scholarly journals Fecal microbiota analysis of polycystic kidney disease patients according to renal function: A pilot study

2018 ◽  
Vol 244 (6) ◽  
pp. 505-513 ◽  
Author(s):  
Rabi Yacoub ◽  
Girish N Nadkarni ◽  
Daniel I McSkimming ◽  
Lee D Chaves ◽  
Sham Abyad ◽  
...  
Keyword(s):  
Renal Function ◽  
Renal Insufficiency ◽  
Metabolic Pathways ◽  
Confounding Factors ◽  
Direct Effects ◽  
Comorbid Conditions ◽  
Bacterial Composition ◽  
Microbiome Composition ◽  
Bacterial Microbiota ◽  
Composition Changes

Gut bacterial microbiota is altered in patients with advanced renal disease and those on dialysis. However, it is not clear yet what bacterial composition changes are due to the renal insufficiency per se, and what are in result of the accompanying interventions and comorbid conditions. Most studies analyzed diabetic nephropathy, hypertensive nephropathy, and glomerulonephritis patients which might have directly influenced the microbiome regardless of alterations in renal function. We present in this report changes in gut bacterial microbiota in a highly selected group of patients with strict inclusion criteria to eliminate the effects of the confounding factors on the microbiome composition. We conducted multiple analysis approaches according to participants’ renal function to further understand microbiome alteration in different degrees of renal insufficiency. An interesting group of bacteria showed a step-wise change in relative abundance in response to the three groups’ analysis. These bacteria either decreased or increased from mild, moderate to severe renal insufficiency indicating strong and direct effects of the uremic milieu on its relative abundance. We also ran a sensitivity analysis that took into account an assembly of the significant taxa observed in an approach to investigate whether these taxa can fully explain the separation noted between the groups. We determined the projected metabolic pathways altered according to the gut microbiota composition changes. This report not only delineates with a higher certainty the effects of alteration in renal function on the microbiome, but also explores the possible role of dysbiosis on comorbid conditions through alterations in the projected metabolic pathways. Impact statement The heterogeneity of the renal disease, therapeutic interventions, and the original cause of the renal failure, all directly affect the microbiota. We delineate in this report the direct effect of decreased renal function on the bacterial composition following stringent criteria to eliminate the possibilities of other confounding factors and dissect the direct effects of the uremic milieu. We analyzed the microbiome following three different approaches to further evaluate the effects of mild, moderate and advanced renal insufficiency on the microbiome. We also present here a detailed functional analysis of the projected altered pathways secondary to changes in the microbiome composition.

T3 concentrations reflect renal function in patients with renal insufficiency

2007 ◽  
Vol 115 (S 1) ◽  
Author(s):  
W Reinhardt ◽  
U Ewerhart ◽  
K Mann ◽  
O Witzke
Keyword(s):  
Renal Function ◽  
Renal Insufficiency

scholarly journals 1157. Clinical Safety, Efficacy, and Pharmacokinetics of Fosmanogepix, a Novel First-in-class Antifungal, in Patients with Renal Insufficiency: Subset Analysis from a Phase 2 Candidemia Trial

2020 ◽  
Vol 7 (Supplement_1) ◽  
pp. S605-S605
Author(s):  
Pierre Bulpa ◽  
Galia Rahav ◽  
Ilana Oren ◽  
Mickaël Aoun ◽  
George R Thompson ◽  
...  
Keyword(s):  
Renal Function ◽  
Renal Insufficiency ◽  
Antifungal Agents ◽  
Research Study ◽  
Scientific Research ◽  
Panel Member ◽  
Antifungal Treatment ◽  
Successful Outcome ◽  
Review Panel ◽  
Study Investigator

