Baseline Urinary Angiotensinogen Excretion Predicts Deterioration of the Kidney Function in Patients with Chronic Kidney Disease

Objective The intrarenal renin-angiotensin system (RAS) is activated in patients with chronic kidney disease (CKD), and urinary angiotensinogen (AGT) levels, a surrogate marker of the intrarenal RAS activation, are associated with blood pressure (BP) and urinary albumin excretion. In addition, it has been shown that changes in urinary AGT levels correlate with annual changes in the estimated glomerular filtration rate (eGFR) in patients with type 2 diabetes and that elevated levels of urinary AGT in type 2 diabetic patients with albuminuria are a high-risk factor for worsening renal and cardiovascular complications. However, whether or not baseline urinary AGT levels predict deterioration of the kidney function in all patients with CKD is unclear. Methods We recruited 62 patients with CKD whose eGFR was ＞15 mL/min/1.73 m². We performed 24-hour ambulatory BP monitoring at 30-min intervals and daily urinary collection to examine the urinary AGT levels and albumin excretion and measured the levels of plasma angiotensin II (Ang II), a surrogate marker of circulating RAS. In addition, annual changes in the eGFR were followed up for 3.4±1.5 years. Results Annual changes in the eGFR were significantly and negatively associated with urinary AGT levels (r=-0.31, p=0.015) as well as the age, systolic BP, and urinary albumin levels. In contrast, annual changes in the eGFR were not correlated with plasma Ang II levels. Furthermore, when dividing patients into quartiles according to urinary AGT levels, patients with the highest urinary AGT levels showed a progressive decline in the eGFR. Conclusion These results suggest that elevated baseline urinary AGT levels can predict renal dysfunction in patients with CKD.     

Subacute Kidney Injury in Hospitalized Patients

Background and objectives

The epidemiology of AKI and CKD has been described. However, the epidemiology of progressively worsening kidney function (subacute kidney injury [s-AKI]) developing over a longer time frame than defined for AKI (7 days), but shorter than defined for CKD (90 days), is completely unknown.

Design, setting, participants, & measurements

This retrospective study used a hospital laboratory and admission database. Adult patients admitted to a teaching hospital in Tokyo, Japan, between April 1, 2008, and October 31, 2011, were included. s-AKI was classified into three grades of severity (mild, moderate, severe) in accordance with the Risk, Injury, and Failure categories of the Risk, Injury, Failure, Risk, Loss, and ESRD classification, but did not use its time frame. Kidney injury (AKI and s-AKI) occurring during each hospital stay was identified, and logistic regression analysis was performed to assess their effect on hospital mortality.

Results

Of 56,567 patients admitted to the hospital during the study period, 49,518 were included. Of these, 87.8% had no evidence of kidney dysfunction, 11.0% had AKI, and 1.1% had s-AKI. Patients with s-AKI had mild renal dysfunction in 82.7% of cases, moderate in 12.1%, and severe in 5.0%. Worsening s-AKI category was linearly correlated with hospital mortality, as previously described for AKI (no injury: 1.2%, mild: 6.5%, moderate: 12.9%, severe: 20.7%). Although mortality (8.0% versus 17.5%) and need for renal replacement therapy (0.2% versus 2.2%) were lower in patients with s-AKI than in those with AKI, multivariable regression analysis confirmed that s-AKI was an independent risk factor for hospital mortality (odds ratio (OR), 5.44; 95% confidence interval [95% CI], 3.89 to 7.44); the OR with AKI was 14.8 (95% CI, 13.2 to 16.7).

Conclusions

Close to 1% of hospitalized patients develop s-AKI. This condition is independently associated with increased hospital mortality, and the risk for death increases with s-AKI severity. Patients with s-AKI had a better outcome and were less likely to require renal replacement therapy than patients with AKI.     

