Severe acute kidney injury in a patient with renal artery stenosis of a single-functioning kidney: A case report of rapid normalisation of the renal function after percutaneous transluminal angioplasty with stent placement.

Revascularisation of renal arterial stenosis in acute settings, such as uncontrolled arterial hypertension, flash pulmonary oedema and/or acute renal failure, has shown controversial results in observational and prospective studies. Current guidelines do not recommend revascularisation in the occurrence of renal failure as revascularisation and best medical treatment have shown similar long-term outcomes on renal function. We describe a case of acute degradation of the renal function (with oligo-anuria and a peak creatinine of 462 µmol/L) after the re-introduction of an angiotensin-II receptor blocker (irbesartan) in a 66-year-old Caucasian diabetic male patient with bilateral renal stenosis and a right-sided single-functioning kidney, with a rapid improvement of the renal function which normalized 5 days after percutaneous angioplasty and stenting of the right renal artery.

Monthly measurement of high-sensitivity cardiac troponins T and creatine kinase in asymptomatic chronic hemodialysis patients: A one-year prospective study.

BACKGROUND: Cardiology guidelines recommend measuring high-sensitivity cardiac troponin (hs-cTn) for the diagnostic work-up of acute coronary syndromes (ACS). Many hospitals measure hs-cTnT, but preliminary data have shown that hs-cTnT is higher than normal in many hemodialysis patients without evidence of ACS. The purpose of this study was therefore to determine the hs-cTnT levels every month for 1 year in asymptomatic hemodialysis patients, in order to assess their changes over time relative to creatine kinase. METHODS: Fourty-four hemodialysis patients (mean age 67 ± 14 years) were included. The predialysis levels of fifth-generation hs-cTnT, CK, and CK-MB were measured every month for 1 year using a Cobas® 6000 analyzer (Roche Diagnostics, Switzerland). RESULTS: Almost 100% of hs-cTnT measurements were higher than normal (N < 14 ng/L); the mean ± SD annual level was 84 ± 59 ng/L, ranging from a minimum of 24 ± 2 to 241 ± 28 ng/L in individual patients. The mean levels of CK and CK-MB were normal. Thirteen myocardial infarctions were analyzed, which were all associated with an initial elevation in hs-cTnT >45% from the individual baseline value. By comparison, CK and CK-MB only increased in 38% and 31% of these myocardial infarctions, respectively. DISCUSSION: hs-cTnT is persistently higher than normal in chronic hemodialysis patients. Standard algorithms for diagnosing ACS can obviously not be used and alternative diagnostic strategies need to be developed. According to our data, and given the huge variation in baseline hs-cTnT levels among patients, the use of higher cut-offs as proposed in the literature cannot be recommended. Instead, we consider that hs-cTnT should be checked at regular intervals (e.g., every 3-6 months) in order to establish individual baseline levels for hs-cTnT. This approach, in most instances, not only makes it possible to more rapidly rule-in but also to rapidly rule-out, cases of ACS in hemodialysis patients who develop cardiac symptoms.

Acute Renal Failure in a Patient with Rivaroxaban-Induced Hypersensitivity Syndrome: A Case Report with a Review of the Literature and of Pharmacovigilance Registries.

Direct oral anticoagulants (DOACs) are among the most commonly prescribed medications, and DOAC-associated kidney dysfunction may be a problem that is underrecognized by clinicians. We report on the case of an 82-year-old patient who, two weeks after the prescription of rivaroxaban for atrial fibrillation, was hospitalized for a drug-induced hypersensitivity syndrome whose main clinical manifestations were low-grade fever with a petechial rash in the legs and acute renal failure (ARF). Within one week after rivaroxaban withdrawal, the patient's clinical condition improved and the renal function normalized. In a review of the literature, we only found five case reports of rivaroxaban-related ARF: two patients had tubulo-interstitial nephritis (TIN), two had anticoagulant-related nephropathy (ARN), and the last one had IgA nephropathy. As some recent publications suggest that kidney injury due to anticoagulation drugs may be largely underdiagnosed, we also analyzed the data from the VigiAccess database, the World Health Organization pharmacovigilance program that collects drug-related adverse events from 134 national registries worldwide. Among all the rivaroxaban-associated adverse events reported in VigiAccess since 2006, 4,323 (3.5%) were renal side effects, of which 2,351 (54.3%) were due to unspecified ARF, 363 (8.4%) were due to renal hemorrhage (characteristically associated with ARN), and 24 (0.6%) were due to TIN. We also compared these results with those reported in VigiAccess for other DOACs and vitamin K antagonists. This analysis suggests that the frequency of renal adverse events associated with rivaroxaban and other DOACs may be appreciably higher than what one might currently consider based only on the small number of fully published cases.

