Renal Hypoperfusion Research Articles

Response to Letter Regarding Article, “Is Worsening Renal Function an Ominous Prognostic Sign in Patients With Acute Heart Failure? The Role of Congestion and Its Interaction With Renal Function”

We thank the authors for their interest in our study. Its main message is that short-term increases in serum creatinine, such as those that can be detected in patients undergoing aggressive diuretic treatment for acutely decompensated heart failure, do not necessarily predict a poor prognosis because they may be secondary to hemodynamic mechanisms (renal hypoperfusion and arterial underfilling) related to aggressive diuretic treatment in the absence of a persistent kidney injury.1 Data in the literature are controversial with respect to the prognostic significance of short-term serum creatinine changes. When serum creatinine levels were not assessed prospectively in every patient,2,3 …

Oxygen transport and mitochondrial function in porcine septic shock, cardiogenic shock, and hypoxaemia

The relevance of tissue oxygenation in the pathogenesis of organ dysfunction during sepsis is controversial. We compared oxygen transport, lactate metabolism, and mitochondrial function in pigs with septic shock, cardiogenic shock, or hypoxic hypoxia. Thirty-two anaesthetized, ventilated pigs were randomized to faecal peritonitis (P), cardiac tamponade (CT), hypoxic hypoxia (HH) or controls. Systemic and regional blood flows, lactate, mitochondrial respiration, and tissue hypoxia-inducible factor 1 alpha (HIF-1α) were measured for 24 h. Mortality was 50% in each intervention group. While systemic oxygen consumption (VO(2) ) was maintained in all groups, hepatic VO(2) tended to decrease in CT [0.84 (0.5-1.3) vs. 0.42 (0.06-0.8)/ml/min/kg; P = 0.06]. In P, fractional hepatic, celiac trunk, and portal vein blood flows, and especially renal blood flow [by 46 (14-91)%; P = 0.001] decreased. In CT, renal blood flow [by 50.4 (23-81)%; P = 0.004] and in HH, superior mesenteric blood flow decreased [by 38.9 (16-100)%, P = 0.009]. Hepatic lactate influx increased > 100% in P and HH, and > 200% in CT (all P < 0.02). Hepatic lactate uptake remained unchanged in P and HH and converted to release in CT. Mitochondrial respiration remained normal. Muscle adenosine triphosphate (ATP) concentrations decreased in P (5.9 ± 1.4 μmol/g wt vs. 2.8 ± 2.7 μmol/g wt, P = 0.04). HIF-1α expression was not detectable in any group. We conclude that despite shock and renal hypoperfusion, tissue hypoxia is not a major pathophysiological issue in early and established faecal peritonitis. The reasons for reduced skeletal muscle tissue ATP levels in the presence of well-preserved in-vitro muscle mitochondrial respiration should be further investigated.

Sphingosine‐1‐phosphate receptor 1 agonist SEW2871 decreases sepsis‐induced renal microvascular permeability but not peritubular capillary hypoperfusion

Renal microcirculatory failure and vascular leakage are hallmarks of sepsis‐induced acute kidney injury (AKI). To investigate the mechanism of renal capillary hypoperfusion, the cecal ligation and puncture (CLP) model of sepsis was used in male 40 wk C57BL/6 mice. Since activation of sphingosine‐1‐phosphate receptor 1 (S1P1) has been reported to enhance endothelial barrier function and decrease vascular permeability, mice were administered the S1P1 agonist SEW2871 (1, 3, 10 or 30mg/kg ip) at the time of CLP. Evans blue dye leakage assay was used to measure renal microvascular permeability and intravital video microscopy was used to quantitate changes in renal peritubular capillary perfusion. CLP caused a rapid increase in capillary permeability at 2h, prior to decreased renal capillary perfusion at 4h. SEW2871 dose‐dependently decreased renal vascular permeability at 6h post CLP. However, peritubular capillary perfusion was not improved compared to CLP mice at 6h. Results suggest that renal microvascular leakage is an early event during the development of sepsis and that activation of S1P1 may decrease vascular permeability but cannot prevent the deterioration of renal capillary perfusion. Overall, our study suggested that the early renal capillary hypoperfusion is independent of the increased vascular permeability in CLP septic mice. Supported by AHA 10PRE4140065 (ZW) and NIH DK075991 (PRM).

