Rise In Serum Creatinine Concentration Research Articles

Kidney Outcomes with Sodium-Glucose Cotransporter-2 Inhibitor Initiation after AKI among Veterans with Diabetic Kidney Disease.

The effect of SGLT2i on kidney function after acute kidney injury (AKI) is unknown. The study population was drawn from a retrospective cohort of Veterans with diabetes mellitus type 2 (DM2) and proteinuria. The study exposure was time-varying use of SGLT2i after an index AKI hospitalization. The two study outcomes were time-to- 1) a sustained decrease in eGFR over at least three months to <60 mL/minute/1.73 m2 and ≥30% below a post-AKI-updated eGFR and 2) recurrent hospitalization with AKI. AKI was defined as a rise in serum creatinine concentration to ≥50% above a moving outpatient creatinine baseline. DM2 was defined by ≥2 billing codes related to DM2 prior to the index AKI; proteinuria was defined by the most recent albuminuria, proteinuria, or urinalysis test. Veterans were required to have a baseline eGFR and an eGFR 3-12 months after the index AKI hospitalization ≥30 mL/minute/1.73 m2. 10,036 Veterans met study inclusion criteria. 2,794 (28%) received a SGLT2i. 775 (8%) had CKD progression and 1,816 (18%) had recurrent AKI over a median follow-up of 1.8 and 1.7 years, respectively, which began one year after the index AKI hospitalization. SGLT2i use was associated with lower risk for CKD progression [adjusted hazard ratio (aHR) 0.72 (95% confidence interval (CI): 0.57-0.91)] and for recurrent AKI [aHR 0.75 (95% CI: 0.65-0.88)]. SGLT2i use was associated with a lower risk for CKD progression and for recurrent AKI among those with diabetic kidney disease and recent AKI.

Global Perspectives in Acute Kidney Injury: Spain.

Global Perspectives in Acute Kidney Injury: Spain.

Assessment of the Renal Angina Index in Determining Acute Kidney Injury

Background: Oliguria or A rise in serum creatinine concentration have been performed to detect acute kidney injury (AKI), however none of these methods is

Contrast Induced Nephropathy in ICU settings

Contrast-Induced Nephropathy (CIN) is defined as acute deterioration of renal function after the administration of Radio-contrast materials, mostly within a period of 24 to 48 hours. Most of cases are non-oliguric and reversible and rarely associated with adverse outcomes. The diagnosis of CIN is based upon the clinical presentation, including the characteristic rise in serum creatinine concentration beginning with the first 24 to 48 hours after contrast exposure, and the exclusion of other causes of acute kidney injury (AKI). Incidence of CIN varies widely depending on the definition of AKI, the presence or absence of risk factors, the amount and type of agent administered, and the type of radiologic procedure. Biomarkers Cystatin C, Neutrophil gelatinase-associated lipocalin (NGAL) in urine and plasma, 2 hr after contrast administration have been shown to be predictive biomarkers of CIN. Most cases of CIN are self-limited. Management is conservative as with any other case of AKI and dialysis is rarely required. Adequate hydration, use of low doses of contrast media especially low-osmolar or iso-osmolar type , will reduce the risk of CIN.

Plasma indoxyl sulfate concentration predicts progression of chronic kidney disease in dogs and cats

Indoxyl sulfate is a protein-bound uremic toxin that increases as the severity of impaired renal function increases in humans, laboratory animals, dogs and cats. An elevation of indoxyl sulfate is related to prognosis among people with chronic kidney disease. However, whether indoxyl sulfate is able to predict the progression of chronic kidney disease in dogs and cats has not been previously studied. In the present study, 58 cats and 36 dogs with chronic kidney disease were enrolled. Plasma indoxyl sulfate was measured by high performance liquid chromatography. Renal progression was defined as an increase by one International Renal Interest Society (IRIS) stage and/or a rise in serum creatinine concentration of 0.5mg/dL during the same stage within a 3-month period.Compared with the non-progression groups, across different stages of renal failure, the baseline plasma indoxyl sulfate concentration was increased in the renal progression group (P<0.05), especially for IRIS stages 2 and 3 animals. The area under the receiver operator characteristic curves of indoxyl sulfate, when predicting renal progression, was above 0.75 for both dogs and cats. Indoxyl sulfate concentrations were also correlated with the increase of blood urea nitrogen, serum creatinine, and phosphate and the decrease of hematocrit among cats; while in dogs, concentrations were only correlated with the increase of phosphate concentrations. Indoxyl sulfate served as a biomarker of progression risk in dogs and cats with chronic kidney disease.

