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Chronic kidney disease is a progressive disease with no cure and high morbidity and mortality that occurs commonly in the general adult population, especially in people with diabetes and hypertension. Preservation of kidney function can improve outcomes and can be achieved through non-pharmacological strategies (eg, dietary and lifestyle adjustments) and chronic kidney disease-targeted and kidney disease-specific pharmacological interventions. A plant-dominant, low-protein, and low-salt diet might help to mitigate glomerular hyperfiltration and preserve renal function for longer, possibly while also leading to favourable alterations in acid-base homoeostasis and in the gut microbiome. Pharmacotherapies that alter intrarenal haemodynamics (eg, renin–angiotensin–aldosterone pathway modulators and SGLT2 [SLC5A2] inhibitors) can preserve kidney function by reducing intraglomerular pressure independently of blood pressure and glucose control, whereas other novel agents (eg, non-steroidal mineralocorticoid receptor antagonists) might protect the kidney through anti-inflammatory or antifibrotic mechanisms. Some glomerular and cystic kidney diseases might benefit from disease-specific therapies. Managing chronic kidney disease-associated cardiovascular risk, minimising the risk of infection, and preventing acute kidney injury are crucial interventions for these patients, given the high burden of complications, associated morbidity and mortality, and the role of non-conventional risk factors in chronic kidney disease. When renal replacement therapy becomes inevitable, an incremental transition to dialysis can be considered and has been proposed to possibly preserve residual kidney function longer. There are similarities and distinctions between kidney-preserving care and supportive care. Additional studies of dietary and pharmacological interventions and development of innovative strategies are necessary to ensure optimal kidney-preserving care and to achieve greater longevity and better health-related quality of life for these patients.

Background Lower-than-normal estimated glomerular filtration rate (eGFR) is associated with the risk for all-cause mortality and adverse cardiovascular events. In this regard, the role of higher-than-normal eGFR is still controversial. Objective Investigate long-term clinical consequences across the levels of eGFR calculated by the creatinine-based Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation among apparently healthy cardiovascular risk subjects. Design Prospective study. Participants Participants ( n =1747) of a population-based screening and intervention program for cardiovascular risk factors in Finland during the years 2005–2007. Main Measures Cardiovascular morbidity and all-cause mortality. Key Results Over the 14-year follow-up, subjects with eGFR ≥105 ml/min/1.73 m 2 ( n =97) had an increased risk for all-cause mortality [HR 2.15 (95% CI: 1.24–3.73)], incident peripheral artery disease [HR 2.62 (95% CI: 1.00–6.94)], and atrial fibrillation/flutter [HR 2.10 (95% CI: 1.21–3.65)] when compared to eGFR category 90–104 ml/min after adjustment for cardiovascular and lifestyle-related risk factors. The eGFR category ≥105 ml/min was also associated with a two-fold increased mortality rate compared to the Finnish general population. Conclusions Renal hyperfiltration defined as eGFR ≥105 ml/min/1.73 m 2 is a frequent and important finding in patients commonly treated in primary care. These patients should be followed closely for timely interventions, such as strict BP and blood glucose regulation.

Chronic kidney disease (CKD) affects >10% of the adult population. Each year, approximately 120,000 Americans develop end-stage kidney disease and initiate dialysis, which is costly and associated with functional impairments, worse health-related quality of life, and high early-mortality rates, exceeding 20% in the first year. Recent declarations by the World Kidney Day and the U.S. Government Executive Order seek to implement strategies that reduce the burden of kidney failure by slowing CKD progression and controlling uremia without dialysis. Pragmatic dietary interventions may have a role in improving CKD outcomes and preventing or delaying dialysis initiation. Evidence suggests that a patient-centered plant-dominant low-protein diet (PLADO) of 0.6–0.8 g/kg/day composed of >50% plant-based sources, administered by dietitians trained in non-dialysis CKD care, is promising and consistent with the precision nutrition. The scientific premise of the PLADO stems from the observations that high protein diets with high meat intake not only result in higher cardiovascular disease risk but also higher CKD incidence and faster CKD progression due to increased intraglomerular pressure and glomerular hyperfiltration. Meat intake increases production of nitrogenous end-products, worsens uremia, and may increase the risk of constipation with resulting hyperkalemia from the typical low fiber intake. A plant-dominant, fiber-rich, low-protein diet may lead to favorable alterations in the gut microbiome, which can modulate uremic toxin generation and slow CKD progression, along with reducing cardiovascular risk. PLADO is a heart-healthy, safe, flexible, and feasible diet that could be the centerpiece of a conservative and preservative CKD-management strategy that challenges the prevailing dialysis-centered paradigm.

