How to Estimate Kidney Growth in Patients with Autosomal Dominant Polycystic Kidney Disease.

Autosomal dominant polycystic kidney disease (ADPKD) is a disease characterized by a progressive kidney growth due to the development of cysts that lead to gradual destruction of the surrounding parenchyma. In the first stage, the estimated GFR will remain stable despite the reduction of the renal parenchyma because of an increase in glomerular hyperfiltration. The total kidney volume (TKV) measured with computed tomography or magnetic resonance imaging is related to the future GFR decline. Thus, TKV has become an early marker to be analyzed in all patients with ADPKD. In addition, in recent years, it has been pointed out that kidney growth rate estimated with a single TKV measurement can be a clear prognostic marker for future glomerular filtration decline. However, there is no consensus on how to measure kidney volume growth in ADPKD, so each author has used different models that, not having the same meaning, have been handled as if they produced similar values. This may lead to erroneous estimates of kidney growth rate with the consequent prognostic error. The Mayo Clinic classification is now the most widely accepted prognostic model in clinical practice to predict patients who will deteriorate faster and to decide what patients should be treated with tolvaptan. However, some aspects of this model have not been discussed in depth. Our aim in this review was to present the models that can be used to estimate kidney volume growth rate in ADPKD, to facilitate their applicability in daily clinical practice.

Hypocitraturia is present when renal function is impaired in diverse nephropathies and is not related with serum bicarbonate levels.

BACKGROUND: In autosomal dominant polycystic kidney disease (ADPKD) it is frequently found a reduction in urinary citrate of unknown origin. It has been suggested that it could be a marker of acid retention in chronic kidney disease. Our aim was to compare urinary citrate in ADPKD with other nephropathies and to show its relation with serum bicarbonate. METHODS: We determined urinary citrate in patients with several nephropathies and varied renal function. We included 291 patients, 119 with glomerular diseases, 116 with ADPKD, 21 with other nephropathies, and 35 patients with normal renal function. RESULTS: Urinary citrate was higher in women and in patients with normal renal function. ADPKD patients showed similar values of urinary citrate to patients with glomerular diseases and with other nephropathies. We observed a progressive reduction in urinary citrate with renal impairment, in a comparable way among patients with ADPKD and glomerular diseases. We did not observe a relationship with serum bicarbonate. Serum uric acid levels were significantly higher in patients with glomerular diseases than in ADPKD patients, even after correction with the degree of renal function. CONCLUSIONS: Hypocitraturia is not specific of ADPKD but it is also present in all tested nephropathies and is related with renal impairment and not with serum bicarbonate. It could be interesting to study urinary citrate as a marker of renal function and as a prognostic factor.

Urinary citrate as a marker of renal function in patients with autosomal dominant polycystic kidney disease.

INTRODUCTION: Autosomal dominant polycystic kidney disease (ADPKD) is frequent to find low urinary citrate levels. Recently, it has been suggested that urinary citrate could be a marker of covert metabolic acidosis in chronic kidney disease. OBJECTIVE: Our aim was to analyze relationship between urinary citrate levels, renal function, and serum bicarbonate in ADPKD patients. METHODS: We determined citrate in 24-h collected urine from ADPKD patients and correlated with glomerular filtration rate (CKD-EPI equation) and serum bicarbonate concentration. RESULTS: We included 120 patients, 60% men, eGFR was 71 ± 32 mL/min/1.73 m2. Urinary citrate/creatinine ratio was 195 ± 152 mg/gCr (range 1.2-689) with levels significantly higher in females. Urinary citrate lower than 300 mg/gCr was present in 75% of patients and when considering chronic kidney stages (CKD), we observed reduced levels in 48.8% in CKD1 stage, in 79.4% in CKD2 stage, in 96.2% in CKD3 stage, and in 94.7% of patients in CKD4 stage. Urinary citrate was correlated with serum creatinine (r = - 0.61, p < 0.001) and eGFR (r = 0.55, p < 0.001) in both gender. We did not find any correlation with serum bicarbonate. Using a general linear modeling analysis, we found as predictors of urinary citrate/creatinine ratio to glomerular filtration rate, gender, and age. Lower levels of urinary citrate were accompanied by a decline in urinary osmolality and in renal excretion of calcium and uric acid. In a subgroup of patients, we measured total kidney volume and we found an inverse correlation with urinary citrate levels that disappeared when it was corrected with glomerular filtration rate. CONCLUSIONS: Urinary citrate is very frequently reduced in ADPKD patients being present from very early CKD stages. Their levels in urine are inversely correlated with glomerular filtration rate and it is not related with serum bicarbonate concentration. We think that it would be interesting to study urinary citrate as a marker of chronic kidney disease in ADPKD patients.

