Small Increases In Serum Creatinine Research Articles

Relative and Absolute Changes in Urinary Neutrophil Gelatinase-Associated Lipocalin and Correlation with Small Increases in Serum Creatinine Levels after Coronary Angiography: An Observational Study

Introduction/Aims: The Acute Kidney Injury Network classification is based on small increases in serum creatinine (sCr) for stage 1. This study investigated whether changes in the urinary concentration of neutrophil gelatinase-associated lipocalin (uNGAL) could predict small increases in sCr in patients undergoing coronary angiography. Methods: The uNGAL was measured before contrast infusion and 2 and 4 h afterwards. Patients were divided into 2 subgroups: G₁ (n = 103), where sCr increased by <0.3 mg/dl, and G₂ (n = 22), where sCr increased by ≥0.3 mg/dl 48 h after the angiography. To determine the sensitivity and specificity for the absolute and relative variations of uNGAL, a receiver operating characteristic curve analysis was performed. Results: In G₂, the uNGAL concentration increased over baseline values (15.9 vs. 9.2 ng/dl; p < 0.05), and it was also 2-fold higher in G₂ versus G₁ (15.9 vs. 8.0 ng/dl; p < 0.001). The uNGAL remains an independent predictor of the small increases in sCr, and, for an increase of 50% over baseline levels, it showed 60% sensitivity and 81% specificity. Conclusion: Changes in uNGAL concentration 2 h after the infusion of contrast media showed marginal sensitivity to predict small increases in sCr.

Clinical Impact of Mild Acute Kidney Injury After Cardiac Surgery

Dialysis-dependent renal failure occurs infrequently after cardiac surgery but leads to substantial morbidity and mortality. In contrast, milder degrees of acute kidney injury (AKI), based on small increases in serum creatinine, occur frequently but the independent impact of mild AKI on outcome remains unclear. Between January 2010 and December 2012, 3,869 consecutive patients undergoing cardiac surgery comprised the study cohort. Acute kidney injury was defined according to the AKI Network criteria as stage I, II, or III. A nonparsimonious multivariable logistic regression model including preoperative and intraoperative variables was constructed to determine a propensity score for the development of stage I AKI followed by a greedy matching algorithm to create 1:1 propensity-matched pairs. The incidence of stage I AKI in the entire cohort was 22.4%. Stage I AKI patients were more likely to be older; to have diabetes mellitus, hypertension, preoperative renal dysfunction, and poorer left ventricle function; and to require more urgent surgery and longer cardiopulmonary bypass. After propensity matching, the 833 matched pairs were similar in terms of all of the above characteristics (all p > 0.5). Within the matched cohort, AKI patients had higher mortality (2.6% versus 1.2%, p = 0.01), higher incidence of neurologic dysfunction (15.2% versus 8.1%, p < 0.001), and longer duration of mechanical ventilation (41.7 ± 125.0 versus 19.3 ± 58.6 hours, p < 0.001). Intensive care unit stay (5.2 ± 10.7 versus 2.7 ± 3.8 days, p < 0.0001), and hospital length of stay (17.9 ± 20.1 versus 14.7 ± 18.3 days, p = 0.0007) was significantly longer for matched AKI patients. Patients with even mild degrees of AKI have increased mortality and morbidity compared with their matched counterparts. Interventions that prevent or mitigate AKI after cardiac surgery can yield substantial clinical benefit.

Definition and biomarkers of acute renal damage: New perspectives

The RIFLE and AKIN criteria have definitely helped out to draw attention to the relationship between a deterioration of renal function that produces a small increase in serum creatinine and a worse outcome. However, the specific clinical utility of using these criteria remains to be well-defined. It is believed that the main use of these criteria is for the design of epidemiological studies and clinical trials to define inclusion criteria and objectives of an intervention.AKI adopting term, re-summoning former ARF terminology, it is appropriate to describe the clinical condition characterized by damage to kidney, in the same way as the term is used to describe acute lung damage where the lung injury situation still has not increased to a situation of organ failure (dysfunction).The serum and urine biomarkers (creatinine, urea, and diuresis) currently in use are not sensitive or specific for detecting kidney damage, limiting treatment options and potentially compromising the outcome. New biomarkers are being studied in order to diagnose an earlier and more specific AKI, with the potential to change the definition criteria of AKI with different stages, currently based in diuresis and serum creatinine.