Impaired Kidney Function and Atrial Fibrillation in Elderly Subjects

BackgroundImpaired kidney function is associated with increased risk for cardiovascular events. We evaluated whether kidney function is associated with atrial fibrillation (AF) risk in elderly persons.Methods and ResultsSubjects were participants in the Cardiovascular Health Study (CHS), a population-based cohort of ambulatory elderly. Measures of kidney function were cystatin C and creatinine-based estimated glomerular filtration rate (eGFR). Among the 4663 participants, 342 (7%) had AF at baseline and 579 (13%) developed incident AF during follow-up (mean 7.4 years). In unadjusted analyses, cystatin C quartiles were strongly associated with prevalent AF with a nearly 3-fold odds in the highest quartile compared with the lowest (HR = 1.19, 95% CI [0.80-1.76] in quartile 2; HR = 2.00, 95% CI [1.38-2.88] in quartile 3; and HR = 2.87, 95% CI [2.03-4.07] in quartile 4). This increased risk for prevalent AF remained significant after multivariate adjustment. The risk for incident AF increased across cystatin C quartiles in the unadjusted analysis (HR = 1.37, 95% CI [1.07-1.75] in quartile 2; HR = 1.43, 95% CI [1.11-1.84] in quartile 3; and HR = 1.88, 95% CI [1.47-2.41] in quartile 4); however, after multivariate adjustment, these findings were no longer significant. An estimated GFR <60 mL·min·1.73 m² was associated with prevalent and incident AF in unadjusted, but not multivariate analyses.ConclusionsImpaired kidney function, as measured by cystatin C, is an independent marker of prevalent AF; however, neither cystatin C nor eGFR are predictors of incident AF.     

高血压合并肾损害患者血管紧张素Ⅱ1型受体和α1受体自身抗体与尿白蛋白

目的 探讨高血压合并肾损害患者血管紧张素Ⅱ1型受体(AT1R)和α1受体自身抗体与蛋白尿的关系.方法 以合成的AT1R和α1受体多肽片段为抗原,应用酶联免疫吸附测定(ELISA)技术,检测高血压合并肾损害患者(A组)71例、高血压无肾损害患者(B组)60例及40例健康者(C组)血清中抗G蛋白偶联型AT1R和α1受体自身抗体.尿白蛋白检测亦用酶联免疫吸附法(ELISA)测定技术检测.A组根据尿白蛋白排泄率(UAER)再分为A1组(UAER≥200 μg/min)与A2组(UAER 20～199 μg/min).结果 A组抗AT1和α1受体抗体阳性率为54.9%(39/71)和54.9%(39/71),明显高于B组的13.3%(7/60)和15.0%(9/60)及C组的12.5%(5/40)和7.5%(3/40),P＜0.01.UAER较高的A1组,抗AT1R和α1受体自身抗体阳性率为87.1%(27/31)和80.6%(25/31),明显高于UAER较低的A2组的30.0%(12/40)和35.0%(14/40),P＜0.01.结论 血清抗G蛋白偶联型AT1R和α1受体自身抗体可能与高血压合并肾损害有关,AT1R和α1受体自身抗体阳性率与尿微量白蛋白排出的严重程度有关.AT1R和α1受体自身抗体在高血压合并肾损害发病中起了重要作用.     

Promoting Kidney Function Recovery in Patients with AKI Requiring RRT

AKI requiring RRT is associated with high mortality, morbidity, and long-term consequences, including CKD and ESRD. Many patients never recover kidney function; in others, kidney function improves over a period of many weeks or months. Methodologic constraints of the available literature limit our understanding of the recovery process and hamper adequate intervention. Current management strategies have focused on acute care and short-term mortality, but new data indicate that long-term consequences of AKI requiring RRT are substantial. Promotion of kidney function recovery is a neglected focus of research and intervention. This lack of emphasis on recovery is illustrated by the relative paucity of research in this area and by the lack of demonstrated effective management strategies. In this article the epidemiologic implications of kidney recovery after AKI requiring RRT are discussed, the available literature and its methodologic constraints are reviewed, and strategies to improve the understanding of factors that affect kidney function recovery are proposed. Measures to promote kidney function recovery are a serious unmet need, with a great potential to improve short- and long-term patient outcomes.     

Urine Microscopy Is Associated with Severity and Worsening of Acute Kidney Injury in Hospitalized Patients

