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Process mining holds promise for analysing longitudinal data in clinical epidemiology, yet its application remains limited. The objective of this study was to propose and evaluate a methodology for applying process mining techniques in observational clinical epidemiology. We propose a methodology that integrates a cohort study design with data-driven process mining, with an eight-step approach, including data collection, data extraction and curation, event-log generation, process discovery, process abstraction, hypothesis generation, statistical testing, and prediction. These steps facilitate the discovery of disease progression patterns. We implemented our proposed methodology in a cohort study comparing new users of proton pump inhibitors (PPI) and H2 blockers (H2B). PPI usage was associated with a higher risk of disease progression compared to H2B usage, including a greater than 30% decline in estimated Glomerular Filtration Rate (eGFR) (Hazard Ratio [HR] 1.6, 95% Confidence Interval [CI] 1.4–1.8), as well as increased all-cause mortality (HR 3.0, 95% CI 2.1–4.4). Furthermore, we investigated the associations between each transition and covariates such as age, gender, and comorbidities, offering deeper insights into disease progression dynamics. Additionally, a risk prediction tool was developed to estimate the transition probability for an individual at a future time. The proposed methodology bridges the gap between process mining and epidemiological studies, providing a useful approach to investigating disease progression and risk factors. The synergy between these fields enhances the depth of study findings and fosters the discovery of new insights and ideas. [ABSTRACT FROM AUTHOR]

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Aims/Introduction: Chronic kidney disease (CKD) is a very important issue globally because of the risk of its progressing to end‐stage renal disease. We aimed to identify factors contributing to long‐term estimated glomerular filtration rate (eGFR) decline to determine an early diagnosis and prevent CKD progression. Materials and Methods: From January 2003 to December 2006, 5,507 individuals underwent health checkups at our hospital's Preventive Medicine Research Center. We ultimately enrolled 2,175 individuals. The eGFR was ≥60 mL/min/1.73 m2 at the start of observation period, which was 20 years. The event onset time was the day that the eGFR became <30 mL/min during the 20‐year period. Baseline risk factors – in particular, the effect of plasma glucose levels on the eGFR – were extracted and evaluated by using Fine and Gray analysis. Results: During the 20‐year observation, the hazard ratio (HR) of CKD progression was examined. A fasting plasma glucose (FPG) level ≥105 mg/dL was significantly associated with the risk of CKD progressing to an eGFR <30 mL/min. This trend was similar in the slope of eGFR. An FPG ≥105 mg/dL or an glycated hemoglobin level ≥6.5% was useful for intervening in CKD progression. Multivariate analysis showed that independent risk factors were an FPG level ≥105 mg/dL (HR 1.9; P < 0.001), age ≥60 years (HR 3.86; P < 0.001), obesity (HR 1.61; P < 0.01) and urinary protein (HR 1.55; P < 0.01). Conclusions: For early intervention against a reduction in the eGFR, detecting mild increases in FPG ≥105 mg/dL in patients with CKD with or without diabetes is useful. [ABSTRACT FROM AUTHOR]

Abstract Process mining holds promise for analysing longitudinal data in clinical epidemiology, yet its application remains limited. The objective of this study was to propose and evaluate a methodology for applying process mining techniques in observational clinical epidemiology. We propose a methodology that integrates a cohort study design with data-driven process mining, with an eight-step approach, including data collection, data extraction and curation, event-log generation, process discovery, process abstraction, hypothesis generation, statistical testing, and prediction. These steps facilitate the discovery of disease progression patterns. We implemented our proposed methodology in a cohort study comparing new users of proton pump inhibitors (PPI) and H2 blockers (H2B). PPI usage was associated with a higher risk of disease progression compared to H2B usage, including a greater than 30% decline in estimated Glomerular Filtration Rate (eGFR) (Hazard Ratio [HR] 1.6, 95% Confidence Interval [CI] 1.4–1.8), as well as increased all-cause mortality (HR 3.0, 95% CI 2.1–4.4). Furthermore, we investigated the associations between each transition and covariates such as age, gender, and comorbidities, offering deeper insights into disease progression dynamics. Additionally, a risk prediction tool was developed to estimate the transition probability for an individual at a future time. The proposed methodology bridges the gap between process mining and epidemiological studies, providing a useful approach to investigating disease progression and risk factors. The synergy between these fields enhances the depth of study findings and fosters the discovery of new insights and ideas.

ABSTRACT Aims/Introduction Chronic kidney disease (CKD) is a very important issue globally because of the risk of its progressing to end‐stage renal disease. We aimed to identify factors contributing to long‐term estimated glomerular filtration rate (eGFR) decline to determine an early diagnosis and prevent CKD progression. Materials and Methods From January 2003 to December 2006, 5,507 individuals underwent health checkups at our hospital's Preventive Medicine Research Center. We ultimately enrolled 2,175 individuals. The eGFR was ≥60 mL/min/1.73 m2 at the start of observation period, which was 20 years. The event onset time was the day that the eGFR became

This study aimed to determine the feasibility of applying machine-learning methods to assess the progression of chronic kidney disease (CKD) in patients with coronavirus disease (COVID-19) and acute renal injury (AKI). The study was conducted on patients aged 18 years or older who were diagnosed with COVID-19 and AKI between April 2020 and March 2021, and admitted to a second-level hospital in Mérida, Yucatán, México. Of the admitted patients, 47.92% died and 52.06% were discharged. Among the discharged patients, 176 developed AKI during hospitalization, and 131 agreed to participate in the study. The study's results indicated that the area under the receiver operating characteristic curve (AUC-ROC) for the four models was 0.826 for the support vector machine (SVM), 0.828 for the random forest, 0.840 for the logistic regression, and 0.841 for the boosting model. Variable selection methods were utilized to enhance the performance of the classifier, with the SVM model demonstrating the best overall performance, achieving a classification rate of 99.8% ± 0.1 in the training set and 98.43% ± 1.79 in the validation set in AUC-ROC values. These findings have the potential to aid in the early detection and management of CKD, a complication of AKI resulting from COVID-19. Further research is required to confirm these results. [ABSTRACT FROM AUTHOR]

