Background
IgA nephropathy (IgAN) may recur in kidney transplant recipients. B‐cell‐activating factor (BAFF), a proliferation‐inducing ligand (APRIL), and α‐defensins are involved in the pathogenesis ...of native IgAN; however, their role on IgAN recurrence has not been previously analyzed.
Methods
Thirty‐five patients with IgAN who received a kidney transplant in our center between January 1, 1993, and December 31, 2015, were included. Recurrence was diagnosed and ruled out in 14 and 11 patients, respectively, by indication biopsies. Pre‐transplant, 6‐month, 1‐, 3‐, and 5‐year sera selected to measure BAFF, APRIL, and defensin by ELISA.
Results
Six months post‐transplantation, APRIL levels (300.1 vs 1203.8 pg/mL, P = 0.033) and the mean APRIL values from 6 months to 3 years (409.8 vs 1258.0 pg/mL, P = 0.003) were higher in recurrent patients. Both 6‐month APRIL levels (AUC‐ROC 0.753, P = 0.033) and mean APRIL values (AUC‐ROC 0.844, P = 0.004) discriminated patients with recurrence risk. By logistic regression, APRIL at 6 months (P = 0.044) and mean APRIL (P = 0.021) related to the risk of IgAN recurrence independently. Neither BAFF nor defensin related to recurrence.
Conclusions
Serum APRIL increased at 6 months and mean APRIL remained higher the first 3 years in patients in whom IgAN was going to recur.
About 25% of patients with IgA nephropathy (IgAN) progress to stage 5 chronic kidney disease (CKD) after years of evolution. Various tools have been developed in recent years designed to predict ...which of the patients will had poorer outcomes. The value of circulating galactosyl-deficient IgA1 (Gd-IgA1) has been related to a worse evolution of IgAN in several studies. There are also some publications that relate higher APRIL values with a worse evolution. Recently, a new method has been developed that allows measuring the value of circulating Gd-IgA1 in a simpler way than those previously available. The objective of this study is to analyze the influence of circulating Gd-IgA1, measured by this method, on the progression of IgAN.
Forty-nine patients with a diagnosis of IgAN demonstrated by renal biopsy were selected in our center, without having received prior immunosuppressive treatment, for whom frozen serum was available. The median follow-up was 4 years. Gd-IgA1 was measured by lectin-independent ELISA with the monoclonal antibody KM55 (IgA1 kit Cat. No. 30111694. IBL Int., Hamburg, Germany). Likewise, APRIL levels were also measured in these patients.
19 (38.8%) patients reached stage 5 CKD. The fourth quartile of circulating Gd-IgA1 was related to a higher cumulative risk of reaching stage 5 CKD in the Kaplan–Meier analysis (risk at the 5th year 39.4% vs. 24.3%, log rank p=0.019). The Gd-IgA1 value was related to an increased risk of CKD stage 5 (HR 1.147, 95% CI 1.035–1.270, p=0.009), regardless of glomerular filtration rate, proteinuria, the percentage of sclerosed glomeruli and the value of segmental sclerosis. We did not find significant differences in the APRIL values.
The value of circulating Gd-IgA1 measured by the monoclonal antibody KM55 is related to a worse evolution of patients with IgAN independently of other variables, so it could be included in the study of patients to improve the prediction of the risk of disease progression.
En torno al 25% de los pacientes con nefropatía IgA (NIgA) progresa hacia el estadio 5 de la enfermedad renal crónica tras años de evolución. En los últimos años se han desarrollado diversas herramientas diseñadas para predecir qué pacientes evolucionan peor. El valor de IgA1 galactosil-deficiente (Gd-IgA1) circulante se ha relacionado con una peor evolución de la NIgA en algunos estudios. También hay varios trabajos que relacionan valores más elevados de APRIL con una peor evolución. Recientemente se ha desarrollado un método que permite medir el valor de Gd-IgA1 circulante de una manera más sencilla que los previamente disponibles. El objetivo de este estudio es analizar la influencia de la Gd-IgA1 circulante, medida por este método, en la progresión de la NIgA.
Se seleccionaron 49 pacientes con diagnóstico de NIgA demostrado mediante biopsia renal en nuestro centro, sin haber recibido tratamiento inmunosupresor previo, de los que se dispusiera de suero congelado. La mediana de seguimiento fue de cuatro años. Se midió Gd-IgA1 mediante ELISA independiente de lectina con el anticuerpo monoclonal KM55 (IgA1 kit Cat. No 30111694. IBL Int., Hamburgo, Alemania). Así mismo también se midieron los niveles de APRIL en estos pacientes.