Definición y biomarcadores de daño renal agudo: nuevas perspectivas

The RIFLE and AKIN criteria have definitely help out to draw attention to the relationship between a deterioration of renal function that produces a small increase in serum creatinine and a worse outcome. However, the specific clinical utility of using these criteria remains to be well-defined. It is believed that the main use of these criteria is for the design of epidemiological studies and clinical trials to define inclusion criteria and objectives of an intervention.AKI adopting term, re-summoning former ARF terminology, it is appropriate to describe the clinical condition characterized by damage to kidney, in the same way as the term is used to describe acute lung damage where the lung injury situation still has not increased to a situation of organ failure (dysfunction).The serum and urine biomarkers (creatinine, urea, and diuresis) currently in use are not sensitive or specific for detecting kidney damage, limiting treatment options and potentially compromising the outcome. New biomarkers are being studied in order to diagnose an earlier and more specific AKI, with the potential to change the definition criteria of AKI with different stages, currently based in diuresis and serum creatinine.

Impact of Mild Acute Kidney Injury Following Cardiac Surgery

Dialysis-dependent renal failure occurs infrequently following cardiac surgery but leads to substantial morbidity and mortality. In contrast, milder degrees of acute kidney injury (AKI), based on small increases in serum creatinine, occur frequently but the independent impact of mild AKI on outcome remains unclear.

LB0005 12-week results of a phase 2B dose-ranging study of LY3009104 (INCB028050), an oral JAK1/JAK2 inhibitor, in combination with traditional dmards in patients with rheumatoid arthritis

BackgroundLY3009104 (LY) is a novel, oral inhibitor of the JAK1/JAK2 signalling pathway known to be important in the pathobiology of rheumatoid arthritis (RA).ObjectivesTo compare efficacy and safety of LY versus...

Contrast-induced acute kidney injury following coronary angiography: a cohort study of hospitalized patients with or without chronic kidney disease

Contrast-induced acute kidney injury (CIAKI) has been linked to unfavorable consequences. In routine clinical practice, small increases in serum creatinine (SCr) following coronary angiography tend to be underestimated, especially in patients without chronic kidney disease (CKD). We conducted a retrospective observational cohort study to analyze in-hospital and long-term outcomes of CIAKI following coronary angiography in patients with or without CKD (eGFR ≥ 60 mL/min/1.73 m(2)) from January 2008 through December 2009. CIAKI was defined as SCr either ≥ 25% or ≥ 0.5 mg/dL from baseline within 72 h after contrast exposure. Multivariable logistic regression for in-hospital mortality and Cox proportional hazards calculations for long-term mortality and requirement for dialysis were performed. A total of 1160 patients were included in the study. CIAKI occurred in 19% of CKD patients and in 18% of non-CKD patients. In CKD and non-CKD patients, CIAKI was more frequent in patients requiring mechanical ventilation or inotropes or in those given furosemide, and it was associated with adverse in-hospital (prolonged hospitalization, acute dialysis and mortality) and long-term (increased creatinine, initiation of dialysis and mortality) outcomes. In multivariable analysis, CKD patients had greater in-hospital mortality if they developed CIAKI (adjusted OR 8, 95% CI 1.9-34.5, P = 0.005), and non-CKD patients had greater long-term mortality if they developed CIAKI (adjusted HR 2.2, 95% CI 1.2-4.1, P = 0.016). CIAKI following coronary angiography was associated with adverse in-hospital and long-term outcomes in both CKD and non-CKD patients.

Effect of Cobicistat on Glomerular Filtration Rate in Subjects With Normal and Impaired Renal Function

This study evaluated the effect of cobicistat (COBI) on glomerular filtration rate in subjects with normal renal function (RF) or with mild/moderate renal impairment, by comparing creatinine clearance [estimated glomerular filtration rate (eGFR)] with actual GFR (aGFR) using iohexol, a probe drug excreted by glomerular filtration. COBI is a potent CYP3A inhibitor (pharmacoenhancer) currently in phase 3 testing with elvitegravir, atazanavir, and darunavir. Normal RF subjects received COBI 150 mg QD, ritonavir (RTV) 100 mg QD, or placebo for 7 days; subjects with mild/moderate renal impairment received COBI 150 mg QD. The eGFR and aGFR were measured on days 0, 7, and 14 and within-subject changes calculated relative to day 0. COBI and RTV pharmacokinetics were analyzed on day 7. All 36 subjects in cohort 1 and 17 of 18 subjects in cohort 2 completed all study treatments. Study treatments were well tolerated. Small increases in serum creatinine with corresponding mean decreases in eGFR (∼10 mL/min or mL/min per 1.73 m) were observed on day 7 relative to day 0 in subjects receiving COBI (P < 0.05). The decreases were reversible on COBI discontinuation; mean eGFR values returned to baseline on day 14 (P > 0.05). No statistically significant changes in aGFR on days 7 or 14 relative to day 0 were seen with COBI (P > 0.05). No statistically significant decreases in aGFR or eGFR were observed with RTV or placebo. COBI affects eGFR but not the actual GFR. The time to onset, magnitude, and time to resolution of changes in eGFR are consistent with altered proximal tubular secretion of creatinine through inhibition of drug transporters.