Introduction: Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic disease of the kidney, leading to end-stage kidney disease (ESKD) in a large proportion of affected individuals. The only approved therapy to slow the progression of chronic kidney disease (CKD) secondary to ADPKD is tolvaptan. The following analysis aimed to present the experience of the centre with tolvaptan used for ADPKD. Materials and methods: Retrospective analysis of single centre data. The study group consisted of 13 patients who started treatment with tolvaptan. The control group consisted of 13 patients who refused to be treated with tolvaptan. Results: In the study group, 2 patients (15%) discontinued tolvaptan due to the side effects. The intention to treat (ITT) analysis showed that among both groups progression of CKD occurred during the observation period. No statistically significant difference in the median change of estimated glomerular filtration rate (eGFR) was noticed between the study and the control group. Moreover, no statistically significant difference in the median change of eGFR was noticed between the pre-study period and the observation period both in the study group and in the control group. Conclusions: According to the following results, tolvaptan is not effective in slowing the progression of CKD in patients with ADPKD in real-life settings. Further observations are needed to confirm these results. [ABSTRACT FROM AUTHOR]

Background: The impact of triglyceride-glucose (TyG) index variations on chronic kidney disease (CKD) progression remains unexplored. To investigate the effects of the TyG index and its dynamic changes on CKD progression. Method: This prospective cohort study included data from 8,418 hypertensive participants. The exposure variable in this study was defined as the difference between the TyG index at the last visit from that at baseline. The study's outcome variable was the progression of CKD, defined as follows: for subjects with an estimated glomerular filtration rate (eGFR) =60 mL/min, a =30% decrease in eGFR with a final follow-up value <60 mL/min; for those with an eGFR <60 mL/min, a =50% decrease in eGFR; or terminal renal failure requiring dialysis. Results: During a median follow-up period of 48 months, 1077 patients were diagnosed with CKD progression. In the fully adjusted Model 3, patients with a change in the TyG index <0 exhibited a significantly decreased 13% risk of CKD progression (HR: 0.87, 95% CI: 0.76-0.98) compared to those with a change in the TyG index=0 group. Subgroup analyses showed that changes in the TyG index significantly increased the risk of CKD progression only in patients with diastolic blood pressure (DBP) <90mmHg. In the path analysis, baseline TyG was associated with follow-up eGFR (the standard regression coefficient was 1.26 [95% CI, 0.45-2.06]). Conclusions: Our findings suggest that TyG variability may serve as a useful tool for identifying individuals at risk of CKD progression, particularly hypertensive patients with normal DBP levels. [ABSTRACT FROM AUTHOR]

Background and Objectives: Several studies revealed a relation between abnormal cardiac remodeling and glomerular filtration rate (GFR) decline, but there are limited data regarding echocardiographic changes in chronic kidney disease (CKD). This study evaluated the abnormal cardiac structures characterizing patients with CKD, assessing the independent association between echocardiographic parameters and the risk of decline in renal function. Materials and Methods: In total, 160 patients with CKD were studied. All patients underwent an echocardiographic exam and 99mTc-DTPA renal scintigraphy to measure the GFR. After the baseline assessments, patients were followed prospectively for 12 months, or until the endpoint achievement, defined as a worsening in renal function (doubling of baseline serum creatinine, GFR decline ≥25%, the start of dialysis). Results: Patients with GFR values of 34.8 ± 15 mL/min, identifying stages III–IV of CKD, were associated with high levels of left ventricular mass index (LVMi) (101.9 ± 12.2 g/m2), which was related to proteinuria, systolic blood pressure, and pulmonary artery systolic pressure in a multiple regression model. During the observational period, 26% of patients reached the endpoint. Regression analysis revealed LVMi as a predictor of change in renal function after adjusting for kidney and cardiac risk factors. Multiple Cox regression indicated that an increase in LVMi was associated with a 12% increased risk of kidney disease progression (HR: 1.12; 95% CI: 1.04–1.16; p = 0.001). Conclusions: In patients with CKD, high LVMi represents an independent predictor of the progressive decline of the renal function, until the start of renal replacement therapy. Echocardiography can help identify patients at high risk for renal disease worsening in patients with CKD independently of clinical cardiac involvement. [ABSTRACT FROM AUTHOR]

Rationale & Objective: The extent to which depression affects the progression of chronic kidney disease (CKD) and leads to adverse clinical outcomes remains inadequately understood. We examined the association of depressive symptoms (DS) and antidepressant medication use on clinical outcomes in 4,839 adults with nondialysis CKD. Study Design: Observational cohort study. Setting and Participants: Adults with mild to moderate CKD who participated in the multicenter Chronic Renal Insufficiency Cohort Study (CRIC). Exposure: The Beck Depression Inventory (BDI) was used to quantify DS. Antidepressant use was identified from medication bottles and prescription lists. Individual effects of DS and antidepressants were examined along with categorization as follows: (1) BDI

Background: In the recent years, pregnancy outcomes in women with primary chronic glomerulonephritis (CGN) have been encouraging despite increased incidence of complications and preterm birth. However, the impact of pregnancy on CKD progression in glomerulonephritis remains understudied. Aim: To evaluate the effect of pregnancy on CKD progression in the postpartum period in patients with primary CGN. Materials and methods: This was an observational longitudinal study. The study group included 40 patients with CGN and CKD G1G3b, who had 40 deliveries from January 2009 to November 2022. The control group included 35 patients with CGN who had no pregnancies after CKD was diagnosed. Serum creatinine and estimated glomerular filtration rate (GFR) were assessed during the follow up, recording the development of CKD G5. Results: The annual rate of GFR decline in the study group was -4.6 [-8.0; -2.5] ml/min/1.73 m2, and in the control group -1.8 [-5.8; +1.5] ml/min/1.73 m2 (p = 0.056). After complicated pregnancy (preeclampsia, placental insufficiency, increase in proteinuria, worsening of arterial hypertension, acute kidney injury), the annual rate of GFR decline was -6.4 [-13.4; -3.5] ml/min/1.73 m2, which was higher than in the controls (p = 0.042). There were no significant differences in survival without GFR decrease by 30%, 50% and without CKD G5 between the study and the control groups. However, CKD G5-free survival in the patients with complicated pregnancy was lower than that in the controls (p = 0.022) and in those with uncomplicated pregnancies (p = 0.009). Eleven (11) of 40 patients in the main group and 3/35 in the control group reached CKD G5. The time from delivery to CKD G5 was 4.83 [2.08; 7.07] years. Among women who reached end-stage renal failure after childbirth, there were significantly more patients with CKD G3, proteinuria 1 g/day during pregnancy, arterial hypertension at baseline and during pregnancy, preeclampsia, acute kidney injury, delivery at less than 37 weeks of gestation, with neonates requiring treatment at intensive care unit, and unfavorable pregnancy outcomes. Conclusion: Renal survival in the women with primary CGN who had been pregnant was not significantly different from that in the women who did not have pregnancies; however, complicated pregnancy increased the rate of kidney function decline.