Predicting Future Renal Function Decline in Patients with Autosomal Dominant Polycystic Kidney Disease Using Mayo Clinic Classification.

INTRODUCTION: Mayo clinic classification (MCC) has been proposed in patients with autosomal dominant polycystic kidney disease (ADPKD) to identify who may experience a rapid decline of renal function. Our aim was to validate this predictive model in a population from southern Spain. METHODS: ADPKD patients with measurements of height-adjusted total kidney volume (HtTKV) and baseline estimated glomerular filtration rate (eGFR) >30 mL/min/1.73 m2 were selected. Last eGFR was estimated with Mayo Clinic (MC) equation and bias and accuracy were studied. We also analyzed predictive capacity of MCC classes using survival analysis and Cox regression models. RESULTS: We included 134 patients with a mean follow-up of 82 months. While baseline eGFR was not different between classes, last eGFR decreased significantly with them. eGFR variation rate was different according to the MCC class with a more rapid decline in 1C, 1D, and 1E classes. Final eGFR predicted was not significantly different from the real one, with an absolute bias of 0.6 ± 17.0 mL/min/1.73 m2. P10 accuracy was low ranging from 37.5 to 59.5% in classes 1C, 1D, and 1E. Using MC equation, the rate of eGFR decline was underestimated in 1C, 1D, and 1E classes. Cox regression analysis showed that MCC class is a predictor of renal survival after adjusting with baseline eGFR, age, sex, and HtTKV, with 1D and 1E classes having the worst prognosis. CONCLUSION: MCC classification is able to identify patients who will undergo a more rapid decline of renal function in a Spanish population. Prediction of future eGFR with MC equation is acceptable as a group, although it shows a loss of accuracy considering individual values. The rate of eGFR decline calculated using MC equation can underestimate the real rate presented by patients of 1C, 1D, and 1E classes.

Nefropatía IgA: efectos a corto plazo del tratamiento con prednisona sobre la proteinuria, función renal y relación con la clasificación de Oxford / IgA nephropathy: Short term effects of prednisone treatment on proteinuria, renal function and relation with Oxford classification

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Osmolalidad urinaria en pacientes con poliquistosis renal: ¿medida o calculada? / Urinary osmolality in patients with polycystic kidney disease: Measured or calculated?

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Comparación de las ecuaciones MDRD y de las antiguas ecuaciones CKD-EPI frente a las nuevas ecuaciones CKD-EPI en pacientes con trasplante renal cuando se emplea 51Cr-EDTA para medir el filtrado glomerular / Comparison of MDRD and the old CKD-EPI equations with the new CKD-EPI equations in kidney transplant patients when glomerular filtration rate is measured with 51Cr-EDTA

INTRODUCCIÓN: Para la estimación del filtrado glomerular renal (FG) en trasplantados renales se emplean las ecuaciones MDRD y CKD-EPI de 2009 que han mostrado diferencias importantes cuando se comparan con el FG medido con técnicas de referencia. OBJETIVO: Analizar el rendimiento de las ecuaciones MDRD, CKD-EPI de 2009 y de 2012 en 270 pacientes trasplantados renales de un año de evolución, comparando con el FG medido con aclaramiento plasmático de 51Cr-EDTA. RESULTADOS: El FG medido fue 43,0 ± 11,4 (18,2-79,4) mL/min/1,73 m2, con niveles de creatinina de 1,42 ± 0,46 (0,60-4,33) mg/dL y de cistatina C de 1,45 ± 0,53 (0,42-3,48) mg/L. El FG medido se correlacionó moderadamente con creatinina (r = -0,61; p < 0,001) y cistatina C (r = - 0,52; p < 0,001). Empleando técnicas de regresión lineal observamos que creatinina, cistatina C, sexo y edad solo explicaban el 52% de la varianza total del FG. Todas las ecuaciones sobrestimaron el FG, con sesgo medio de +11,1 mL/min/1,73 m2 para MDRD, +16,4 mL/min/1,73 m2 para CKD-EPI de 2009, +15 mL/min/1,73 m2 para CKD-EPI con cistatina C y +14,1 mL/min/1,73 m2 para CKD-EPI con creatinina y cistatina C de 2012. Las estimaciones con MDRD y CKD-EPI de 2009 se correlacionaron mejor con 51Cr-EDTA que CKD-EPI con creatinina y/o cistatina C. Las sobrestimaciones se correlacionaron negativamente con los niveles de creatinina y cistatina C, siendo más importantes para CKD-EPI con creatinina y/o cistatina C cuando el FG fue mayor de 60 mL/min/1,73 m2. CONCLUSIONES: Las ecuaciones CKD-EPI de 2012 con creatinina y/o cistatina C sobrestiman el FG de forma muy marcada en estadios 1 y 2 de la enfermedad renal crónica, por lo que en ellos sería recomendable emplear la ecuación MDRD. La técnica de referencia empleada para medir el FG parece tener una influencia muy importante en el sesgo de las ecuaciones