Preventable Risk Factors for Acute Kidney Injury in Patients Undergoing Cardiac Surgery

f s c t t ACUTE KIDNEY INJURY (AKI) develops in 5% to 42% of patients who undergo cardiac surgery depending on the efinition of AKI, and 1% to 4% of patients require dialysis.1-6 AKI requiring dialysis after cardiac surgery is associated with an increased incidence of infection, length of critical care unit stay, and long-term need for dialysis.7-9 Chertow et al10 have shown that AKI requiring dialysis is an independent risk factor for mortality after cardiac surgery. Recent studies have shown that even small increases in serum creatinine ( 0.3 mg/dL) postoperatively are associated with increased mortality.11-13 The presence of stage-3 chronic kidney disease (CKD) at baseline (serum creatinine 1.47 mg/dL or glomerular filtration rate [GFR] 60 mL/min/1.73 m2) has been associated ith an increased incidence of postoperative AKI, a longer ospital stay, increased hospital mortality, and a poorer ong-term outcome.14-16 CKD is now defined in stages acording to the estimated GFR derived from serum creatinine evels (Table 1).17 Given the significant morbidity and mortality risk associated with postoperative AKI, the prevention of renal dysfunction is of paramount importance. This has led to the formulation and validation of many clinical risk scores to predict post–cardiac surgery AKI requiring renal replacement therapy (RRT).18-21 Chertow et al18 were among the first to develop a preoperative enal risk stratification algorithm based on the Veterans Affairs oronary Artery Surgery Study experience.18 Subsequently, a umber of investigators derived and validated equations to stimate the risk of post–cardiac surgery AKI requiring RRT Table 2). Finally, Palomba et al22 designed the Acute Kidney Injury After Cardiac Surgery Score based on a cohort of patients who underwent elective surgery at a Brazilian center.22 The Palomba study predicted the risk for post–cardiac surgery AKI not requiring dialysis. Most of the factors used in the development of prediction equations are nonmodifiable. These include female sex, congestive heart failure, a low ejection fraction ( 35%), diabetes mellitus, CKD, chronic obstructive pulmonary disease, peripheral vascular disease, combined valve surgery, and emergency surgery.18-22 Preoperative assessment increases the awareness of risk for AKI and can be used when obtaining consent and in planning for the perioperative period. Most importantly, the identification of high-risk patients provides an opportunity to optimize preoperative care. There are both modifiable and nonmodifiable risk factors associated with the development of AKI in cardiac surgery. This review focuses on modifiable risk factors to prevent the occurrence of AKI. These have been classified as preoperative, intraoperative, and postoperative modifiable risk factors (Table

Subtle change of cystatin C, with or without acute kidney injury, associated with increased mortality in the intensive care unit

Purpose Recent epidemiologic studies suggest a significant association between small increases in serum creatinine (sCr) and adverse outcomes. The Acute Kidney Injury Network (AKIN) sought to increase the sensitivity of the AKIN criteria for acute kidney injury (AKI) by recommending the use of small changes in sCr for the diagnosis of AKI. Several recent studies have reported that serum cystatin C (cysC) is more accurate than sCr as a surrogate for the glomerular filtration rate. This study was performed to determine whether small increases in cysC (≥0.3 mg/L within 48 hours) are associated with clinical outcomes in critically ill patients. Materials and Methods This was a prospective study of 274 consecutive patients admitted to the intensive care unit. Clinical data, including urine output, sCr, cysC, and outcomes, were collected for up to 3 months. Kaplan-Meier curves were used to determine the 90-day survival rate. Mortality was adjusted according to the Cox proportional hazards model. Results Acute kidney injury developed in 84 (30.7%) patients based on the AKIN criteria. Among these patients, 42 (50%) had stage 1; 8 (9.5%), stage 2; and 34 (40.4%), stage 3 disease. Fourteen patients with increased cysC did not have AKI by AKIN criteria. The overall 90-day mortality was 20.8%. When mortality was stratified by group, it was 5.7% for the no-AKI-without-cysC-increment group, 28.6% for the no-AKI-with-increased-cysC group, 33.3% for the AKIN stage 1 group, 62.5% for the AKIN stage 2 group, and 70.6% for the AKIN stage 3 group ( P < .001). Kaplan-Meier curves were constructed for each group based on stage and 90-day survival. The Cox analysis showed that patients who met AKIN criteria and patients with increases of cysC without AKI had associated mortality. In addition, patients with increases in cysC without AKI had outcomes similar to the patients with stage 1 AKI. Conclusions Small increases of cysC were associated with increased mortality in intensive care unit patients independent of diagnosis of AKI by AKIN criteria.