This study aimed to determine the feasibility of applying machine-learning methods to assess the progression of chronic kidney disease (CKD) in patients with coronavirus disease (COVID-19) and acute renal injury (AKI). The study was conducted on patients aged 18 years or older who were diagnosed with COVID-19 and AKI between April 2020 and March 2021, and admitted to a second-level hospital in Mérida, Yucatán, México. Of the admitted patients, 47.92% died and 52.06% were discharged. Among the discharged patients, 176 developed AKI during hospitalization, and 131 agreed to participate in the study. The study’s results indicated that the area under the receiver operating characteristic curve (AUC-ROC) for the four models was 0.826 for the support vector machine (SVM), 0.828 for the random forest, 0.840 for the logistic regression, and 0.841 for the boosting model. Variable selection methods were utilized to enhance the performance of the classifier, with the SVM model demonstrating the best overall performance, achieving a classification rate of 99.8% ± 0.1 in the training set and 98.43% ± 1.79 in the validation set in AUC-ROC values. These findings have the potential to aid in the early detection and management of CKD, a complication of AKI resulting from COVID-19. Further research is required to confirm these results.

Summary: Background: Urinary biomarkers may improve the prediction of chronic kidney disease (CKD) progression. Yet, data reporting the applicability of most commercial biomarker assays to the detection of their target analyte in urine together with an evaluation of their predictive performance are scarce. Methods: 30 commercial assays (ELISA) were tested for their ability to quantify the target analyte in urine using strict (FDA-approved) validation criteria. In an exploratory analysis, LASSO (Least Absolute Shrinkage and Selection Operator) logistic regression analysis was used to identify potentially complementary biomarkers predicting fast CKD progression, determined as the 51CrEDTA clearance-based measured glomerular filtration rate (mGFR) decline (>10% per year) in a subsample of 229 CKD patients (mean age, 61 years; 66% men; baseline mGFR, 38 mL/min) from the NephroTest prospective cohort. Findings: Among the 30 assays, directed against 24 candidate biomarkers, encompassing different pathophysiological mechanisms of CKD progression, 16 assays fulfilled the FDA-approved criteria. LASSO logistic regressions identified a combination of five biomarkers including CCL2, EGF, KIM1, NGAL, and TGF-α that improved the prediction of fast mGFR decline compared to the kidney failure risk equation variables alone: age, gender, mGFR, and albuminuria. Mean area under the curves (AUC) estimated from 100 re-samples was higher in the model with than without these biomarkers, 0.722 (95% confidence interval 0.652–0.795) vs. 0.682 (0.614–0.748), respectively. Fully-adjusted odds-ratios (95% confidence interval) for fast progression were 1.87 (1.22, 2.98), 1.86 (1.23, 2.89), 0.43 (0.25, 0.70), 1.10 (0.71, 1.83), 0.55 (0.33, 0.89), and 2.99 (1.89, 5.01) for albumin, CCL2, EGF, KIM1, NGAL, and TGF-α, respectively. Interpretation: This study provides a rigorous validation of multiple assays for relevant urinary biomarkers of CKD progression which combination may improve the prediction of CKD progression. Funding: This work was supported by Institut National de la Santé et de la Recherche Médicale, Université de Paris, Assistance Publique Hôpitaux de Paris, Agence Nationale de la Recherche, MSDAVENIR, Pharma Research and Early Development Roche Laboratories (Basel, Switzerland), and Institut Roche de Recherche et Médecine Translationnelle (Paris, France).

Background and Objectives: Several studies revealed a relation between abnormal cardiac remodeling and glomerular filtration rate (GFR) decline, but there are limited data regarding echocardiographic changes in chronic kidney disease (CKD). This study evaluated the abnormal cardiac structures characterizing patients with CKD, assessing the independent association between echocardiographic parameters and the risk of decline in renal function. Materials and Methods: In total, 160 patients with CKD were studied. All patients underwent an echocardiographic exam and 99mTc-DTPA renal scintigraphy to measure the GFR. After the baseline assessments, patients were followed prospectively for 12 months, or until the endpoint achievement, defined as a worsening in renal function (doubling of baseline serum creatinine, GFR decline ≥25%, the start of dialysis). Results: Patients with GFR values of 34.8 ± 15 mL/min, identifying stages III–IV of CKD, were associated with high levels of left ventricular mass index (LVMi) (101.9 ± 12.2 g/m2), which was related to proteinuria, systolic blood pressure, and pulmonary artery systolic pressure in a multiple regression model. During the observational period, 26% of patients reached the endpoint. Regression analysis revealed LVMi as a predictor of change in renal function after adjusting for kidney and cardiac risk factors. Multiple Cox regression indicated that an increase in LVMi was associated with a 12% increased risk of kidney disease progression (HR: 1.12; 95% CI: 1.04–1.16; p = 0.001). Conclusions: In patients with CKD, high LVMi represents an independent predictor of the progressive decline of the renal function, until the start of renal replacement therapy. Echocardiography can help identify patients at high risk for renal disease worsening in patients with CKD independently of clinical cardiac involvement.