Editor's Choice- What do small serum creatinine changes tell us about outcomes after acute myocardial infarction?

Acute kidney injury (AKI), mostly defined as a rise in serum creatinine concentration of more than 0.5 mg/dl, is a common, serious, and potentially preventable complication of percutaneous coronary intervention and is associated with adverse outcomes including an increased risk of inhospital mortality. Recent data from the National Cardiovascular Data Registry/Cath-PCI registry including 985,737 consecutive patients undergoing percutaneous coronary intervention suggest that approximately 7% experienced AKI with a reported incidence of 3-19%. In patients undergoing primary percutaneous coronary intervention for acute myocardial infarction (AMI), AKI occurs more frequently with rates up to 20% depending on patient and procedural characteristics. However, varying definitions of AKI limit comparisons of AKI rates across different studies. Recently, most studies have adopted the Acute Kidney Injury Network (AKIN) criteria for definition and classification of AKI. Beyond the AKIN criteria for AKI, other classifications such as the risk, injury, failure, loss and end-stage kidney disease (RIFLE) and kidney disease: improving global outcomes (KDIGO) criteria are used to define AKI. Notably, even small increases in serum creatinine beyond AKI may be associated with adverse outcomes including increased hospital length of stay and excess. Acute kidney injury (AKI) is a serious and potentially preventable complication of percutaneous coronary intervention (PCI). Worsening renal function is associated with adverse outcomes including a higher rate of in-hospital mortality. In patients undergoing primary PCI for acute myocardial infarction (AMI), AKI occurs up to 20% of such individuals. Varying definitions of AKI limit comparisons of AKI rates across different studies. Additionally, even small increases in serum creatinine beyond lavels meeting AKI definitions may be associated with adverse outcomes including increased hospital length of stay.

Unique Transcriptional Programs Identify Subtypes of AKI.

Two metrics, a rise in serum creatinine concentration and a decrease in urine output, are considered tantamount to the injury of the kidney tubule and the epithelial cells thereof (AKI). Yet neither criterion emphasizes the etiology or the pathogenetic heterogeneity of acute decreases in kidney excretory function. In fact, whether decreased excretory function due to contraction of the extracellular fluid volume (vAKI) or due to intrinsic kidney injury (iAKI) actually share pathogenesis and should be aggregated in the same diagnostic group remains an open question. To examine this possibility, we created mouse models of iAKI and vAKI that induced a similar increase in serum creatinine concentration. Using laser microdissection to isolate specific domains of the kidney, followed by RNA sequencing, we found that thousands of genes responded specifically to iAKI or to vAKI, but very few responded to both stimuli. In fact, the activated gene sets comprised different, functionally unrelated signal transduction pathways and were expressed in different regions of the kidney. Moreover, we identified distinctive gene expression patterns in human urine as potential biomarkers of either iAKI or vAKI, but not both. Hence, iAKI and vAKI are biologically unrelated, suggesting that molecular analysis should clarify our current definitions of acute changes in kidney excretory function.

Pregnancy Outcomes after Clinical Recovery from AKI.

The effect of clinically recovered AKI (r-AKI) on future pregnancy outcomes is unknown. We retrospectively studied all women who delivered infants between 1998 and 2007 at Massachusetts General Hospital to assess whether a previous episode of r-AKI associated with subsequent adverse maternal and fetal outcomes, including preeclampsia. AKI was defined as rise in serum creatinine concentration to 1.5-fold above baseline. We compared pregnancy outcomes in women with r-AKI without history of CKD (eGFR>90 ml/min per 1.73 m2 before conception; n=105) with outcomes in women without kidney disease (controls; n=24,640). The r-AKI and control groups had similar prepregnancy serum creatinine measurements (0.70±0.20 versus 0.69±0.10 mg/dl; P=0.36). However, women with r-AKI had increased rates of preeclampsia compared with controls (23% versus 4%; P<0.001). Infants of women with r-AKI were born earlier than infants of controls (37.6±3.6 versus 39.2±2.2 weeks; P<0.001), with increased rates of small for gestational age births (15% versus 8%; P=0.03). After multivariate adjustment, r-AKI associated with increased risk for preeclampsia (adjusted odds ratio [aOR], 5.9; 95% confidence interval [95% CI], 3.6 to 9.7) and adverse fetal outcomes (aOR, 2.4; 95% CI, 1.6 to 3.7). When women with r-AKI and controls were matched 1:2 by age, race, body mass index, diastolic BP, parity, and diabetes status, r-AKI remained associated with preeclampsia (OR, 4.7; 95% CI, 2.1 to 10.1) and adverse fetal outcomes (OR, 2.1; 95% CI, 1.2 to 3.7). Thus, a past episode of AKI, despite return to normal renal function before pregnancy, associated with adverse outcomes in pregnancy.