Background and objectives: Serum creatinine concentration at the time of nephrology consultation is not necessarily indicative of the severity of acute kidney injury (AKI). Although urine microscopy is useful to differentiate AKI, its role in predicting adverse clinical outcomes has not been well described.Design, setting, participants, & measurements: The relationship between urine microscopy findings at the time of nephrology consultation for AKI and clinical outcomes was evaluated prospectively. A urinary sediment scoring system was created on the basis of the number of renal tubular epithelial cells and granular casts. The primary outcome was worsening of AKI (progressing to higher AKI Network stage, dialysis, or death) during hospitalization.Results: Of 249 patients consulted for AKI, 197 had acute tubular necrosis or prerenal AKI and were included in the analysis. At consultation, 80 (40%) had stage 1, 53 (27%) had stage 2, and 66 (33%) had stage 3 AKI. The urinary sediment combined scores were lowest in those with stage 1 and highest in stage 3 AKI. Seventy-nine patients (40%) experienced worsening of AKI from the time of consultation. The urinary scoring system was significantly associated with increased risk of worsening AKI (adjusted relative risk: 7.3; 95% confidence interval: 4.5 to 9.7 for worsening with score of ≥3 versus score of 0) and was more predictive than AKI Network stage at the time of consultation.Conclusions: The urinary sediment score may be a useful tool to predict worsening of AKI due to either acute tubular necrosis or prerenal AKI during hospitalization.Currently, diagnosis of acute kidney injury (AKI) is based on serum creatinine concentration and urine output. The Acute Kidney Injury Network (AKIN) definition is based on these two parameters and uses various cutoffs to define three distinct AKI stages (1). Urine microscopy and biochemistry are complementary to these diagnostic parameters and provide information that facilitates the differentiation of AKI into traditional categories, including prerenal AKI and acute tubular necrosis (ATN), the most common causes of hospital-acquired AKI (2–4). Urinary microscopy in patients with ATN classically is described as containing renal tubular epithelial (RTE) cells, RTE cell casts, granular casts, or mixed cellular casts, whereas sediment in patients with prerenal AKI usually is bland or contains occasional hyaline casts (5–9). In fact, we recently demonstrated that urine microscopy at the time of nephrology consultation, on the basis of the number of RTE cells and granular casts (10). We believe this is important because both prognosis and therapies for prerenal AKI and ATN differ substantially, making early clinical differentiation fundamental to AKI management.

Table 1.

Scoring system based on number of granular casts and RTE cells

高胆固醇血症患者高密度脂蛋白损伤血管功能

目的观察高胆固醇血症患者高密度脂蛋白性质改变及其对血管功能的影响,探讨高胆固醇血症患者中高密度脂蛋白促进动脉粥样硬化的可能机制。方法分别取20名健康志愿者(男12例,女8例)和20例高胆固醇血症患者(男11例,女9例)作为观察对象,年龄均在18~60岁;测定其血浆中总胆固醇、甘油三酯、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇水平,并对高密度脂蛋白的趋炎性进行分析。用血浆提取的高密度脂蛋白处理小鼠的主动脉,观察血管的收缩与舒张功能。结果高胆固醇血症患者血浆总胆固醇、甘油三酯、低密度脂蛋白胆固醇水平明显高于健康志愿者(P0.05),高密度脂蛋白胆固醇水平与健康志愿者比较无明显差异(P0.05)。高胆固醇血症患者与健康志愿者相比高密度脂蛋白趋炎性增加,趋炎的高密度脂蛋白明显抑制内皮依赖的血管舒张功能。结论高胆固醇血症状态下高密度脂蛋白处于炎症状态,失去对血管的保护作用,抑制内皮依赖的血管舒张功能,可能是促进动脉粥样硬化形成的一个重要原因。     

D-dimer Testing in Patients with Suspected Pulmonary Embolism and Impaired Renal Function

Background

Determination of pretest probability and D-dimer tests are the first diagnostic steps in patients with suspected pulmonary embolism, which can be ruled out when clinical probability is unlikely and D-dimer level is normal. We evaluated the utility of D-dimer testing in patients with impaired renal function.

Methods

D-dimer tests were performed in consecutive patients with suspected pulmonary embolism and an unlikely clinical probability. Creatinine levels were assessed as clinical routine. Glomerular filtration rate was calculated using the Modification of Diet in Renal Disease formula. Correlation between D-dimer level and renal function and proportions of patients with normal D-dimer in different categories of estimated glomerular filtration rate (eGFR) were assessed. Different categories of decreasing eGFR were defined as: normal renal function (eGFR >89 mL/min), mild decrease in eGFR (eGFR 60-89 mL/min), and moderate decrease in eGFR (eGFR 30-59 mL/min).

Results

Creatinine levels were assessed in 351 of 385 patients (91%). D-dimer levels significantly increased in 3 categories of decreasing eGFR (P = .027 and P = .021 for moderate renal impairment compared with mild renal impairment and normal renal function, respectively). Normal D-dimer levels were found in 58% of patients with eGFR >89 mL/min, in 54% with eGFR 60-89 mL/min, and in 28% with eGFR 30-59 mL/min.