Focal segmental glomerulosclerosis (FSGS) is a major cause of end-stage renal disease and remains without specific treatment. To identify new events during FSGS progression, we used an experimental model of FSGS associated with nephroangiosclerosis in rats injected with L-NAME (Nω-nitro-L-arginine methyl ester). After transcriptomic analysis we focused our study on the role of Isthmin-1 (ISM1, an anti-angiogenic protein involved in endothelial cell apoptosis. We studied the renal expression of ISM1 in L-NAME rats and other models of proteinuria, particularly at the glomerular level. In the L-NAME model, withdrawal of the stimulus partially restored basal ISM1 levels, along with an improvement in renal function. In other four animal models of proteinuria, ISM1 was overexpressed and localized in podocytes while the renal function was degraded. Together these facts suggest that the glomerular expression of ISM1 correlates directly with the progression-recovery of the disease. Further in vitro experiments demonstrated that ISM1 co-localized with its receptors GRP78 and integrin αvβ5 on podocytes. Treatment of human podocytes with low doses of recombinant ISM1 decreased cell viability and induced caspase activation. Stronger ISM1 stimuli in podocytes dropped mitochondrial membrane potential and induced nuclear translocation of apoptosis-inducing factor (AIF). Our results suggest that ISM1 participates in the progression of glomerular diseases and promotes podocyte apoptosis in two different complementary ways: one caspase-dependent and one caspase-independent associated with mitochondrial destabilization. [ABSTRACT FROM AUTHOR]

Objective: Familial Mediterranean fever is an autosomal recessive genetic disease characterized by fever and serositis attacks. The most important complication is amyloidosis. In Familial Mediterranean fever patients, chronic kidney disease can develop without amyloid development. The aim of the study is to evaluate the development of chronic kidney disease in familial Mediterranean fever patients and to determine the factors that are involved in this development. Methods: One hundred seventy-eight familial Mediterranean fever patients who were followed up between 2000 and 2020 were included in the study. Familial Mediterranean fever diagnosis was made according to the Tel-Hashomer criteria. Genetic tests were obtained in cases in which there was suspicion of diagnosis. Clinical and demographic characteristics of patients and all laboratory data including urea, creatinine, estimated glomerular filtration rate, and proteinuria in 24-hour urine at the time of first and last admission were evaluated. Results: The mean age of the patients was 34.53 ± 10.72, the follow-up period was 6.12 ± 3.94, and the diagnosis age was 21.7 ± 11.5 years. The percentage of chronic kidney disease development at first and last admission was 13.5% and 19.1%, respectively. The risk factors associated with the development of chronic kidney disease were early disease onset and arthritis attacks. Conclusion: The role of genotype characteristics in the development of chronic kidney disease has not been determined. Patients diagnosed with familial Mediterranean fever disease at an early age and especially with arthritis attacks should be closely monitored in terms of the risk of developing chronic kidney disease. [ABSTRACT FROM AUTHOR]

Background: Elevated blood pressure and proteinuria are well-established risk factors for chronic kidney disease (CKD) progression in children. This study aimed to analyze risk factors for CKD progress, emphasizing detailed ambulatory blood pressure (ABPM) data. Methods: In 55 children with CKD II–V, observed for ≥1 year or until initiation of kidney replacement therapy, we analyzed ABPM, clinical, and biochemical parameters. Results: At the beginning, the glomerular filtration rate (eGFR) was 66 (interquartile range—IQR: 42.8–75.3) mL/min/1.73 m2, and the observation period was 27 (16–36) months. The mean eGFR decline was 2.9 ± 5.7 mL/min/1.73 m2/year. eGFR decline correlated (p < 0.05) with age (r = 0.30), initial proteinuria (r = 0.31), nighttime systolic and mean blood pressure (r = 0.27, r = 0.29), and systolic and diastolic blood pressure dipping (r = −0.37, r = −0.29). There was no relation between mean arterial pressure during 24 h (MAP 24 h Z-score) and eGFR decline and no difference in eGFR decline between those with MAP 24 h < and ≥50 th percentile. In multivariate analysis, systolic blood pressure dipping (beta = −0.43), presence of proteinuria (beta = −0.35), and age (beta = 0.25) were predictors of eGFR decline. Conclusions: Systolic blood pressure dipping may be a valuable indicator of CKD progression in children. [ABSTRACT FROM AUTHOR]

Background: Chronic kidney disease (CKD) progression is presumably related to inflammatory response. The modified Glasgow prognostic score (mGPS), based on a combination of albumin and C‐reactive protein, has been derived from oncology and validated in multiple diseases. Aims: To evaluate the relationship between the mGPS and CKD progression. Methods: The present retrospective unicentric cohort study included 547 CKD patients (age 60.2 years; 53% male; estimated glomerular filtration (eGFR) 42.0 mL/min; mean change −2 mL/min/year) admitted between 1 January 2007 and 31 December 2012. Patients' records were reviewed from the CKD diagnosis to one of the four outcomes: end‐stage kidney disease (ESKD), death, loss to follow up or until 31 July 2017. Results: The mGPS score was 0 for 420 (78%), 1 for 110 (19%) and 2 for 17 (3%) patients. More patients with rapid CKD progression were found in the group with the highest mGPS (P = 0.05). mGPS was negatively correlated with baseline eGFR and positively with albuminuria. In the multivariate analysis, mGPS was associated with the eGFR slope. During the study period, 130 (24%) patients died and 109 (20%) reached ESKD. The mean kidney survival time was 8.1 (95% confidence interval 7.9–8.4) years. Patients with zero mGPS had better kidney survival than those with the score of 1 and 2 (Kaplan–Meier, P = 0.02). However, the kidney survival differences were not present after adjusting for CKD progression risk factors. Conclusion: The inflammation‐based mGPS score was associated with eGFR decline in CKD patients. Therefore, could prove useful in improving risk stratification of CKD patients. [ABSTRACT FROM AUTHOR]

Background and Aim: Associations of morning hypertension with chronic kidney disease are rarely investigated in prospective studies. We aim to investigate the predictive value of uncontrolled morning hypertension (UMH) to chronic kidney disease (CKD) progression and cardiovascular (CV) events in patients with CKD and hypertension.Methods and Results: In this prospective two-center observational study, 304 hypertensive patients with CKD were enrolled. Time to total mortality, CKD progression and CV events was recorded; Kaplan-Meier survival function estimates and Multivariable Cox proportional hazard model were used to investigate associations between UMH and outcomes. The study protocol was approved by the Institutional Review Board (http://www.thaiclinicaltrials.org; TCTR20180313004). After a follow-up for median 30 months, 23 (7.6%) patients died, 34 (11.2%) had CKD progression, and 95 (31.3%) occurred new-onset CV events, respectively. UMH was shown to be a strong predictor of CKD progression [hazard ratio (HR) 2.46, 95% confidence interval (CI) 1.22-4.94] and CV events (HR 1.69, 95% CI 1.12-2.53). When morning hypertension was analyzed as a continuous variable, morning systolic blood pressure (per 10 mmHg) was also shown to be predictive to CKD progression (HR 1.28, 95% CI 1.07-1.53, P < 0.01) and CV events (HR 1.15, 95% CI 1.03-1.28, P < 0.01).Conclusions: UMH is strongly associated with CKD progression and CV events in patients with CKD and hypertension. UMH in CKD patients deserves further attentions. [ABSTRACT FROM AUTHOR]