Although the connection between decreased kidney function and hypertension is commonly acknowledged, there is insufficient research examining the relationship between renal hyperfiltration (higher-than-normal estimated glomerular filtration rate (eGFR)) and the incidence risk of hypertension. Therefore, through a nationwide longitudinal study, our research aimed to explore the relationship between the eGFR and the incidence risk of hypertension in the general population. This research used the cohort records for the National Health Insurance Service in Korea, analyzing records from 1,873,550 individuals between the ages of 20 and 79 who underwent health check-ups between 2010 and 2011. The eGFR levels, determined by applying the 2009 Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation, were employed to evaluate the renal function. An incidence of hypertension was confirmed when a diagnosis of (primary or secondary) hypertension (International Classification of Diseases (ICD)-10 codes I10-I11) was noted at least once per year during outpatient or inpatient care with a prescription for antihypertensive medication or at least one more surpassing 140/90 mmHg from a health examination after the index date after excluding diagnosis of secondary hypertension. The mean age of subjects was 46.03 ± 11.24 years. The 411,029 (21.9%) hypertension cases were identified over a median follow-up of 9.53 years. In the multivariable Cox regression analysis, compared with the 5th decile, the 10th eGFR deciles (≥ 115.58 mL/min/1.73 m²) (hazard ratio (HR): 0.87, 95% confidence interval (CI)(0.85–0.88), p  < 0.001) demonstrated a significant association with a reduced incidence of hypertension. Moreover, an eGFR exceeding 120 mL/min/1.73 m² was linked to a lowered likelihood of hypertension (HR: 0.78, 95% CI (0.76–0.80), p  < 0.001) compared to normal eGFR levels (90 ~ 120 mL/min/1.73 m²). In contrast, in the subgroup analysis of ages over 70 years old, renal hyperfiltration was not associated with a reduced incidence of hypertension. In our study, renal hyperfiltration were associated with a reduced risk of hypertension, and this association was particularly significant in those younger than 70 years old. The association between renal hyperfiltration and a lower risk of hypertension incidence was likely to vary with age.

Background: Glomerular hyperfiltration has been reported to be associated with adverse renal outcomes in general population. It is not known whether drinking pattern is associated with the risk of glomerular hyperfiltration in healthy individuals.Methods: We prospectively followed middle-aged 8,640 Japanese men with normal renal function, no proteinuria, no diabetes, and no use of antihypertensive medications at entry. Data on alcohol consumption were gathered by questionnaire. Glomerular hyperfiltration was defined as estimated glomerular filtration rate (eGFR) ≥117 mL/min/1.73 m2, which was the upper 2.5th percentile value of eGFR in the entire cohort.Results: During 46,186 person-years of follow-up, 330 men developed glomerular hyperfiltration. In a multivariate model, for men who consumed alcohol on 1–3 days per week, alcohol consumption of ≥69.1g ethanol/drinking day was significantly associated with the risk of glomerular hyperfiltration (hazard ratio (HR), 2.37 (95% CI, 1.18–4.74)) compared with non-drinkers. For those who consumed alcohol on 4–7 days per week, higher alcohol consumption per drinking day was associated with a higher risk of glomerular hyperfiltration: the HRs (95% CI) for alcohol consumption of 46.1–69.0, and ≥69.1 g ethanol/drinking day were 1.55 (1.01–2.38), and 1.78 (1.02–3.12), respectively.Conclusions: For high drinking frequency per week, more alcohol intake per drinking day was associated with an increased risk of glomerular hyperfiltration, while for low drinking frequency per week, only very high alcohol intake per drinking day was associated with an increased risk of glomerular hyperfiltration in middle-aged Japanese men.

Abstract Context Glomerular hyperfiltration may represent a direct pathogenetic link between obesity and kidney disease. The most widely used methods to estimate creatine clearance such as Cockroft–Gault (CG), Modification of Diet in Renal Disease (MDRD), and Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) have not been validated in subjects with obesity. Objective The performance of prediction formulas was compared with measured creatinine clearance (mCrCl) in subjects with obesity. Methods The study population included 342 patients with obesity (mean BMI 47.6 kg/m2) without primary kidney disease. A urine collection was performed over 24 hours for measurement of CrCl. Results mCrCl increased with body weight. The CG formula showed an overestimation at high CrCl, whereas an underestimation resulted from CKD-EPI and MDRD. To improve the accuracy of estimated CrCl (eCrCl), a new CG-based formula was developed:53+0.7×(140−Age)×Weight/(96xSCr)×(0.85iffemale)A cut-off point for BMI of 32 kg/m2 was identified, at which the new formula may be applied to improve eCrCl. Conclusion In patients with obesity the glomerular filtration rate increases with body weight, and it is associated with the presence of albuminuria, suggesting an early kidney injury. We propose a novel formula that improves the accuracy of eCrCl to avoid missed diagnoses of hyperfiltration in patients with obesity.

