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Khan and Lanktree discuss glucagon-like peptide-1 (GLP-1) receptor agonists for treating chronic kidney disease in patients with type 2 diabetes. GLP-1 receptor agonists (also called \"glutides\") are an effective treatment for patients with type 2 diabetes and chronic kidney disease. They are a second-line treatment for patients with type 2 diabetes and chronic kidney disease. GLP-1 receptor agonists should not be used in combination with dipeptidyl peptidase 4 inhibitors.

In patients without diabetes, sodium-glucose cotransporter-2 (SGLT2) inhibitors (or \"flozins\") should be considered for moderate chronic kidney disease or clinical heart failure regardless of ejection fraction. Benefits of SGLT2 inhibitors include improved blood pressure, albuminuria and weight loss. Testing eGFR is not required after starting SGLT2 inhibitors except in patients at risk of volume depletion (i.e., orthostatic hypotension, high-dose diuretics). Women are 2-3 times more likely than men to have a genital mycotic infection while taking SGLT2 inhibitors. No cases of severe hypoglycemia or euglycemic diabetic ketoacidosis were reported in SGLT2 inhibitor clinical trials that included 5877 patients without diabetes.

Using age- and height-adjusted total kidney volume, the Mayo Clinic Imaging Classification provides a validated approach to assess the risk of chronic kidney disease (CKD) progression in autosomal dominant polycystic kidney disease (ADPKD), but requires excluding patients with atypical imaging patterns, whose clinical characteristics have been poorly defined. We report an analysis of the prevalence, clinical and genetic characteristics of patients with atypical polycystic kidney disease by imaging. Patients from the extended Toronto Genetic Epidemiology Study of Polycystic Kidney Disease recruited between 2016 and 2018 completed a standardized clinical questionnaire, kidney function assessment, genetic testing, and kidney imaging by magnetic resonance or computed tomography. We compared the prevalence, clinical features, genetics, and renal prognosis of atypical versus typical polycystic kidney disease by imaging. Forty-six of the 523 (8.8%) patients displayed atypical polycystic kidney disease by imaging; they were older (55 vs. 43 years; P  < 0.001), and less likely to have a family history of ADPKD (26.1% vs. 74.6%; P  < 0.001), a detectable PKD1 or PKD2 mutation (9.2% vs. 80.4%; P  < 0.001), or progression to CKD stage 3 or stage 5 ( P  < 0.001). Patients with atypical polycystic kidney disease by imaging represent a distinct prognostic group with a low likelihood of progression to CKD.

Adiponectin, a secretagogue exclusively produced by adipocytes, has been associated with metabolic features, but its role in the development of the metabolic syndrome remains unclear. We investigated the association between serum adiponectin level and metabolic traits, using both observational and genetic epidemiologic approaches in a multiethnic population assembled in Canada. Clinical data and serum adiponectin level were collected in 1,157 participants of the SHARE/SHARE-AP studies. Participants were genotyped for the functional rs266729 and rs1260326 SNPs in ADIPOQ and GCKR genes. Adiponectin level was positively associated with HDL cholesterol and negatively associated with body mass index, waist-to-hip ratio, triglycerides, fasting glucose, fasting insulin, systolic and diastolic pressure (all P<0.002). The rs266729 minor G allele was associated with lower adiponectin and higher HOMA-IR (P = 0.004 and 0.003, respectively). The association between rs266729 SNP and HOMA-IR was no longer significant after adjustment for adiponectin concentration (P = 0.10). The rs266729 SNP was associated with HOMA-IR to an extent that exceeded its effect on adiponectin level (0.15 SD 95% C.I. [0.06, 0.24], P<0.001). There was no significant interaction between rs266729 SNP and ethnicity on adiponectin or HOMA-IR. In contrast, the SNP rs1260326 in GCKR was associated with HOMA-IR (P<0.001), but not with adiponectin level (P = 0.67). The association of the functional promoter polymorphism rs266729 with lower serum adiponectin and increased insulin resistance in diverse ethnic groups may suggest a causal relationship between adiponectin level and insulin resistance.

