Epidemiología de la hiperpotasemia en la enfermedad renal crónica / Epidemiology of hyperkalemia in chronic kidney disease

ANTECEDENTES: La hiperpotasemia constituye un importante desequilibrio electrolítico en la enfermedad renal crónica (ERC). Los inhibidores del sistema renina-angiotensina-aldosterona (iSRAA) tienen propiedades beneficiosas cardiorrenales, aunque son causa importante de hiperpotasemia. OBJETIVO: Examinar la prevalencia de la hiperpotasemia en la ERC, identificar factores asociados a su aparición y la relación entre hiperpotasemia y mortalidad. PACIENTES Y MÉTODOS: Estudio observacional retrospectivo en pacientes con ERC en el período 1971-2017. La población se categorizó en 3 grupos: grupo 1, pacientes con ERC sin tratamiento renal sustitutivo; grupo 2, pacientes en hemodiálisis, y grupo 3, pacientes en diálisis peritoneal continua ambulatoria. RESULTADOS: Se evaluó a 2.629 pacientes. La prevalencia observada en los distintos grupos fue del 9,6, el 16,4 y el 10,6%, respectivamente. Los factores de riesgo relacionados con la aparición de hiperpotasemia en el grupo de ERC fueron la tasa de filtrado glomerular (FG) (p < 0,001), la creatinina plasmática (p < 0,001), el sodio plasmático (p < 0,001), la hemoglobina (p = 0,028), la presión arterial diastólica (p = 0,012), la ingesta de inhibidores de la enzima de conversión de la angiotensina o antagonistas de receptores de angiotensina II (p = 0,008), el tratamiento con metformina (p < 0,001) y la diabetes (p = 0,045). El tratamiento con iSRAA incrementó de forma relevante la hiperpotasemia a medida que disminuía el FG, así como en pacientes con diabetes o insuficiencia cardiaca. CONCLUSIONES: La hiperpotasemia es una alteración metabólica frecuente en pacientes con ERC que aumenta en presencia de fármacos con propiedades beneficiosas cardiorrenales (iSRAA), por lo que en muchos casos los pacientes pierden el beneficio asociado a estos fármacos. Nuevos compuestos no absorbibles de reciente aparición, que se unen al potasio en el tracto gastrointestinal potenciando su excreción fecal, manteniendo el beneficio cardiorrenal de los iSRAA, pudieran ser relevantes en la evolución de los pacientes con ERC

BACKGROUND: Hyperkalaemia is a significant electrolyte imbalance in chronic kidney disease (CKD). Renin-angiotensin-aldosterone system inhibitors (RAASi) have beneficial cardio-renal properties, although they can often cause hyperkalaemia. OBJECTIVE: To examine the prevalence of hyperkalaemia in CKD, identify factors associated with its appearance and the relationship between hyperkalaemia and mortality. PATIENTS AND METHODS: Retrospective observational study on patients with CKD in the period 1971-2017. The population was categorised into 3 groups: Group 1, patients with CKD without renal replacement therapy; Group 2, patients on haemodialysis; and Group 3, patients on continuous ambulatory peritoneal dialysis. RESULTS: A total of 2,629 patients were evaluated. The prevalence observed in the different groups was: 9.6%, 16.4% and 10.6%, respectively. Risk factors related to the appearance of hyperkalaemia in the CKD group were glomerular filtration rate (GFR) (P<.001), plasma creatinine (P<.001), plasma sodium (P<.001), haemoglobin (P=.028), diastolic blood pressure (P=.012), intake of ACE inhibitors and/or angiotensin II receptor blockers (P=.008), treatment with metformin (P<.001) and diabetes (P=.045). Treatment with RAASi significantly increased hyperkalaemia as GFR decreased, as well as in patients with diabetes or heart failure. CONCLUSIONS: Hyperkalaemia is a frequent metabolic alteration in CKD patients that increases in the presence of drugs with beneficial cardio-renal properties (RAASi), which means that patients often lose the benefit associated with these drugs. New, recently-appearing non-absorbable compounds, which bind to potassium in the gastrointestinal tract, enhancing faecal excretion and thus maintaining the cardio-renal benefit of the RAASi, could be relevant in the progress of patients with CKD

Epidemiology of hyperkalemia in chronic kidney disease. / Epidemiología de la hiperpotasemia en la enfermedad renal crónica.

BACKGROUND: Hyperkalaemia is a significant electrolyte imbalance in chronic kidney disease (CKD). Renin-angiotensin-aldosterone system inhibitors (RAASi) have beneficial cardio-renal properties, although they can often cause hyperkalaemia. OBJECTIVE: To examine the prevalence of hyperkalaemia in CKD, identify factors associated with its appearance and the relationship between hyperkalaemia and mortality. PATIENTS AND METHODS: Retrospective observational study on patients with CKD in the period 1971-2017. The population was categorised into 3groups: Group 1, patients with CKD without renal replacement therapy; Group 2, patients on haemodialysis; and Group 3, patients on continuous ambulatory peritoneal dialysis. RESULTS: A total of 2,629 patients were evaluated. The prevalence observed in the different groups was: 9.6%, 16.4% and 10.6%, respectively. Risk factors related to the appearance of hyperkalaemia in the CKD group were glomerular filtration rate (GFR) (P<.001), plasma creatinine (P<.001), plasma sodium (P<.001), haemoglobin (P=.028), diastolic blood pressure (P=.012), intake of ACE inhibitors and/or angiotensin ii receptor blockers (P=.008), treatment with metformin (P<.001) and diabetes (P=.045). Treatment with RAASi significantly increased hyperkalaemia as GFR decreased, as well as in patients with diabetes or heart failure. CONCLUSIONS: Hyperkalaemia is a frequent metabolic alteration in CKD patients that increases in the presence of drugs with beneficial cardio-renal properties (RAASi), which means that patients often lose the benefit associated with these drugs. New, recently-appearing non-absorbable compounds, which bind to potassium in the gastrointestinal tract, enhancing faecal excretion and thus maintaining the cardio-renal benefit of the RAASi, could be relevant in the progress of patients with CKD.

