Evaluation of renal microperfusion in hyperuricemic nephropathy by contrast-enhanced ultrasound imaging.

Diagnostic tools for the early detection of renal injury caused by hyperuricemia are still lacking. Here, we investigated whether contrast-enhanced ultrasound (CEUS) could be used as a diagnostic tool for hyperuricemic nephropathy (HN). In the HN rat model, CEUS detected a significant decline in renal cortical perfusion compared with that in control rats. Peak intensity (PI) values correlated significantly with serum KIM-1 levels and fibrosis scores in HN rats. An early decline in PI values was also observed in chronic kidney disease (CKD) stage 1 patients with HN compared with the controls (61.1±4.52 dB versus 65.80±7.10 dB) and correlated with renal function in the patients with HN. In contrast, an increase in time to reach PI values was detected in HN patients with stage 1 CKD (15.14±1.75 s versus 14.52±4.75 s) and was more pronounced in CKD stage 4 patients (67.32±3.29 s). CEUS was able to detect abnormal renal perfusion in early CKD with HN, which correlated with renal function decline, suggesting that CEUS could be used as a noninvasive tool for assessing renal function in patients with HN.

Clinical and Histological Predictors of Renal Survival in Patients with Biopsy-Proven Diabetic Nephropathy.

INTRODUCTION: Clinical indicators or pathological features alone cannot reliably predict renal survival in patients with biopsy-confirmed diabetic nephropathy (DN). Therefore, this analysis sought to develop and validate a predictive model incorporating both clinical and pathological markers to predict renal outcomes in patients with biopsy-confirmed DN. METHODS: A predictive nomogram was developed based upon data pertaining to 194 patients with biopsy-confirmed DN. The prognostic relevance of individual clinicopathological variables was assessed through univariate and multivariate Cox regression analyses. A prognostic nomogram was then developed and validated based upon concordance (C)-index values and calibration curves. Internal validation was conducted through bootstrap resampling, while the clinical utility of this model was assessed via a decision curve analysis (DCA) approach. RESULTS: Nephrotic-range 24-h proteinuria, late-stage CKD, glomerular classification III-IV, and IFTA score 2-3 were all identified as independent predictors of poor renal outcomes in DN patients and were incorporated into our final nomogram. Calibration curves revealed good agreement between predicted and actual 3- and 5-year renal survival in DN patients with the C-index value for this nomogram at 0.845 (95% CI: 0.826-0.864). DCA revealed that our nomogram was superior to models based solely upon clinical indicators. CONCLUSION: A predictive nomogram incorporating clinical and pathological indicators was developed and validated for the prediction of renal survival outcomes in patients with biopsy-confirmed DN. This model will be of value to clinicians, as it can serve as an easy-to-use and reliable tool for physicians to guide patient management based on individualized risk.

Nicotinamide retains Klotho expression and ameliorates rhabdomyolysis-induced acute kidney injury.

OBJECTIVES: Acute kidney injury (AKI) is a severe complication of rhabdomyolysis that significantly increases mortality. Unfortunately, the therapeutic approach is limited. Inflammation plays a critical role in the pathogenesis of rhabdomyolysis-induced AKI, which is a potential therapeutic target. Nicotinamide, a form of vitamin B3 and a precursor of nicotinamide adenine dinucleotide, has been shown to have potent antiinflammation effects. Klotho is a tubular highly expressed renoprotective protein. Therefore, we explored the effect of nicotinamide on rhabdomyolysis-induced AKI and the underlying mechanisms. METHODS: We intramuscularly injected glycerol to induce rhabdomyolysis, and intraperitoneally administrated nicotinamide to observe the effect on kidney injury. Interleukin-1 beta, tumor necrosis factor alpha, nuclear factor kappa B (NF-κB), and Klotho were determined by Western blot. Chromatin immunoprecipitation was used to assess the interaction of NF-κB, nuclear receptor corepressor, and histone deacetylase 1 with Klotho promoters. Small interfering RNA was used to evaluate the role of Klotho in nicotinamide-related renoprotection. RESULTS: The results showed that nicotinamide attenuated renal pathologic morphology, kidney functional abnormalities, and kidney inflammatory response in rhabdomyolysis. Moreover, nicotinamide effectively blocked the recruitment of NF-κB, nuclear receptor corepressor, and histone deacetylase 1 to the promoter of Klotho, and preserved Klotho expression. More importantly, the renoprotection effect of nicotinamide was abrogated when Klotho was knocked down by small interfering RNA in rhabdomyolysis mice. CONCLUSIONS: Our study demonstrated that Klotho preservation is essential for the renoprotection effect of nicotinamide, and provides a new preventive strategy for rhabdomyolysis-induced AKI.