Peri-operative renal protection: The strategies revisited.

Postoperative acute renal failure (ARF) is a serious complication which can result in a prolonged hospital stay and a high mortality and morbidity. Underlying renal disease, cardiac diseases, nephrotoxin exposure and renal hypoperfusion are the possible predisposing risk factors which can create a high probability for the development of ARF. The incidence of ARF is highest after major vascular, cardiac and high-risk thoraco-abdominal surgery. Among the various renal protection strategies, adequate peri-operative volume expansion and avoidance of hypovolemia is the most accepted and practiced strategy. Numerous bio-markers of renal injury are used to estimate the presence and extent of renal insult and various new are currently under trial. Traditional pharmacological interventions like dopamine, diuretics and calcium antagonists are not currently the first line of reno-protective agents. The new non-pharmacological and pharmacological methods may improve outcome in renal transplantation, contrast-induced nephropathy and in various other settings of ARF. The current review is an attempt to refresh the knowledge and put forth the various renal protection strategies during the peri-operative period.

Pathophysiology of ischemic acute tubular necrosis

Ischemia is an important cause of acute tubular necrosis. In spite of fluctuations in hydration and blood pressure, kidney tries to auto regulate glomerular perfusion with the help of myogenic reflex, tubuloglomerular feedback, and renin- angiotensin system. Other protective features are medullary pericytes, higher capacity for glycolysis in medulla, and capacity of kidney to be preconditioned. Poor fluid intake or increased fluid loss, bleeding, low cardiac output state, and sepsis-induced vasodilatation cause renal hypoperfusion. Diseased renal vessels, old age, diabetes, nonsteroidal anti-inflammatory drug (NSAID) predispose to ischemia. When ischemia is severe, compensatory renal mechanisms are overwhelmed and renal failure ensues. In pre-renal failure, function quickly normalizes if perfusion is restored. But with worse insult, renal tubular cells actually get injured and necrosed. In its most extreme form, ischemia leads to bilateral renal patchy or complete cortical necrosis. Pathophysiology of ischemic acute renal failure is not as simple as ischemia. Today it is considered an inflammatory disease. Innate and acquired immunity, tubular and endothelial factors, leukocytes, mitochondrial biogenesis, apoptosis, all are involved. Organ cross-talk of acute kidney injury (AKI) explains multiorgan involvement and increased mortality. After a maintenance phase, restoration of tubular epithelium takes place after dedifferentiation and proliferation of surviving tubular cells. Resolving and protectins may initiate resolution. When new tubular cell regains polarization and function, renal function gradually returns to normal. Sometimes recovery may be incomplete. The detailed understanding of pathophysiology and underlying mediators is helping in identifying various biomarkers for early diagnosis of AKI and also in exploring novel therapeutic options.

Inflammation and Microvasculopathy in Renal Ischemia Reperfusion Injury

Acute renal failure (ARF) severely worsens prognosis of hospitalized patients. The most frequent cause of intrarenal ARF is transient or prolonged renal hypoperfusion (ischemia). Ischemia primarily affects the function and structure of tubular epithelial cells, which, in severe cases, is characterized by epithelial cell necrosis. Nevertheless, ischemia does not exclusively lead to alterations of epithelial cells but also causes interstitial inflammation and interstitial microvasculopathy. Both inflammation and microvasculopathy are particularly important in terms of postischemic kidney repair. Postischemic microvasculopathy is characterized by endothelial cell swelling with subsequent microvascular occlusion. Thus, reperfusion is inhibited (no-reflow phenomenon). Such endothelial cell dysfunction offers new therapeutic perspectives in ischemic ARF. Newer observations point towards the role of the so-called endothelial progenitor cells (EPCs) in the treatment of ARF. Systemic administration of EPCs to mice with bilateral renal ischemia mitigates postischemic endothelial cell dysfunction and protects animals from acute renal failure.