BackgroundWhereas several longitudinal metabolomics studies have been conducted in individuals with normal estimated glomerular filtration rate (eGFR) at baseline, disease progression among individuals with established chronic kidney disease (CKD) has not been rigorously examined.MethodsWe performed a nested case-control study of rapid CKD progression in the Chronic Renal Insufficiency Cohort Study, profiling baseline plasma from 200 individuals each with eGFR slope

Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenetic hereditary renal disease, promoting end-stage renal disease (ESRD). Klinefelter syndrome (KS) is a consequence of an extra copy of the X chromosome in males. Main symptoms in KS include hypogonadism, tall stature, azoospermia, and a risk of cardiovascular diseases, among others. Gitelman syndrome (GS) is an autosomal recessive disorder caused by SLC12A3 variants, and is associated with hypokalemia, hypomagnesemia, hypocalciuria, normal or low blood pressure, and salt loss. The three disorders have distinct and well-delineated clinical, biochemical, and genetic findings. We here report a male patient with ADPKD who developed early chronic renal failure leading to ESRD, presenting with an intracranial aneurysm and infertility. NGS identified two de novo PKD1 variants, one known (likely pathogenic), and a previously unreported variant of uncertain significance, together with two SLC12A3 pathogenic variants. In addition, cytogenetic analysis showed a 47, XXY karyotype. We investigated the putative impact of this rare association by analyzing possible clinical, biochemical, and/or genetic interactions and by comparing the evolution of renal size and function in the proband with three age-matched ADPKD (by variants in PKD1) cohorts. We hypothesize that the coexistence of these three genetic disorders may act as modifiers with possible synergistic actions that could lead, in our patient, to a rapid ADPKD progression. [ABSTRACT FROM AUTHOR]

ObjectiveStudies on the association between urinary protein-to-creatinine ratio (UPCR) and chronic kidney disease (CKD) progression are limited. This study aimed to investigate the relationship between UPCR and CKD progression in a Japanese population.MethodsThe present research was a secondary analysis of a prospective cohort study. Eight hundred and ninety-six subjects from the research of CKD-ROUTE in Japan were included. All the patients were new visitors or first referred to the participating centers of nephrology between October 2010 and December 2011. The target-independent variable was UPCR measured at baseline. The dependent variable was CKD progression and the estimated glomerular filtration rate (eGFR) changes during follow-up. We used Cox proportional hazards regression to investigate the association between UPCR and CKD progression risk. To address UPCR and CKD progression's non-linearity, a multivariate Cox proportional hazards regression analysis with cubic spline functions model and smooth curve fitting (penalized spline method) were conducted. We further used a generalized linear mixed model to explore the relationship between UPCR and the changes of eGFR.ResultThe mean age of the included patients was 67.2 ± 13.4 years old. Two hundred and thirty-four people occurred CKD progression during follow-up. The present study showed that UPCR was independently associated with CKD progression in the multivariate analysis [HR = 1.164, 95% CI (1.116, 1.215)]. The non-linear relationship between UPCR and CKD progression was explored in a dose-dependent manner, with an obvious inflection point of 1.699. Furthermore, our findings indicated that the tendency of the effect sizes on both the left and right sides of the inflection point was not consistent [left HR: 4.377, 95% CI (2.956, 6.483); right HR: 1.100, 95% CI (1.049–1.153)]. Using the linear mixed-effects regression model, we found that UPCR was an independent predictor of the longitudinal changes in eGFR (p < 0.001 for the interaction term with time).ConclusionThis study demonstrates a nonlinear positive relationship between UPCR and CKD progression in the Japanese population. UPCR is also an independent predictor of the longitudinal changes in eGFR.

Rationale & Objective: Potential surrogate end points for kidney failure have been proposed in chronic kidney disease (CKD); however, they must be evaluated to ensure accurate, powerful, and harmonized research, particularly among patients with advanced CKD. The aim of the current study was to investigate the power and predictive ability of surrogate kidney failure end points in a population with moderate-to-advanced CKD. Study Design: Analysis of longitudinal data of a large multinational CKD observational study (Chronic Kidney Disease Outcomes and Practice Patterns Study). Setting & Participants: CKD stage 3-5 patients from Brazil, France, Germany, and the United States. Outcomes: Reaching an estimated glomerular filtration rate (eGFR) < 15 mL/min/1.73 m2 or eGFR decline of ≥40%, and composite end points of these individual end points. Analytical Approach: Each end point was used as a time-varying indicator in the Cox model to predict the time to kidney replacement therapy (KRT; dialysis or transplant) and was compared by the number of events and prediction accuracy. Results: 8,211 patients had a median baseline eGFR of 27 mL/min/1.73 m2 (interquartile range, 21-36 mL/min/1.73 m2) and 1,448 KRT events over a median follow-up of 2.7 years (interquartile range, 1.2-3.0 years). Among CKD stage 4 patients, the eGFR < 15 mL/min/1.73 m2 end point had higher prognostic ability than 40% eGFR decline, but the end points were similar for CKD stage 3 patients. The combination of eGFR < 15 mL/min/1.73 m2 and 40% eGFR decline had the highest prognostic ability for predicting KRT, regardless of the CKD stage. Including KRT in the composite can increase the number of events and, therefore, the power. Limitations: Variable visit frequency resulted in variable eGFR measurement frequency. Conclusions: The composite end point can be useful for CKD progression studies among patients with advanced CKD. Harmonized use of this approach has the potential to accelerate the translation of new discoveries to clinical practice by identifying risk factors and treatments for kidney failure.