Diabetic nephropathy (DN) is a common complication of Diabetes Mellitus (DM) Types 1 and 2, and prevention of end stage renal disease (ESRD) remains a major challenge. Despite its high prevalence, the pathogenesis of DN is still controversial. Initial glomerular disease manifested by hyperfiltration and loss of glomerular size and charge permselectivity may initiate a cascade of injuries, including tubulo-interstitial disease. Clinically, ‘microalbuminuria’ is still accepted as an early biomarker of glomerular damage, despite mounting evidence that its predictive value for DN is questionable, and findings that suggest the proximal tubule is an important link in the development of DN. The concept of ‘diabetic tubulopathy’ has emerged from recent studies, and its causative role in DN is supported by clinical and experimental evidence, as well as plausible pathogenetic mechanisms. This review explores the ‘tubulocentric’ view of DN. The recent finding that inhibition of proximal tubule (PT) glucose transport (via SGLT2) is nephro-protective in diabetic patients is discussed in relation to the tubule’s potential role in DN. Studies with a tubulocentric view of DN have stimulated alternative clinical approaches to the early detection of diabetic kidney disease. There are tubular biomarkers considered as direct indicators of injury of the proximal tubule (PT), such as N-acetyl-β-D-glucosaminidase, Neutrophil Gelatinase-Associated Lipocalin and Kidney Injury Molecule-1, and other functional PT biomarkers, such as Urine free Retinol-Binding Protein 4 and Cystatin C, which reflect impaired reabsorption of filtered proteins. The clinical application of these measurements to diabetic patients will be reviewed in the context of the need for better biomarkers for early DN.

Introduction: The pandemic of obesity is strongly related to increase of chronic kidney disease (CKD) prevalence. The currently recommended CKD epidemiology collaboration (CKD EPI) equation has several serious limitations, particularly in obese subjects who have high body surface area (BSA). The aim of our study was to analyze differences in the prevalence of CKD between CKD EPI and de-indexed equations where individual BSA was used. Methods: In a total of 2,058 subjects (random sample from a general rural population, 29.65% obese), BSA was estimated using DuBois and DuBois and Moesteller equations and included into the de-indexed equations (CKD DBi, CKD Mi). CKD was classified according to the KDIGO guidelines, and glomerular hyperfiltration (GHF) was defined as 95th percentile, according to the gender and age decade. Results: In obese subjects, prevalence of CKD was significantly higher with CKD EPI than with CKD DBi and CKD Mi equations (9.5%, 6.1%, 5.3%, respectively; p < 0.001), while prevalence of GHF was significantly lower (3.8%, 12.3%, 12.8%, respectively; p < 0.001). Opposite results were observed in subjects with a body mass index <25 kg/m 2 for CKD (5%, 7.1%, 7.2%; p = 0.07) and GHF prevalence (6.1%, 1%, 0.6%; p < 0.001). Discussion/Conclusions: The prevalence of CKD is overestimated, and the prevalence of GHF is underestimated in obese subjects using the CKD EPI equation, i.e., the CKD EPI equation is unreliable in one-third of the population. De-indexed equations should be recommended instead of the CKD EPI equation in epidemiological studies until direct measurement of the glomerular filtration rate becomes more available.

Introduction Renal hyperfiltration (RHF) has been found to be an independent predictor of adverse cardiovascular outcome. However, it remains uncertain whether it is precursor of chronic kidney disease (CKD) in a healthy population. Materials and methods To determine relative risks and identify the predictor of incident proteinuria and decline of estimated glomerular filtration rate (eGFR) in subjects with RHF. A total of 55,992 subjects aged ≥20 years who underwent health check-up during 2004–2017 were included. Among them, 16,946 subjects who completed at least two health checkups were analyzed. Results A total of 949 (5.6%) subjects developed proteinuria and 98 (0.6%) subjects showed ≥ 30% of eGFR decline. The risk of incident proteinuria was significantly higher in those with RHF (RR: 1.644; 95% CI: 1.064–2.541). Those with RHF showed 8.720 fold (95% CI: 4.205–18.081) increased risk for ≥30% decline. ESR, CRP, and monocyte count showed reversed J shaped curve according to the increase of eGFR. The adjusted mean of monocyte count was significantly higher in participants with eGFR ≥90ml/min/1.73m2 or < 60ml/min/1.73m2 compared to that in patients with eGFR 75-89ml/min/1.73m2. Compared to subjects with the lowest tertile of monocyte and no RHF, those with the highest tertile of monocyte count in the RHF group had 3.314-fold (95% CI: 1.893–5.802) higher risk of incident proteinuria and 3.822-fold (95% CI, 1.327–11.006) risk of 30% eGFR decline. Conclusions RHF had significantly increased risk of developing proteinuria and CKD in healthy subjects. Higher monocyte count might be used as a predictor of CKD in subjects with RHF.