Conclusions

The specificity of D-dimer testing in patients with suspected pulmonary embolism and decreased GFR is significantly decreased. Nonetheless, performing D-dimer tests is still useful because computed tomography scanning can be withheld in a significant proportion of these patients.     

Effects of Quinapril Hydrochloride in Patients with Essential Hypertension and Impaired Renal Function

The short-term effects of administration of an angiotensin-converting enzyme (ACE) inhibitor, quinapril hydrochloride (quinapril) (5–10mg/day), for 12 weeks on blood pressure and renal function were evaluated in 8 patients (60.5±7.3 years old, mean±SD) with mild to moderate essential hypertension and mild impairment of renal function due to nephrosclerosis. Systolic blood pressure and diastolic blood pressure were significantly reduced from 163.0± 4.0 to 132.3± 17.6 mmHg (p<0.01) and from 98.3± 4.6 to 81.5± 6.4 mmHg (p<0.001), respectively, before to after treatment. Both renal plasma flow (RPF) and glomerular filtration rate (GFR) were significantly increased in all patients, from 203.9 ± 33.3 to 245.4 ± 36.7 ml/min/1.73m² (p<0.01), and from 43.4± 6.4 to 53.5± 4.6 ml/min/1.73m² (p<0.05), respectively.

Short-term quinapril administration was beneficial to renal function in patients with essential hypertension and impaired renal function.     

Chronic Renal Insufficiency Cohort (CRIC) Study: Baseline Characteristics and Associations with Kidney Function

Background and objectives: The Chronic Renal Insufficiency Cohort (CRIC) Study was established to examine risk factors for the progression of chronic kidney disease (CKD) and cardiovascular disease (CVD) in patients with CKD. We examined baseline demographic and clinical characteristics.Design, setting, participants, & measurements: Seven clinical centers recruited adults who were aged 21 to 74 yr and had CKD using age-based estimated GFR (eGFR) inclusion criteria. At baseline, blood and urine specimens were collected and information regarding health behaviors, diet, quality of life, and functional status was obtained. GFR was measured using radiolabeled iothalamate in one third of participants.Results: A total of 3612 participants were enrolled with mean age ± SD of 58.2 ± 11.0 yr; 46% were women, and 47% had diabetes. Overall, 45% were non-Hispanic white, 46% were non-Hispanic black, and 5% were Hispanic. Eighty-six percent reported hypertension, 22% coronary disease, and 10% heart failure. Mean body mass index was 32.1 ± 7.9 kg/m², and 47% had a BP >130/80 mmHg. Mean eGFR was 43.4 ± 13.5 ml/min per 1.73 m², and median (interquartile range) protein excretion was 0.17 g/24 h (0.07 to 0.81 g/24 h). Lower eGFR was associated with older age, lower socioeconomic and educational level, cigarette smoking, self-reported CVD, peripheral arterial disease, and elevated BP.Conclusions: Lower level of eGFR was associated with a greater burden of CVD as well as lower socioeconomic and educational status. Long-term follow-up of participants will provide critical insights into the epidemiology of CKD and its relationship to adverse outcomes.The prevalence of ESRD that requires renal replacement therapy has risen dramatically in the United States during the past three decades (1). Non–dialysis-requiring chronic kidney disease (CKD) is substantially more common than ESRD, with an estimated 15 million adults in the United States having CKD of stage 3 or worse (as defined by an estimated GFR [eGFR] of <60 ml/min per 1.73 m²) (2) Furthermore, CKD frequently progresses in severity, but the factors that are responsible for accelerated decline need further elucidation. In addition, recent studies have highlighted an important association between even mild CKD and increased risk for cardiovascular disease (CVD) (3), but the mechanisms for this association remain unclear.In response to the epidemic of CKD and our incomplete understanding of factors that govern its progression and associated morbidity, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) established the Chronic Renal Insufficiency Cohort (CRIC) Study in 2001. The broad aims of the CRIC Study are to examine risk factors for the progression of kidney disease and CVD in patients with CKD and to develop predictive models to identify high-risk subgroups. The design and methods of the CRIC Study have been previously reported (4). In this article, we characterize the eligibility and recruitment methods, describe the baseline characteristics of patients enrolled in the cohort, and report initial analyses of correlates of level of eGFR.     