BACKGROUND: When estimating the glomerular filtration rate (GFR) in kidney transplant patients, significant differences have been found between MDRD and the 2009 CKD-EPI equations, and reference techniques. OBJECTIVE: To analyse and compare the performance of MDRD and the 2009 and 2012 CKD-EPI equations against 51Cr-EDTA plasma clearance in measuring GFR in 270 kidney transplant patients after one year. RESULTS: The mean measured GFR was 43.0 ± 11.4 (18.2-79.4) ml/min/1.73 m2, with creatinine levels of 1.42 ± 0.46 (0.60-4.33) mg/dl and cystatin C levels of 1.45 ± 0.53 (0.42-3.48) mg/l. This correlated moderately with creatinine (r = -0.61, P < .001) and cystatin C (r = -0.52, P < .001). Using linear regression techniques, it was found that creatinine, cystatin C, gender and age only explained 52% of GFR total variance. All equations overestimated GFR, with a mean bias of +11.1 ml/min/1.73 m2 for MDRD, + 16.4 ml/min/1.73 m2 for 2009-CKD-EPI, +15 ml/min/1.73m2 for CKD-EPI with cystatin C, and +14.1 ml/min/1.73 m2 for 2012-CKD-EPI with creatinine and cystatin C. eGFR by MDRD and the 2009 CKD-EPI equation correlated better with 51Cr-EDTA than CKD-EPI with creatinine and/or cystatin C. The overestimations were negatively correlated with creatinine and cystatin C levels, most significantly for CKD-EPI with creatinine and/or cystatin C when GFR was greater than 60 ml/min/1.73 m2. CONCLUSIONS: The 2012 CKD-EPI equations with creatinine and/or cystatin C significantly overestimate GFR in stage 1 and 2 chronic kidney disease. The MDRD equations is therefore recommended in these cases. The reference method used to measure GFR seems to heavily influence the bias of the equations

Comparison of MDRD and the old CKD-EPI equations with the new CKD-EPI equations in kidney transplant patients when glomerular filtration rate is measured with 51Cr-EDTA. / Comparación de las ecuaciones MDRD y de las antiguas ecuaciones CKD-EPI frente a las nuevas ecuaciones CKD-EPI en pacientes con trasplante renal cuando se emplea 51Cr-EDTA para medir el filtrado glomerular.

BACKGROUND: When estimating the glomerular filtration rate (GFR) in kidney transplant patients, significant differences have been found between MDRD and the 2009 CKD-EPI equations, and reference techniques. OBJECTIVE: To analyse and compare the performance of MDRD and the 2009 and 2012 CKD-EPI equations against 51Cr-EDTA plasma clearance in measuring GFR in 270 kidney transplant patients after one year. RESULTS: The mean measured GFR was 43.0±11.4 (18.2-79.4)ml/min/1.73m2, with creatinine levels of 1.42±0.46 (0.60-4.33)mg/dl and cystatin C levels of 1.45±0.53 (0.42-3.48)mg/l. This correlated moderately with creatinine (r=-0.61, P<.001) and cystatin C (r=-0.52, P<.001). Using linear regression techniques, it was found that creatinine, cystatin C, gender and age only explained 52% of GFR total variance. All equations overestimated GFR, with a mean bias of +11.1ml/min/1.73m2 for MDRD, +16.4ml/min/1.73m2 for 2009-CKD-EPI, +15ml/min/1.73m2 for CKD-EPI with cystatin C, and +14.1ml/min/1.73m2 for 2012-CKD-EPI with creatinine and cystatin C. eGFR by MDRD and the 2009 CKD-EPI equation correlated better with 51Cr-EDTA than CKD-EPI with creatinine and/or cystatin C. The overestimations were negatively correlated with creatinine and cystatin C levels, most significantly for CKD-EPI with creatinine and/or cystatin C when GFR was greater than 60ml/min/1.73m2. CONCLUSIONS: The 2012 CKD-EPI equations with creatinine and/or cystatin C significantly overestimate GFR in stage 1 and 2 chronic kidney disease. The MDRD equations is therefore recommended in these cases. The reference method used to measure GFR seems to heavily influence the bias of the equations.