This study aimed to evaluate the association between obesity, evaluated by fat mass index (FMI) with the risk of microvascular diseases in patients with type 2 diabetes mellitus (T2DM) and compare the magnitude of associations of FMI, body mass index (BMI), and waist circumference (WC) with the risk of microvascular diseases. We performed a post-hoc analysis of the Action to Control Cardiovascular Risk in Diabetes study. The primary microvascular outcomes of the present study included chronic kidney disease (CKD) progression, retinopathy, and neuropathy. Cox proportional-hazards models were performed to evaluate the association of FMI with microvascular diseases. A discordant analysis was performed to compare the magnitude of associations of FMI, BMI, and WC with the risk of microvascular diseases. Our study included 10,251 T2DM participants with a median of 5 years (interquartile range, 4.2–5.7) of follow-up. A total of 6,184 participants developed CKD progression, 896 participants had retinopathy, and 3,213 participants developed neuropathy (Michigan Neuropathy Screening Instrument, >2.0). After the confounding factors were adjusted for, patients in the highest FMI quartile had a higher risk of CKD progression (HR: 1.26, 95%CI: 1.16–1.36) and neuropathy (HR: 1.93, 95% CI: 1.74–2.15), except for retinopathy (HR: 1.17, 95% CI: 0.96–1.43), than those in the lowest quartile. Discordant analyses found that FMI and WC are better in identifying individuals with obesity-related risk of neuropathy, compared with BMI; neither is better in identifying individuals with obesity-related risk of CKD progression and retinopathy. Obesity is associated with CKD progression and neuropathy in T2DM participants. Further randomized trials are needed to test whether obesity control can improve the outcomes of T2DM participants with CKD or neuropathy. FMI and WC are more useful in identifying obesity-related risk of neuropathy compared with BMI in T2DM patients. Clinical Trial Registration: http://www.clinicaltrials.gov , NCT00000620. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the association between obesity, evaluated by fat mass index (FMI) with the risk of microvascular diseases in patients with type 2 diabetes mellitus (T2DM) and compare the magnitude of associations of FMI, body mass index (BMI), and waist circumference (WC) with the risk of microvascular diseases. We performed a post-hoc analysis of the Action to Control Cardiovascular Risk in Diabetes study. The primary microvascular outcomes of the present study included chronic kidney disease (CKD) progression, retinopathy, and neuropathy. Cox proportional-hazards models were performed to evaluate the association of FMI with microvascular diseases. A discordant analysis was performed to compare the magnitude of associations of FMI, BMI, and WC with the risk of microvascular diseases. Our study included 10,251 T2DM participants with a median of 5 years (interquartile range, 4.2–5.7) of follow-up. A total of 6,184 participants developed CKD progression, 896 participants had retinopathy, and 3,213 participants developed neuropathy (Michigan Neuropathy Screening Instrument, >2.0). After the confounding factors were adjusted for, patients in the highest FMI quartile had a higher risk of CKD progression (HR: 1.26, 95%CI: 1.16–1.36) and neuropathy (HR: 1.93, 95% CI: 1.74–2.15), except for retinopathy (HR: 1.17, 95% CI: 0.96–1.43), than those in the lowest quartile. Discordant analyses found that FMI and WC are better in identifying individuals with obesity-related risk of neuropathy, compared with BMI; neither is better in identifying individuals with obesity-related risk of CKD progression and retinopathy. Obesity is associated with CKD progression and neuropathy in T2DM participants. Further randomized trials are needed to test whether obesity control can improve the outcomes of T2DM participants with CKD or neuropathy. FMI and WC are more useful in identifying obesity-related risk of neuropathy compared with BMI in T2DM patients.Clinical Trial Registrationhttp://www.clinicaltrials.gov, NCT00000620.

Background: Chronic kidney disease (CKD) is a public health priority of increasing concern worldwide. Sleep apnea (SA) of moderate-to-severe degree has a 3–9% prevalence in women and 10–17% in men in the general population. Summary: In CKD patients, the prevalence of SA parallels the decline of the GFR being 27% in CKD patients with a GFR of >60 mL/min/1.73 m2 and 57% in patients with end-stage kidney disease (ESKD). In the early CKD stages, fluid overload is probably the sole risk factor for SA in this population. At more severe CKD stages, disturbed central and peripheral chemosensitivity and the accumulation of uremic toxins might contribute to SA. Still, there is no direct evidence supporting this hypothesis in human studies. Observational studies coherently show that SA is a risk factor for CKD incidence and CKD progression as well as for cardiovascular disease and death in this population. However, there is no randomized clinical trial testing continuous positive airway pressure or other interventions documenting that attenuation of SA may have a favorable effect on renal and cardiovascular outcomes in CKD and ESKD patients. However, most likely, the causal nature of the association between SA and cardiorenal outcomes remains unproven. Renal transplantation is the most effective treatment of SA in patients with ESKD, but this disturbance re-emerges on long-term observation in this population. However, after renal transplantation, SA does not seem to be a predictor of adverse health outcomes. [ABSTRACT FROM AUTHOR]

Background: Elevated blood pressure and proteinuria are well-established risk factors for chronic kidney disease (CKD) progression in children. This study aimed to analyze risk factors for CKD progress, emphasizing detailed ambulatory blood pressure (ABPM) data. Methods: In 55 children with CKD II–V, observed for ≥1 year or until initiation of kidney replacement therapy, we analyzed ABPM, clinical, and biochemical parameters. Results: At the beginning, the glomerular filtration rate (eGFR) was 66 (interquartile range—IQR: 42.8–75.3) mL/min/1.73 m2, and the observation period was 27 (16–36) months. The mean eGFR decline was 2.9 ± 5.7 mL/min/1.73 m2/year. eGFR decline correlated (p < 0.05) with age (r = 0.30), initial proteinuria (r = 0.31), nighttime systolic and mean blood pressure (r = 0.27, r = 0.29), and systolic and diastolic blood pressure dipping (r = −0.37, r = −0.29). There was no relation between mean arterial pressure during 24 h (MAP 24 h Z-score) and eGFR decline and no difference in eGFR decline between those with MAP 24 h < and ≥50 th percentile. In multivariate analysis, systolic blood pressure dipping (beta = −0.43), presence of proteinuria (beta = −0.35), and age (beta = 0.25) were predictors of eGFR decline. Conclusions: Systolic blood pressure dipping may be a valuable indicator of CKD progression in children.