Association between Serum Potassium and Outcomes in Patients with Reduced Kidney Function

Background and objectives

Patients with CKD are more likely than others to have abnormalities in serum potassium (K⁺). Aside from severe hyperkalemia, the clinical significance of K⁺ abnormalities is not known. We sought to examine the association of serum K⁺ with mortality and hospitalization rates within narrow eGFR strata to understand how the burden of hyperkalemia varies by CKD severity. Associations were examined between serum K⁺ and discontinuation of medications that block the renin-angiotensin-aldosterone system (RAAS), which are known to increase serum K⁺.

Design, setting, participants, & measurements

A cohort of patients with CKD (eGFR<60 ml/min per 1.73 m²) with serum K⁺ data were studied (n=55,266) between January 1, 2009, and June 30, 2013 (study end). Serum K⁺, eGFR, and covariates were considered on a time-updated basis. Mortality, major adverse cardiovascular events (MACE), hospitalization, and discontinuation of RAAS blockers were considered per time at risk.

Results

During the study, serum K⁺ levels of 5.5–5.9 and ≥6.0 mEq/L were most prevalent at lower eGFR: they were present, respectively, in 1.7% and 0.2% of patient-time for eGFR of 50–59 ml/min per 1.73 m² versus 7.6% and 1.8% of patient-time for eGFR<30 ml/min per 1.73 m². Serum K⁺ level <3.5 mEq/L was present in 1.2%–1.4% of patient-time across eGFR strata. The median follow-up time was 2.76 years. There was a U-shaped association between serum K⁺ and mortality; pooled adjusted incidence rate ratios were 3.05 (95% confidence interval, 2.53 to 3.68) and 3.31 (95% confidence interval, 2.52 to 4.34) for K⁺ levels <3.5 mEq/L and ≥6.0 mEq/L, respectively. Within eGFR strata, there were U-shaped associations of serum K⁺ with rates of MACE, hospitalization, and discontinuation of RAAS blockers.

Conclusions

Both hyperkalemia and hypokalemia were independently associated with higher rates of death, MACE, hospitalization, and discontinuation of RAAS blockers in patients with CKD who were not undergoing dialysis. Future studies are needed to determine whether interventions targeted at maintaining normal serum K⁺ improve outcomes in this population.     

Ventricular Tachycardia in Patients with Impaired Left Ventricular Function: The Role of Propafenone

The combined occurrence of left ventricular dysfunction and -ventricular tachyarrhythmias portends a high annual mortality. Anti arrhythmic drugs can ameliorate ventricular arrhythmia and may reduce the risk of sudden cardiac death. We administered propafenone to 15 patients with ventricular tachyarrhythmias and left ventricular ejection fractions 40%. Propafenone significantly reduced isolated ventricular premature depolarizations, couplets, and ventricular tachycardia on ambulatory monitoring. Propafenone eliminated all exercise provocable ventricular tachycardia. Propafenone additionally abolished ventricular tachycardia inducible by programmed stimulation in 4 of 7 patients. In 8 patients studied before and during therapy, there was no significant change in left ventricular ejection fraction as determined by nuclear ventriculography. Propafenone was discontinued in 4 patients due to side effects. Seven patients receiving continuing propafenone therapy remain alive with only one patient suffering arrhythmia recurrence. Propafenone is an effective drug for the management of ventricular tachyarrhythmias and may be used for patients with impaired left ventricular function.     

糖耐量减低患者血小板活化和血管内皮功能的变化

为观察糖耐量减低对血小板活化和血管内皮功能的影响,选择40例糖耐量减低患者,测定血小板α－颗粒膜蛋白浓度,并应用高分辨超声测量右肱动脉在静息时（基础内径）,反应性充血（流量介导血管舒张）,舌下含服硝酸甘油（硝酸甘油介导血管舒张）时的舒张期内径。取30例查体健康者作对照组,结果发现,糖耐量减低组空腹血糖与对照组无显著差异（P＞0．05）,而空腹时血小板α－颗粒膜蛋白较对照组显著升高（P＜0．01）,流量介导血管舒张时内径较对照组显著降低（P＜0．01）,而两组间硝酸甘油介导血管舒张内径和基础内径无显著差异（P＞0．05）。口服75g葡萄糖负荷后2h,糖耐量减低组血糖浓度显著高于对照组,血小板α－糖粒膜蛋白较空腹状态时显著升高（P＜0．01）,同时2h流量介导血管舒张时内径较空腹时进一步降低,差异显著IP＜0．01）,相关分析表明,糖耐量减低组空腹血糖与血小板α－糖粒膜蛋白和流量介导血管舒张时内径无显著相关,而糖负荷后,血糖变化程度与血小板α－颗粒膜蛋白变化程度显著正相关（P＜0．01）,与流量介导血管舒张时内径的变化程度显著负相关（P＜0．01）,血小板活化增强和血管内皮功能受损,并且在糖负荷后病程程度进一步加重。     