Rituximab Versus Cyclophosphamide for ANCA-Associated Vasculitis with Renal Involvement

Rituximab (RTX) is non-inferior to cyclophosphamide (CYC) followed by azathioprine (AZA) for remission-induction in severe ANCA-associated vasculitis (AAV), but renal outcomes are unknown. This is a post hoc analysis of patients enrolled in the Rituximab for ANCA-Associated Vasculitis (RAVE) Trial who had renal involvement (biopsy proven pauci-immune GN, red blood cell casts in the urine, and/or a rise in serum creatinine concentration attributed to vasculitis). Remission-induction regimens were RTX at 375 mg/m(2) × 4 or CYC at 2 mg/kg/d. CYC was replaced by AZA (2 mg/kg/d) after 3-6 months. Both groups received glucocorticoids. Complete remission (CR) was defined as Birmingham Vasculitis Activity Score/Wegener's Granulomatosis (BVAS/WG)=0 off prednisone. Fifty-two percent (102 of 197) of the patients had renal involvement at entry. Of these patients, 51 were randomized to RTX, and 51 to CYC/AZA. Mean eGFR was lower in the RTX group (41 versus 50 ml/min per 1.73 m(2); P=0.05); 61% and 75% of patients treated with RTX and 63% and 76% of patients treated with CYC/AZA achieved CR by 6 and 18 months, respectively. No differences in remission rates or increases in eGFR at 18 months were evident when analysis was stratified by ANCA type, AAV diagnosis (granulomatosis with polyangiitis versus microscopic polyangiitis), or new diagnosis (versus relapsing disease) at entry. There were no differences between treatment groups in relapses at 6, 12, or 18 months. No differences in adverse events were observed. In conclusion, patients with AAV and renal involvement respond similarly to remission induction with RTX plus glucocorticoids or CYC plus glucocorticoids.

The Impact of Routine Norepinephrine Infusion on Hemodilution and Blood Transfusion in Cardiac Surgery

Background: Hemodilution and blood transfusion are associated with poor outcome after cardiac surgery. We hypothesized that routine norepinephrine infusion commenced prior to anesthesia induction during on-bypass cardiac surgery would reduce intraoperative hemodilution and red cell transfusion. Methods: Two cohorts of consecutive cardiac surgery patients at different time periods were retrospectively reviewed for perioperative hemoglobin, creatinine concentrations and units of red cells transfused. Patients in group NE (n=72, in 2010) all received standardized hemodynamic management by a single anesthesiologist with low dose norepinephrine infusion commenced at 3-5 μg.min-1 (18-30 nmol.min-1, 0.24-0.4 nmol.kg-1.min-1) commencing prior to anesthetic induction and continued into the postoperative period. In the absence of blood loss, hemodynamic stability was achieved using vasopressors and inotropes rather than fluid administration, in an attempt to reduce hemodilutional anemia and trigger for red cell transfusion. Controls (n=94, in 2005) received selective norepinephrine infusion post cardiopulmonary bypass for persistent hypotension and vasodilation. There were no major changes to surgical or perfusion technique in the time period between cohorts, and the transfusion trigger remained the same at Hb<70 g/L. Results: Intraoperatively, hemoglobin concentrations were higher in group NE compared with controls (p<0.0001) despite lower baseline values (139 ± 19 vs 133 ± 15, P=0.028). Additionally, fewer units of red cells were transfused in the NE group intraoperatively (0.2 ± 0.6 units/patient) compared with controls (0.53 ± 1.47, p=0.041). Maximum postoperative rise in serum creatinine concentration (μmol.L-1) was not significantly different (NE 26 ± 32, controls 30 ± 57, p=0.49 and at discharge 3 ± 53 vs. 5 ± 30, p=0.39). NE group patients were at increased risk of bleeding, having received more extensive surgery (p=0.042), longer clamp-time (p=0.009) and no aprotinin compared to 74% of controls. Conclusions: This study shows proof of concept that during on-bypass cardiac surgery, routine low dose norepinephrine infusion is associated with reduced hemodilution and intraoperative red cell transfusion without increasing postoperative serum creatinine.

