Page kidney is a rare cause of hypertension and kidney injury; it results from extrinsic compression of the kidney due to fluid accumulation in the subcapsular space. Hypertensive crisis may be the only presenting clinical sign in patients with Page kidney. Urinomas are a very rare cause of Page kidney with very few cases reported in the literature. Urinoma should be suspected in patients presenting in hypertensive crisis who have a history of recent abdominal trauma, genitourinary malignancy, and renal instrumentation. Patients diagnosed with Page kidney from a urinoma should be managed with the least invasive means possible.

Cardiac tamponade is a rare manifestation of relapsing extramedullary multiple myeloma and portends poor prognosis. No cases of cardiac tamponade with co-occurring renal obstruction from plasmacytoma have been reported in the literature, making this case a unique presentation of relapsing multiple myeloma. The presence of known malignancy should not limit our differential diagnosis when evaluating patients with signs of cardiac tamponade.

Introduction: An accurate measurement of blood pressure (BP) is critical to diagnosing and treating hypertension (HTN). Manual office BP (MOBP) often results in higher readings than automated office BP (AOBP). In previous studies, a repeat MOBP by a physician resulted in a lower BP than the initial MOBP by nursing staff. We evaluated our hypothesis that a repeat MOBP by a physician is statistically equivalent to AOBP. Methods: In an ambulatory outpatient setting, patients were roomed and at least a 5-minute interval lapsed before an AOBP was performed using a Welch Allyn Connex Vital Signs Monitor. The physician was blinded to the AOBP. The physician then entered the room and obtained a MOBP with a manual aneroid sphygmomanometer. The difference between the AOBP and the MOBP was calculated. A Wilcoxon signed rank sum test was used to determine if a significant difference between AOBP and MOBP exists. Results: A total of 186 patients (112 females, 74 male) had BP measured with a mean age of 66 years. AOBP resulted in a median systolic BP (SBP) 136 mmHg (IQR 121-150 mmHg) and median diastolic BP (DBP) of 78 mmHg (IQR 72-85 mmHg). MOBP SBP had a median of 132 mmHg (IQR 120-142 mmHg) and DBP had a median of 76 mmHg (IQR 70-81 mmHg). SBP and DBP were significantly lower in the MOBP group with a mean difference between AOBP and MOBP of 4.0 and 2.7 mmHg respectively (p-value of <0.0001). Conclusions: Repeat MOBP performed by the physician resulted in a significantly lower BP compared to AOBP. The lower BP may be due to an overall longer interval between the AOBP measurement and MOBP measurement. MOBP may be a viable option for accurate diagnosis and treatment of HTN clinics without access to a AOBP machine.

Background: Cardiac troponins I and T are highly sensitive and specific markers for acute myocardial infarction (AMI). However, a wide range of non-AMI conditions can also cause significant elevations in cardiac troponins. Given the deleterious impact of misdiagnosis of AMI, the ability to risk-stratify patients who present with an elevated troponin is paramount. We hypothesized that the maximum troponin level would be more predictive of mortality and the diagnosis of AMI than the initial troponin level or change in troponin level. Methods: Patient records from a 9-hospital system (n=30,173) in Texas were reviewed during a 24-month period in 2016-2017. Data collected for patients aged ࣙ40 years included International Classification of Diseases, Tenth Revision diagnoses, troponin I, demographic data (age, sex, smoking history, and chronic medical conditions), and death during hospitalization. We used logistic regression with the Firth penalized likelihood approach to determine the predictive ability of initial, maximum, and change in troponin level for mortality and the diagnosis of AMI. Results: Demographic characteristics of our cohort included a median age of 70 years, with 48.05% male and 51.95% female. The most common preexisting risk factor was hypertension in 78.81% of the cohort. Notable findings from the logistic regression include the predictive ability of maximum troponin on the odds of death by 0.7% for each unit of increase in troponin value. Also, the odds of AMI increased by 3.1% for each unit of increase in the maximum troponin value. Conclusion: Regardless of the level, a detectable amount of troponin in the serum results in a significantly elevated risk of mortality. Many patients with elevated troponin levels leave the hospital without a specific diagnosis, which can lead to poor outcomes because a detectable troponin does not represent a no-risk population. Our study demonstrates that maximum troponin level is a more sensitive and specific predictor of mortality than initial or change in troponin. Similarly, maximum troponin is the most predictive of AMI vs other causes of troponin elevation, likely because of the correlation between rising troponin levels and cardiomyocyte damage. Further studies are needed to correlate maximum troponin levels and clinical manifestations, which may be helpful in redefining AMI so that AMI can be distinguished more easily from non-AMI diagnoses.