Background: Soluble suppression of tumorigenicity-2 (sST2) and galectin-3, novel biomarkers of heart failure and cardiovascular stress, predict cardiovascular events (CVEs) and mortality. However, their relationship with kidney function and adverse outcomes in CKD are uncertain. The purpose of this study was to determine the association between sST2 and galectin-3 with CKD progression and adverse clinical outcomes.Methods: We measured baseline sST2 and galectin-3 levels in the CKD patient cohort at our institution between October 2013 and December 2014. The primary outcome was CKD progression (kidney failure with replacement therapy or ≥50% reduction in estimated glomerular filtration rate from the baseline). The secondary outcome was the composite of CVEs and death. We used a Cox proportional hazards model to evaluate the associations between sST2 and galectin-3 levels, with kidney and clinical outcomes.Results: In total, 352 patients were enrolled in this study. At baseline, log sST2 and galectin-3 were directly associated with the serum creatinine (Cr) and urine protein-to-Cr ratio. Cox regression analysis showed that the baseline log sST2 level independently predicted CKD progression and composite outcome after adjustment for age, sex, smoking, diabetes mellitus, hypertension, cardiovascular disease, renin-angiotensin system blocker, calcium channel blocker, β-blocker, diuretics, antiplatelet agents, anemia, and hypoalbuminemia. The baseline log galectin-3 level was independently associated with CKD progression, but not with the composite outcome after adjustment for confounding variables.Conclusions: Elevated levels of sST2 and galectin-3 are significantly associated with CKD progression, but only sST2 is associated with adverse clinical outcomes. [ABSTRACT FROM AUTHOR]

Metabolic acidosis is commonly found in patients with chronic kidney disease (CKD), and its causes are: impaired ammonia excretion, reduced tubular bicarbonate reabsorption and insufficient renal bicarbonate production in relation to the amount of acids synthesised by the body and ingested with food. As the consequence, numerous metabolic abnormalities develop, which may lead to dysfunction of several organs. In observational studies, it has been found that CKD patients with metabolic acidosis are characterised by faster progression of kidney disease towards end stage kidney failure, and by increased mortality. Results of interventional studies suggest that alkali therapy in CKD patients slows progression of kidney disease. In view of these facts, the members of “The Working Group of the Polish Society of Nephrology on Metabolic and Endocrine Abnormalities in Kidney Diseases” have prepared the following statement and guidelines for the diagnosis and treatment of metabolic acidosis in CKD patients. Measurement of bicarbonate concentration in venous plasma or venous blood to check for metabolic acidosis should be performed in all CKD patients and metabolic acidosis in these patients should be diagnosed when the venous plasma or venous blood bicarbonate concentration is lower than 22 mmol/l. In patients with metabolic acidosis and CKD, oral sodium bicarbonate administration is recommended. The goal of such a treatment is to achieve a plasma or blood bicarbonate concentration equal to or greater than 22 mmol/l.

Autosomal dominant polycystic kidney disease (ADPKD) is a heterogeneous inherited disease characterized by renal and extrarenal manifestations with progressive fluid‐filled cyst development leading to end‐stage renal disease. The rate of disease progression in ADPKD exhibits high inter‐ and intrafamilial variability suggesting involvement of modifier genes and/or environmental factors. Renal hypouricemia (RHUC) is an inherited disorder characterized by impaired tubular uric acid transport with severe complications, such as acute kidney injury and chronic kidney disease (CKD). However, the two disorders have distinct and well‐delineated genetic, biochemical, and clinical findings. Only a few cases of coexistence of ADPKD and RHUC (type 1) in a single individual have been reported. We report a family with two members: an ADPKD 24‐year‐old female which presented bilateral renal cysts in utero and hypouricemia since age 5, and her mother with isolated hypouricemia. Next‐generation sequencing identified two mutations in two genes PKD1 and SLC2A9 in this patient and one isolated SLC2A9 mutation in her mother, showing RHUC type 2, associated to CKD. The coexistence of these two disorders provides evidence of SLC2A9 variant could act as a modifier change, with synergistic actions, that could promote cystogenesis and rapid ADPKD progression. This is the first case of coexistence of PKD1 and SLC2A9 mutations treated with tolvaptan. [ABSTRACT FROM AUTHOR]

Background Beverages are a source of calories and other bioactive constituents but are an understudied aspect of the diet. Different beverages have varying effects on health outcomes. Objectives We created the Healthy Beverage Score (HBS) to characterize participants' beverage patterns and examined its association with chronic kidney disease (CKD) progression, incident cardiovascular disease (CVD), and all-cause mortality among individuals with CKD. Methods We conducted a prospective analysis of 2283 adults aged 21–74 y with a baseline estimated glomerular filtration rate of 20–70 mL · min−1 · 1.73 m−2 from the Chronic Renal Insufficiency Cohort. Diet was assessed using a 124-item FFQ at visit 1 (2003–2008). The HBS, ranging from 7 to 28 possible points, consisted of 7 components, each scored from 1 to 4 based on rank distribution by quartile, except alcohol, which was based on sex-specific cutoffs. Participants were given more points for higher consumption of low-fat milk and of coffee/tea, for moderate alcohol, and for lower consumption of 100% fruit juice, whole-fat milk, artificially sweetened beverages, and sugar-sweetened beverages. CKD progression, incident CVD, and mortality were ascertained through January 2018. We conducted multivariable Cox proportional hazards models. Results There were 815 cases of CKD progression, 285 cases of incident CVD, and 725 deaths over a maximum of 14 y of follow-up. Compared with participants in the lowest tertile of the HBS, participants in the highest tertile had a 25% lower likelihood of CKD progression (HR: 0.75; 95% CI: 0.63, 0.89; P -trend = 0.001) and a 17% lower likelihood of all-cause mortality (HR: 0.83; 95% CI: 0.69, 1.00; P -trend = 0.04) after adjusting for sociodemographic, clinical, and dietary factors. There was no significant trend for incident CVD. Conclusions Among individuals with CKD, a healthier beverage pattern was inversely associated with CKD progression and all-cause mortality. Beverage intake may be an important modifiable target in preventing adverse outcomes for individuals with CKD. [ABSTRACT FROM AUTHOR]

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Abstract Background Chronic kidney disease (CKD) is a major contributor to mortality in the general population. Understanding the factors that drive this process will help delay progression of CKD. The study aimed to estimate the risks of kidney failure and death prior to and after the development of kidney failure among patients with pre-existing CKD, and to identify potential prognostic factors. Method Data were obtained from patients with CKD from Ubon Ratchathani province, Thailand from 1997 to 2011. The probability of each transition (i.e., CKD➔death (T1), CKD➔kidney failure (T2), and kidney failure➔death (T3)) was estimated using a competing risk model. A parametric survival model with restricted cubic spline function was applied to assess prognostic factors. Illness-death models were constructed for the 3 transitions. Among 32,106 patients with CKD, 5576 (17.4%), 4768 (14.9%), and 3056 (9.5%) respectively moved through T1, T2, and T3. Results Diabetics had 22.6%, 13.5%, and 60.7% higher risks of T1, T2, and T3 than non-diabetics respectively (p