Clinical Impact of Renal Dysfunction in Heart Failure

Renal impairment in heart failure (HF) patients has been increasingly recognized as an independent risk factor for morbidity and mortality. In the most recent European and American guidelines for HF management, renal dysfunction was considered an index of poor prognosis independent of the presence of other traditionally investigated risk factors. Different mechanisms appear to be implicated in worsening renal function in patients with acute decompensated HF (ADHF) in contrast to chronic HF. In patients with acute ADHF, renal impairment has been attributed to renal hypoperfusion due to reduced cardiac output and decreased systemic blood pressure. In these patients, neurohormonal activation of the renin-angiotensin and sympathetic nervous systems plays a key role. In chronic and clinically stable HF, other mechanisms, including microvascular damage, oxidative stress, inflammation, and fibrosis, lead to a reduced number of functioning nephrons. Differentiating transient functional changes in renal filtration and acute renal tubular injury with loss of functioning nephrons is a critical step in understanding cardiorenal syndromes and selection of patients for novel therapeutic approaches.

Spectrum of mutations in the renin-angiotensin system genes in autosomal recessive renal tubular dysgenesis

Autosomal recessive renal tubular dysgenesis (RTD) is a severe disorder of renal tubular development characterized by early onset and persistent fetal anuria leading to oligohydramnios and the Potter sequence, associated with skull ossification defects. Early death occurs in most cases from anuria, pulmonary hypoplasia, and refractory arterial hypotension. The disease is linked to mutations in the genes encoding several components of the renin-angiotensin system (RAS): AGT (angiotensinogen), REN (renin), ACE (angiotensin-converting enzyme), and AGTR1 (angiotensin II receptor type 1). Here, we review the series of 54 distinct mutations identified in 48 unrelated families. Most of them are novel and ACE mutations are the most frequent, observed in two-thirds of families (64.6%). The severity of the clinical course was similar whatever the mutated gene, which underlines the importance of a functional RAS in the maintenance of blood pressure and renal blood flow during the life of a human fetus. Renal hypoperfusion, whether genetic or secondary to a variety of diseases, precludes the normal development/ differentiation of proximal tubules. The identification of the disease on the basis of precise clinical and histological analyses and the characterization of the genetic defects allow genetic counseling and early prenatal diagnosis.

The role of renal hypoperfusion in development of renal microcirculatory dysfunction in endotoxemic rats: reply to Ji et al.

Dear Editor, We would like to thank Ji et al. [1] for their comments regarding our recently published study [2]. The authors raised two very interesting and relevant points of concern. First, they point out that we might have missed the initial peak in TNF-α expression shortly after LPS infusion and therefore cannot conclude that neither immediate nor late fluid could prevent systemic inflammatory activation. However, although we may have missed the peak expression, we could still detect increased TNF-α levels at the end of our protocol group which evidently indicates that neither immediate nor late fluid resuscitation could completely prevent systemic inflammatory activation. Furthermore, plasma TNF-α may not accurately reflect TNF-α kinetics in tissue. For instance, Detmer et al. [3] found that TNF-α increased until 360 min after LPS exposure in smooth muscle cells. The kinetics of TNF-α release may also been modified by interaction of TNF-α with other cytokines. Andersson et al. [4] found a reciprocal functional relationship between cytokines with HMG-1 extending and amplifying the secretion of TNF-α. Thus, if anything, the point raised by Ji et al. does not preclude our conclusion. Nonetheless, we must acknowledge that the main aim of our study was not to investigate the whole picture of the LPS-induced cytokine response spectrum, but to investigate the role of LPS-induced hypotension and renal hypoperfusion in the development of renal microcirculatory dysfunction and systemic and renal inflammatory activation. The method we used fits this goal. Second, Ji et al. raised concerns regarding the relatively small sample size. This might be a valid point here. However, although we can not exclude a lack of power, we believe that increasing the sample size would not show a different result with respect to the very similar TNF-α plasma levels in the immediately and delayed resuscitated groups. The authors also pointed out that there was a clerical error in the abstract of the article. For this we would like to apologize. Finally, the authors state that the data presented in our study should be interpreted with some caution. Of course, as should the data presented in every study. Furthermore, the authors state that more research is needed. Again, we agree. Although we could explore the role of renal hypoperfusion in the development of renal microcirculatory failure, application of immediate fluid resuscitation is clinically impossible. Hence, future research could focus on developing therapeutic strategies protecting the renal microcirculation in endotoxemia, hemorrhage, ischemia/reperfusion injury, and other scenarios in which the kidney might suffer from hypoperfusion and inflammation.

