The relationship between hyperuricemia, gout, and renal disease has been investigated for several years. From the beginning, kidney disease has been considered a complication of gout; however, the viewpoints changed, claiming that hypertension and elevated uric acid (UA) levels are caused by decreased urate excretion in patients with renal impairment. To date, several examples of evidence support the role of hyperuricemia in cardiovascular or renal diseases. Several mechanisms have been identified that explain the relationship between hyperuricemia and chronic kidney disease, including the crystal effect, renin–angiotensin–aldosterone system activation, nitric oxide synthesis inhibition, and intracellular oxidative stress stimulation, and urate-lowering therapy (ULT) has been proven to reduce renal disease progression in the past few years. In this comprehensive review, the source and physiology of UA are introduced, and the mechanisms that explain the reciprocal relationship between hyperuricemia and kidney disease are reviewed. Lastly, current evidence supporting the use of ULT to postpone renal disease progression in patients with hyperuricemia and gout are summarized.

The relationship between change of gut microbiota and host serum metabolomics associated with low protein diet (LPD) has been unraveled incompletely in CKD patients. Fecal 16S rRNA gene sequencing and serum metabolomics profiling were performed. We reported significant changes in the β-diversity of gut microbiota in CKD patients having LPD (CKD-LPD, n = 16). We identified 19 genera and 12 species with significant differences in their relative abundance among CKD-LPD patients compared to patients receiving normal protein diet (CKD-NPD, n = 27) or non-CKD controls (n = 34), respectively. CKD-LPD had a significant decrease in the abundance of many butyrate-producing bacteria (family Lachnospiraceae and Bacteroidaceae) associated with enrichment of functional module of butanoate metabolism, leading to concomitant reduction in serum levels of SCFA (acetic, heptanoic and nonanoic acid). A secondary bile acid, glyco λ-muricholic acid, was significantly increased in CKD-LPD patients. Serum levels of indoxyl sulfate and p-cresyl sulfate did not differ among groups. The relationship between abundances of microbes and metabolites remained significant in subset of resampling subjects of comparable characteristics. Enrichment of bacterial gene markers related to D-alanine, ketone bodies and glutathione metabolism was noted in CKD-LPD patients. Our analyses reveal signatures and functions of gut microbiota to adapt dietary protein restriction in renal patients.

Recent studies have demonstrated that red cell distribution width (RDW) is associated with cardiovascular (CV) events and mortality. Patients with chronic kidney disease (CKD) are often anemic and have high RDW levels. In this study, we investigated the effect of RDW on major composite CV outcomes among patients with CKD. We retrospectively analyzed patients with CKD who were admitted to the department of cardiology of a tertiary hospital in 2011. The patients were divided into 2 groups: normal RDW (RDW < 14.5%) and elevated RDW (RDW ≥ 14.5%). Demographic characteristics, comorbidities, blood investigation results, prescriptions, and outcomes were analyzed after a 3-year follow-up period. Six adjustment levels were performed to evaluate the effect of RDW on outcomes. This study involved 282 patients with CKD: 213 in the elevated RDW group and 69 in the normal RDW group. The elevated RDW group had older patients, a lower proportion of male patients, lower left ventricular ejection fraction (LVEF) values, lower hemoglobin levels, lower serum albumin levels, and higher creatinine levels, compared with the normal RDW group. A linear trend was observed toward higher RDW in patients with deteriorating renal function. In the final adjusted model, RDW ≥ 14.5%, older age, and lower LVEF were associated with an increased risk of major composite CV outcomes. RDW is a potentially useful cost-effective indicator of major composite CV outcomes in patients with CKD.

Mortality after coronary artery bypass grafting (CABG) is generally associated with underlying disease and surgical factors overlooked in preoperative prognostic models. Sequential Organ Failure Assessment (SOFA) and Acute Physiology and Chronic Health Evaluation (APACHE II) scores are widely used in intensive care units for outcome prediction. This study investigated the accuracy of these models in predicting mortality. Between January 2010 and April 2013, 483 patients who underwent isolated CABG were enrolled. The clinical characteristics, outcomes, and prognostic model scores of the patients were collected. Discrimination was assessed using the area under the curve approach. Both SOFA and APACHE II scores were effective for predicting in-hospital mortality. Among the organ systems examined in the SOFA, the cardiac and renal systems were the strongest predictors of CABG mortality. Multivariate analysis identified only the SOFA score as being an independent risk factor for mortality. In summary, the SOFA score can be used to accurately identify mortality after isolated CABG.

Renal leptospirosis caused by leptospiral infection is characterised by tubulointerstitial nephritis and tubular dysfunction, resulting in acute and chronic kidney injury. Metabolomic and transcriptomic data from a murine model of Leptospira infection were analysed to determine whether metabolomic data from urine were associated with transcriptome changes relevant to kidney injury caused by Leptospira infection. Our findings revealed that 37 metabolites from the urine of L. interrogans-infected mice had significantly different concentrations than L. biflexa-infected and non-infected control mice. Of these, urinary L-carnitine and acetyl-L-carnitine levels were remarkably elevated in L. interrogans-infected mice. Using an integrated pathway analysis, we found that L-carnitine and acetyl-L-carnitine were involved in metabolic pathways such as fatty acid activation, the mitochondrial L-carnitine shuttle pathway, and triacylglycerol biosynthesis that were enriched in the renal tissues of the L. interrogans-infected mice. This study highlights that L-carnitine and acetyl-L-carnitine are implicated in leptospiral infection-induced kidney injury, suggesting their potential as metabolic modulators.

Acute kidney injury is a common and complex complication that has high morality and the risk for chronic kidney disease among survivors. The accuracy of current AKI biomarkers can be affected by water retention and diuretics. Therefore, we aimed to identify a urinary non-recovery marker of acute kidney injury in patients with acute decompensated heart failure. We used the isobaric tag for relative and absolute quantification technology to find a relevant marker protein that could divide patients into control, acute kidney injury with recovery, and acute kidney injury without recovery groups. An enzyme-linked immunosorbent assay of the endothelial cell protein C receptor (EPCR) was used to verify the results. We found that the EPCR was a usable marker for non-recovery renal failure in our setting with the area under the receiver operating characteristics 0.776 ± 0.065; 95%CI: 0.648–0.905, (p < 0.001). Further validation is needed to explore this possibility in different situations.