19 (38,8%) pacientes alcanzaron ERC estadio 5. El cuarto cuartil de Gd-IgA1 circulante se relacionaba con un mayor riesgo acumulado de llegar a ERC estadio 5 en el análisis de Kaplan–Meier (riesgo al 5 año 39,4% vs. 24,3%; log rank p=0,019). El valor de Gd-IgA1 se relacionaba con un mayor riesgo de ERC estadio 5 (HR 1,147; IC 95%: 1,035–1,270; p=0,009), independientemente del filtrado glomerular, la proteinuria, el porcentaje de glomérulos esclerosados y el valor de esclerosis segmentaria. No encontramos diferencias significativas en los valores de APRIL.
El valor de Gd-IgA1 circulante medido mediante el anticuerpo monoclonal KM55 se relaciona con una peor evolución de los pacientes con NIgA independientemente de otras variables, por lo que se podría incluir en el estudio de los pacientes para mejorar la predicción del riesgo de progresión de la enfermedad.
ITGAM–ITGAX (rs11150612, rs11574637), VAV3 rs17019602, CARD9 rs4077515, DEFA (rs2738048, rs10086568), and HORMAD2 rs2412971 are mucosal immune defence polymorphisms, that have an impact on IgA ...production, described as risk loci for IgA nephropathy (IgAN). Since IgAN and Immunoglobulin-A vasculitis (IgAV) share molecular mechanisms, with the aberrant deposit of IgA1 being the main pathophysiologic feature of both entities, we assessed the potential influence of the seven abovementioned polymorphisms on IgAV pathogenesis. These seven variants were genotyped in 381 Caucasian IgAV patients and 997 matched healthy controls. No statistically significant differences were observed in the genotype and allele frequencies of these seven polymorphisms when the whole cohort of IgAV patients and those with nephritis were compared to controls. Similar genotype and allele frequencies of all polymorphisms were disclosed when IgAV patients were stratified according to the age at disease onset or the presence/absence of gastrointestinal or renal manifestations. Likewise, no ITGAM–ITGAX and DEFA haplotype differences were observed when the whole cohort of IgAV patients, along with those with nephritis and controls, as well as IgAV patients, stratified according to the abovementioned clinical characteristics, were compared. Our results suggest that mucosal immune defence polymorphisms do not represent novel genetic risk factors for IgAV pathogenesis.
Preeclampsia (PE) is a hypertensive disorder of pregnancy associated with high maternal and fetal morbidity and mortality and increased future risk of cardiovascular complications.
To analyze whether ...women who have had PE with severe features in their pregnancy have higher arterial stiffness (AS) parameters than those whose PE course was without signs of severity.
Sixty-five women who developed PE during their gestation were evaluated, divided into two groups: PE group without severe features or non-severe PE (n=30) and PE group with severe features or severe PE (n=35). Carotid-femoral pulse wave velocity (cfPWV), central augmentation index corrected to a heart rate of 75 beats per minute (AIxc75) and central augmentation pressure (cAP) were determined one month and six months postpartum. Comparison of proportions was carried out using the chi-square test, comparison of means between groups using the Student’s t-test or the Mann–Whitney test, and comparison of means of the same group at different evolutionary moments, using the t-test or the Wilcoxon test. Correlation, with and between hemodynamic parameters, was carried out with Spearman’s correlation coefficient and the association between demographic variables, personal history and hemodynamic parameters, and altered arterial stiffness parameters was carried out using linear and logistic regression models.
Women with severe PE presented, both at 1 and 6 months postpartum, higher values of blood pressure, both central and peripheral, as well as AR and pulse amplification parameters, than those women whose PE was not severe. Central augmentation index (cAIx) values at 1 month and 6 months postpartum were higher, although not significantly, in the severe PE group compared to the non-severe PE group (24.0 (16.5–34.3) vs. 19.0% (14–29) and 24.0 (14.0–30.0) vs. 20.0% (12.3–26.8), respectively). Carotid-femoral pulse wave velocity (cfPWV) was significantly higher at both 1 and 6 months postpartum in the severe PE group compared to the non-severe PE group (10.2 (8.8−10.7) vs. 8.8m/s (8.3−9.6) and 10.0 (8.8−10.6) vs. 8.8m/s (8.3−9.3), respectively). Central systolic pressure and central pulse pressure amplification were also higher, although not significantly, in the severe PE group in comparison with the non-severe PE group.
