 - 25 This enzyme serves an identical function in non-hepatic tissues such as the brain and skeletal muscle. 2 , 7 - 9 , 22 Gln can then be used for energy production in the gut or be excreted in the urine. 24 Secondarily, NH 3 is produced by deamination in skeletal muscle 2 , 7 - 9 , 22 and the kidneys.…”

Section: Pathophysiologymentioning

confidence: 99%

“… 2 , 7 - 9 , 22 Gln can then be used for energy production in the gut or be excreted in the urine. 24 Secondarily, NH 3 is produced by deamination in skeletal muscle 2 , 7 - 9 , 22 and the kidneys. 2 , 7 - 9 , 22 , 26 The kidneys are able to regulate NH 3 levels by shifting their production to excretion ratio to favor excretion in times of elevated NH 3 .…”

Section: Pathophysiologymentioning

confidence: 99%

“… 1 , 6 The most common cause of the disorder in adults is hepatic dysfunction—particularly cirrhosis. 7 - 9 In children, it is classically associated with inborn-errors-of-metabolism concerning urea cycle enzymes and transporters, 1 , 10 , 11 collectively called urea cycle disorders (UCDs). More recently, however, hyperammonemia has been increasingly linked to organ transplantation—particularly in lung transplant recipients.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Hyperammonemia Post Lung Transplantation: A Review

Leger

Silverman

Hauck

et al. 2020

Clin Med Insights Circ Respir Pulm Med

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Hyperammonemia is the pathological accumulation of ammonia in the blood, which can occur in many different clinical settings. Most commonly in adults, hyperammonemia occurs secondary to hepatic dysfunction; however, it is also known to be associated with other pathologies, surgeries, and medications. Although less common, hyperammonemia has been described as a rare, but consistent complication of solid organ transplantation. Lung transplantation is increasingly recognized as a unique risk factor for the development of this condition, which can pose grave health risks—including long-term neurological sequelae and even death. Recent clinical findings have suggested that patients receiving lung transplantations may experience postoperative hyperammonemia at rates as high as 4.1%. A wide array of etiologies has been attributed to this condition. A growing number of case studies and investigations suggest disseminated opportunistic infection with Ureaplasma or Mycoplasma species may drive this metabolic disturbance in lung transplant recipients. Regardless of the etiology, hyperammonemia presents a severe clinical problem with reported mortality rates as high as 75%. Typical treatment regimens are multimodal and focus on 3 main avenues of management: (1) the reduction of impact on the brain through the use of neuroprotective medications and decreasing cerebral edema, (2) augmentation of mechanisms for the elimination of ammonia from the blood via hemodialysis, and (3) the diminishment of processes producing predominantly using antibiotics. The aim of this review is to detail the pathophysiology of hyperammonemia in the setting of orthotopic lung transplantation and discuss methods of identifying and managing patients with this condition.

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Hyperammonemia and lactic acidosis in adults: Differential diagnoses with a focus on inborn errors of metabolism

Tchan

2018

Rev Endocr Metab Disord

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The adult endocrinologist may be asked to consult on a patient for unexplained biochemical disturbances that could be caused by an underlying inborn error of metabolism. A genetic disorder is generally less likely to be the cause as these disorders are individually rare, however inborn errors of metabolism are collectively not infrequent and important to consider as they may be treatable and tragic outcomes avoided. Hyperammonemia or lactic acidosis are most often secondary markers of an acquired primary disease process, but they may be a clue to the presence of a genetic disorder. Herein is presented an approach to the differential diagnosis of elevated ammonia and lactate, and a brief discussion of management for when an inborn error is diagnosed.

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Hyperammonemia associated with distal renal tubular acidosis or urinary tract infection: a systematic review

Abstract: This study reveals that both altered distal renal tubular acidification and urinary tract infection may be associated with relevant hyperammonemia in both children and adults.

Cited by 20 publications

References 48 publications

Impaired consciousness, hypokalaemia and renal tubular acidosis in sustained Nurofen Plus abuse

Impaired consciousness, hypokalaemia and renal tubular acidosis in sustained Nurofen Plus abuse

Hyperammonemia Post Lung Transplantation: A Review

Hyperammonemia and lactic acidosis in adults: Differential diagnoses with a focus on inborn errors of metabolism

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