Kidney transplant outcomes are influenced by donor and recipient age, sex, HLA mismatch, donor type, anti-rejection medication adherence and disease recurrence, but variability in transplant outcomes remains unexplained. We hypothesise that donor and recipient polygenic burden for traits related to kidney function may also influence graft function. We assembled a cohort of 6,060 living and deceased kidney donor-recipient pairs. We calculated polygenic risk scores (PRSs) for kidney function-related traits in both donors and recipients. We investigated the association between these PRSs and recipient eGFR at 1- and 5-year post-transplant as well as graft failure. Donor: hypertension PRS ( P < 0.001), eGFR PRS ( P < 0.001), and intracranial aneurysm PRS ( P = 0.01), along with recipient eGFR PRS ( P = 0.001) were associated with eGFR at 1-year post-transplantation. Clinical factors explained 25% of the variation in eGFR at 1-year and 13% at 5-year, with PRSs cumulatively adding 1% in both cases. PRSs were not associated with long-term graft survival. We demonstrate a small, but statistically significant association between donor and recipient PRSs and recipient graft function at 1- and 5-year post-transplant. This effect is, at present, unlikely to have clinical application and further research is required to improve PRS performance.

Background: Loin pain hematuria syndrome (LPHS) is a poorly understood clinical syndrome characterized by hematuria and either unilateral or bilateral severe kidney pain in the absence of identifiable urological disease. Loin pain hematuria syndrome imposes a significant health and economic impact with a loss of productivity and quality of life in a young population. Owing to an incomplete understanding of its pathophysiology, treatment has been limited to nonspecific pain management. Nearly 60 years after its initial description, we are no further ahead in understanding the molecular pathways involved in LPHS. Objective: To outline the study design for exome sequencing in adults with LPHS and their families. Methods: In this single-center case series, 24 patients with LPHS and 2 additional first-degree family members per participant will be recruited. DNA extracted from venous blood samples will undergo exome sequencing on the Illumina NovaSeq 6000 System at 100× depth and will be assessed for pathogenic variants in genes associated with hematuria (number of genes in: glomerular endothelium [n = 10] and basement membrane [n = 8]), and pain pathways (number of genes in: pain transduction [n = 17], conduction [n = 8], synaptic transmission [n = 37], and modulation [n = 27]). We will further examine identified potentially pathogenic variants that co-segregate with LPHS features among affected families. Conclusions: This pilot study may identify new directions for an investigation into the molecular mechanisms underlying LPHS.

Chronic kidney disease (CKD) causes skeletal muscle wasting, resulting in reduced function and inability to live independently. This systematic review critically appraised the scientific literature regarding the effects of full‐body resistance training on clinically‐relevant functional capacity measures in CKD. The study population included studies of people with Stage 4 or 5 CKD and a mean age of 40+ years old. Eight databases were searched for eligible studies: Pubmed, Embase, Cochrane, CINAHL, Scopus, Web of Science, MEDLINE, and AGELINE. MeSH terms and keyword combinations were used for screening following the PRISMA conduct. Inclusion criteria were based on PICO principles and no date of publication filter was applied. The intervention was training 2 days/week of structured resistance exercises using major upper and lower muscle groups. Minimum intervention period was 7 weeks. Comparison groups maintained their habitual activity without structured exercise training. Outcome measures of interest were: 6‐min walk test, grip strength, timed up‐and‐go test, and sit‐to‐stand. Eight randomized controlled trials and one nonequivalent comparison‐group study fulfilled the inclusion criteria and underwent data extraction. All studies were of hemodialysis patients. The evidence indicates that full‐body resistance exercise significantly improved grip strength, timed up and go and sit to stand tests; metrics associated with enhanced quality and quantity of life.