Mild acute kidney injury is associated with increased mortality after cardiac surgery in patients with eGFR < 60 mL/min/1.73 m2

Background: A small increase in serum creatinine after cardiac surgery has been associated with increased mortality. However, it is unclear whether this association varies with baseline renal function. Methods: We retrospectively reviewed data on 1359 patients who underwent cardiac surgery over a 4-year period in two tertiary care hospitals including demographic data, comorbid conditions, and intra- and postoperative complications using a standardized form. We followed patients for 90 days postoperatively and death rates and length of hospital stay were noted. Results: The incidence of acute kidney injury (AKI) after cardiac surgery was 40.2%. Patients were grouped into terciles based on change in serum creatinine. Kaplan–Meier survival analysis and Cox regression analysis showed that the development of AKI with a small increase in serum creatinine of more than 0.3 mg/dL from baseline (tercile 3) was associated with a higher risk of mortality within 90 days and 7 days longer hospitalization following a cardiac surgery. Stratified analysis showed that only patients with baseline eGFR < 60 mL/min/1.73 m had fivefold higher mortality with rise of serum creatinine >0.3 mg/dL. Conclusions: Patients with baseline eGFR < 60 mL/min/1.73 m2 had increased risk of mortality after cardiac surgery with a small increase in serum creatinine whereas a similar increase in serum creatinine in those with eGFR ≥ 60 mL/min/1.73 m2 did not increase mortality.

Small increases in serum creatinine are associated with prolonged ICU stay and increased hospital mortality in critically ill patients with cancer

Declining kidney function has been associated with adverse hospital outcome in cancer patients. ICU literature suggests that small changes in serum creatinine are associated with poor outcome. We hypothesized that reductions in renal function previously considered trivial would predict a poor outcome in critically ill patients with malignant disease. We evaluated the effects on hospital mortality and ICU length of stay of small changes in creatinine following admission to the intensive care unit. We conducted a retrospective cohort study utilizing clinical, laboratory and pharmacy data collected from 3,795 patients admitted to the University of Texas M.D. Anderson Cancer Center's Intensive Care Unit. We conducted univariate and multivariate regression analysis to determine those factors associated with adverse ICU and hospital outcome. Increases in creatinine as small as 10% (0.2 mg/dl) were associated with prolonged ICU stay (5 days vs 6.6 days, p < 0.001) and increased mortality (14.6% vs 25.5%, p < 0.0001). Patients with a 25% rise in creatinine during the first 72 h of ICU admission were twice as likely to die in the hospital (14.3% vs 30.1%, p < 0.001). RIFLE criteria were accurate predictors of outcome, though they missed much of the risk of even smaller increases in creatinine. Even small rises in serum creatinine following admission to the ICU are associated with increased morbidity and mortality in oncologic patients. The poor outcome in those with rising creatinine could not be explained by severity of illness or other risk factors. These small changes in creatinine may not be trivial, and should be regarded as evidence of a decline in an individual patient's condition.