Should monitoring of vancomycin be delayed? A case of likely nephrotoxicity occasioned by morbid obesity and minimal monitoring

Should monitoring of vancomycin be delayed? A case of likely nephrotoxicity occasioned by morbid obesity and minimal monitoring

Diagnostic Value of Urinary Sodium, Chloride, Urea, and Flow

Up to 30% of hospitalized critically ill patients may have a rise in serum creatinine concentration. In addition to history and physical examination, there is diagnostic value in assessing urinary electrolytes, solute excretion, and urine flow in these patients. The correct interpretation of these urinary parameters can avoid unnecessary volume overload and mechanical ventilation, risk factors for increased mortality in patients with rising serum creatinine. The present article also discusses the role of arterial underfilling in causing prerenal azotemia in the presence of an increase in total body sodium and extracellular fluid expansion. As with extracellular fluid volume depletion, arterial underfilling secondary to impaired cardiac function or primary arterial vasodilation can delay or prevent recovery from ischemic or toxic acute tubular necrosis. The present brief review discusses the various aspects of the correct interpretation of urinary electrolytes, solute excretion, and urine flow in the setting of a rising serum creatinine concentration.

Curbing the Use of Ultrasonography in the Diagnosis of Acute Kidney Injury: Penny Wise or Pound Foolish?

Curbing the Use of Ultrasonography in the Diagnosis of Acute Kidney Injury: Penny Wise or Pound Foolish?

Acute renal failure after myeloablative allogeneic hematopoietic stem cell transplantation: incidence, risk factors, and relationship with the quantity of transplanted cells

Aim: Acute renal failure (ARF) after hematopoietic stem cell transplantation (HSCT) is a widespread complication leading to considerable morbidity and mortality. The present study aims to determine the incidence and risk factors of ARF and to investigate whether there exists a relationship between the renal injury indicators and quantity of the transplanted stem cells in a uniform patient population after allogeneic myeloablative HSCT. Methods: Patients undergoing myeloablative allogeneic HSCT from 2007 to 2008 were monitored prospectively in terms of their renal functions during the first 100 days after transplantation. ARF was defined as a twofold rise in serum creatinine concentration of baseline value or a >50% decrease in creatinine clearance and classified into three grades. Results: ARF occurred in 51.3% of patients over a period of 100 days after HSCT. ARF developed in 12 (60.0%) patients within the first 2 weeks, whereas in 8 (40.0%) of them ARF development was observed within 2–4 weeks. No correlation was found between ARF development and the quantity of the infused hematopoietic stem cells. Additionally, we were not able to identify a particular cause which was significantly associated with the occurrence of ARF after HSCT. Conclusion: A 51.3% incidence of ARF was found in patients after myeloablative allogeneic HSCT. ARF in HSCT patients could not be linked to a single cause. Rather a combination of multiple risk factors seems to be responsible for ARF development.

Effects of cyclooxygenase inhibitor treatment on the renal toxicity of cisplatin in rats

The purpose of this study was to determine the effects of a nonselective cyclooxygenase (cox) inhibitor and of a selective cox-2 inhibitor on the renal toxicity of cisplatin. Cisplatin with or without a cox-1 inhibitor (SC560), a cox-2 inhibitor (SC236), or a nonselective cox inhibitor (piroxicam) was administered to Sprague-Dawley rats. Renal toxicity was assessed by serum creatinine concentration (SCR), urine specific gravity (USG), and histopathologic lesion score (HLS). Acutely, the SCR was significantly higher in rats receiving cisplatin/SC560 (1.62+/-0.34 mg/dl) or cisplatin/piroxicam (2.0+/-0.41 mg/dl) than in rats receiving cisplatin alone (1.09+/-0.40 mg/dl). The apparent increase in SCR in the rats receiving cisplatin/SC236 (1.58+/-0.31) was not significantly different from that of rats receiving cisplatin alone (1.09+/-0.40 mg/dl). No significant differences in USG or HLSs were noted between rats receiving cisplatin alone and cisplatin combined with any cox inhibitor. In a chronic study, no differences in renal toxicity were found between rats treated with cisplatin alone and cisplatin/SC236 or cisplatin/piroxicam. The acute rise in SCR following cisplatin treatment can be worsened by the addition of cox inhibitors, especially those that inhibit cox-1.