Incorporation of Urinary Neutrophil Gelatinase-Associated Lipocalin and Computed Tomography Quantification to Predict Acute Kidney Injury and In-Hospital Death in COVID-19 Patients.

BACKGROUND: The prevalence of acute kidney injury (AKI) in COVID-19 patients is high, with poor prognosis. Early identification of COVID-19 patients who are at risk for AKI and may develop critical illness and death is of great importance. OBJECTIVE: The aim of this study was to develop and validate a prognostic model of AKI and in-hospital death in patients with COVID-19, incorporating the new tubular injury biomarker urinary neutrophil gelatinase-associated lipocalin (u-NGAL) and artificial intelligence (AI)-based chest computed tomography (CT) analysis. METHODS: A single-center cohort of patients with COVID-19 from Wuhan Leishenshan Hospital were included in this study. Demographic characteristics, laboratory findings, and AI-assisted chest CT imaging variables identified on hospital admission were screened using least absolute shrinkage and selection operator (LASSO) and logistic regression to develop a model for predicting the AKI risk. The accuracy of the AKI prediction model was measured using the concordance index (C-index), and the internal validity of the model was assessed by bootstrap resampling. A multivariate Cox regression model and Kaplan-Meier curves were analyzed for survival analysis in COVID-19 patients. RESULTS: One hundred seventy-four patients were included. The median (±SD) age of the patients was 63.59 ± 13.79 years, and 83 (47.7%) were men.u-NGAL, serum creatinine, serum uric acid, and CT ground-glass opacity (GGO) volume were independent predictors of AKI, and all were selected in the nomogram. The prediction model was validated by internal bootstrapping resampling, showing results similar to those obtained from the original samples (i.e., 0.958; 95% CI 0.9097-0.9864). The C-index for predicting AKI was 0.955 (95% CI 0.916-0.995). Multivariate Cox proportional hazards regression confirmed that a high u-NGAL level, an increased GGO volume, and lymphopenia are strong predictors of a poor prognosis and a high risk of in-hospital death. CONCLUSIONS: This model provides a useful individualized risk estimate of AKI in patients with COVID-19. Measurement of u-NGAL and AI-based chest CT quantification are worthy of application and may help clinicians to identify patients with a poor prognosis in COVID-19 at an early stage.

Dl-3-n-butylphthalide pretreatment attenuates renal ischemia/reperfusion injury.

BACKGROUND: Renal ischemia reperfusion injury (IRI) has become a growing concern in clinical practice with high morbidity and mortality rates. There is currently no effective prophylactic regimen available to prevent its occurrence and to improve its clinical prognosis. Dl-3-n-butylphthalide (NBP) has been used for stroke treatment in China for years. Little is known about its role in preventing kidney injury. METHODS: The kidneys of male C57BL/6J mice were subjected to 33 min of ischemia followed by 24 h of reperfusion. NBP was administered by gavage prior to surgery. The reno-protective effect of NBP was evaluated by serum creatinine, kidney injury markers and renal pathological changes. Furthermore, the inflammation, oxidative stress, and apoptosis markers in kidney tissue were examined. In vitro, HK2 cells were treated prophylactically with NBP and then exposed to hypoxia/reoxygenation (H/R). Cell viability and apoptosis related protein were quantified to verify the protective effect of NBP. Pro-inflammation genes expression as well as ROS generation were further investigated also. RESULTS: NBP pretreatment significantly improved renal dysfunction and alleviated pathological injury, renal inflammation response, oxidative stress and cell apoptosis. Consistently, NBP attenuated H/R induced increases in ROS, pro-inflammatory genes expression, apoptosis and cleaved caspase-3 levels in HK2 cells. CONCLUSION: Our promising results validated for the first time that NBP could ameliorate renal IRI via attenuating inflammation, oxidative stress, and apoptosis, which indicated that NBP might be a good candidate against AKI.