No Impaired Cognitive Function in Treated Patients with Mild-Moderate Hypertension Compared to Normotensive Controls

Hypertension is a predictor for impaired cognitive function and dementia in several prospective studies. It is currently under debate whether treatment of hypertension, and thus blood pressure lowering, is another risk factor for cognitive decline. We recruited a sample of 123 treated hypertensive patients and 76 normotensive controls, from a population-based study in primary health care, for screening of blood pressure, metabolic variables and cognitive function, as measured by the Mini-Mental State Examination (MMSE). Treated hypertensives had higher blood pressure but did not differ in cognitive function from the normotensives. Neither educational level nor metabolic variables confounded the findings. In conclusion, treated hypertensives did not differ in cognitive function from normotensive controls. This does not support the notion that pharmacological blood pressure reduction impairs cognitive function.     

Diagnostic Value of Urine Microscopy for Differential Diagnosis of Acute Kidney Injury in Hospitalized Patients

Background and objectives: Urine microscopy is the oldest and one of the most commonly used tests for differential diagnosis of acute kidney injury (AKI), but its performance has not been adequately studied in the setting of AKI.Design, setting, participants, & measurements: Fresh urine samples were obtained from 267 consecutive patients with AKI, and urinary sediment was examined. The cause of AKI was assessed at two time points: (1) Before urine microscopy diagnosis and (2) after patient discharge or death (final diagnosis). A urinary scoring system also was created on the basis of casts and renal tubular epithelial cells (RTEC) to differentiate acute tubular necrosis (ATN) from prerenal AKI.Results: The urinary sediment scoring system was highly predictive of the final diagnosis of ATN. In patients with a high pretest probability of ATN (initial diagnosis of ATN), any casts or RTEC (score ≥2) resulted in very high positive predictive value and low negative predictive value for a final diagnosis of ATN. In patients with a low pretest probability of ATN (initial diagnosis of prerenal AKI), lack of casts or RTEC on urinary sediment examination had a sensitivity of 0.73 and specificity of 0.75 for a final diagnosis of prerenal AKI. The negative predictive value of lack of casts or RTEC in patients with low pretest probability of disease was 91%.Conclusions: Urine sediment examination is a valuable diagnostic tool for confirming the diagnosis of ATN. A score of ≥2 on an ATN urinary sediment scoring system is an extremely strong predictor of ATN.Urine microscopy is the oldest and one of the most commonly used tests for differential diagnosis of acute kidney injury (AKI). The diagnosis of AKI is currently and primarily based on measurement of serum creatinine, blood urea nitrogen, and urine output. In addition to these parameters, urine biochemistry and microscopy provide the vital information in the differentiation of AKI into traditional categories of prerenal azotemia and acute tubular necrosis (ATN) (1–5). Therapies and prognosis for prerenal AKI and ATN differ substantially; therefore, early clinical differentiation is important. Although urine microscopy with sediment examination is commonly suggested for patients with AKI in the literature, its precise diagnostic value is not clearly known. Furthermore, there has been a gradual trend away from routine urine microscopy in the clinical evaluation of AKI.Urinary microscopy in patients with ATN classically is described as containing renal tubular epithelial cells (RTEC), RTEC casts, granular casts, and muddy brown or mixed cellular casts, whereas sediment in patients with prerenal AKI usually demonstrates occasional hyaline or fine granular casts (6–10). Because urine microscopy is readily available, rapid, and inexpensive, valuable information that will improve the differential diagnosis of AKI might be quickly obtained from this test. The aims of this study were to describe the urinary sediment findings in a cohort of patients with AKI and to determine the performance of urinary sediment examination for differentiation between ATN and prerenal AKI, the most common causes of AKI in the hospital.