Women who have had severe PE have more pronounced arterial stiffness parameters than those in whom PE was not particularly severe. The determination of cAIx and cfPWV, as a strategy for the assessment of cardiovascular risk, should be evaluated among women who have had PE.
La preeclampsia (PE) es un trastorno hipertensivo del embarazo asociado a una elevada morbimortalidad materna y fetal, y un mayor riesgo futuro de complicaciones cardiovasculares.
Analizar si las mujeres que han tenido PE grave en su embarazo presentan parámetros de rigidez arterial (RA) superiores a las de aquellas cuya PE cursó sin signos de gravedad.
Se evaluaron 65 mujeres que habían desarrollado PE durante su gestación, divididas en 2 grupos: grupo de PE sin criterios de gravedad o PE no grave (n=30) y grupo de PE con criterios de gravedad o PE grave (n=35). Se determinó la velocidad de onda de pulso carótida-femoral (VOPcf), el índice de aumento central normalizado a 75 latidos por minuto (IAc75) y presión de aumento central (PAc) al mes y a los 6 meses posparto. La comparación de proporciones se llevó a cabo mediante la prueba de Chi-cuadrado, la comparación de medias entre grupos se utilizaron la prueba t de Student o la prueba de Mann-Whitney, y la comparación de medias de un mismo grupo en momentos evolutivos diferentes, la prueba t para o el test de Wilcoxon. La correlación, con y entre parámetros hemodinámicos, se llevó a cabo con el coeficiente de correlación de Spearman y la asociación entre variables demográficas, antecedentes personales y parámetros hemodinámicos, y valores alterados de RA se llevó a cabo mediante modelos de regresión lineal y logística.
Las mujeres con PE grave presentaban, al mes y a los 6 meses posparto, valores de presión arterial, tanto central como periférica, así como parámetros de RA y amplificación de pulso, superiores a aquellas mujeres cuya PE no revistió gravedad. Los valores del índice de aumento central (IAc) al mes y a los 6 meses posparto fueron superiores, aunque no de forma significativa, en el grupo de PE grave respecto al grupo de PE no grave (24,0 16,5–34,3 vs. 19,0% 14–29 y 24,0 14,0–30,0 vs. 20,0% 12,3–26,8, respectivamente). La velocidad onda de pulso carótida-femoral (VOPcf) fue superior de forma significativa, tanto al mes como a los 6 meses posparto en el grupo de PE grave respecto al grupo de PE no grave (10,2 8,8–10,7 vs. 8,8m/s 8,3–9,6 y 10,0 8,8–10,6 vs. 8,8m/s 8,3–9,3, respectivamente). La amplificación de la presión sistólica central y de la presión de pulso central fueron también superiores, aunque no de forma significativa, en el grupo de PE grave respecto al de PE no grave.
Las mujeres que han tenido PE grave presentan parámetros de RA más acusados que los de aquellas en las que la PE no revistió especial gravedad. Debiera evaluarse la conveniencia de incluir de forma rutinaria entre las mujeres que han tenido PE la determinación del IAc y especialmente la VOPcf, como estrategia de evaluación del riesgo cardiovascular.
La preeclampsia (PE) es un trastorno hipertensivo del embarazo asociado a una elevada morbimortalidad materna y fetal, y un mayor riesgo futuro de complicaciones cardiovasculares.
Analizar si las ...mujeres que han tenido PE grave en su embarazo presentan parámetros de rigidez arterial (RA) superiores a las de aquellas cuya PE cursó sin signos de gravedad.
Se evaluaron 65 mujeres que habían desarrollado PE durante su gestación, divididas en 2 grupos: grupo de PE sin criterios de gravedad o PE no grave (n=30) y grupo de PE con criterios de gravedad o PE grave (n=35). Se determinó la velocidad de onda de pulso carótida-femoral (VOPcf), el índice de aumento central normalizado a 75 latidos por minuto (IAc75) y presión de aumento central (PAc) al mes y a los 6 meses posparto. La comparación de proporciones se llevó a cabo mediante la prueba de Chi-cuadrado, la comparación de medias entre grupos se utilizaron la prueba t de Student o la prueba de Mann-Whitney, y la comparación de medias de un mismo grupo en momentos evolutivos diferentes, la prueba t para o el test de Wilcoxon. La correlación, con y entre parámetros hemodinámicos, se llevó a cabo con el coeficiente de correlación de Spearman y la asociación entre variables demográficas, antecedentes personales y parámetros hemodinámicos, y valores alterados de RA se llevó a cabo mediante modelos de regresión lineal y logística.