Wnt5a promotes renal tubular inflammation in diabetic nephropathy by binding to CD146 through noncanonical Wnt signaling.

Immune and inflammatory factors have emerged as key pathophysiological mechanisms in the progression of diabetic renal injury. Noncanonical Wnt5a signaling plays an essential role in obesity- or diabetes-induced metabolic dysfunction and inflammation, but its explicit molecular mechanisms and biological function in diabetic nephropathy (DN) remain unknown. In this study, we found that the expression of Wnt5a and CD146 in the kidney and the level of soluble form of CD146 (sCD146) in serum and urine samples were upregulated in DN patients compared to controls, and this alteration was correlated with the inflammatory process and progression of renal impairment. Blocking the activation of Wnt5a signaling with the Wnt5a antagonist Box5 prevented JNK phosphorylation and high glucose-induced inflammatory responses in db/db mice and high glucose-treated HK-2 cells. Similar effects were observed by silencing Wnt5a with small-interfering RNA (siRNA) in cultured HK-2 cells. Knockdown of CD146 blocked Wnt5a-induced expression of proinflammatory cytokines and activation of JNK, which suggests that CD146 is essential for the activation of the Wnt5a pathway. Finally, we confirmed that Wnt5a directly interacted with CD146 to activate noncanonical Wnt signaling in HK-2 cells. Taken together, our findings suggest that by directly binding to CD146, Wnt5a-induced noncanonical signaling is a contributing mechanism for renal tubular inflammation in diabetic nephropathy. The concentration of sCD146 in serum and urine could be a potential biomarker to predict renal outcomes in DN patients.

Sitagliptin ameliorates renal tubular injury in diabetic kidney disease via STAT3-dependent mitochondrial homeostasis through SDF-1α/CXCR4 pathway.

Mitochondrial abnormalities play critical roles in diabetic tubular injury progression. Dipeptidyl peptidase-4 (DPP4) inhibitors are widely used antihyperglycemic agents that exert renal protective and positive effects against mitochondrial dysfunction in diabetic kidney disease (DKD). However, their underlying mechanism remains unclear. In this study, DPP4 upregulation, mitochondrial fragmentation, and altered mitochondrial dynamics-associated protein expression were observed in the tubules of DBA2/J (D2) diabetic mice with unilateral nephrectomy and in albumin-stimulated tubular cells. The inhibition of DPP4 by sitagliptin (Sita) ameliorated these mitochondrial perturbations both in vivo and in vitro, whereas DPP4 overexpression aggravated mitochondrial fusion-fission disorder and tubular cell injury in albumin-treated HK-2 cells. Downstream of DPP4, the SDF-1α/CXCR4 pathway was significantly suppressed in diabetic tubules. After Sita treatment, this signaling pathway was restored, and the mitochondrial dynamics was improved. Furthermore, a direct interaction between STAT3 and OPA1 was found in the mitochondria of tubular cells, and this effect was weakened by overloading albumin and by CXCR4 siRNA treatment, suggesting a possible link between DPP4-mediated SDF-1α/CXCR4/STAT3 signaling and mitochondrial dysfunction in diabetic tubular cells. The results suggest that a novel mechanism links the DPP4 enzyme to impaired mitochondrial dynamics homeostasis during tubular injury in DKD and highlight that the SDF-1α/CXCR4/STAT3 signaling pathway could become a potential target for managing DKD.

Poor Renal and Cardiovascular Outcomes in Patients with Biopsy-Proven Diabetic Nephropathy.