Developmental abnormalities, blood pressure variability and renal disease in Riley Day syndrome

Riley Day syndrome, commonly referred to as familial dysautonomia (FD), is a genetic disease with extremely labile blood pressure due to baroreflex deafferenation. Chronic renal disease is very frequent in these patients and was attributed to recurrent arterial hypotension and renal hypoperfusion. Aggressive treatment of hypotension, however, has not reduced its prevalence.We evaluated the frequency of kidney malformations as well as the impact of hypertension, hypotension and blood pressure variability on the severity of renal impairment. We also investigated the effect of fludrocortisone treatment on the progression of renal disease.Patients with FD appeared to have an increased incidence of hydronephrosis/reflux and patterning defects. Patients younger than 4 years old had hypertension and normal eGFR. Patients with more severe hypertension and greater variability in their blood pressure had worse renal function (both, p<0.01). In contrast, there was no relationship between eGFR and the lowest blood pressure recorded during upright tilt. The progression of renal disease was faster in patients receiving fludrocortisone (p<0.02).Hypertension precedes kidney disease in these patients. Moreover, increased blood pressure variability as well as mineralocorticoid treatment accelerate the progression of renal disease. No association was found between hypotension and renal disease in patients with FD.

Cardio-renal syndrome: an entity cardiologists and nephrologists should be dealing with collegially

Heart failure may lead to acute kidney injury and vice versa. Chronic kidney disease may affect the clinical outcome in terms of cardiovascular morbidity and mortality while chronic heart failure may cause CKD. All these disorders contribute to the composite definition of cardio-renal syndromes. Renal impairment in HF patients has been increasingly recognized as an independent risk factor for morbidity and mortality; however, the most important clinical trials in HF tend to exclude patients with significant renal dysfunction. The mechanisms whereby renal insufficiency worsens the outcome in HF are not known, and several pathways could contribute to the "vicious heart/kidney circle." Traditionally, renal impairment has been attributed to the renal hypoperfusion due to reduced cardiac output and decreased systemic pressure. The hypovolemia leads to sympathetic activity, increased renin-angiotensin-aldosterone pathways and arginine-vasopressin release. All these mechanisms cause fluid and sodium retention, peripheral vasoconstriction and an increased congestion as well as cardiac workload. Therapy addressed to improve renal dysfunction, reduce neurohormonal activation and ameliorate renal blood flow could lead to a reduction in mortality and hospitalization in patients with cardio-renal syndrome.

TEVAR in Acute Complicated Type B Dissection-Ammunition for Complex Aortic Pathology

Open surgery for acute, complicated type B dissection is associated with an operative mortality in excess of 20% and considerable morbidity including spinal cord ischaemia. Furthermore a mortality of 17% has recently been reported after percutaneous flap fenestration for acute type B associated malperfusion. There has therefore been considerable contemporary interest in the role of TEVAR in both acute uncomplicated and complicated type B dissection. The precise definition of acute complicated type B dissection has been recently clarified and has been defined as symptom onset of 14 days or less, with rupture, defined as haemorrhage outside the aortic wall or malperfusion, defined as visceral, renal, lower extremity or spinal cord hypoperfusion. The mortality and morbidity results reported in this manuscript are excellent in comparison to historic open repair results and contemporary TEVAR results. The authors report a 30-day mortality rate of 4.4% and an overall survival of 95.6% at 1 and 3 years respectively. These are considerably better than the recently reported multicenter US data, with a 30-day mortality of 10.8% and 1-year survival of 70.6%. The 3-yr survival figures are also

The role of renal hypoperfusion in development of renal microcirculatory dysfunction in endotoxemic rats