Las mujeres con PE grave presentaban, al mes y a los 6 meses posparto, valores de presión arterial, tanto central como periférica, así como parámetros de RA y amplificación de pulso, superiores a aquellas mujeres cuya PE no revistió gravedad. Los valores del índice de aumento central (IAc) al mes y a los 6 meses posparto fueron superiores, aunque no de forma significativa, en el grupo de PE grave respecto al grupo de PE no grave (24,0 16,5-34,3 vs. 19,0% 14-29 y 24,0 14,0-30,0 vs. 20,0% 12,3-26,8, respectivamente). La velocidad onda de pulso carótida-femoral (VOPcf) fue superior de forma significativa, tanto al mes como a los 6 meses posparto en el grupo de PE grave respecto al grupo de PE no grave (10,2 8,8-10,7 vs. 8,8m/s 8,3-9,6 y 10,0 8,8-10,6 vs. 8,8m/s 8,3-9,3, respectivamente). La amplificación de la presión sistólica central y de la presión de pulso central fueron también superiores, aunque no de forma significativa, en el grupo de PE grave respecto al de PE no grave.
Las mujeres que han tenido PE grave presentan parámetros de RA más acusados que los de aquellas en las que la PE no revistió especial gravedad. Debiera evaluarse la conveniencia de incluir de forma rutinaria entre las mujeres que han tenido PE la determinación del IAc y especialmente la VOPcf, como estrategia de evaluación del riesgo cardiovascular.
Preeclampsia (PE) is a hypertensive disorder of pregnancy associated with high maternal and fetal morbidity and mortality and increased future risk of cardiovascular complications.
To analyze whether women who have had PE with severe features in their pregnancy have higher arterial stiffness (AS) parameters than those whose PE course was without signs of severity.
Sixty-five women who developed PE during their gestation were evaluated, divided into two groups: PE group without severe features or non-severe PE (n=30) and PE group with severe features or severe PE (n=35). Carotid-femoral pulse wave velocity (cfPWV), central augmentation index corrected to a heart rate of 75 beats per minute (AIxc75) and central augmentation pressure (cAP) were determined one month and six months postpartum. Comparison of proportions was carried out using the chi-square test, comparison of means between groups using the Student's t-test or the Mann-Whitney test, and comparison of means of the same group at different evolutionary moments, using the t-test or the Wilcoxon test. Correlation, with and between hemodynamic parameters, was carried out with Spearman's correlation coefficient and the association between demographic variables, personal history and hemodynamic parameters, and altered arterial stiffness parameters was carried out using linear and logistic regression models.
Women with severe PE presented, both at 1 and 6 months postpartum, higher values of blood pressure, both central and peripheral, as well as AR and pulse amplification parameters, than those women whose PE was not severe. Central augmentation index (cAIx) values at 1 month and 6 months postpartum were higher, although not significantly, in the severe PE group compared to the non-severe PE group (24.0 (16.5-34.3) vs. 19.0% (14-29) and 24.0 (14.0-30.0) vs. 20.0% (12.3-26.8), respectively). Carotid-femoral pulse wave velocity (cfPWV) was significantly higher at both 1 and 6 months postpartum in the severe PE group compared to the non-severe PE group (10.2 (8.8-10.7) vs. 8.8m/s (8.3-9.6) and 10.0 (8.8-10.6) vs. 8.8m/s (8.3-9.3), respectively). Central systolic pressure and central pulse pressure amplification were also higher, although not significantly, in the severe PE group in comparison with the non-severe PE group.
Women who have had severe PE have more pronounced arterial stiffness parameters than those in whom PE was not particularly severe. The determination of cAIx and cfPWV, as a strategy for the assessment of cardiovascular risk, should be evaluated among women who have had PE.
Abstract
BAFF, APRIL and BAFF-R are key proteins involved in the development of B-lymphocytes and autoimmunity. Additionally,
BAFF, APRIL
and
BAFFR
polymorphisms were associated with immune-mediated ...conditions, being
BAFF
GCTGT>A a shared insertion-deletion genetic variant for several autoimmune diseases. Accordingly, we assessed whether
BAFF, APRIL
and
BAFFR
represent novel genetic risk factors for Immunoglobulin-A vasculitis (IgAV), a predominantly B-lymphocyte inflammatory condition.
