The National Kidney Foundation's Kidney Disease Outcomes Quality Initiative (KDOQI) has provided evidence-based guidelines for nutrition in kidney diseases since 1999. Since the publication of the first KDOQI nutrition guideline, there has been a great accumulation of new evidence regarding the management of nutritional aspects of kidney disease and sophistication in the guidelines process. The 2020 update to the KDOQI Clinical Practice Guideline for Nutrition in CKD was developed as a joint effort with the Academy of Nutrition and Dietetics (Academy). It provides comprehensive up-to-date information on the understanding and care of patients with chronic kidney disease (CKD), especially in terms of their metabolic and nutritional milieu for the practicing clinician and allied health care workers. The guideline was expanded to include not only patients with end-stage kidney disease or advanced CKD, but also patients with stages 1-5 CKD who are not receiving dialysis and patients with a functional kidney transplant. The updated guideline statements focus on 6 primary areas: nutritional assessment, medical nutrition therapy (MNT), dietary protein and energy intake, nutritional supplementation, micronutrients, and electrolytes. The guidelines primarily cover dietary management rather than all possible nutritional interventions. The evidence data and guideline statements were evaluated using Grading of Recommendations, Assessment, Development and Evaluation (GRADE) criteria. As applicable, each guideline statement is accompanied by rationale/background information, a detailed justification, monitoring and evaluation guidance, implementation considerations, special discussions, and recommendations for future research.

Renal disease variability in autosomal dominant polycystic kidney disease (ADPKD) is strongly influenced by the gene locus (PKD1 versus PKD2). Recent studies identified nontruncating PKD1 mutations in approximately 30% of patients who underwent comprehensive mutation screening, but the clinical significance of these mutations is not well defined. We examined the genotype-renal function correlation in a prospective cohort of 220 unrelated ADPKD families ascertained through probands with serum creatinine #1.4 mg/dl at recruitment. We screened these families for PKD1 and PKD2 mutations and reviewed the clinical outcomes of the probands and affected family members. Height-adjusted total kidney volume (htTKV) was obtained in 161 affected subjects. Multivariate Cox proportional hazard modeling for renal and patient survival was performed in 707 affected probands and family members. Overall, we identified pathogenic mutations in 84.5% of our families, in which the prevalence of PKD1 truncating, PKD1 in-frame insertion/deletion, PKD1 nontruncating, and PKD2 mutations was 38.3%, 4.3%, 27.1%, and 30.3%, respectively. Compared with patients with PKD1 truncating mutations, patients with PKD1 in-frame insertion/deletion, PKD1 nontruncating, or PKD2 mutations have smaller htTKV and reduced risks (hazard ratio Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease worldwide, responsible for 5%-10% of ESRD. 1,2 Mutations in two genes (PKD1 and PKD2) account for most patients with ADPKD. 2,3 Previous studies of European families ascertained through probands enriched with renal failure reported that approximately 85% and approximately 15% of ADPKD families were linked to the PKD1 and PKD2 loci, respectively. 3 However, a higher prevalence of PKD2 of 26% has been recently reported in a population-based study. 4 Disease progression of ADPKD is highly variable, in part because of a strong gene locus effect. [5][6][7][8] Adjusted for age, patients with PKD1 have larger kidneys and earlier onset of ESRD than patients with PKD2 (mean age at ESRD, 53.4 versus 72.7 years old, respectively). 5,6,8 Additionally, significant intrafamilial renal disease variability in ADPKD suggests a modifier effect. [9][10][11] [

The clinical use of conventional ultrasonography (US) in autosomal dominant polycystic kidney disease (ADPKD) is currently limited by reduced diagnostic sensitivity, especially in at-risk subjects younger than 30 years of age. In this single-center prospective study, we compared the diagnostic performance of MRI with that of high-resolution (HR) US in 126 subjects ages 16-40 years born with a 50% risk of ADPKD who underwent both these renal imaging studies and comprehensive PKD1 and PKD2 mutation screening. Concurrently, 45 healthy control subjects without a family history of ADPKD completed the same imaging protocol. We analyzed 110 at-risk subjects whose disease status was unequivocally defined by molecular testing and 45 unaffected healthy control subjects. Using a total of .10 cysts as a test criterion in subjects younger than 30 years of age, we found that MRI provided both a sensitivity and specificity of 100%. Comparison of our results from HR US with those from a previous study of conventional US using the test criterion of a total of three or more cysts found a higher diagnostic sensitivity (approximately 97% versus approximately 82%) with a slightly decreased specificity (approximately 98% versus 100%) in this study. Similar results were obtained in test subjects between the ages of 30 and 40 years old. These results suggest that MRI is highly sensitive and specific for diagnosis of ADPKD. HR US has the potential to rival the diagnostic performance of MRI but is both center-and operator-dependent.