BACKGROUND: Despite the high mortality of cardiovascular disease (CVD) in diabetic patients with renal injury, few studies have compared cardiovascular characteristics and outcomes between patients with diabetic nephropathy (DN) and non-diabetic renal disease (NDRD). METHODS: A total of 326 type 2 diabetes mellitus patients with renal biopsy were assigned to DN and NDRD groups. Echocardiography and Doppler ultrasound were performed to evaluate left ventricular hypertrophy (LVH) and peripheral atherosclerosis disease (PAD). Renal and cardiovascular survival rates were compared between the DN and NDRD groups by Kaplan-Meier analysis. Risk factors for renal and cardiovascular events in DN patients were identified by a Cox proportional hazards model. RESULTS: In total, 179 patients entered the DN group (54.9%) and 147 made up the NDRD group (45.1%). The presence of diabetic retinopathy, family history of diabetes, and dependence on insulin therapy were associated with the presence of DN. DN patients had more CVD with more severe LVH and PAD. Poorer renal (log-rank χ2 = 26.534, p < 0.001) and cardiovascular (log-rank χ2 = 16.257, p < 0.001) prognoses were seen in the DN group. DR (HR 1.539, 95% CI 1.332-1.842), eGFR (HR 0.943, 95% CI 0.919-0.961), and 24-h proteinuria (HR 1.211, 95% CI 1.132-1.387) were identified as risk factors for renal endpoints. Age (HR 1.672, 95% CI 1.487-1.821), HbA1C (HR 1.398, 95% CI 1.197-1.876), and 24-h proteinuria (HR 1.453, 95% CI 1.289-1.672) were associated with cardiovascular endpoints. CONCLUSION: Patients with DN had more severe CVD along with poorer renal and cardiovascular prognoses than those with NDRD.

Comparison of Kidney Transcriptomic Profiles of Early and Advanced Diabetic Nephropathy Reveals Potential New Mechanisms for Disease Progression.

To identify the factors mediating the progression of diabetic nephropathy (DN), we performed RNA sequencing of kidney biopsy samples from patients with early DN, advanced DN, and normal kidney tissue from nephrectomy samples. A set of genes that were upregulated at early but downregulated in late DN were shown to be largely renoprotective, which included genes in the retinoic acid pathway and glucagon-like peptide 1 receptor. Another group of genes that were downregulated at early but highly upregulated in advanced DN consisted mostly of genes associated with kidney disease pathogenesis, such as those related to immune response and fibrosis. Correlation with estimated glomerular filtration rate (eGFR) identified genes in the pathways of iron transport and cell differentiation to be positively associated with eGFR, while those in the immune response and fibrosis pathways were negatively associated. Correlation with various histopathological features also identified the association with the distinct gene ontological pathways. Deconvolution analysis of the RNA sequencing data set indicated a significant increase in monocytes, fibroblasts, and myofibroblasts in advanced DN kidneys. Our study thus provides potential molecular mechanisms for DN progression and association of differential gene expression with the functional and structural changes observed in patients with early and advanced DN.

Ischemic Duration and Frequency Determines AKI-to-CKD Progression Monitored by Dynamic Changes of Tubular Biomarkers in IRI Mice.

Ischemia reperfusion injury (IRI) is one of the most common causes of acute kidney injury (AKI). However, the pathogenesis and biomarkers predicting the progression of IRI-induced AKI to chronic kidney disease (CKD) remain unclear. A side-by-side comparison between different IRI animal models with variable ischemic duration and episodes was performed. The dynamic changes of KIM-1 and NGAL continuously from AKI to CKD phases were studied as well. Short-term duration of ischemia induced mild renal tubule-interstitial injury which was completely reversed at acute phase of kidney injury, while long-term duration of ischemia caused severe tubular damage, cell apoptosis and inflammatory infiltration at early disease stage, leading to permanent chronic kidney fibrosis at the late stage. Repeated attacks of moderate IRI accelerated the progression of AKI to CKD. Different from serum and urine levels of KIM-1 that increased at acute phase of IRI then declined gradually in chronic phase, NGAL increased continuously during AKI-to-CKD transition. Severity and frequency of ischemia injury determines the progression and outcome of ischemia-induced AKI. Inflammation, apoptosis and fibrogenesis likely participate in the progression of AKI to CKD. Both KIM-1 and NGAL enable noninvasive and early detection of AKI, but NGAL is associated better with the process of AKI-to-CKD progression.