Bilateral Ureteral Stenosis with Hydronephrosis as First Manifestation of Granulomatosis with Polyangiitis (Wegener's Granulomatosis): A Case Report and Review of the Literature.

Ureteral stenosis is a rare manifestation of granulomatosis with polyangiitis (formerly known as Wegener's granulomatosis). We report the case of a 76-year-old woman with progressive renal failure in which bilateral hydronephrosis due to ureteral stenosis was the first manifestation of the disease. Our patient also had renal involvement with pauci-immune crescentic glomerulonephritis associated with high titers of anti-proteinase 3 c-ANCAs, but no involvement of the upper or lower respiratory tract. The hydronephrosis and renal function rapidly improved under immunosuppressive therapy with high-dose corticosteroids and intravenous pulse cyclophosphamide. We reviewed the literature and found only ten other reported cases of granulomatosis with polyangiitis/Wegener's granulomatosis and intrinsic ureteral stenosis: in two cases, the presenting clinical manifestation was unilateral hydronephrosis and in only two others was the hydronephrosis bilateral, but this complication developed during a relapse of the disease. This case emphasizes the importance of including ANCA-related vasculitis in the differential diagnosis of unusual cases of unilateral or bilateral ureteral stenosis.

Three-times-weekly, post-dialysis cefepime therapy in patients on maintenance hemodialysis: a retrospective study.

BACKGROUND: In hemodialysis patients, post-dialysis treatment with intravenous antibiotics permits even severe infections to be managed on an outpatient basis. Cefepime is a fourth-generation cephalosporin with a broad spectrum of action in monotherapy. We report on the pharmacokinetics of cefepime in post-dialysis therapy. METHODS: Since June 2012, twelve infections were treated with post-dialysis cefepime in 9 patients on high-flux hemodialysis. The initial post-dialysis dose of cefepime was approximately 15 mg/kg. The following doses were adapted according to the trough serum levels obtained before the subsequent dialysis in order to be above the EUCAST breakpoints for susceptible organisms and above the MIC90. Residual plasma concentrations were determined before (n = 30) and after (n = 17) dialysis by liquid chromatography-mass spectrometry. RESULTS: Overall, the mean ± SD dose of cefepime was 920 ± 270 mg (14.5 ± 5.1 mg/kg), but it was significantly lower before the 48 h interval (775 ± 210 mg or 12.7 ± 4.5 mg/kg) compared to the 72 h interval (1125 ± 225 mg or 17.2 ± 4.9 mg/kg) (p < 0.05). The mean trough pre-dialysis concentrations were 10.7 ± 3.9 mg/l and 11.3 ± 5.6 mg/l at 48 and 72 h, respectively. These levels always largely exceeded the EUCAST susceptibility breakpoints for all the targeted bacteria (>1 mg/l) with the exception of Pseudomonas aeruginosa (>8 mg/l). Cefepime concentrations were higher in anuric patients compared to those with preserved diuresis (15.6 ± 3.5 vs 9.25 ± 3.6 mg/l; p < 0.001) and decreased on average by 81 % during dialysis (from 10.5 ± 3.7 to 1.96 ± 1.2 mg/l; p < 0.001). The clinical outcome of all patients was good. CONCLUSIONS: Outpatient treatment with cefepime administered post-dialysis three-times-weekly was effective and well-tolerated in our patients. According to our data, in patients infected by highly susceptible pathogens a fixed dose of cefepime of 1 g before every 48-h interval and of 1.5 g before every 72-h interval should be recommended, without need of routine monitoring of the cefepime blood levels. In patients having an infection with less susceptibles pathogens as P. aeruginosa, and particularly in those among them exhibiting residual renal function, higher initial doses are necessary (1.5 g before a 48-h interval and 2.0 g before a 72-h interval) with adaption according to the subsequent pre-dialysis trough serum levels.