Abstract Background Fosmanogepix (FMGX) is a first-in-class antifungal agent, with a unique MOA targeting the fungal enzyme Gwt1, and broad-spectrum activity against yeasts and molds, including fungi resistant to other antifungal agents. Patients with candidemia often have underlying renal insufficiency or are receiving medications that affect renal function. This analysis evaluated outcomes in patients with varying degrees of renal insufficiency. Methods This global, multicenter, open-label, non-comparative study evaluated the safety and efficacy of FMGX for first-line treatment of candidemia. Patients with a recent diagnosis of candidemia defined as positive blood culture for Candida spp within 96 hrs prior to study entry with ≤ 2 days of prior antifungal treatment were eligible, including those with renal insufficiency. Patients with neutropenia, C. krusei infection, deep-seated Candida infections or receiving hemodialysis were excluded. Subjects were treated with FMGX for up to 14 days: 1000 mg IV BID for 1 day, then 600 mg IV QD for at least 2 days, followed by either 600 mg IV QD or 700 mg PO QD. Patients requiring antifungal treatment beyond 14 days received fluconazole. The primary efficacy endpoint was outcome at end of study treatment (EOST) as determined by an independent data review committee. Successful outcome was defined as survival with clearance of Candida from blood cultures with no additional antifungal treatment. Results 14/21 (66%) subjects had some degree of renal insufficiency: 7 had mild renal insufficiency (GFR:60-89), 5 had moderate renal insufficiency (GFR:30-59), and 2 had severe renal insufficiency (GFR:15-29). 12/14 (86%) completed study treatment, and treatment was successful at EOST in 12/14 (86%) subjects. Decline in renal function was not observed at EOST. 4 had worsening of renal function during the follow-up period; none required dialysis. Renal impairment did not increase exposure of FMGX. There were no treatment-related adverse events. Conclusion FMGX demonstrated high level treatment success with no evidence of drug-related nephrotoxicity, with no dose adjustments required. These preliminary data support the continued evaluation of FMGX in patients with candidemia and renal dysfunction as an alternative to potentially nephrotoxic antifungal agents. Disclosures Pierre Bulpa, MD, Amplyx Pharmaceuticals (Scientific Research Study Investigator) Galia Rahav, MD, AstraZeneca (Scientific Research Study Investigator) Mickaël Aoun, MD, Amplyx Pharmaceuticals (Scientific Research Study Investigator) Peter Pappas, MD, SCYNEXIS, Inc. (Consultant, Advisor or Review Panel member, Research Grant or Support) Bart Jan Kullberg, MD, FRCP, FIDSA, Amplyx (Advisor or Review Panel member) Sara Barbat, BSN, RN, Amplyx Pharmaceuticals (Employee) Pamela Wedel, BSc, Amplyx Pharmaceuticals (Employee) Haran T. Schlamm, MD, Amplyx (Consultant) Michael Hodges, BSc. MD, Amplyx Pharmaceuticals Inc. (Employee)

scholarly journals Contrast-Induced Acute Kidney Injury: Definition, Epidemiology, and Outcome

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Felix G. Meinel ◽  
Carlo N. De Cecco ◽  
U. Joseph Schoepf ◽  
Richard Katzberg
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Renal Insufficiency ◽  
Time Window ◽  
Contrast Material ◽  
Kidney Injury ◽  
Preventive Strategy ◽  
Iodinated Contrast ◽  
Contrast Enhanced Ct ◽  
Contrast Enhanced

Contrast-induced acute kidney injury (CI-AKI) is commonly defined as a decline in kidney function occurring in a narrow time window after administration of iodinated contrast material. The incidence of AKI after contrast material administration greatly depends on the specific definition and cutoff values used. Although self-limiting in most cases, postcontrast AKI carries a risk of more permanent renal insufficiency, dialysis, and death. The risk of AKI from contrast material, in particular when administered intravenously for contrast-enhanced CT, has been exaggerated by older, noncontrolled studies due to background fluctuations in renal function. More recent evidence from controlled studies suggests that the risk is likely nonexistent in patients with normal renal function, but there may be a risk in patients with renal insufficiency. However, even in this patient population, the risk of CI-AKI is probably much smaller than traditionally assumed. Since volume expansion is the only preventive strategy with a convincing evidence base, liberal hydration should be encouraged to further minimize the risk. The benefits of the diagnostic information gained from contrast-enhanced examinations will still need to be balanced with the potential risk of CI-AKI for the individual patient and clinical scenario.

scholarly journals Erythrocyte Sedimentation Rate in Patients with Renal Insufficiency and Renal Replacement Therapy

2021 ◽  
Author(s):  
Anna Buckenmayer ◽  
Lotte Dahmen ◽  
Joachim Hoyer ◽  
Sahana Kamalanabhaiah ◽  
Christian S. Haas
Keyword(s):  
Renal Function ◽  
Peritoneal Dialysis ◽  
Renal Replacement Therapy ◽  
Kidney Disease ◽  
Renal Insufficiency ◽  
Replacement Therapy ◽  
Sedimentation Rate ◽  
Inflammatory Markers ◽  
Erythrocyte Sedimentation ◽  
Esrd Patients

Abstract Background: The erythrocyte sedimentation rate (ESR) is a simple laboratory diagnostic tool for estimating systemic inflammation. It remains unclear, if renal function affects ESR, thereby compromising its validity. This pilot study aims to compare prevalence and extent of ESR elevations in hospitalized patients with or without kidney disease. In addition, the impact of renal replacement therapy (RRT) modality on ESR was determined.Methods: In this single-center, retrospective study, patients were screened for ESR values. ESR was compared in patients with and without renal disease and/or RRT. In addition, ESR was correlated with other inflammatory markers, the extent of renal insufficiency and clinical characteristics.Results: A total of 203 patients was identified, showing an overall elevated ESR in the study population (mean 51.7±34.6 mm/h). ESR was significantly increased in all patients with severe infection, active vasculitis or cancer, respectively, independent from renal function. Interestingly, there was no difference in ESR between patients with and without kidney disease or those having received a prior renal transplant or being on hemodialysis. However, ESRD patients treated with peritoneal dialysis presented with a significantly higher ESR (78.3±33.1 mm/h, p<0.001), while correlation with other inflammatory markers was not persuasive.Conclusions: We showed that ESR: (1) does not differ between various stages of renal insufficiency; (2) may be helpful as a screening tool also in patients with renal insufficiency; and (3) is significantly increased in ESRD patients on peritoneal dialysis per se, while it seems not to be affected by hemodialysis or renal transplantation (see graphical abstract as supplementary material).

