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1.  Kidney Biomarkers and Differential Diagnosis of Patients With Cirrhosis and Acute Kidney Injury 
Hepatology (Baltimore, Md.)  2014;60(2):622-632.
Acute kidney injury (AKI) is common in patients with cirrhosis and associated with significant mortality. The most common etiologies of AKI in this setting are pre-renal azotemia (PRA), acute tubular necrosis (ATN) and hepatorenal syndrome (HRS). Accurately distinguishing the etiology of AKI is critical as treatments differ markedly. However, establishing an accurate differential diagnosis is extremely challenging. Urinary biomarkers of kidney injury distinguish structural from functional causes of AKI and may facilitate more accurate and rapid diagnoses. We conducted a multi-center, prospective cohort study of patients with cirrhosis and AKI assessing multiple biomarkers for differential diagnosis of clinically adjudicated AKI. Patients (n=36) whose creatinine returned to within 25% of their baseline within 48 hours were diagnosed with PRA. 76 patients with progressive AKI were diagnosed via blinded retrospective adjudication. Of these progressors, thirty-nine (53%) patients were diagnosed with ATN, 19 (26%) with PRA and 16 (22%) with HRS. Median values for neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1), liver-type fatty acid binding protein (L-FABP) and albumin differed between etiologies and were significantly higher in patients adjudicated with ATN. The fractional excretion of sodium (FENa) was lowest in patients with HRS, 0.10%, but did not differ between those with PRA, 0.27%, or ATN, 0.31%, p=0.54. The likelihood of being diagnosed with ATN increased step-wise with number of biomarkers above optimal diagnostic cutoffs.
Urinary biomarkers of kidney injury are elevated in patients with cirrhosis and AKI due to ATN. Incorporating biomarkers into clinical decision making has the potential to more accurately guide treatment by establishing which patients have structural injury underlying their AKI. Further research is required to document biomarkers specific to HRS.
PMCID: PMC4065642  PMID: 24375576
AKI; etiology; adjudication; urinary markers; ATN
2.  Crystalline-induced kidney disease: a case for urine microscopy 
Clinical Kidney Journal  2014;8(2):131-136.
PMCID: PMC4370296  PMID: 25815167
calcium oxalate; light chains; methotrexate; uric acid; urine microscopy
3.  Diagnosing drug-induced AIN in the hospitalized patient: A challenge for the clinician  
Clinical Nephrology  2014;81(6):381-388.
Drug-induced acute interstitial nephritis (AIN) is a relatively common cause of hospital-acquired acute kidney injury (AKI). While prerenal AKI and acute tubular necrosis (ATN) are the most common forms of AKI in the hospital, AIN is likely the next most common. Clinicians must differentiate the various causes of hospital-induced AKI; however, it is often difficult to distinguish AIN from ATN in such patients. While standardized criteria are now used to classify AKI into stages of severity, they do not permit differentiation of the various types of AKI. This is not a minor point, as these different AKI types often require different therapeutic interventions. Clinicians assess and differentiate AIN from these other AKI causes by utilizing clinical assessment, various imaging tests, and certain laboratory data. Gallium scintigraphy has been employed with mixed results. While a few serum tests, such as eosinophilia may be helpful, examination of the urine with tests such as dipstick urinalysis, urine chemistries, urine eosinophils, and urine microscopy are primarily utilized. Unfortunately, these tools are not always sufficient to definitively clinch the diagnosis, making it a challenging task for the clinician. As a result, kidney biopsy is often required to accurately diagnose AIN and guide management.
PMCID: PMC4326856  PMID: 24691017
urine microscopy; eosinophiluria; leukocytes; white blood cell cast; acute kidney injury; acute interstitial nephritis; acute tubular necrosis
4.  ACE-I/ARB Therapy prior to Contrast Exposure: What Should the Clinician Do? 
BioMed Research International  2014;2014:423848.
Contrast-induced nephropathy (CIN) is now one of the three leading causes of acute kidney injury in the world. A lot is known about the risk factors of CIN, yet it remains a major cause of morbidity, end stage renal disease, prolonged hospital stay, and increased costs as well as a high mortality. Many patients undergoing contrast-based radiological investigations are treated with angiotensin converting inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs) for their cardiac and renal benefits and their known mortality benefits. However, controversy exists among clinicians as to whether ACE-Is and ARBs should be continued or discontinued prior to contrast media exposure. In this paper we review the current evidence on ACE-I/ARB therapy for patients undergoing procedures involving use of contrast media and provide recommendations as to whether these drugs should be continued or held prior to contrast exposure.