Oral postdialysis cholecalciferol supplementation in patients on maintenance hemodialysis: a dose-response approach.

The aim of the present study was to evaluate the dose of postdialysis cholecalciferol needed to maintain the 25-hydroxyvitamin D [25(OH)D] levels in the optimal range of 75-150 nmol/L. Twenty-six patients who had low baseline 25(OH)D levels (mean 27.5 ± 14.9 nmol/L) were studied. The 25(OH)D levels were measured every 2 months for one year. During the first two months, all the patients received 2000 IU of cholecalciferol after each hemodialysis (=6000 IU/wk). Thereafter, the dose was individualized and adapted every 2 months by administering 1 to 6 cholecalciferol tablets (2000 IU each) per week (total weekly dose = 2000-12000 IU/wk). During cholecalciferol supplementation, the 25(OH)D concentrations rapidly increased from baseline to 140.1 ± 28.3 nmol/L at month 6 and 95.6 ± 20.9 nmol/L at month 12. At month twelve, 86% of the patients had 25(OH)D levels within the target range with a mean dose of 5917 ± 4106 IU/wk of cholecalciferol; however, the amount needed to maintain these levels varied widely from 0 (n = 2) to 12000 IU/wk (n = 5). In conclusion, postdialysis cholecalciferol prescription is quite effective in correcting vitamin D deficiency/insufficiency, but the amount of cholecalciferol needed to maintain the 25(OH)D levels within the optimal range over the long-term varies widely among patients and must be individualized.

Urinary Neutrophil Gelatinase-Associated Lipocalin (uNGAL) and contrast-induced acute kidney injury after coronary angiogram.

QUESTIONS UNDER STUDY: Diagnosis of acute kidney injury (AKI) relies on measurement of serum creatinine (SCr). SCr is a late marker of impaired renal function. Urinary Neutrophil Gelatinase-Associated Lipocalin (uNGAL) has given encouraging results for an early and sensitive detection of AKI. This cohort study was conducted (1) to assess the value of uNGAL as early marker of contrast-induced AKI (CI-AKI) in unselected patients undergoing percutaneous coronary procedure (PCP) and (2) to investigate whether uNGAL levels correlate with the volume of contrast medium (CM) used during the procedure. METHODS: We enrolled 244 consecutive adult patients undergoing PCP done with the low-osmolar CM Iomeprolum (median volume of CM 122 [88-168] ml per procedure). uNGAL was measured at its peak with a standardised clinical laboratory platform (ARCHITECT uNGAL assay, Abbott). RESULTS: Overall, the post-PCP uNGAL levels were extremely low in our cohort with a median value of 7.7 [4.0-14.5] ng/ml (N ≤132 ng/ml). Twenty-five (10%) patients developed CI-AKI according to the classical diagnostic criteria (≥25% or ≥44.2 µmol/l increase in SCr) and 8 (3.3%) patients according to the AKIN criteria. Regardless of the definition considered, uNGAL levels did not significantly differ in patients with or without CI-AKI. Similarly, we found no significant correlation between the volume of CM used and the post-PCP uNGAL levels (r = -0.11). CONCLUSIONS: In a large cohort of unselected adult patients, uNGAL measured four to six hours after PCP was ineffective to predict the risk of CI-AKI and did not correlate with the volume of CM used during the procedure.

Contrast-induced nephropathy in invasive cardiology.