PurposeTo study the role of renal hypoperfusion in development of renal microcirculatory dysfunction in endotoxemic rats.MethodsRats were randomized into four groups: a sham group (n = 6), a lipopolysaccharide (LPS) group (n = 6), a group in which LPS administration was followed by immediate fluid resuscitation which prevented the drop of renal blood flow (EARLY group) (n = 6), and a group in which LPS administration was followed by delayed (i.e., a 2-h delay) fluid resuscitation (LATE group) (n = 6). Renal blood flow was measured using a transit-time ultrasound flow probe. Microvascular perfusion and oxygenation distributions in the renal cortex were assessed using laser speckle imaging and phosphorimetry, respectively. Interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-α were measured as markers of systemic inflammation. Furthermore, renal tissue samples were stained for leukocyte infiltration and inducible nitric oxide synthase (iNOS) expression in the kidney.ResultsLPS infusion worsened both microvascular perfusion and oxygenation distributions. Fluid resuscitation improved perfusion histograms but not oxygenation histograms. Improvement of microvascular perfusion was more pronounced in the EARLY group compared with the LATE group. Serum cytokine levels decreased in the resuscitated groups, with no difference between the EARLY and LATE groups. However, iNOS expression and leukocyte infiltration in glomeruli were lower in the EARLY group compared with the LATE group.ConclusionsIn our model, prevention of endotoxemia-induced systemic hypotension by immediate fluid resuscitation (EARLY group) did not prevent systemic inflammatory activation (IL-6, IL-10, TNF-α) but did reduce renal inflammation (iNOS expression and glomerular leukocyte infiltration). However, it could not prevent reduced renal microvascular oxygenation.Electronic supplementary materialThe online version of this article (doi:10.1007/s00134-011-2267-4) contains supplementary material, which is available to authorized users.

Hemodynamic changes in the kidney in a pediatric rat model of sepsis-induced acute kidney injury

Sepsis is a leading cause of acute kidney injury (AKI) and mortality in children. Understanding the development of pediatric sepsis and its effects on the kidney are critical in uncovering new therapies. The goal of this study was to characterize the development of sepsis-induced AKI in the clinically relevant cecal ligation and puncture (CLP) model of peritonitis in rat pups 17-18 days old. CLP produced severe sepsis demonstrated by time-dependent increase in serum cytokines, NO, markers of multiorgan injury, and renal microcirculatory hypoperfusion. Although blood pressure and heart rate remained unchanged after CLP, renal blood flow (RBF) was decreased 61% by 6 h. Renal microcirculatory analysis showed the number of continuously flowing cortical capillaries decreased significantly from 69 to 48% by 6 h with a 66% decrease in red blood cell velocity and a 57% decline in volumetric flow. The progression of renal microcirculatory hypoperfusion was associated with peritubular capillary leakage and reactive nitrogen species generation. Sham adults had higher mean arterial pressure (118 vs. 69 mmHg), RBF (4.2 vs. 1.1 ml·min(-1)·g(-1)), and peritubular capillary velocity (78% continuous flowing capillaries vs. 69%) compared with pups. CLP produced a greater decrease in renal microcirculation in pups, supporting the notion that adult models may not be the most appropriate for studying pediatric sepsis-induced AKI. Lower RBF and reduced peritubular capillary perfusion in the pup suggest the pediatric kidney may be more susceptible to AKI than would be predicted using adults models.

How Valid is the AHRQ Patient Safety Indicator “Postoperative Physiologic and Metabolic Derangement”?