PMCID: PMC3925541  PMID: 24605330
5.  Perceptions and use of the national kidney foundation KDOQI guidelines: a survey of U.S. renal healthcare providers 
BMC Nephrology  2013;14:230.
The National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (KDOQI) developed guidelines to care for patients with chronic kidney disease (CKD). While these are disseminated through the NKF’s website and publications, the guidelines’ usage remains suboptimal. The KDOQI Educational Committee was formed to identify barriers to guideline implementation, determine provider and patient educational needs and develop tools to improve care of patients with CKD.
An online survey was conducted from May to September 2010 to evaluate renal providers’ familiarity, current use of and attitudes toward the guidelines and tools to implement the guidelines.
Most responders reported using the guidelines often and felt that they could be easily implemented into clinical practice; however, approximately one-half identified at least one barrier. Physicians and physician extenders most commonly cited the lack of evidence supporting KDOQI guidelines while allied health professionals most commonly listed patient non-adherence, unrealistic guideline goals and provider time-constraints. Providers thought that the guidelines included too much detail and identified the lack of a quick resource as a barrier to clinical implementation. Most were unaware of the Clinical Action Plans.
Perceived barriers differed between renal clinicians and allied health professionals; educational and implementation tools tailored for different providers are needed.
PMCID: PMC4016578  PMID: 24152744
KDOQI; Chronic kidney disease; Guidelines; Survey
6.  Macrophages at work: phagocytosis of urinary fungi 
Clinical Kidney Journal  2013;6(2):233-234.
PMCID: PMC4432439  PMID: 26019856
urine microscopy; macrophages; fungi; pyuria
7.  Nephrotoxicity of HAART 
AIDS Research and Treatment  2011;2011:562790.
Highly active antiretroviral therapy (HAART) and other medical therapies for HIV-related infections have been associated with toxicities. Antiretroviral therapy can contribute to renal dysfunction directly by inducing acute tubular necrosis, acute interstitial nephritis, crystal nephropathy, and renal tubular disorders or indirectly via drug interactions. With the increase in HAART use, clinicians must screen patients for the development of kidney disease especially if the regimen employed increases risk of kidney injury. It is also important that patients with chronic kidney disease (CKD) are not denied the best combinations, especially since most drugs can be adjusted based on the estimated GFR. Early detection of risk factors, systematic screening for chronic causes of CKD, and appropriate referrals for kidney disease management should be advocated for improved patient care. The interaction between immunosuppressive therapy and HAART in patients with kidney transplants and the recent endorsement of tenofovir/emtricitabine by the Centers for Disease Control (CDC) for preexposure prophylaxis bring a new dimension for nephrotoxicity vigilance. This paper summarizes the common antiretroviral drugs associated with nephrotoxicity with particular emphasis on tenofovir and protease inhibitors, their risk factors, and management as well as prevention strategies.
PMCID: PMC3157198  PMID: 21860787
9.  Recurrent flank pain from ‘lobster claw’ 
NDT Plus  2011;4(4):274-275.
PMCID: PMC4421448  PMID: 25949502
computed tomographic urogram (CTU); papillary necrosis; sickle cell
10.  Plasma neutrophil gelatinase-associated lipocalin is an early biomarker for acute kidney injury in an adult ICU population 
Intensive Care Medicine  2009;36(3):444-451.
Neutrophil gelatinase-associated lipocalin (NGAL) is a useful marker for acute kidney injury (AKI), particularly when the timing of renal insult is known. However, its performance in an adult critical care setting has not been well described. We performed this study to estimate the diagnostic accuracy of plasma NGAL for early detection of AKI and need for renal replacement therapy (RRT) in an adult intensive care unit (ICU).
We enrolled 307 consecutive adult patients admitted to a general medical-surgical ICU; 301 were included in the final analysis. Serial blood samples were analyzed for plasma NGAL using a standardized clinical platform. The primary outcome was AKI, defined as an increase in creatinine of at least 50% from baseline or a reduction in urine output to <0.5 ml/kg/h for >6 h.
Of 301 patients, 133 (44%) had AKI during their ICU stay. Plasma NGAL was a good diagnostic marker for AKI development within the next 48 h (area under ROC 0.78, 95% CI 0.65–0.90), and for RRT use (area under ROC 0.82, 95% CI 0.70–0.95). Peak plasma NGAL concentrations increased with worsening AKI severity (R = 0.554, P < 0.001).
Plasma NGAL is a useful early marker for AKI in a heterogeneous adult ICU population, in which the timing of renal insult is largely unknown. It allows the diagnosis of AKI up to 48 h prior to a clinical diagnosis based on AKI consensus definitions. Additionally, it predicts need for RRT and correlates with AKI severity. Early identification of high risk patients may allow potentially beneficial therapies to be initiated early in the disease process before irreversible injury occurs.