Markers of inflammation before and during peritoneal dialysis.

In this study, we compared changes in inflammatory markers-C-reactive protein (CRP), pentraxin 3 (PTX3), serum component of amyloid A (SAA), and procalcitonin (PCT)-in 182 subjects: 69 from the general population (GP), 47 with CKD, 19 with an implanted intra-abdominal catheter for peritoneal dialysis ("prePD"), and 47 on peritoneal dialysis (PD). These were the results [median (95% confidence interval)] for the GP CKD, prePD, and PD groups respectively: CRP: 1.40 mg/L (1.15-2.10 mg/L), 5.30 mg/L (3.04-8.06 mg/L), 3.33 mg/L (2.15-12.58 mg/L), 7.25 mg/L (4.43-15.16 mg/L). SAA: 3.10 mg/L (2.90-3.53 mg/L), 7.77 mg/L (4.17-15.83 mg/L), 7.30 mg/L (4.81-10.96 mg/L), 9.14 mg/L (5.31-23.54 mg/L). PCT: 0.028 ng/mL (0.022-0.032 ng/mL), 0.121 ng/mL (0.094-0.166 ng/mL), 0.160 ng/mL (0.090-0.277 ng/mL), 0.363 ng/mL (0.222-0.481 ng/mL). PTX3: 0.54 ng/mL (0.33-0.62 ng/mL), 0.71 ng/ mL (0.32-1.50 ng/mL), 0.56 ng/mL (0.44-1.00 ng/ mL), 1.04 ng/mL (0.65-1.56 ng/mL). After catheter insertion, CRP showed a nonsignificant declining trend that disappeared throughout PD. The behavior of SAA was similar to that of CRP and was not modified by the changes induced by the start of PD. An increase in PTX3 was observed only with PD, which may be related to a local proinflammatory state caused by PD solution. We can conclude that catheter insertion for PD does not account for most of the local inflammatory changes observed in PD patients.

Inflammation markers, chronic kidney disease, and renal replacement therapy.

Chronic kidney disease (CKD) is associated with a proinflammatory state and an excess of cardiovascular risk. In this work, we describe changes in inflammatory markers-C-reactive protein (CRP), pentraxin 3 (PTX3), serum component of amyloid A (SAA), and procalcitonin (PCT)--in CKD patients compared with a control group of subjects with a normal estimated glomerular filtration rate (eGFR). Blood samples were obtained from 69 healthy individuals (GP) and 70 end-stage CKD patients--25 not yet on dialysis, 22 on peritoneal dialysis (PD), and 23 on hemodialysis (HD). These were the results [median (95% confidence interval)] for the GP CKD, PD, and HD groups respectively: CRP: 1.40 mg/L (1.19-2.11 mg/L), 6.50 mg/L (3.57-8.32mg/L), 7.60 mg/L (2.19-22.10mg/L), 9.60 mg/L (6.62-16.38 mg/L). SAA: 3.10 mg/L (2.90-3.53 mg/L), 7.11 mg/L (3.81-15.40mg/L), 9.69 mg/L (5.07-29.47mg/L), 15.90 mg/L (6.80-37.48 mg/L). PCT: 0.03 ng/mL (0.02-0.03 ng/mL), 0.12 ng/mL (0.09-0.16 ng/mL), 0.32 ng/mL (0.20-0.46 ng/ mL), 0.79 ng/mL (0.45-0.99 ng/mL). PTX3: 0.54 ng/mL (0.33-0.62 ng/mL), 0.71 ng/ mL (0.32-1.50 ng/mL), 1.52 ng/mL (0.65-2.13 ng/mL), 1.67 ng/mL (1.05-2.27 ng/mL). Compared with levels in the GP group, levels of SAA and CRP (systemic response) were significantly higher in CKD patients on and not on dialysis. Levels of PTX3 were higher only in dialyzed patients, significantly so in those on HD (greatly different from the CRP levels). These differing levels might be related to a local reaction caused by an invasive intervention (PD or HD). As eGFR declines and with the start of renal replacement therapy, PCT increases. Levels of PCT could potentially cause confusion when these patients are being evaluated for the presence of infection, and may also demonstrate some microvascular implications of dialysis therapy.

Biliopancreatic diversion in a renal transplant patient.

Surgery is usually the only solution to modify the evolution of morbid obesity and resolve the associated co-morbidities. There is very little written regarding malabsorptive surgery and transplantation. A 48-year-old male with hypertension, hyperuricemia and obesity underwent renal transplantation in 1994 for renal amyloidosis. He was maintained on oral immunosuppressive cyclosporine. The patient developed uncontrollable hypertension, hyperlipemia, hyperglycemia and increasing weight to a BMI of 44. Thus, in December 2004, he underwent biliopancreatic diversion (BPD). After 18 months follow-up, he has lost 85% of his excess weight, and his hypertension, hyperglycemia and hyperlipemia are markedly improved. Renal function was not modified, nor were the levels of cyclosporine. He has had no complications derived from the BPD, and has a better quality of life.

Reproducibilidad del test de equilibrio peritoneal / No disponible

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