Inhibition of JAK kinases in patients with rheumatoid arthritis: scientific rationale and clinical outcomes

CP-690,550 is an orally active and selective inhibitor of the janus kinase (JAK) molecules. The molecular pathways through which the JAK moieties function are described along with the clinical mechanisms associated with their inhibition. Animal models of JAK inhibition are reviewed as a background for the possible inhibition of JAK in humans. The pharmacokinetics of CP-690,550 in humans is described, and the Phase IIA and IIB trials are reviewed in some detail. These trials were dose-ranging and showed a general dose response with relatively robust American College of Rheumatology 20 (ACR20) responses. A proof-of-concept 6-week trial in which CP-690,550 was given as monotherapy was associated with highly efficacious responses at the mid and higher twice-daily dose ranges employed. A subsequent 24 week dose-ranging trial in which CP-690,550 was administered in combination with methotrexate showed ACR20 responses, which were also statistically significant versus placebo interventions. CP-690,550 treatment was associated with side effects, which included headache and nausea. Infections were more common versus placebo as were elevations in transaminase enzymes when administered in combination with methotrexate, and increases in low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol. Decreases in haemoglobin and white blood cell (WBC) counts were also observed along with small increases in serum creatinine. Occasional significant decreases of haemoglobin (>2 g dl(-1)) were observed, although decreases of WBC to less than 1000 per mm(3) were not seen. Plans for long-term follow-up of the described trials are described along with the features of five presently ongoing Phase III trials of the CP-690,550 janus kinase (JAK) inhibitor. Future directions include completion and publication of these trials along with study of JAK inhibition for other indications.

Acute Renal Syndrome/Renal Angina

Acute kidney injury (AKI) is a widespread problem in the intensive care unit (ICU) that heralds increased morbidity, mortality, and ICU length and cost of stay, independent of other factors (1–3). Unfortunately, there are few, if any, specific interventions proven to prevent or treat AKI. Renal replacement therapy is a reactionary, supportive therapy that almost by definition is started long after the inciting process and well into the pathophysiologic cascade of AKI. Although renal replacement therapy is effective at treating the sequelae of AKI such as electrolyte, fluid, and acid-base disorders, it does not address the underlying disease and is rather a bridge to hoped-for spontaneous renal recovery. Although many interventions have been studied to treat AKI and prevent its progression (4), nothing has been clearly beneficial, and we are left with the obvious yet nonspecific interventions: Maintain renal perfusion, avoid nephrotoxic drugs, and correct the underlying process (sepsis, hypovolemia). Many have suggested that at least one reason for the futility of interventions for AKI is late disease detection using conventional markers of renal function (4–7). That is, by the time azotemia and its sequelae are detected, renal injury is well established and may be outside the window for mitigation by an intervention (8). Part of the problem is that in contrast to many other acute disease states in which patients present with acute symptoms, patients with AKI are relatively asymptomatic until the disease is advanced. For example, in the case of acute myocardial infarction, patients typically present with symptoms of disease (chest pain, …

Prerenal failure: from old concepts to new paradigms

Prerenal failure is used to designate a reversible form of acute renal dysfunction. However, the terminology encompasses several different conditions that vary considerably. The lack of a widely accepted definition for prerenal failure makes it impossible to determine the epidemiology, natural history, and association with adverse outcomes. New diagnostic and staging criteria for acute kidney injury proposed by the Acute Kidney Injury (AKI) Network recognize that small increases in serum creatinine are associated with increased mortality. However, these criteria have not determined specific diagnostic criteria to classify prerenal conditions. As a consequence of the lack of standardized definitions and the difficulty in assessing reversibility of AKI, the concept of prerenal failure has been recently challenged. The difference in the pathophysiology and manifestations of prerenal failure suggests that our current approach needs to be reevaluated. Prerenal failure state needs to be classified depending on the underlying capacity for compensation, the nature and the timing of the insult and the adaptation to chronic comorbidities. Identification of high-risk states and high-risk processes associated with the use of new biomarkers for AKI will provide new tools to distinguish between the prerenal failure and the established AKI. This review provides an appraisal of the current status and recommendations for future research in this field.

Long-term outcomes after small increases in serum creatinine during hospitalization

Long-term outcomes after small increases in serum creatinine during hospitalization

Progression From Acute Kidney Injury to Chronic Kidney Disease: A Pediatric Perspective

Although emerging evidence indicates that the incidence of both acute kidney injury (AKI) and chronic kidney disease (CKD) in children is rising and the etiologies are dramatically changing, relatively little is currently known regarding the potential for transition from AKI to CKD. In both situations, early intervention can significantly improve the dismal prognosis. However, the lack of a uniform AKI definition and the paucity of early, predictive biomarkers have impaired our ability diagnose AKI early to institute potentially effective therapies in a timely manner. Fortunately, recent data has validated a multidimensional AKI classification system for children. In addition, the application of innovative technologies has identified candidates that are emerging as early biomarkers of both AKI and CKD. These include neutrophil gelatinase-associated lipocalin, liver-type fatty acid-binding protein, and kidney injury molecule-1. Studies to validate the sensitivity and specificity of these biomarkers in clinical samples from large cohorts and from multiple clinical situations are currently in progress, facilitated by the development of commercial tools for the reproducible measurement of these biomarkers across different laboratories.

