Objective
Higher body mass index (BMI) is associated with increased risk of acute kidney injury (AKI) after major trauma. Since BMI is non-specific, reflecting lean, fluid, and adipose mass, we evaluated the use of computed tomography (CT) to determine if abdominal adiposity underlies the BMI-AKI association.
Design
Prospective cohort study.
Setting
Level I Trauma Center of a university hospital.
Patients
Patients older than 13 years with an Injury Severity Score ≥16 admitted to the trauma intensive care unit were followed for development of AKI over five days. Those with isolated severe head injury or on chronic dialysis were excluded.
Interventions
None
Measurements and Main Results
Clinical, anthropometric, and demographic variables were collected prospectively. CT images at the level of the L4-5 intervertebral disc space were extracted from the medical record and used by two operators to quantitate visceral and subcutaneous adipose tissue (VAT and SAT, respectively) areas. AKI was defined by Acute Kidney Injury Network (AKIN) creatinine and dialysis criteria. Of 400 subjects, 327 (81.8%) had CT scans suitable for analysis: 264/285 (92.6%) blunt trauma subjects, 63/115 (54.8%) penetrating trauma subjects. VAT and SAT areas were highly correlated between operators (ICC>0.999, p<0.001 for each) and within operator (ICC>0.999, p<0.001 for each). In multivariable analysis, the standardized risk of AKI was 15.1% (95% CI 10.6%,19.6%), 18.1% (14%,22.2%), and 23.1% (18.3%,27.9%) at the 25th, 50th, and 75th percentiles of VAT area, respectively (p=0.001), with similar findings when using SAT area as the adiposity measure.
Conclusions
Quantitation of abdominal adiposity using CT scans obtained for clinical reasons is feasible and highly reliable in critically ill trauma patients. Abdominal adiposity is independently associated with AKI in this population, confirming that excess adipose tissue contributes to the BMI-AKI association. Further studies of the potential mechanisms linking adiposity with AKI are warranted.
Endocrine tumors are a less common but important component of the clinical spectrum of a number of hereditary tumor syndromes such as neurofibromatosis type 1, Peutz-Jeghers syndrome, Beckwith-Wiedemann syndrome, the tuberous sclerosis complex, Li-Fraumeni syndrome, PTEN hamartoma tumor syndrome, and APC-associated polyposis. It is important to recognize the often unique clinical presentations of these tumors and possible strategies for presymptomatic screening and early diagnosis.
We report a case of acute kidney injury as the initial manifestation of sarcoidosis. A 55-year-old male was sent from his primary care physician's office with incidental lab findings significant for hypercalcemia and acute kidney injury with past medical history significant for nephrolithiasis. Initial treatment with intravenous hydration did not improve his condition. The renal biopsy subsequently revealed granulomatous interstitial nephritis (GIN). Treatment with the appropriate dose of glucocorticoids improved both the hypercalcemia and renal function. Our case demonstrates that renal limited GIN due to sarcoidosis, although a rare entity, can cause severe acute kidney injury and progressive renal failure unless promptly diagnosed and treated.
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