Background: The impact of triglyceride-glucose (TyG) index variations on chronic kidney disease (CKD) progression remains unexplored. To investigate the effects of the TyG index and its dynamic changes on CKD progression., Method: This prospective cohort study included data from 8,418 hypertensive participants. The exposure variable in this study was defined as the difference between the TyG index at the last visit from that at baseline. The study's outcome variable was the progression of CKD, defined as follows: for subjects with an estimated glomerular filtration rate (eGFR) ≥60 mL/min, a ≥30% decrease in eGFR with a final follow-up value <60 mL/min; for those with an eGFR <60 mL/min, a ≥50% decrease in eGFR; or terminal renal failure requiring dialysis., Results: During a median follow-up period of 48 months, 1077 patients were diagnosed with CKD progression. In the fully adjusted Model 3, patients with a change in the TyG index <0 exhibited a significantly decreased 13% risk of CKD progression (HR: 0.87, 95% CI: 0.76-0.98) compared to those with a change in the TyG index≥0 group. Subgroup analyses showed that changes in the TyG index significantly increased the risk of CKD progression only in patients with diastolic blood pressure (DBP) <90mmHg. In the path analysis, baseline TyG was associated with follow-up eGFR (the standard regression coefficient was 1.26 [95% CI, 0.45-2.06])., Conclusions: Our findings suggest that TyG variability may serve as a useful tool for identifying individuals at risk of CKD progression, particularly hypertensive patients with normal DBP levels., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Yu, Shi, Wang, Zhu, Zhou, Bao and Cheng.)

Rationale & Objective: The extent to which depression affects the progression of chronic kidney disease (CKD) and leads to adverse clinical outcomes remains inadequately understood. We examined the association of depressive symptoms (DS) and antidepressant medication use on clinical outcomes in 4,839 adults with nondialysis CKD., Study Design: Observational cohort study., Setting and Participants: Adults with mild to moderate CKD who participated in the multicenter Chronic Renal Insufficiency Cohort Study (CRIC)., Exposure: The Beck Depression Inventory (BDI) was used to quantify DS. Antidepressant use was identified from medication bottles and prescription lists. Individual effects of DS and antidepressants were examined along with categorization as follows: (1) BDI <11 and no antidepressant use, (2) BDI <11 with antidepressant use, (3) BDI ≥11 and no antidepressant use, and (4) BDI ≥11 with antidepressant use., Outcomes: CKD progression, incident cardiovascular disease composite, all-cause hospitalizations, and mortality., Analytic Approach: Cox regression models were fitted for outcomes of CKD progression, incident cardiovascular disease, and all-cause mortality, whereas hospitalizations used Poisson regression., Results: At baseline, 27.3% of participants had elevated DS, and 19.7% used antidepressants. Elevated DS at baseline were associated with significantly greater risk for an incident cardiovascular disease event, hospitalization, and all-cause mortality, but not CKD progression, adjusted for antidepressants. Antidepressant use was associated with higher risk for all-cause mortality and hospitalizations, after adjusting for DS. Compared to participants without elevated DS and not using antidepressants, the remaining groups (BDI <11 with antidepressants; BDI ≥11 and no antidepressants; BDI ≥11 with antidepressants) showed higher risks of hospitalization and all-cause mortality., Limitations: Inability to infer causality among depressive symptoms, antidepressants, and outcomes. Additionally, the absence of nonpharmacological data, and required exploration of generalizability and alternative analytical approaches., Conclusions: Elevated DS increased adverse outcome risk in nondialysis CKD, unattenuated by antidepressants. Additionally, investigation into the utilization and counterproductivity of antidepressants in this population is warranted., (© 2024 The Authors.)

Background: Markers currently used to predict the likelihood of rapid disease progression in patients with autosomal dominant polycystic kidney disease (ADPKD) are expensive and time consuming to assess and often have limited sensitivity. New, easy-to-measure markers are therefore needed that alone or in combination with conventional risk markers can predict the rate of disease progression. In the present study, we investigated the ability of tubular damage and inflammation markers to predict kidney function decline.Methods: At baseline, albumin, immunoglobulin G, kidney injury molecule 1, β2 microglobulin (β2MG), heart-type fatty acid-binding protein, neutrophil gelatinase-associated lipocalin, and monocyte chemotactic protein-1 -(MCP-1) were measured in 24-h urine samples of patients participating in a study investigating the therapeutic efficacy of lanreotide in ADPKD. Individual change in estimated glomerular filtration rate (eGFR) during follow-up was calculated using mixed-model analysis taking into account 13 -eGFRs (chronic kidney disease EPIdemiology) per patient. Logistic regression analysis was used to select urinary biomarkers that had the best association with rapidly progressive disease. The predictive value of these selected urinary biomarkers was compared to other risk scores using C-statistics.Results: Included were 302 patients of whom 53.3% were female, with an average age of 48 ± 7 years, eGFR of 52 ± 12 mL/min/1.73 m2, and a height-adjusted total kidney volume (htTKV) of 1,082 (736-1,669) mL/m. At baseline, all urinary damage and inflammation markers were associated with baseline eGFR, also after adjustment for age, sex and baseline htTKV. For longitudinal analyses only patients randomized to standard care were considered (n = 152). A stepwise backward analysis revealed that β2MG and MCP-1 showed the strongest association with rapidly progressive disease. A urinary biomarker score was created by summing the ranking of tertiles of β2MG and MCP-1 excretion. The predictive value of this urinary biomarker score was higher compared to that of the Mayo htTKV classification (area under the curve [AUC] 0.73 [0.64-0.82] vs. 0.61 [0.51-0.71], p = 0.04) and comparable to that of the predicting renal outcomes in -ADPKD score (AUC 0.73 [0.64-0.82] vs. 0.65 [0.55-0.75], p = 0.18). In a second independent cohort with better kidney function, similar results were found for the urinary biomarker score.Conclusion: Measurement of urinary β2MG and MCP-1 excretion allows selection of ADPKD patients with rapidly progressive disease, with a predictive value comparable to or even higher than that of TKV or PKD mutation. Easy and inexpensive to measure urinary markers therefore hold promise to help predict prognosis in ADPKD. [ABSTRACT FROM AUTHOR]