Electronic supplementary material
The online version of this article (doi:10.1007/s00134-009-1711-1) contains supplementary material, which is available to authorized users.
PMCID: PMC2820221  PMID: 19956925
Acute kidney injury; Acute renal failure; Adult; Biomarker; Diagnostic accuracy; Intensive care unit; NGAL; Renal replacement therapy; Sensitivity; Specificity
11.  Effectiveness of polymyxin B-immobilized fiber column in sepsis: a systematic review 
Critical Care  2007;11(2):R47.
Severe sepsis and septic shock are common problems in the intensive care unit and carry a high mortality. Endotoxin, one of the principal components on the outer membrane of gram-negative bacteria, is considered important to their pathogenesis. Polymyxin B bound and immobilized to polystyrene fibers (PMX-F) is a medical device that aims to remove circulating endotoxin by adsorption, theoretically preventing the progression of the biological cascade of sepsis. We performed a systematic review to describe the effect in septic patients of direct hemoperfusion with PMX-F on outcomes of blood pressure, use of vasoactive drugs, oxygenation, and mortality reported in published studies.
We searched PubMed, the Cochrane Collaboration Database, and bibliographies of retrieved articles and consulted with experts to identify relevant studies. Prospective and retrospective observational studies, pre- and post-intervention design, and randomized controlled trials were included. Three authors reviewed all citations. We identified a total of 28 publications – 9 randomized controlled trials, 7 non-randomized parallel studies, and 12 pre-post design studies – that reported at least one of the specified outcome measures (pooled sample size, 1,425 patients: 978 PMX-F and 447 conventional medical therapy).
Overall, mean arterial pressure (MAP) increased by 19 mm Hg (95% confidence interval [CI], 15 to 22 mm Hg; p < 0.001), representing a 26% mean increase in MAP (range, 14% to 42%), whereas dopamine/dobutamine dose decreased by 1.8 μg/kg per minute (95% CI, 0.4 to 3.3 μg/kg per minute; p = 0.01) after PMX-F. There was significant intertrial heterogeneity for these outcomes (p < 0.001), which became non-significant when analysis was stratified for baseline MAP. The mean arterial partial pressure of oxygen/fraction of inspired oxygen (PaO2/FiO2) ratio increased by 32 units (95% CI, 23 to 41 units; p < 0.001). PMX-F therapy was associated with significantly lower mortality risk (risk ratio, 0.53; 95% CI, 0.43 to 0.65). The trials assessed had suboptimal method quality.
Based on this critical review of the published literature, direct hemoperfusion with PMX-F appears to have favorable effects on MAP, dopamine use, PaO2/FiO2 ratio, and mortality. However, publication bias and lack of blinding need to be considered. These findings support the need for further rigorous study of this therapy.
PMCID: PMC2206475  PMID: 17448226
12.  Hyperkalemia in the Elderly 
To review the pathophysiology underlying the predisposition to hyperkalemia in the elderly; the medications that disrupt potassium balance and promote the development of hyperkalemia in the elderly; the prevention of hyperkalemia in elderly patients treated with potassium-altering medications; and the appropriate management of hyperkalemia when it develops.
A MEDLINE search of the literature (1966 –1996) using the terms hyperkalemia, drugs, elderly, and treatment was conducted and pertinent review articles, textbooks, and personal files were consulted. Elderly subjects appear to be predisposed to the development of hyperkalemia on the basis of both innate disturbances in potassium homeostasis and comorbid disease processes that impair potassium handling. Hyperkalemia in the elderly is most often precipitated by medications that impair cellular uptake or renal disposal of potassium. This electrolyte disorder is best prevented by recognition of at-risk physiology in the aged, avoidance of therapy with certain high-risk medications, and monitoring of plasma potassium concentration and renal function at intervals appropriate for the medication prescribed. Management of hyperkalemia entails identification of the clinical manifestations of severe hyperkalemia, stabilization of cardiac tissue, promotion of cellular potassium uptake, and ultimately removal of potassium from the body.
Geriatric patients should be considered at risk of developing hyperkalemia, especially when they are prescribed certain medications. Potassium levels should be monitored at appropriate intervals when these patients are treated with potassium-altering medications. Appropriate management of hyperkalemia in the elderly can avoid life-threatening neuromuscular and cardiac complications.
PMCID: PMC1497179  PMID: 9346463
hyperkalemia; elderly; drugs; hypoaldosteronism; treatment

Results 1-12 (12)