Effects of sulindac on renal function and prostaglandin synthesis in patients with moderate chronic renal insufficiency

1986 ◽  
Vol 70 (5) ◽  
pp. 501-505 ◽  
Author(s):  
C. D. Mistry ◽  
C. J. Lote ◽  
R. Gokal ◽  
W. J. C. Currie ◽  
M. Vandenburg ◽  
...  
Keyword(s):  
Renal Function ◽  
Renal Insufficiency ◽  
Creatinine Clearance ◽  
Chronic Renal Disease ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Breakdown Product ◽  
Predisposing Factor ◽  
A Minor ◽  
Therapeutic Doses

1. The renal effects of therapeutic doses of sulindac were studied in nine patients with stable renal insufficiency, mean creatinine clearance 37.0 ± 2.2 ml min−1 1.73 m−2 (range 24.7–54.6 ml min−1 1.73 m−2). 2. Nine days' treatment with sulindac produced a small, but significant, reduction in the mean creatinine clearance (37.0 ± 2.2 to 34.7 ± 2.2 ml min−1 1.73 m−2; P < 0.02) and 99mTc diethylenetriaminepenta-acetate (DTPA) clearance (35.5 ± 3.4 to 31.4 ± 3.6 ml min−1 1.73 m−2; P < 0.02) without altering body weight, effective renal plasma flow [131I]hippuran clearance), plasma renin activity (PRA), 24 h urinary volume or electrolyte excretion. 3. After discontinuation of sulindac, creatinine clearance returned to pretreatment values. 4. In five female patients, pretreatment urinary excretion of the 6-ketoprostaglandin F1α (6-keto-PGF1α), a stable breakdown product of prostacyclin (PGI2), was significantly reduced (P < 0.02) when compared with four healthy controls, whereas prostaglandin E2 (PGE2) was unchanged. Administration of sulindac did not significantly alter the excretion rate of PGE2 or 6-ketoPGF1α in this group of patients. 5. In chronic renal disease with moderate renal impairment, reduced renal prostacyclin synthesis may be an important predisposing factor to the renal toxicity associated with the use of nonsteroidal anti-inflammatory drugs (NSAID). Short term use of sulindac in therapeutic doses does not appear to influence the excretion of prostaglandins and produces only a minor reversible change in renal function; used cautiously it may have advantages over other NSAID in these patients.-

scholarly journals Acute-on-Chronic Kidney Injury in Thyroid Hormone Withdrawal: A Case with Possible Implications for Radioactive Iodine Planning

2015 ◽  
Vol 2015 ◽  
pp. 1-3 ◽  
Author(s):  
Elizabeth A. McAninch ◽  
Violet S. Lagari
Keyword(s):  
Renal Function ◽  
Thyroid Cancer ◽  
Thyroid Hormone ◽  
Renal Insufficiency ◽  
Radioactive Iodine ◽  
Kidney Injury ◽  
Unilateral Renal Agenesis ◽  
Thyroid Hormone Withdrawal ◽  
Ckd Stage ◽  
Acute Hypothyroidism

The association between renal dysfunction and hypothyroidism is of increasing clinical importance as thyroid hormone replacement may attenuate decline in renal function and improve cardiovascular outcomes in patients with chronic kidney disease (CKD). Although multiple mechanisms for the induction of renal insufficiency in hypothyroidism have been described, the renal impact of short-term, acute hypothyroidism is unknown, which has possible implications for thyroid cancer patients preparing to receive radioactive iodine (RAI). A 56-year-old gentleman with history of unilateral renal agenesis and CKD stage III presented with intermediate-risk papillary thyroid cancer. In preparation for RAI, he underwent thyroid hormone withdrawal (THW) associated with acute kidney injury (AKI), as marked by a decrease in his estimated GFR from 53 to 32 mL/min/1.73 m2. Upon resumption of thyroid hormone, renal function returned to baseline within months. Although AKI in this case was not otherwise associated with adverse outcome and reversed upon resumption of thyroid hormone, it is possible that this phenomenon could result in potential harm, particularly in the patient with baseline renal insufficiency. In CKD patients, preparation for RAI therapy may require special consideration; future studies should address the role of recombinant TSH to mitigate deleterious renal effects of acute hypothyroidism in this setting.

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