Interprofessional geriatric and palliative care intervention associated with fewer hospital days.

Background: With increasing complexity of our aging inpatient population, we implemented an interprofessional geriatric and palliative care intervention on a hospitalist service. This study aimed to measure the intervention's impact on length of stay (LOS), 30-day readmission, and the daily intensity of inpatient services utilization.

Methods: Using a nonrandomized controlled intervention at a 1000-bed U.

Critical timing of ACEi initiation prevents compensatory glomerular hypertrophy in the remaining single kidney.

Increasing evidence suggests that single in kidney states (e.g., kidney transplantation and living donation) progressive glomerulosclerosis limits kidney lifespan.

Effect of a Multifactorial Fall Injury Prevention Intervention on Patient Well-Being: The STRIDE Study.

Background/objectives: In the Strategies to Reduce Injuries and Develop Confidence in Elders (STRIDE) study, a multifactorial intervention was associated with a nonsignificant 8% reduction in time to first serious fall injury but a significant 10% reduction in time to first self-reported fall injury relative to enhanced usual care. The effect of the intervention on other outcomes important to patients has not yet been reported. We aimed to evaluate the effect of the intervention on patient well-being including concern about falling, anxiety, depression, physical function, and disability.

A Randomized Trial of a Multifactorial Strategy to Prevent Serious Fall Injuries.

Background: Injuries from falls are major contributors to complications and death in older adults. Despite evidence from efficacy trials that many falls can be prevented, rates of falls resulting in injury have not declined.

Methods: We conducted a pragmatic, cluster-randomized trial to evaluate the effectiveness of a multifactorial intervention that included risk assessment and individualized plans, administered by specially trained nurses, to prevent fall injuries.

Interprofessional Intervention to Improve Geriatric Consultation Timing on an Acute Medical Service.

Objectives: To determine whether an interprofessional intervention would improve the use and timing of a geriatric consultation on a hospitalist service.

Design: Difference-in-differences (DID), which measures the difference in improvement over time between intervention and control team patients attributable to the intervention.

Setting: 1,000-bed U.

Strategies to Reduce Injuries and Develop Confidence in Elders (STRIDE): A Cluster-Randomized Pragmatic Trial of a Multifactorial Fall Injury Prevention Strategy: Design and Methods.

Background: Fall injuries are a major cause of morbidity and mortality among older adults. We describe the design of a pragmatic trial to compare the effectiveness of an evidence-based, patient-centered multifactorial fall injury prevention strategy to an enhanced usual care.

Methods: Strategies to Reduce Injuries and Develop Confidence in Elders (STRIDE) is a 40-month cluster-randomized, parallel-group, superiority, pragmatic trial being conducted at 86 primary care practices in 10 health care systems across United States.

FSGS as an Adaptive Response to Growth-Induced Podocyte Stress.

Glomerular sclerotic lesions develop when the glomerular filtration surface area exceeds the availability of podocyte foot process coverage, but the mechanisms involved are incompletely characterized. We evaluated potential mechanisms using a transgenic (podocin promoter-AA-4E-BP1) rat in which podocyte capacity for hypertrophy in response to growth factor/nutrient signaling is impaired. FSGS lesions resembling human FSGS developed spontaneously by 7 months of age, and could be induced earlier by accelerating kidney hypertrophy by nephrectomy.

Aging, the Medical Subspecialties, and Career Development: Where We Were, Where We Are Going.

Historically, the medical subspecialties have not focused on the needs of older adults. This has changed with the implementation of initiatives to integrate geriatrics and aging research into the medical and surgical subspecialties and with the establishment of a home for internal medicine specialists within the annual American Geriatrics Society (AGS) meeting. With the support of AGS, other professional societies, philanthropies, and federal agencies, efforts to integrate geriatrics into the medical and surgical subspecialties have focused largely on training the next generation of physicians and researchers.

Quantitative podocyte parameters predict human native kidney and allograft half-lives.

Background: Kidney function decreases with age. A potential mechanistic explanation for kidney and allograft half-life has evolved through the realization that linear reduction in glomerular podocyte density could drive progressive glomerulosclerosis to impact both native kidney and allograft half-lives.

Methods: Predictions from podometrics (quantitation of podocyte parameters) were tested using independent pathologic, functional, and outcome data for native kidneys and allografts derived from published reports and large registries.

Aging Biology in the Kidney.

The notion that kidney function declines with age in the general population is well known in the Nephrology community and the average loss of glomerular filtration rate (GFR) about 1ml per year in most longitudinal studies. There is much debate within the community about whether this represents "normal aging" or whether this constitutes a form of renal disease. However this debate turns out, the real question is whether this decline is preventable - can it be modified or slowed? Efforts to find drivers of this decline are still in the very earliest stages, but have shown some promise at elucidating some of the pathologies involved.

Glomerular Aging and Focal Global Glomerulosclerosis: A Podometric Perspective.

Kidney aging is associated with an increasing proportion of globally scarred glomeruli, decreasing renal function, and exponentially increasing ESRD prevalence. In model systems, podocyte depletion causes glomerulosclerosis, suggesting age-associated glomerulosclerosis could be caused by a similar mechanism. We measured podocyte number, size, density, and glomerular volume in 89 normal kidney samples from living and deceased kidney donors and normal poles of nephrectomies.