Contrast-induced nephropathy (CIN) is an acute renal injury due to the renal toxicity of iodinated contrast media. It is classically defined as a relative (≥25%) or absolute (≥0.5 mg/dl; 44 µmol/l) increase in serum creatinine from baseline value. CIN accounts for 10 to 15% of hospital-acquired acute renal failure and may rarely lead to irreversible renal function loss. Following percutaneous coronary intervention, reported incidence of CIN varies between 0 to more than 20%, depending on the prevalence of risk factors and used definition. Nowadays, the diagnosis of CIN relays on serum creatinine monitoring, although it is a late marker of acute kidney injury. Given the expanding number of percutaneous coronary interventions made in outpatient settings and the morbidity and mortality associated with CIN, early detection of CIN is of utmost clinical relevance. Several plasmatic and urinary biomarkers have been studied in that view, with plasmatic cystatine-C and urinary NGAL being the most promising. As no treatment specifically targets CIN once it develops, the main goal for clinicians remains prevention, with hydration status optimisation being the only proven strategy to date. Here, we will review the recent evidence concerning CIN, its incidence, proposed early diagnostic biomarkers, as well as its treatment and prognostic implication.

Contrast-induced acute kidney injury following iodine opacification other than by intravascular injection.

Contrast-induced acute kidney injury (CI-AKI) classically occurs following the intravascular administration of iodinated contrast medium (CM). However, some cases of iodine-induced nephrotoxicity have been reported in patients who did not receive intravascular CM, as a consequence of iodine absorption through mucosae, burned skin or interstitial tissues. Recently, we observed the first case of CI-AKI occurring after an enteroclysis without any direct intravascular injection of CM. Here, we report this case, and review other clinical situations in which renal toxicity has been reported following the non-intravascular use of iodinated compounds.

[Hematuria: which algorithm for an effective diagnostic strategy?]. / Hématurie: quel algorithme pour une stratégie diagnostique efficace?

Microscopic hematuria is common in medical practice; its prevalence in the adult population varies between 2.5 and 13%. Currently available data are insufficient to determine an algorithm based on evidence of the most effective diagnostic strategy of hematuria. Avoid invasive tests for the patient and expensive for the community, determine whether the hematuria of glomerular origin or not, facilitate the clinician referral to a nephrologist or urologist for the etiological diagnosis, should be the basic principles of any approach to develop such an algorithm. We try to answer on this question in this article.

Cardiac findings in asymptomatic chronic hemodialysis patients with persistently elevated cardiac troponin I levels.

BACKGROUND: The prevalence and significance of higher than normal cardiac troponin I (cTnI) levels in asymptomatic chronic hemodialysis (HD) patients remains a source of discussion. The aim of the present study was to evaluate the prevalence of higher than normal cTnI levels in asymptomatic HD patients, as determined by the last generation of immunoassay, and to perform further cardiological investigations in those patients with persistently elevated cTnI levels. METHODS: All chronic HD patients in our center who had exhibited no symptoms of coronary artery disease (CAD) during the previous four weeks were screened. cTnI levels were determined before dialysis in all patients using the last generation AccuTnI assay (UniCel DxI 800, Beckman Coulter). The cTnI levels of those patients with elevated cTnI at the screening evaluation were then measured monthly for six months. We were thus able to identify a group of patients with persistently elevated cTnI levels (> 3 consecutive months) who subsequently underwent cardiac echography and dipyridamole-exercise (D-E) thallium testing. If stress myocardial ischemia was detected, a coronary angiography was then performed. RESULTS: Fifty patients (32 males) were included: mean age 62.8 +/- 13.6 years, 20 (40%) with a history of CAD, and 21 (42%) diabetic. At the initial screening, the mean cTnI concentration was 0.05 +/- 0.06 microg/L and the cTnI levels were higher than normal (> 0.09 microg/L) in six patients (12%). In the follow-up, the cTnI normalized immediately in two patients but remained persistently elevated (range, 0.10-0.48 microg/L) in four (8%). These four patients (all males, one diabetic) had a mean age of 70.2 +/- 6.6 years, and all had heart failure with a history of severe CAD with previous myocardial infarction (n = 4), coronary stenting (n = 3), and/or bypass (n = 2). D-E thallium imaging showed reversible myocardial ischemia in all. The stress ischemia involved one to four cardiac segments and was slight to moderate in three patients and severe in the diabetic patient. A coronary angiogram was performed in all patients, and showed lesions of variable severity: severe three-vessel CAD with severe systolic dysfunction in two patients (including the diabetic), and non-critical/peripheral coronary stenosis in the other two. CONCLUSIONS: Among the asymptomatic HD patients in our center, we identified four (8%) with persistently elevated cTnI levels, as determined using the last generation AccuTnI assay. All of them had a history of severe CAD with heart failure and exhibited reversible myocardial ischemia upon D-E thallium imaging; coronary angiography revealed coronary lesions of variable severity. Overall, our data indicate that persistent low-grade cTnI elevation occurs in HD patients having longstanding severe cardiac disease, but, from our data, it is difficult to reach a conclusion as to the best clinical approach for this group of patients.