Effect of paricalcitol on mineral bone metabolism in kidney transplant recipients with secondary hyperparathyroidism.

INTRODUCTION: Secondary hyperparathyroidism is highly prevalent in kidney transplant recipients, and commonly results in hypercalcaemia; an association to osteopenia and bone fractures has also been observed. Paricalcitol has proved effective to control secondary hyperparathyroidism in chronic kidney disease in both dialysed and non-dialysed patients, with a low hypercalcaemia incidence. Currently available experience on paricalcitol use in kidney transplant recipients is scarce. Our main aim was to show the effect of paricalcitol on mineral bone metabolism in kidney transplant recipients with secondary hyperparathyroidism. MATERIAL AND METHODS: A retrospective multicentre study in kidney transplant recipients aged>18 years with a 12-month or longer post-transplantation course, stable renal function, having received paricalcitol for more than 12 months, with available clinical follow-up for a 24-month period. RESULTS: A total of 69 patients with a 120 ± 92-month post-transplantation course were included. Baseline creatinine was 2.2 ± 0.9 mg/dl y GFR-MDRD was 36 ± 20 ml/min/1.73 m(2). Paricalcitol doses were gradually increased during the study: baseline 3.8 ± 1.9 µg/week, 12 months 5.2 ± 2.4 µg/week; 24 months 6.0 ± 2.9 µg/week (P<.001). Serum PTH levels showed a significant fast decline: baseline 288 ± 152 pg/ml; 6 months 226 ± 184 pg/ml; 12 months 207 ± 120; 24 months 193 ± 119 pg/ml (P<.001). Reduction from baseline PTH was ≥30% in 42.4% of patients at 12 months y in 65.2% of patients at 24 months. Alkaline phosphatase showed a significant decrease in first 6 months followed by a plateau: baseline 92 ± 50 IU/l; 6 months 85 ± 36 IU/l, 12 months 81 ± 39 IU/l (P<.001). Overall, no changes were observed in serum calcium and phosphorus, and in urine calcium excretion. PTH decline was larger in patients with higher baseline levels. Patients with lower baseline calcium levels showed significantly increased levels (mean increase was 0.5-0.6 mg/dl) but still within normal range, whereas patients with baseline calcium>10mg/dl showed gradually decreasing levels. Fifteen (21.7%) patients had received prior calcitriol therapy. When shifted to paricalcitol, such patients required paricalcitol doses significantly larger than those not having received calcitriol. Paricalcitol was used concomitantly to cinacalcet in 11 patients with significant PTH reductions being achieved; clinical course was similar to other patients and paricalcitol doses were also similar. CONCLUSIONS: Paricalcitol is an effective therapy for secondary hyperparathyroidism in kidney transplant recipients. Overall, no significant changes were observed in calcium and phosphorus levels or urinary excretion. Patients having previously received calcitriol required higher paricalcitol doses. When used in patients receiving cinacalcet, paricalcitol results in a significant PTH fall, with paricalcitol doses being similar to those used in patients not receiving cinacalcet.

Efecto de paricalcitol sobre el metabolismo mineralóseo en pacientes trasplantados renales con hiperparatiroidismo secundario / Effect of paricalcitol on mineral bone metabolism in kidney transplant recipients with secondary hyperparathyroidism