Urine podocyte mRNAs, proteinuria, and progression in human glomerular diseases.

Model systems demonstrate that progression to ESRD is driven by progressive podocyte depletion (the podocyte depletion hypothesis) and can be noninvasively monitored through measurement of urine pellet podocyte mRNAs. To test these concepts in humans, we analyzed urine pellet mRNAs from 358 adult and pediatric kidney clinic patients and 291 controls (n=1143 samples). Compared with controls, urine podocyte mRNAs increased 79-fold (P<0.

Slowing the aging process.

Research into the aging process is very new. For many years aging was thought to be the natural and inevitable consequence of a life of wear and tear. The idea that aging could be influenced by the genetic code and had a modifiable biologic component is less than 20 years old.

Geriatric assessment for the nephrologist.

Dialysis providers are increasingly being presented with progressively older and frailer patients, in all healthcare settings from the acute hospital to the community dialysis center. These patients commonly bring more than kidney failure with them, with a complex constellation of chronic illness, comorbidity, and functional and cognitive impairment. Navigating these challenges and coordinating the care of these highly complex patients significantly increase the work of the whole dialysis team.

Urine podocin:nephrin mRNA ratio (PNR) as a podocyte stress biomarker.

Background: Proteinuria and/or albuminuria are widely used for noninvasive assessment of kidney diseases. However, proteinuria is a nonspecific marker of diverse forms of kidney injury, physiologic processes and filtration of small proteins of monoclonal and other pathologic processes. The opportunity to develop new glomerular disease biomarkers follows the realization that the degree of podocyte depletion determines the degree of glomerulosclerosis, and if persistent, determines the progression to end-stage kidney disease (ESKD).

Aging in the glomerulus.

Kidney function declines with age in the majority of the population. Although very few older people progress to end stage, the consequences of doing so are burdensome for the patient and very expensive for the society. Although some of the observed decline is likely due to changes in the vasculature, much is associated with the development of age-associated glomerulosclerosis.

Growth-dependent podocyte failure causes glomerulosclerosis.

Podocyte depletion leads to glomerulosclerosis, but whether an impaired capacity of podocytes to respond to hypertrophic stress also causes glomerulosclerosis is unknown. We generated transgenic Fischer 344 rats that express a dominant negative AA-4E-BP1 transgene driven by the podocin promoter; a member of the mammalian target of rapamycin complex 1 (mTORC1) pathway, 4E-BP1 modulates cap-dependent translation, which is a key determinant of a cell's hypertrophic response to nutrients and growth factors. AA-4E-BP1 rat podocytes expressed the transgene and had normal kidney histology and protein excretion at 100 g of body weight but developed ESRD by 12 months.

Angiotensin II-dependent persistent podocyte loss from destabilized glomeruli causes progression of end stage kidney disease.

Podocyte depletion is a major mechanism driving glomerulosclerosis. Progression is the process by which progressive glomerulosclerosis leads to end stage kidney disease (ESKD). In order to determine mechanisms contributing to persistent podocyte loss, we used a human diphtheria toxin transgenic rat model.

Why do our kidneys get old?

The majority of the human population shows a decline in renal clearance with age and a loss of renal physiologic reserve. Kidneys are increasingly less able to deal with stressful challenges such as a salt or acid load. It is not clear what underlies this aging-related change and whether it is inevitable or can be modified in such a way as to preserve renal function throughout the life span.

NFkappaB promotes inflammation, coagulation, and fibrosis in the aging glomerulus.

The peak prevalence of ESRD from glomerulosclerosis occurs at 70 to 79 years. To understand why old glomeruli are prone to failure, we analyzed the Fischer 344 rat model of aging under ad libitum-fed (rapid aging) and calorie-restricted (slowed aging) conditions. All glomerular cells contained genes whose expression changed "linearly" during adult life from 2 to 24 months: mesangial cells (e.

Podocytes and glomerular function with aging.

Kidney function declines with age in association with the development of age-associated glomerulosclerosis. The well-established structural and functional changes with age are reviewed briefly. The modification of aging pathology by calorie restriction is discussed.

Antibodies to protein tyrosine phosphatase receptor type O (PTPro) increase glomerular albumin permeability (P(alb)).

Glomerular capillary filtration barrier characteristics are determined in part by the slit-pore junctions of glomerular podocytes. Protein tyrosine phosphatase receptor-O (PTPro) is a transmembrane protein expressed on the apical surface of podocyte foot processes. Tyrosine phosphorylation of podocyte proteins including nephrin may control the filtration barrier.

Urine podocyte mRNAs mark progression of renal disease.

Because loss of podocytes associates with glomerulosclerosis, monitoring podocyte loss by measuring podocyte products in urine may be clinically useful. To determine whether a single episode of podocyte injury would cause persistent podocyte loss, we induced limited podocyte depletion using a diphtheria toxin receptor (hDTR) transgenic rat. We monitored podocyte loss by detecting nephrin and podocin mRNA in urine particulates with quantitative reverse transcriptase-PCR.