The importance of comorbidity in nephrologists' assessment of acute renal failure

To study the features of acute renal failure (ARF) in our hospital and to determine prognosis and mortality associated factors. Retrospective study of ARF episodes during a two years period (2005-2007). ARF was considered when a sudden rise in serum creatinine concentration was more than 0,5 mg/dl in patients with normal renal function and more than 1 mg/dl in patients with previous mild to moderate chronic renal failure. We analyzed epidemiologic, clinical, laboratories results, therapeutics and prognosis factors. Two hundred and one patients were evaluated (62,7% males; Age= 67,35 16,38 years (63,68%>65 years); Comorbility Index of Charlson 3,49 2,43). 115 episodes presented in patients with previous renal failure. ARF was pre-renal in 52,7%, renal in 34,8% and post-renal in 8,5%. 35,8% of ARF patients had oliguria or anuria. The mean duration of ARF/hospitalization was 22,47 days (22,47 21,83). The percentage of resolved ARF was 70,1%. Mortality was 30,8%. The univariated analysis showed comorbility Index of Charlson, oliguria, low serum albumin and cholesterol, and anemia were significantly associated with mortality (p<0,05). The lineal regression analysis found three factors associated to the mortality rate: Comorbility Index of Charlson, oliguria and low serum cholesterol. Mortality predictive model was carried out. Highest basal comorbility of patients, oliguria and malnutrition-inflammation dates are princess prognosis and mortality factors in ARF today A new approach is needed in ARF because this new type/class of population.

Use of Isotonic Sodium Bicarbonate to Prevent Radiocontrast Nephropathy in Patients with Mild Pre-Existing Renal Impairment: A Meta-Analysis

Acute renal dysfunction after radiocontrast in patients with pre-existing renal impairment is not uncommon and is associated with significant morbidity and mortality. Isotonic sodium bicarbonate solution was first reported to reduce radiocontrast nephropathy in 2004. This first study was, however; limited by its small sample size and as such, the use of isotonic sodium bicarbonate to prevent radiocontrast nephropathy is still not widely used by many anaesthetists and intensivists. We meta-analysed relevant randomised controlled studies sourced from the Cochrane Controlled Trial Register (2007 issue 4), EMBASE and MEDLINE databases (1966 to April 15, 2008) without any language restriction. The use of isotonic sodium bicarbonate was associated with a significant reduction in risk of an incremental rise in serum creatinine concentration 25% above baseline (relative risk 0.22, 95% confidence interval [CI]: 0.11 to 0.44, P < 0.0001; 2 = 0%) and had a protective effect on the absolute change in serum creatinine concentration (weighted-mean-difference -9.4 micromol/l, 95% CI: -17.2 to -1.7, P = 0.02; F = 0%) and creatinine clearance (weighted-mean-difference 3.7 ml/min, 95% CI: 0.55 to 6.80, P = 0.02; F = 57.1%) after radiocontrast. The incidence of acute renal failure requiring dialysis was low (1.4%) and was not significantly different after the use of isotonic sodium bicarbonate (relative risk 0.59, 95% CI: 0.15 to 2.42, P = 0.47; F = 0%). With the limited data available, isotonic sodium bicarbonate appears to be safe and very effective in reducing radiocontrast nephropathy in patients with mild pre-existing renal impairment. A large randomised controlled study is needed to confirm whether isotonic bicarbonate can improve patient centred clinical outcomes.