Fatigue is common and pervasive in clinically stable KTRs. It is strongly associated with reduced QoL. This study identified modifiable fatigue predictors and sets the scene for future interventional studies.

Objective: Sarcopenia, defined as loss of both muscle strength and mass, is associated with inferior clinical outcomes and quality of life (QoL) in chronic kidney disease, but its effects are unknown in kidney transplantation. Obesity confers increased mortality risk and compromises QoL in kidney transplant recipients (KTRs), but the impacts of sarcopenic obesity remain unexplored. This study aimed to evaluate the associations of muscle strength and mass, sarcopenia, and sarcopenic obesity with clinical outcomes and QoL in KTRs. Methods: This prospective longitudinal study enrolled 128 KTRs ³1-year posttransplantation. Low muscle strength (by handgrip strength) and mass (by bio-impedance analysis), and a combination of both (sarcopenia) were defined as reference cutoffs , and 3) waist circumference >World Health Organisation cutoffs. Prospective follow-up data on mortality and hospitalisation were collected. QoL was evaluated using Medical Outcomes Study Short Form-36 questionnaire. Results: Median follow-up duration was 64 (60-72) months. Low muscle strength and mass, sarcopenia, and sarcopenic obesity were observed in 64%, 36%, 29% and 16% of KTRs respectively. Low muscle strength was independently associated with the composite endpoint of mortality and hospitalisation (HR=2.45; 95% CI=1.30, 4.64; p=0.006), and QoL (physical-related: β=-12.2; 95% CI=-23.6,-0.8; p=0.04; mental-related: β=-9.9; 95% CI=-19.6,-0.3; p=0.04). Low muscle mass (β=-8.8; 95% CI=-16.9,-0.8; p=0.04) and sarcopenia (β=-14.7; 95% CI=-27.2,-2.5; p=0.03) were associated with physical-related QoL only. No independent associations were found between muscle mass, sarcopenia, and sarcopenic obesity with the composite outcome of mortality and hospitalisation. Conclusion: Low muscle strength is common among KTRs, conferring poor prognosis in the medium term. Future research on strength training may prove valuable in improving kidney transplantation outcomes.

Kidney transplantation is the preferred modality of renal replacement therapy. Long-term patient and graft survival have only improved marginally over the recent decade, mainly because of the development of cardiovascular disease after transplantation. Obesity is a risk factor for cardiovascular disease and is common before and after transplantation. This article reviews the literature assessing the role of pre- and post-transplant obesity on patient and graft survival, discusses the underlying obesity-related mechanisms leading to inferior kidney transplant outcomes, and explores the role of nutritional intervention on improving long-term outcomes of transplantation. Although the role of pretransplant obesity remains uncertain, post-transplant obesity increases the risk of graft failure and mortality. Nutritional intervention is effective in achieving post-transplant weight loss, but the effect on long-term outcomes has not been established. Future research should focus on conducting nutritional intervention studies aiming to improve long-term outcomes of kidney transplantation.

This study confirms the utility of fDGF as an early marker of subsequent inferior allograft outcomes, suggesting superiority over the traditional (often subjective) dialysis-based definition. Wider adoption of the fDGF definition should be considered, both as a risk-stratification tool in clinical practice and a clinical trial endpoint.

The purpose of these experiments was to further elucidate the effect of the trace element, zinc, on vitamin A metabolism. Three experiments were conducted at two different locations using different sources of animals. A total of 95 rats were used; 71 specific pathogen free and 24 germfree. The results indicate that plasma vitamin A is depressed in zinc deficient animals or animals severely restricted in food and growth. Liver stores of vitamin A were adequate in both groups. Thus, the normal mechanism for maintaining plasma vitamin A appears to be altered by either zinc deficiency and/or severe food and growth restriction.