Long-Term Outcomes of Acute Kidney Injury

Acute kidney injury (AKI) is common in the intensive care unit and is associated with significant morbidity and mortality. Based on the RIFLE criteria, AKI occurs in up to 67% of patients in the intensive care unit (ICU), with approximately 4% of critically ill patients requiring renal replacement therapy (RRT). It is well known that this subset of AKI patients who require RRT have an in-hospital mortality rate exceeding 50%. However, long-term outcomes of survivors of AKI requiring RRT remain poorly described. Long-term mortality is greater in those patients who survived AKI when compared with critically ill patients without AKI. Long-term morbidity, renal and extrarenal, is a frequent and underappreciated complication of AKI. Among survivors of AKI at long-term follow-up (1-10 years), approximately 12.5% are dialysis dependent (wide range of 1%-64%, depending on the patient population) and 19% to 31% have chronic kidney disease. According to the United States Renal Data System, "acute tubular necrosis without recovery" as a cause of end-stage kidney disease increased from 1.2% in 1994 to 1998 to 1.7% in 1999 to 2003. The incidence will likely continue to rise with the aging population, increase in comorbidities, and expansion of intensive care unit capabilities. AKI is an underrecognized cause of chronic kidney disease (CKD) and patients who survive should be followed closely for new CKD and/or progression of underlying CKD.

ACUTE KIDNEY INJURY IN THE ICU: TIME HAS COME FOR AN EARLY BIOMARKER KIT!

Early recognition of acute kidney injury (AKI) in the intensive care unit (ICU) remains a critical problem, with a rising incidence and a high mortality rate. As a consequence, the actual lack of an early and effective biomarker results in a significant delay in initiating appropriate therapy. The accurate diagnosis of AKI is especially problematic in critically-ill patients, in whom we know that renal function is in an unsteady state; therefore the validity of creatinine- based baseline assessment measures is reduced. Because the rationale for assessing AKI markers in critically-ill patients is strong at the present time, researchers are stimulated to establish a multidimensional AKI classification system. This system should in essence grade AKI severity. The most widely referenced classification is the RIFLE system. Thus, early recognition of AKI, well before changes in serum creatinine occur, has come under intensive research, because it is evidenced that even small increases in serum creatinine are associated with an increase in patient mortality. The development of a biomarker kit in which several early markers with different characteristics are combined, is essential. Multi-centre, randomized studies indicate a potential for early biomarkers able to diagnose AKI 48 hours before creatinine changes. In conclusion, time has come to leave serum creatinine behind as a marker of renal function in patients with AKI on the ICU. Only then will we be able to offer early goal-directed therapy for the kidney in the ICU setting.

Safety of Gentamicin Bladder Irrigations in Complex Urological Cases

Recurrent urinary tract infections are common in complex pediatric urological cases, particularly those requiring clean intermittent catheterization. At our institution gentamicin bladder irrigations have been used for antimicrobial prophylaxis and to treat symptomatic bacteriuria, particularly when the infection does not involve the upper urinary tract. The purpose of this study was to assess the safety of this therapy. A retrospective study was performed of all children treated with gentamicin bladder irrigations from 1999 to 2004. The dose was 14 mg gentamicin in 30 ml saline instilled via catheter once or twice daily. Serum creatinine and random gentamicin levels were obtained according to a protocol based on risk of gentamicin toxicity. Patient demographics, laboratory results and outcomes were abstracted from the medical records. A total of 80 patients (38 males and 42 females) were identified. Median patient age was 10 years and median duration of treatment was 90 days. No patient had detectable serum gentamicin levels greater than 0.4 mg/dl. Small increases in serum creatinine were seen in 3 patients, all of whom had chronic renal insufficiency. A total of 21 patients (26%) had breakthrough UTIs, of which 5 (24%) were gentamicin resistant. No adverse events were documented. Gentamicin bladder irrigations are a helpful adjunct in the management of complex pediatric urological cases involving recurrent symptomatic bacteriuria. We no longer require intensive laboratory monitoring of low risk patients at our institution.