The Agency for Healthcare Research and Quality Patient Safety Indicator postoperative physiologic and metabolic derangement (PMD) uses ICD-9-CM codes to screen for potentially preventable acute kidney injury (AKI) requiring dialysis plus diabetes-related complications after elective surgery. Data on PMD's accuracy in identifying true events are limited. We examined the indicator's positive predictive value (PPV) in the Veterans Health Administration (VA). Trained abstractors reviewed medical records of 119 PSI software-flagged PMD cases. We calculated PPVs overall and separately for renal- and diabetes-related complications. We also examined false positives to determine reasons for incorrect identification, and true positives to determine PMD-related outcomes and risk factors. Overall 75 cases were true positives (PPV 63%, 95% CI 54% to 72%); 73 of 104 AKI cases were true positives (PPV 70%, 60% to 79%); only 2 of 15 diabetes cases were true positives (PPV 13%, 2% to 40%). Of all false positives, 70% represented nonelective admissions and 23% had the complication present on admission. Of AKI true positives, 37% died and 26% were discharged on dialysis; 55% had chronic kidney disease (≥ stage 3) present on admission. Cardiac surgery represented the largest category of AKI-associated index procedures (30%). AKI was most commonly attributed to perioperative renal hypoperfusion (84% of true positives), followed by nephrotoxins (33%) including contrast (11%). Due to its low PPV, we recommend removing diabetes complications from the indicator and focusing on AKI. PMD's PPV could be significantly improved by using present-on-admission codes, and specific to the VA, by introduction of admission status codes. Many PMD-identified cases appeared to be at high risk based on patient- and procedure-related factors. The degree to which such cases are truly preventable events requires further assessment.

Renal microcirculatory perfusion in a pediatric model of sepsis‐induced acute kidney injury in the rat

Sepsis is a leading cause of acute kidney injury (AKI) and mortality in children. Understanding the development of pediatric sepsis and its effects on the kidney are critical to finding new therapies. The goal of this study was to characterize the development of sepsis-induced AKI in a clinically relevant cecal ligation and puncture (CLP) model of peritonitis in 17–18 day old rat pups. CLP produced severe sepsis demonstrated by a time-dependent increase in serum cytokines, NO, markers of multi-organ injury including creatinine, and renal microcirculatory hypoperfusion. Although blood pressure and heart rate remained unchanged after CLP, renal blood flow (RBF) was decreased. Renal microcirculatory analysis showed the number of continuously flowing cortical capillaries decreased along with red blood cell velocity and volumetric flow. This was also accompanied by induction ICAM-1 and inducible nitric oxide synthase in the kidney with subsequent peroxynitrite generation. In contrast to sham pups, sham adults had higher blood pressure, RBF, and microcirculatory perfusion. With the exception of blood pressure, CLP produced a greater decrease in these hemodynamic parameters in pups compared to adults, suggesting that the pediatric kidney may be more susceptible to not only sepsis-induced AKI, but also to other forms of AKI due to its relatively low blood flow and microcirculatory perfusion. Supported by DK075991.

569 Right Atrial Enlargement Is an Echocardiographic Marker for Cardiorenal Syndrome

Purpose: Impaired renal failure is an independent risk factor for all cause mortality in patients with congestive heart failure (CHF). This has been attributed to renal hypoperfusion secondary to a reduction in cardiac output. More recent data suggests that venous congestion may play a more substantial role over cardiac index in the deterioration of renal function. We hypothesize that increased right atrial size in CHF will correlate with the development of cardiorenal syndrome. Methods and Materials: Data collected from a total of 39 consecutive patients with CHF was retrospectively analyzed. Group I consisted of 21 patients with systolic dysfunction (EF 50%), pulmonary hypertension (right ventricular systolic pressure (RVSP) 35 mm Hg) and renal insufficiency with a glomerular filtration rate (GFR) 60 ml/min/1.73 m2. Group II consisted of 18 patients with systolic dysfunction (EF 50%), pulmonary hypertension (RVSP 35 mm Hg) and normal renal function (GFR 60 ml/min/1.73 m2). Echocardiographic data of the 2 groups were analyzed. Results: Group I had a significantly larger right atrial size(P 0.03). Those with a right atrial size greater than 17.2 cm, were four times more likely to have cardiorenal syndrome(95% Confidence Interval 1.05 to 15.21). All other echocardiographic parameters were similar between the two groups.