Activation of the Nrf2-ARE Pathway Ameliorates Hyperglycemia-Mediated Mitochondrial Dysfunction in Podocytes Partly Through Sirt1.

BACKGROUND/AIMS: Previously we have shown that activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-antioxidant response element (ARE) attenuated hyperglycemia-induced damage in podocytes, but the molecular mechanism remains unknown. METHODS: Tert-butylhydroquinone (t-BHQ) and small interfering RNAs (siRNAs) were used to regulate Nrf2 expression, while nicotinamide and siRNAs were used to regulate sirtuin 1 (Sirt1) activity and expression, respectively. Mitochondrial superoxide, membrane potential and ATP levels were measured to assess changes in mitochondrial function. Nephrin and synaptopodin expression were measured by western blot analysis. Human podocytes and db/db diabetic mice were used in this study. RESULTS: t-BHQ pretreatment of human podocytes exposed to high glucose (HG) alleviated mitochondrial dysfunction, enhanced the expression of Sirt1, nephrin and synaptopodin and lowered BSA permeability compared with podocytes exposed to HG without t-BHQ pretreatment (p< 0.05). Human podocytes exposed to HG had more severe mitochondrial dysfunction, lower expression of Sirt1, synaptopodin and nephrin and higher BSA permeability than podocytes exposed to HG when Nrf2 expression was downregulated by siRNAs (p< 0.05). The protection provided by activation of the Nrf-ARE pathway in podocytes exposed to HG was partially diminished when Sirt1 expression or activity was decreased by siRNAs or inhibitor compared with podocytes exposed to HG and pretreated with t-BHQ (p< 0.05). When nicotinamide and t-BHQ were both administered to db/db mice, we observed higher levels of urinary albumin/creatinine, lower nephrin and synaptopodin expression, more severe mesangial matrix deposition, collagen deposition on pathological slides and mitochondrial structural damage in podocytes compared to db/db mice treated only with t-BHQ. CONCLUSIONS: Our findings suggest that crosstalk between Sirt1 and the Nrf2-ARE anti-oxidative pathway forms a positive feedback loop and that protection provided by t-BHQ activation of the Nrf2-ARE pathway in db/db mice is partly dependent on Sirt1.

Prevalence of Homocysteine-Related Hypertension in Patients With Chronic Kidney Disease.

Patients with both hypertension and hyperhomocysteinemia, termed H-type hypertension, have a high risk for cardiocerebrovascular diseases. However, little is known about the prevalence of H-type hypertension or its role in target organ damage in patients with chronic kidney disease (CKD). The authors recruited 1042 patients with CKD who were admitted to their hospital division. Multiple linear regression analyses were used to evaluate the association between H-type hypertension and renal/cardiovascular parameters. A total of 460 (44.14%) CKD patients had H-type hypertension. Multivariate logistic regression analysis showed that H-type hypertension is associated with serum albumin, uric acid, estimated glomerular filtration rate (eGFR), and 24-hour systolic blood pressure. Patients with H-type hypertension had the worst renal function and left ventricular hypertrophy among all patients, while the levels of carotid intima-media thickness (cIMT) in patients with H-type hypertension were only slightly higher than in patients with normotension and normohomocysteinemia (P<.05). H-type hypertension was associated with eGFR, left ventricular mass index, and cIMT according to multiple linear regression analyses. The prevalence of H-type hypertension was high and H-type hypertension was associated with target organ damage in patients with CKD.

Prognostic Effect of Isolated Nocturnal Hypertension in Chinese Patients With Nondialysis Chronic Kidney Disease.

