Publications

BACKGROUND AND OBJECTIVES

Awareness of chronic kidney disease (CKD) among providers and patients is low. Whether clinical cues prompt recognition of CKD is unknown. We examined whether markers of kidney disease that should trigger CKD recognition among providers are associated with higher individual CKD awareness.

DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS

CKD awareness was assessed in 1852 adults with an estimated GFR <60 ml/min per 1.73 m(2) using 1999 to 2008 National Health and Nutrition Examination Survey data. CKD awareness was a "yes" answer to "Have you ever been told you have weak or failing kidneys?" Participants were grouped by distribution of the following abnormal markers of CKD: hyperkalemia, acidosis, hyperphosphatemia, elevated blood urea nitrogen, anemia, albuminuria, and uncontrolled hypertension. Odds of CKD awareness associated with each abnormal marker and groupings of markers were estimated by multivariable logistic regression.

RESULTS

Among individuals with kidney disease, only those with albuminuria had greater odds of CKD awareness (adjusted odds ratio, 4.0, P < 0.01) than those without. Odds of CKD awareness increased with each additional manifested clinical marker of CKD (adjusted odds ratio, 1.3, P = 0.05). Nonetheless, 90% of individuals with two to four markers of CKD and 84% of individuals with ≥5 markers of CKD were unaware of their disease.

CONCLUSIONS

Although individuals who manifest many markers of kidney dysfunction are more likely to be aware of their CKD, their CKD awareness remains low. A better understanding of mechanisms of awareness is required to facilitate earlier detection of CKD and implement therapy to minimize associated complications.

We have reported that pyrroloquinoline quinone (PQQ) improves reproduction, neonatal development, and mitochondrial function in animals by mechanisms that involve mitochondrial related cell signaling pathways. To extend these observations, the influence of PQQ on energy and lipid relationships and apparent protection against ischemia reperfusion injury are described herein. Sprague-Dawley rats were fed a nutritionally complete diet with PQQ added at either 0 (PQQ-) or 2 mg PQQ/Kg diet (PQQ+). Measurements included: 1) serum glucose and insulin, 2) total energy expenditure per metabolic body size (Wt(3/4)), 3) respiratory quotients (in the fed and fasted states), 4) changes in plasma lipids, 5) the relative mitochondrial amount in liver and heart, and 6) indices related to cardiac ischemia. For the latter, rats (PQQ- or PQQ+) were subjected to left anterior descending occlusions followed by 2 h of reperfusion to determine PQQ's influence on infarct size and myocardial tissue levels of malondialdehyde, an indicator of lipid peroxidation. Although no striking differences in serum glucose, insulin, and free fatty acid levels were observed, energy expenditure was lower in PQQ- vs. PQQ+ rats and energy expenditure (fed state) was correlated with the hepatic mitochondrial content. Elevations in plasma di- and triacylglyceride and β-hydroxybutryic acid concentrations were also observed in PQQ- rats vs. PQQ+ rats. Moreover, PQQ administration (i.p. at 4.5 mg/kg BW for 3 days) resulted in a greater than 2-fold decrease in plasma triglycerides during a 6-hour fast than saline administration in a rat model of type 2 diabetes. Cardiac injury resulting from ischemia/reperfusion was more pronounced in PQQ- rats than in PQQ+ rats. Collectively, these data demonstrate that PQQ deficiency impacts a number of parameters related to normal mitochondrial function.

In this case of secondary syphilis, pustular lesions progressed rapidly to painful ulcerative lesions in a patient with early HIV infection. This rapidly progressive form of early syphilis has historically been called lues maligna praecox, a severe form of noduloulcerative secondary syphilis. Serologic tests for syphilis were positive and biopsy showed forms consistent with Treponema pallidum in the lesions. This case demonstrates how HIV infection may affect presentation and diagnosis of secondary syphilis.

In vitro spine flexibility testing has been performed using a variety of laboratory-specific loading apparatuses and conditions, making test results across laboratories difficult to compare. The application of pure moments has been well established for spine flexibility testing, but to our knowledge there have been no attempts to quantify differences in range of motion (ROM) resulting from laboratory-specific loading apparatuses. Seven fresh-frozen lumbar cadaveric motion segments were tested intact at four independent laboratories. Unconstrained pure moments of 7.5 Nm were applied in each anatomic plane without an axial preload. At laboratories A and B, pure moments were applied using hydraulically actuated spinal loading fixtures with either a passive (A) or controlled (B) XY table. At laboratories C and D, pure moments were applied using a sliding (C) or fixed ring (D) cable-pulley system with a servohydraulic test frame. Three sinusoidal load-unload cycles were applied at laboratories A and B while a single quasistatic cycle was applied in 1.5 Nm increments at laboratories C and D. Non-contact motion measurement systems were used to quantify ROM. In all test directions, the ROM variability among donors was greater than single-donor ROM variability among laboratories. The maximum difference in average ROM between any two laboratories was 1.5° in flexion-extension, 1.3° in lateral bending and 1.1° in axial torsion. This was the first study to quantify ROM in a single group of spinal motion segments at four independent laboratories with varying pure moment systems. These data support our hypothesis that given a well-described test method, independent laboratories can produce similar biomechanical outcomes.