Acute Kidney Injury Definition in Traumatic Brain Injury Patients Only Based on Serum Creatinine Criteria and Not Together With Urine Output Criteria: Are We Missing Some Acute Kidney Injury Patients?

2021 ◽  
Vol 49 (5) ◽  
pp. e553-e554
Author(s):  
Patrick M. Honore ◽  
Sebastien Redant ◽  
Keitiane Kaefer ◽  
Leonel Barreto Gutierrez ◽  
Luc Kugener ◽  
...  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Markus B. Skrifvars ◽  
Michael Bailey ◽  
Elizabeth Moore ◽  
Johan Mårtensson ◽  
Craig French ◽  
...  

2021 ◽  
Vol Volume 14 ◽  
pp. 4571-4580
Author(s):  
Ruoran Wang ◽  
Jing Zhang ◽  
Jing Xu ◽  
Min He ◽  
Jianguo Xu

2015 ◽  
Vol 33 (4) ◽  
pp. 539-547 ◽  
Author(s):  
Florence Wong

Background: Acute kidney injury (AKI) is a common complication of advanced cirrhosis. Type 1 hepatorenal syndrome is the best-known and most severe form of AKI, and it has a precise definition and a set of specific diagnostic criteria. More recently, it has become recognized that milder degrees of renal dysfunction also have a negative impact on patient outcome in various patient populations. Key Messages: Several definitions and criteria for staging the severity of AKI have been proposed, including the RIFLE (Risk, Injury, Failure, Loss of Function and End-Stage Renal Disease) group, the Acute Kidney Injury Network (AKIN), and the Kidney Disease: Improving Global Outcome (KDIGO) group. All of them incorporate some changes of serum creatinine and urine output in the definition and staging of AKI. The hepatology community has mostly embraced the AKIN diagnostic and staging criteria and has applied them in the prognostication of patients with advanced cirrhosis. However, the AKIN criteria have not been strictly applied in all studies on cirrhosis. This is partly related to the fact that changes in urine output are difficult to assess in advanced cirrhosis, and partly related to the difficulty in defining the baseline serum creatinine from which the change in serum creatinine is calculated. This has led to some confusion in the interpretation of results of the various studies on AKI in cirrhosis. More recently, some investigators have suggested incorporating the AKIN criteria with setting a lower limit of serum creatinine of 1.5 mg/dl in determining the diagnosis and prognosis of AKI in cirrhosis. Conclusions: This is an ongoing debate as to how best to define AKI in cirrhosis. In the near future there should be prospective clinical trials that will clarify which diagnostic and staging criteria of AKI will best serve the cirrhotic population.


2018 ◽  
Vol 63 (2) ◽  
pp. 200-207 ◽  
Author(s):  
Markus B. Skrifvars ◽  
Elizabeth Moore ◽  
Johan Mårtensson ◽  
Michael Bailey ◽  
Craig French ◽  
...  

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jane Rhyu ◽  
Jeffrey Wei ◽  
Christine Hema Darwin

Abstract Background: Parathyroid storm, also known as parathyroid crisis, is a rare and under-recognized endocrine emergency due to severe hypercalcemia in patients with primary hyperparathyroidism. It is characterized by significantly elevated parathyroid hormone (PTH) levels even up to 20 times above the normal limit along with calcium levels >15 mg/dl, leading to multiorgan dysfunction, notably altered mental status and acute kidney injury. Risk of mortality is high without urgent parathyroidectomy. We describe a case of a patient with acute traumatic brain injury and parathyroid storm with PTH >1700 pg/ml (11-51) and Ca 15.4 mg/dl (8.6-10.4) in whom resection of a parathyroid adenoma reversed the comatose state. Clinical Case: Our patient is a 68 year-old male with no significant past medical history who sustained a fall off a 12-foot ladder complicated by right intracranial bleed s/p hemicraniectomy and multiple fractures, including left clavicle fracture with possible subclavian artery injury, left rib fractures, and right hip fracture s/p ORIF. The patient had a brief, partial improvement of mental status, followed by comatose state in the setting of rapidly rising calcium levels and acute kidney injury. In the setting of blood transfusions, the patient had an initial Ca of 8.8 mg/dl (8.6-10.4) on admission. The calcium levels rose over a week to 15.4 mg/dl with albumin of 2.4 g/dl (3.9-5.0), PTH levels from 953 pg/ml to >1700 pg/ml (11-51) after tracheostomy, and creatinine from 0.69 mg/dl to peak of 2.0 mg/dl (0.60-1.30). In spite of IV hydration, calcitonin, cinacalcet up to 90mg twice daily, pamidronate 60mg IV, and several sessions of hemodialysis, the patient’s calcium did not normalize, and the patient remained comatose. Other labs showed phosphorus nadir of 1.4 mg/dl (2.3-4.4), 25-OH VitD 13 ng/ml (20-50), 1,25-OH VitD 9.8 pg/ml (19.9-79.3), VitA 0.6 mg/L (0.3-0.9), PTHrP <2.0 pmol/L (0.0-2.3), normal SPEP/UPEP, and peak CK of 569 U/L (63-474). Sestamibi scan showed intense tracer uptake within a nodule near the suprasternal notch, and parathyroid 4D-CT showed a left 17mm pretracheal lesion with cystic degeneration along the superior margin of the manubrium. The patient subsequently underwent parathyroidectomy of an ectopic cystic mass with normalization of calcium and PTH levels. Pathology revealed a 0.8 gram, 1.5 x 1.0 x 0.3 cm enlarged, hypercellular parathyroid. The patient woke up from his comatose state immediately after surgery with progressive improvement in mental status back to baseline, other than left-sided weakness. Conclusion: Our case highlights the importance of surgical management as an effective cure for parathyroid crisis and underscores the associated critical and significant rise in calcium and PTH levels, which was resistant to medical treatment.


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