BAFF
rs374039502, which colocalizes with
BAFF
GCTGT>A, and two tag variants within
APRIL
(rs11552708 and rs6608) and
BAFFR
(rs7290134 and rs77874543) were genotyped in 386 Caucasian IgAV patients and 806 matched healthy controls. No genotypes or alleles differences were observed between IgAV patients and controls when
BAFF, APRIL
and
BAFFR
variants were analysed independently. Likewise, no statistically significant differences were found in the genotype and allele frequencies of
BAFF, APRIL
or
BAFFR
when IgAV patients were stratified according to the age at disease onset or to the presence/absence of gastrointestinal (GI) or renal manifestations. Similar results were disclosed when
APRIL
and
BAFFR
haplotypes were compared between IgAV patients and controls and between IgAV patients stratified according to the clinical characteristics mentioned above. Our results suggest that
BAFF, APRIL
and
BAFFR
do not contribute to the genetic network underlying IgAV.
Abstract
Cytokines signalling pathway genes are crucial factors of the genetic network underlying the pathogenesis of Immunoglobulin-A vasculitis (IgAV), an inflammatory vascular condition. An ...influence of the
interleukin (IL)33- IL1 receptor like (IL1RL)1
signalling pathway on the increased risk of several immune-mediated diseases has been described. Accordingly, we assessed whether the
IL33-IL1RL1
pathway represents a novel genetic risk factor for IgAV. Three tag polymorphisms within
IL33
(rs3939286, rs7025417 and rs7044343) and three within
IL1RL1
(rs2310173, rs13015714 and rs2058660), that also were previously associated with several inflammatory diseases, were genotyped in 380 Caucasian IgAV patients and 845 matched healthy controls. No genotypes or alleles differences were observed between IgAV patients and controls when
IL33
and
IL1RL1
variants were analysed independently. Likewise, no statistically significant differences were found in
IL33
or
IL1RL1
genotype and allele frequencies when IgAV patients were stratified according to the age at disease onset or to the presence/absence of gastrointestinal (GI) or renal manifestations. Similar results were disclosed when
IL33
and
IL1RL1
haplotypes were compared between IgAV patients and controls and between IgAV patients stratified according to the clinical characteristics mentioned above. Our results suggest that the
IL33-IL1RL1
signalling pathway does not contribute to the genetic network underlying IgAV.
En torno al 25% de los pacientes con nefropatía IgA (NIgA) progresa hacia el estadio 5 de la enfermedad renal crónica tras años de evolución. En los últimos años se han desarrollado diversas ...herramientas diseñadas para predecir qué pacientes evolucionan peor. El valor de IgA1 galactosil-deficiente (Gd-IgA1) circulante se ha relacionado con una peor evolución de la NIgA en algunos estudios. También hay varios trabajos que relacionan valores más elevados de APRIL con una peor evolución. Recientemente se ha desarrollado un método que permite medir el valor de Gd-IgA1 circulante de una manera más sencilla que los previamente disponibles. El objetivo de este estudio es analizar la influencia de la Gd-IgA1 circulante, medida por este método, en la progresión de la NIgA.
Se seleccionaron 49 pacientes con diagnóstico de NIgA demostrado mediante biopsia renal en nuestro centro, sin haber recibido tratamiento inmunosupresor previo, de los que se dispusiera de suero congelado. La mediana de seguimiento fue de cuatro años. Se midió Gd-IgA1 mediante ELISA independiente de lectina con el anticuerpo monoclonal KM55 (IgA1 kit Cat. No 30111694. IBL Int., Hamburgo, Alemania). Así mismo también se midieron los niveles de APRIL en estos pacientes.
19 (38,8%) pacientes alcanzaron ERC estadio 5. El cuarto cuartil de Gd-IgA1 circulante se relacionaba con un mayor riesgo acumulado de llegar a ERC estadio 5 en el análisis de Kaplan-Meier (riesgo al 5 año 39,4% vs. 24,3%; log rank p = 0,019). El valor de Gd-IgA1 se relacionaba con un mayor riesgo de ERC estadio 5 (HR 1,147; IC 95%: 1,035-1,270; p = 0,009), independientemente del filtrado glomerular, la proteinuria, el porcentaje de glomérulos esclerosados y el valor de esclerosis segmentaria. No encontramos diferencias significativas en los valores de APRIL.