BACKGROUND: Isolated nocturnal hypertension (INH) has been studied among the general population and hypertensive patients. However, little insight is available on the prognostic effect of INH in patients with chronic kidney disease (CKD). This study investigated the prognostic effect of INH in a cohort of Chinese patients with nondialysis CKD. METHODS AND RESULTS: A total of 588 Chinese CKD patients who were admitted to the Third Affiliated Hospital of Sun Yat-Sen University were enrolled in this study. We monitored blood pressure (BP) throughout the day and followed health outcomes in the 588 CKD patients admitted to our hospital division. We recorded time to total mortality, cardiovascular mortality, renal events, and cardiovascular events. A total of 370 (62.92%) individuals had nocturnal hypertension, which included 136 (23.13%) patients with INH. Multivariable Cox regression analyses showed that nocturnal BP was a significant risk factor for renal events and cardiovascular events in CKD patients, even when adjusted for clinic BP, 24-hour BP, or daytime BP. Patients with nocturnal hypertension showed a worse prognosis compared with patients with nocturnal normotension (P<0.05), and nocturnal hypertension (versus nocturnal normotension) was associated with an increased risk for renal events (hazard ratio [HR], 3.81; 95% CI, 1.74-8.36) and cardiovascular events (HR, 8.34; 95% CI, 1.98-35.07). In addition, patients with INH had a worse prognosis than patients with normotension (P<0.017), whereas INH (versus normotension) was associated with a higher risk of renal events (HR, 2.78; 95% CI, 1.16-6.65) and cardiovascular events (HR, 6.82; 95% CI, 1.52-30.63). CONCLUSIONS: INH was associated with a poor prognosis in Chinese nondialysis CKD patients.

Prognostic Value of Reverse Dipper Blood Pressure Pattern in Chronic Kidney Disease Patients not Undergoing Dialysis: Prospective Cohort Study.

The "reverse dipping" blood pressure (BP) pattern has been studied among the general population and in individuals suffering from hypertension. However, the prognosis of this pattern in chronic kidney disease (CKD) patients is not known. We monitored BP throughout the day and followed health outcomes in 588 CKD patients admitted to our hospital. Time to all-cause mortality, cardiovascular mortality, renal events and cardiovascular events was recorded. Multivariate-adjusted Cox regression analyses were carried out to detect the prognostic value of a reverse dipping BP pattern. Prevalence of a "dipper", "non-dipper" and "reverse dippers" was 34.69%, 43.54% and 18.03%, respectively. Patients with a reverse dipping pattern had a higher prevalence of total mortality, cardiovascular mortality, renal events and cardiovascular events than patients with a dipping pattern (P < 0.025). Multivariate-adjusted Cox regression analyses showed that reverse dippers (versus dippers) were associated with a higher risk of total mortality (hazard ratio [HR], 5.08; 95% confidence interval [CI], 1.79~14.47), cardiovascular mortality (4.17; 1.25~13.88), renal events (3.00; 1.59~5.65) and cardiovascular events (4.12; 1.78~9.51) even after adjustment by 24-h systolic BP. These data suggest that a reverse dipping BP pattern, independent of 24-h levels of systolic BP, has prognostic value in CKD patients not undergoing dialysis.

High Prevalence of Hyperhomocysteinemia and Its Association with Target Organ Damage in Chinese Patients with Chronic Kidney Disease.

Hyperhomocysteinemia (HHcy) is recognized as a risk factor for cardiovascular disease. However, the prevalence of HHcy and its role in association with target organ damage in patients with chronickidney disease (CKD) are not well understood. This cross-sectional study included 1042 CKD patients who were admitted to our hospital. Patients were divided into two groups: hyperhomocysteinemia and normohomocysteinemia. Multivariable linear regression analyses were used to evaluate the association between plasma homocysteine and renal/cardiovascular parameters. The prevalence of HHcy in patients with CKD was 52.78%, and the prevalence in CKD stage 1, stage 2, stage 3, stage 4 and stage 5 patients was 10.73%, 29.22%, 58.71%, 75.23% and 83.75%, respectively. Patients with HHcy had higher incidences of renal damage, left ventricular hypertrophy, left ventricular diastolic dysfunction and abnormal carotid intima-media thickness compared with patients with normohomocysteinemia (p < 0.05), while multivariable linear regression analyses showed plasma homocysteine was only associated with the estimated glomerular filtration rate (eGFR). eGFR, uric acid, albumin, gender, hemoglobin and calcium×phosphate were associated with levels of plasma homocysteine in these CKD patients. The prevalence of HHcy in Chinese patients with CKD was high, and serum homocysteine levels were associated with impaired renal function in these patients.