Introducción: El hiperparatiroidismo secundario es muy prevalente en pacientes trasplantados renales. Cursa con frecuencia con hipercalcemia y se ha asociado al desarrollo de osteopenia y fracturas óseas. El paricalcitol ha mostrado su eficacia en el control del hiperparatiroidismo secundario en la enfermedad renal crónica con y sin diálisis, con una baja incidencia de hipercalcemia. La experiencia con paricalcitol en trasplantados renales es muy escasa. El objetivo de este trabajo fue mostrar el efecto sobre el metabolismo mineralóseo del paricalcitol en trasplantados renales con hiperparatiroidismo secundario. Material y métodos: Estudio retrospectivo multicéntrico con trasplantados renales de más de 18 años de edad y más de 12 meses de evolución postrasplante, con función renal estable, que hayan sido tratados con paricalcitol durante más de 12 meses, con seguimiento clínico hasta los 24 meses de tratamiento. Resultados: Se incluyó a 69 pacientes, con 120±92 meses postrasplante, con creatinina inicial de 2,2±0,9mg/dl y FG-MDRD 36±20ml/min/1,73 m2. La dosis de paricalcitol se incrementó progresivamente durante el estudio: basal 3,8±1,9μg/semana, 12 meses 5,2±2,4μg/semana; 24 meses 6,0±2,9μg/semana (p<0,001). Los niveles séricos de PTH descendieron de forma rápida y significativa: basal 288±152 pg/ml; 6 meses 226±184 pg/ml; 12 meses 207±120; 24 meses 193±119 pg/ml (p<0,001). Observamos una reducción sobre PTH basal ≥30% en el 42,4% de los pacientes a los 12 meses y en el 65,2% de los pacientes a los 24 meses. La fosfatasa alcalina descendió también significativamente en los 6 primeros meses para luego estabilizarse: basal 92±50 UI/l; 6 meses 85±36 UI/l, 12 meses 81±39 UI/l (p<0,001). Globalmente no hubo modificaciones en el calcio o fósforo séricos ni en la excreción urinaria de calcio. La reducción de PTH fue más importante en trasplantados con niveles séricos más elevados de partida. Observamos que los pacientes con calcio basal más bajo mostraron un incremento significativo de sus cifras de 0,5-0,6 mg/dl en promedio aunque manteniéndose en rango de normalidad, mientras que pacientes con calcio basal > 10 mg/dl mostraron una reducción progresiva de sus cifras. Quince (21,7%) pacientes seguían tratamiento previo con calcitriol y al cambiarlos a paricalcitol precisaron dosis significativamente mayores que los pacientes que no habían recibido calcitriol. El paricalcitol fue asociado a cinacalcet en 11 pacientes, con reducciones significativas de PTH, con evolución similar al resto de la población y con dosis de paricalcitol también similares. Conclusiones: Paricalcitol es eficaz en el tratamiento del hiperparatiroidismo secundario de trasplantados renales. Globalmente no observamos modificaciones significativas de los niveles de calcio ni de fósforo, ni en su excreción urinaria. Los pacientes en tratamiento previo con calcitriol precisaron dosis mayores de paricalcitol. Cuando el paricalcitol se administra a pacientes tratados con cinacalcet, se observa un descenso significativo de la PTH con dosis de paricalcitol similar a pacientes sin cinacalcet (AU)

Introduction: Secondary hyperparathyroidism is highly prevalent in kidney transplant recipients, and commonly results in hypercalcaemia; an association to osteopenia and bone fractures has also been observed. Paricalcitol has proved effective to control secondary hyperparathyroidism in chronic kidney disease in both dialysed and non-dialysed patients, with a low hypercalcaemia incidence. Currently available experience on paricalcitol use in kidney transplant recipients is scarce. Our main aim was to show the effect of paricalcitol on mineral bone metabolism in kidney transplant recipients with secondary hyperparathyroidism. Material and methods: A retrospective multicentre study in kidney transplant recipients aged > 18 years with a 12-month or longer post-transplantation course, stable renal function, having received paricalcitol for more than 12 months, with available clinical follow-up for a 24-month period. Results: A total of 69 patients with a 120 ± 92-month post-transplantation course were included. Baseline creatinine was 2.2 ± 0.9 mg/dl y GFR-MDRD was 36 ± 20 ml/min/1.73m2. Paricalcitol doses were gradually increased during the study: baseline 3.8 ± 1.9 g/week, 12 months 5.2 ± 2.4 g/week; 24 months 6.0 ± 2.9 g/week (P<.001). Serum PTH levels showed a significant fast decline: baseline 288 ± 152 pg/ml; 6 months 226 ± 184 pg/ml; 12 months 207 ± 120; 24 months 193 ± 119 pg/ml (P<.001). Reduction from baseline PTH was ≥30% in 42.4% of patients at 12 months y in 65.2% of patients at 24 months. Alkaline phosphatase showed a significant decrease in first 6 months followed by a plateau: baseline 92 ± 50 IU/l; 6 months 85 ± 36 IU/l, 12 months 81 ± 39 IU/l (P<.001). Overall, no changes were observed in serum calcium and phosphorus, and in urine calcium excretion. PTH decline was larger in patients with higher baseline levels. Patients with lower baseline calcium levels showed significantly increased levels (mean increase was 0.5-0.6 mg/dl) but still within normal range, whereas patients with baseline calcium > 10 mg/dl showed gradually decreasing levels. Fifteen (21.7%) patients had received prior calcitriol therapy. When shifted to paricalcitol, such patients required paricalcitol doses significantly larger than those not having received calcitriol. Paricalcitol was used concomitantly to cinacalcet in 11 patients with significant PTH reductions being achieved; clinical course was similar to other patients and paricalcitol doses were also similar. Conclusions: Paricalcitol is an effective therapy for secondary hyperparathyroidism in kidney transplant recipients. Overall, no significant changes were observed in calcium and phosphorus levels or urinary excretion. Patients having previously received calcitriol required higher paricalcitol doses. When used in patients receiving cinacalcet, paricalcitol results in a significant PTH fall, with paricalcitol doses being similar to those used in patients not receiving cinacalcet (AU)