Adult hemolytic-uremic syndrome associated with urosepsis due to Shigatoxin-producing Escherichia coli O138:H-.

We report the case of a 62-year-old man without prodromal symptoms who developed a hemolytic-uremic syndrome (HUS) one week after the diagnosis of an acute bacteremic urinary infection (UTI). In this patient, the E. coli isolated in blood cultures was a non-O157:H7 Shigatoxin-producing strain that could subsequently be identified as O138:H-. This is a strain that is normally found in pigs and that has never been isolated in humans previously. UTI-related HUS is a rare event, as until now, only 14 pediatric and 3 adult cases have been reported. Indeed, this new case, besides its interesting microbiological aspects, should heighten our awareness of UTI-related HUS as a rare but real condition, not only in young children but also in adult patients. This should emphasize the necessity to search actively for other sources of Shigatoxin-producing E. coli in patients presenting with HUS without gastrointestinal symptoms.

[Differences in cardiac troponin I and T levels measured in asymptomatic hemodialysis patients with last generation immunoassays]. / Comparaison des taux de troponines cardiaques I et T mesurés chez des patients hémodialysés asymptomatiques selon différents immunodosages de dernière génération.

Previous studies reported cardiac troponin I (cTnI) and T (cTnT) levels to be higher than normal in a significant proportion of asymptomatic chronic hemodialysis (HD) patients without evidence of acute myocardial injury. We have therefore evaluated in such patients the accuracy of cTnI and cTnT determinations measured with last generation assays. Fifty chronic HD patients (34 males) without symptoms of acute myocardial ischemia were studied. Their mean age (+/-SD) was 64.4+/-12.7 years, 22 patients (44%) had an history of cardiac ischemic disease and 19 (38%) were diabetics. Serum cardiac markers were measured with last generation assays before and after a single HD session and in a control group including 30 hospitalized patients without renal failure. The cTnI were determined with Dimension RxL "Improved method" assay (Dade Behring), the cTnT with Elecys "Third generation" assay (Roche Diagnostics) and the creatine kinase (CK) with Integra (Roche Diagnostics). The cTnI were also simultaneously determined with the assay previously used at our institution (Dimension RxL, Dade Behring), indicated as old-method-cTnI. With the last generation assay only 1 patient (2%) had elevated cTnI (>0.1 microg/l) in the study group compared to none in the control group (P=NS). Instead, with the old-method-cTnI assay 11 patients (22%) had elevated (>0.3 microg/l) predialysis cTnI levels (P<0.01 compared to the "Improved method" assay). The predialysis cTnT levels were higher than normal (>0.1 microg/l) in 23 patients (46%), compared to none in the control group (P<0.01). The CK levels were elevated (>170 IU/L) in 4 dialysis patients (8%) compared to one (3,3%) in the control group (P=NS). The cTnT levels slightly but non-significantly diminished during dialysis (from 0.102+/-0.070 to 0.085+/-0.067 mug/l, P=NS), while in the same time no changes were observed for cTnI and CK levels. In conclusion, the specificity of cTnI determinations in HD patients is greatly improved by the last generation assay (from 78 to 98%), and is actually similar to that observed in a population with normal renal function. Therefore cTnI, determined with the last generation assay used in the present study, can be reliably used for the diagnosis of acute coronary syndromes in HD patients. Instead, cTnT levels remain higher than normal in a significant proportion of asymptomatic HD patients (46%) and the reasons for this fact need further investigations.