Prevalence, determinants, and clinical significance of masked hypertension and white-coat hypertension in patients with chronic kidney disease.

BACKGROUND: Masked hypertension and white-coat hypertension have been studied among the general population and in hypertensive patients. However, little insight is available on masked and white-coat hypertension among patients with chronic kidney disease (CKD). METHODS: We recruited 1322 CKD patients admitted to our hospital division. Patients were divided into four groups: normotension; white-coat hypertension (WCHT); masked hypertension (MHT); sustained hypertension. Multivariable logistic regression analyses were used to evaluate the correlation between WCHT, MHT and renal/cardiovascular parameters. RESULTS: The prevalence of WCHT and MHT was 10.21% and 16.11%, respectively. Patients with WCHT and MHT had more severe target-organ damage (TOD) than patients with normotension, but had less severe TOD than patients with sustained hypertension. MHT correlated with impaired renal function and left-ventricular hypertrophy, whereas WCHT was associated with abnormal carotid intima media thickness. Age, body mass index, clinic and 24-h systolic blood pressure correlated with MHT, whereas clinic, 24-h diastolic blood pressure and night-time systolic blood pressure was associated with WCHT. CONCLUSIONS: Prevalence of WCHT and MHT was 10.21% and 16.11%, respectively. WCHT and MHT show a close relationship with TOD in CKD patients.

High prevalence of isolated nocturnal hypertension in Chinese patients with chronic kidney disease.

BACKGROUND: Isolated nocturnal hypertension (INH) has been studied among the general population and hypertensive patients. However, little insight is available on the prevalence of INH and its role in target-organ damage among patients with chronic kidney disease (CKD). METHODS AND RESULTS: We recruited 1282 CKD patients admitted to our hospital division. Patients were divided into 4 groups: INH; isolated daytime hypertension; day-night sustained; and ambulatory normotension. Multiple linear regression analyses were used to evaluate the correlation between INH and renal/cardiovascular parameters. A total of 262 (20.44%) CKD patients had isolated nocturnal hypertension and 651 (50.78%) had day-night sustained hypertension, whereas only 350 (27.30%) patients showed normotension and 19 (1.48%) had isolated daytime hypertension. Multivariate logistic regression analysis showed that INH was associated mainly with age, estimated glomerular filtration rate, clinic diastolic blood pressure, and that INH was determined only by age, estimated glomerular filtration rate, and clinic diastolic blood pressure. The prevalence of impaired renal function, left ventricular hypertrophy, and carotid intima-media thickness in patients with INH were higher than in normotensive patients (P<0.05), whereas impaired renal function and left ventricular hypertrophy in these patients were lower than patients in the day-night sustained hypertension group (P<0.05). INH was correlated with estimated glomerular filtration rate, left ventricular mass index, and carotid intima-media thickness according to multiple linear regression analyses. CONCLUSIONS: The prevalence of INH in CKD patients was high, and INH was correlated with target-organ damage in CKD patients.

Nocturnal Hypertension Correlates Better With Target Organ Damage in Patients With Chronic Kidney Disease than a Nondipping Pattern.

Both nocturnal hypertension and nondipping pattern are associated with target organ damages (TODs); however, no data exist with respect to Chinese patients with chronic kidney disease (CKD). The authors recruited 1322 patients with CKD admitted to our hospital division and referred with data in this cross-sectional study. Patients with nocturnal systolic hypertension had a lower estimated glomerular filtration rate (eGFR) and higher left ventricular mass index (LVMI) and carotid intima-media thickness (cIMT) compared with patients with normal nocturnal systolic blood pressure (SPB; all, P<.001), while patients in the dipper and nondipper groups had similar levels of eGFR, LVMI, and cIMT when the patients had a similar nocturnal SBP. Factorial-designed analysis of variance indicated that the main effect of nocturnal SBP was significant for all TOD differences (all, P<.001), but no significance existed with respect to the main effect of the dipper pattern and an interaction between the two factors (all, P>.05). Nocturnal systolic hypertension, rather than nondipping pattern, was an independent risk factor for TOD in CKD patients. Nocturnal hypertension, rather than a nondipping pattern, was better associated with TOD in CKD patients.