Evaluación global subjetiva y escala de malnutrición-inflamación para valorar el estado nutricional de pacientes en diálisis peritoneal con hipoalbuminemia / Subjective global assessment and malnutritioninflammation scale to assess the nutritional status of patients on peritoneal dialysis with hypoalbuminaemia

Los pacientes con insuficiencia renal crónica en diálisis peritoneal con frecuencia están mal nutridos o en riesgo de desnutrición, por sus especiales características y favorecido por múltiples factores, como otras patologías asociadas, diálisis inadecuada, estado inflamatorio, pérdida de nutrientes por el dializado, etc. Se han descrito numerosos métodos para evaluar el estado nutricional, siendo las medidas antropométricas y determinaciones de laboratorio las más utilizadas, pero cuando las aplicamos a pacientes renales los resultados obtenidos son muy variables, además algunos de ellos plantean problemas a la hora de su aplicación, por las especiales características de los pacientes en diálisis. Una forma de prevenir la malnutrición es identificar a aquellos pacientes en riesgo de desnutrición y evitar su deterioro progresivo. Nuestro objetivo, es evaluar el estado nutricional de los pacientes en diálisis peritoneal con hipoalbuminemia. Hemos seleccionado 21 pacientes con más de 3 meses en diálisis peritoneal y con tendencia a tener hipoalbuminemia < 3,6 g/ dl. Hemos evaluado su estado nutricional mediante la escala de evaluación global subjetiva y escala de malnutrición-inflamación. Hemos encontrado que la mayoría de los pacientes presentan bajo riesgo de malnutrición estimado tanto por la evaluación global subjetiva donde el 85,7% tienen bajo riesgo de malnutrición o estado de nutrición normal y por la escala de malnutrición-inflamación igualmente el 85% tienen un estado de nutrición normal. Por tanto, debemos utilizar la combinación de varios métodos para evaluar adecuadamente el estado nutricional e identificar aquellos con riesgo de malnutrición (AU)

Patients with chronic renal deficiency on peritoneal dialysis are often poorly nourished or at risk of malnutrition due to their special characteristics, and this is exacerbated by a range of factors, including other associated pathologies, unsuitable dialysis, inflammatory state, loss of nutrients due to the dialysate, etc. Numerous methods for assessing nutritional status have been described, among which anthropometric measurements and laboratory determinations are the most widely-used. However, when these are applied to renal patients the results obtained are highly variable, and moreover problems arise with putting some of them into practice, due to the special features of dialysis patients. One way of preventing malnutrition is to identify the patients at risk and avoid their gradual deterioration. The aim here is to assess the nutritional status of patients on peritoneal dialysis with hypoalbuminaemia. We selected 21 patients with over 3 months on peritoneal dialysis and with a tendency to suffer hypoalbuminaemia < 3.6g/dl. We appraised their nutritional status using the subjective overall assessment scale and the malnutritioninflammation scale. We found that most patients had a low estimated risk of malnutrition according to both the subjective global assessment where 85.7% had a low risk of malnutrition or a normal nutritional status and the malnutrition-inflammation scale, which likewise gave 85% with a normal nutritional status. We must therefore use a combination of different methods to properly assess nutritional status and identify those at risk of malnutrition (AU)

Interpretación del aumento de peso tras un suplemento nutricional en diálisis peritoneal: a propósito de dos casos / No disponible

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Púrpura trombótica trombocitopénica y endometriosis ovárica / Thrombocytopenic thrombotic purpura and ovaric endometriosis

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