Síndrome de aorta media

Introduction Mid-aortic syndrome (MAS) describes a narrowing segment of the abdominal aorta and the branches arising from there. This narrowing frequently involves the renal arteries, with the only clinical sign being arterial hypertension. Objective To review the cases of MAS diagnosed in the Paediatric Nephrology Department of the Vall D’Hebron Hospital (Barcelona). Methods and materials A retrospective study was conducted on 5 patients aged from 8 days to 12 years old. We analysed the onset, diagnostic examinations, treatment and outcome. Results Hypertension was the common reason behind the study. In two of the five cases, it was associated with renal failure. The definitive diagnostic was made using angiography and angio-MR, observing, in all the cases, that the renal arteries were affected (in 3 cases unilateral). The treatment was by medication in 3 cases, 1 required surgery and 1 died at 7 months. Conclusions MAS, although uncommon, is a very important cause of AHT in infancy. Angiography is the only technique to diagnose it. It is important to rule out cerebral involvement, which could lead to a fatal outcome. Hypertension is very difficult to control through medication. Surgery is required only when the hypertension is not controllable through medication, when there is intermittent claudication, intestinal angina, and renal hypoperfusion. Ideally, it is better to opt for medication as treatment, as the narrowing is progressive up to the end of puberty, after which, the narrowing stabilises.

Diagnostic performance of fractional excretion of urea in the evaluation of critically ill patients with acute kidney injury: a multicenter cohort study

IntroductionSeveral factors, including diuretic use and sepsis, interfere with the fractional excretion of sodium, which is used to distinguish transient from persistent acute kidney injury (AKI). These factors do not affect the fractional excretion of urea (FeUrea). However, there are conflicting data on the diagnostic accuracy of FeUrea.MethodsWe conducted an observational, prospective, multicenter study at three ICUs in university hospitals. Unselected patients, except those with obstructive AKI, were admitted to the participating ICUs during a six-month period. Transient AKI was defined as AKI caused by renal hypoperfusion and reversal within three days. The results are reported as medians (interquartile ranges).ResultsA total of 203 patients were included. According to our definitions, 67 had no AKI, 54 had transient AKI and 82 had persistent AKI. FeUrea was 39% (28 to 40) in the no-AKI group, 41% (29 to 54) in the transient AKI group and 32% (22 to 51) in the persistent AKI group (P = 0.12). FeUrea was of little help in distinguishing transient AKI from persistent AKI, with the area under the receiver operating characteristic curve being 0.59 (95% confidence interval, 0.49 to 0.70; P = 0.06). Sensitivity was 63% and specificity was 54% with a cutoff of 35%. In the subgroup of patients receiving diuretics, the results were similar.ConclusionsFeUrea may be of little help in distinguishing transient AKI from persistent AKI in critically ill patients, including those receiving diuretic therapy. Additional studies are needed to evaluate alternative markers or strategies to differentiate transient from persistent AKI.

Clinical significance of periportal tracking as an extrarenal manifestation of acute pyelonephritis

The purpose of this study was to evaluate whether hepatic periportal tracking (PPT) in patients with acute pyelonephritis correlates with the severity of pyelonephritis. A database search was conducted of patients with clinically suspected acute pyelonephritis who underwent abdominal computed tomography (CT) between January 2004 and June 2009 for disease evaluation. The final study group consisted of 274 patients (221 women, 53 men) with a mean age of 43 ± 20 years. The abdominal CT studies were retrospectively reviewed by two radiologists by consensus to assess PPT, renal wedge-shaped hypoperfusion areas, and renal abscesses. The laboratory reports obtained on the day of the CT examinations were reviewed for C-reactive protein (CRP), white blood cell count (WBCC), and leukocytes in urine. Presence of PPT was correlated with the presence of renal abscess, extension of renal hypoperfusion areas as well with levels of CRP, leukocytosis, and urine leukocytes using the Fisher's exact Test and the Wilcoxon Test. All patients showed renal hypoperfusion areas consistent with the clinical diagnosis of acute pyelonephritis. Twenty-nine patients (11%) showed PPT which was significantly associated with the extension of the wedge-shaped renal hypoperfusion areas (P < 0.001), the presence of a renal abscess (P < 0.01), as well as the level of CRP (P < 0.001) and urine leukocytes (P < 0.01). A renal abscess was observed in 36% of patients with PPT compared with 14% of patients without PPT. The PPT should be kept in mind as an extrarenal finding in acute pyelonephritis and may indicate a more serious clinical course of the disease.