El valor de Gd-IgA1 circulante medido mediante el anticuerpo monoclonal KM55 se relaciona con una peor evolución de los pacientes con NIgA independientemente de otras variables, por lo que se podría incluir en el estudio de los pacientes para mejorar la predicción del riesgo de progresión de la enfermedad.
About 25% of patients with IgA nephropathy (IgAN) progress to stage 5 chronic kidney disease (CKD) after years of evolution. Various tools have been developed in recent years designed to predict which of the patients will had poorer outcomes. The value of circulating galactosyl-deficient IgA1 (Gd-IgA1) has been related to a worse evolution of IgAN in several studies. There are also some publications that relate higher APRIL values with a worse evolution. Recently, a new method has been developed that allows measuring the value of circulating Gd-IgA1 in a simpler way than those previously available. The objective of this study is to analyze the influence of circulating Gd-IgA1, measured by this method, on the progression of IgAN.
Forty-nine patients with a diagnosis of IgAN demonstrated by renal biopsy were selected in our center, without having received prior immunosuppressive treatment, for whom frozen serum was available. The median follow-up was 4 years. Gd-IgA1 was measured by lectin-independent ELISA with the monoclonal antibody KM55 (IgA1 kit Cat. No. 30111694. IBL Int., Hamburg, Germany). Likewise, APRIL levels were also measured in these patients.
19 (38.8%) patients reached stage 5 CKD. The fourth quartile of circulating Gd-IgA1 was related to a higher cumulative risk of reaching stage 5 CKD in the Kaplan–Meier analysis (risk at the 5th year 39.4% vs. 24.3%, log rank p=0.019). The Gd-IgA1 value was related to an increased risk of CKD stage 5 (HR 1.147, 95% CI 1.035–1.270, p=0.009), regardless of glomerular filtration rate, proteinuria, the percentage of sclerosed glomeruli and the value of segmental sclerosis. We did not find significant differences in the APRIL values.
The value of circulating Gd-IgA1 measured by the monoclonal antibody KM55 is related to a worse evolution of patients with IgAN independently of other variables, so it could be included in the study of patients to improve the prediction of the risk of disease progression.
Key Points
Kidney survival in C3 glomerulopathy is significantly higher in patients with a disease chronicity score <4 and proteinuria <3.5 g/d, regardless of baseline eGFR.
A faster eGFR decline in ...C3 glomerulopathy is associated with higher probability of kidney failure.
Patients with glomerulopathy with a progressive reduction in proteinuria over time did not reach kidney failure.
Background
C3 glomerulopathy is a rare kidney disease, which makes it difficult to collect large cohorts of patients to better understand its variability. The aims of this study were to describe the clinical profiles and patterns of progression of kidney disease.
Methods
This was a retrospective, observational cohort study. Patients diagnosed with C3 glomerulopathy between 1995 and 2020 were enrolled. Study population was divided into clinical profiles by combining the following predictors: eGFR under/above 30 ml/min per 1.73 m
2
, proteinuria under/above 3.5 g/d, and histologic chronicity score under/above 4. The change in eGFR and proteinuria over time was evaluated in a subgroup with consecutive measurements of eGFR and proteinuria.
Results
One hundred and fifteen patients with a median age of 30 years (interquartile range 19–50) were included. Patients were divided into eight clinical profiles. Kidney survival was significantly higher in patients with a chronicity score <4 and proteinuria <3.5 g/d, both in those presenting with an eGFR under/above 30 ml/min per 1.73 m
2
. The median eGFR slope of patients who reached kidney failure was −6.5 ml/min per 1.73 m
2
per year (interquartile range −1.6 to −17). Patients who showed a reduction in proteinuria over time did not reach kidney failure. On the basis of the rate of eGFR decline, patients were classified as faster eGFR decline (≥5 ml/min per 1.73 m
2
per year), slower (<5 ml/min per 1.73 m
2
per year), and those without decline. A faster eGFR decline was associated with higher probability of kidney failure.
Conclusions
Kidney survival is significantly higher in patients with a chronicity score <4 and proteinuria <3.5 g/d regardless of baseline eGFR, and a faster rate of decline in eGFR is associated with higher probability of kidney failure.
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