The measurement of whole blood pre-treatment cyclosporine A: metabolite ratios predicts the onset of renal dysfunction in recipients of allogeneic stem cell transplantation

In the context of post-transplant immunosuppression, cyclosporine A (CSA) is dose adjusted in accordance with whole blood drug monitoring. While currently available immunoassay systems primarily target the parent drug, cross-reactivity results in the detection of the major circulating CSA metabolites, though their contribution to both immunosuppression and toxicity remain unclear. This study examines the relationship of CSA metabolites to hepatic and renal dysfunction and the incidence of graft-versus-host disease (GvHD) through parallel assaying of parent drug and drug/metabolites expressed as a metabolite ratio (Cp:mR). Sequential pre-treatment (trough) whole blood samples (n=527) were collected from 31 allo-stem cell transplantation (SCT) recipients. Both parent drug and drug/metabolite levels were determined using the Abbott fluorescence polarization immunoassay. The average mean Cp:mR was significantly higher in patients with hepatic (P=0.004) and renal dysfunction (P=0.004) than in those without. Significantly higher Cp:mR were also found in patients with grades II-IV GvHD (P=0.001) than were observed in patients who did not experience significant GvHD. When measured prospectively, an increasing Cp:mR predated the rise in serum creatinine concentration by a median of two weeks. This study demonstrates a clinically useful CSA metabolite ratio that shows association with hepatic and renal dysfunction and with GvHD. The measure can be used to predict those patients on CSA therapy who are likely to develop renal dysfunction.

Propylene glycol-associated renal toxicity from lorazepam infusion.

Using data from patients who developed elevations in serum creatinine concentrations while receiving continuous-infusion lorazepam, we sought to determine the correlations between the magnitude of serum creatinine concentration rise and each of the following variables: serum propylene glycol level, cumulative lorazepam dose, and duration of lorazepam administration. An additional objective was to identify clinical markers for propylene glycol toxicity. Retrospective chart review. Medical-surgical intensive care unit and burn unit at a university hospital. Eight patients who developed elevations in serum creatinine concentrations while receiving continuous-infusion lorazepam (range 2-28 mg/hr). The mean cumulative dose of lorazepam was 4305 mg (range 1200-10,920 mg), and the mean propylene glycol level determined at the time of peak serum creatinine concentration was 1103 microg/ml (range 186-3450 microg/ml). Serum creatinine concentrations increased in all eight patients during lorazepam infusion and decreased in seven within 3 days after stopping infusion. A weak-to-moderate correlation existed between the magnitude of the rise in serum creatinine concentration and propylene glycol level (r=0.53). A weak-to-moderate correlation also was identified between cumulative lorazepam dose and magnitude of serum creatinine concentration rise (r=0.43), and a strong-to-moderate correlation was found between duration of lorazepam infusion and magnitude of serum creatinine concentration rise (r=0.60). Propylene glycol levels were strongly correlated with both serum osmolality and osmol gap. The patients' increased serum creatinine concentrations are likely to have resulted from exposure to propylene glycol as a result of lorazepam infusion. Serum osmolality and osmol gap may be useful markers for propylene glycol toxicity.

Nephrotoxicity of iopamidol in pediatric, adolescent, and young adult patients who have undergone allogeneic bone marrow transplantation.

To assess the effects of the low-osmolar contrast agent iopamidol and antimicrobial drugs on renal function in pediatric, adolescent, and young adult patients who have undergone bone marrow transplantation (BMT). A retrospective review of records of 120 consecutive pediatric patients who underwent allogeneic BMT in 1997 or 1998 was performed. Eighty-nine patients (median age, 8.1 years) fulfilled study eligibility criteria. Cumulative doses of nephrotoxic antimicrobial drugs were recorded, as well as serum creatinine and blood urea nitrogen concentrations from 24 hours before to 72 hours after each administration of iopamidol during a computed tomographic examination performed within 100 days after BMT. Random coefficient models were used to estimate nephrotoxic effects. Mean baseline glomerular filtration rate was 130.2 mL/min/1.73 m(2), and mean baseline creatinine concentration was 0.51 mg/dL (45 micro mol/L). Older age at BMT (P <.001), use of foscarnet (P =.003), and receipt of iopamidol (P =.073) each prompted a rise in serum creatinine concentration. The antiviral drug foscarnet was associated with the largest increase in the creatinine level; the use of iopamidol effected a relatively small rise in creatinine level. Iopamidol nephrotoxicity was negligible in this cohort of pediatric patients who had undergone allogeneic BMT, even in the presence of elevated renal function levels.