Renal calcium, phosphorus, magnesium and uric acid handling: comparison between stage III chronic kidney disease patients and healthy oldest old

Abstract

Serum levels and FE of calcium, phosphorus, magnesium and uric acid were significantly higher in CKD patients compared to healthy very old people with similar GFR, except for serum magnesium and FE of uric acid, which were similar in both groups.

Association between allopurinol and mortality among Japanese hemodialysis patients: results from the DOPPS

“…Hyperuricemia has been consistently associated with cardiovascular disease (CVD) [1] and with other CVD risk factors, such as hypertension, chronic kidney disease (CKD), and metabolic syndrome [2–4]. Furthermore, hyperuricemia is a risk factor for acute kidney injury in patients undergoing cardiovascular surgery such that when uric acid levels were decreased using rasburicase prior to cardiovascular (CV) surgery in patients with GFR <45 mL/min/1.73 m 2 , subsequent risk of acute kidney injury and markers of renal tubular injury were significantly lower versus hyperuricemic patients not receiving rasburicase [5].…”

Impact of renal aging on drug therapy

“…Serum calcium and magnesium levels and their urinary fractional excretion are similar in the healthy young, old and very old [6,36]. However, since elderly people usually have low vitamin D diet, reduced sun light exposure, decreased renal vitamin D hydroxylation (activation), poor calcium intestinal absorption and low serum levels of sexual hormones, they have a tendency to develop calcium metabolism disorders [36,37].…”

“…However, since elderly people usually have low vitamin D diet, reduced sun light exposure, decreased renal vitamin D hydroxylation (activation), poor calcium intestinal absorption and low serum levels of sexual hormones, they have a tendency to develop calcium metabolism disorders [36,37]. Even though magnesium renal reabsorption is preserved in old and very old people, magnesium urine excretion is significantly increased in volume expansion.…”

“…Even though magnesium renal reabsorption is preserved in old and very old people, magnesium urine excretion is significantly increased in volume expansion. Further, elderly people often need magnesium supplements probably due to a combination of diminished spontaneous intake of magnesium, and poor intestinal absorption [6,36,37]. Because of the divalent cations handling characteristics in the elderly mentioned above, hypocalcemia can easily be induced by loop diuretics, and hypomagnesemia by thiazides, cisplatin, amphotericin, aminoglycosides and calcineurin inhibitors (cyclosporine and tacrolimus) in this population [35][36][37][38].…”

Hiperfosfatemia en la enfermedad renal crónica: incrementar la excreción renal de fósforo tal vez sea la clave para su tratamiento

“…), b) reducir el pasaje del fósforo del compartimiento óseo al plasmático (bifosfonatos, control del hiperparatiroidismo secundario, etc. ), c) incrementar la excreción corporal de fósforo, ya sea por vía urinaria o dialítica 1,2 .Con respecto a la estrategia de incrementar la excreción urinaria de fósforo, es precisamente el mecanismo que, en general, preserva al paciente enfermo renal crónico de presentar hiperfosfatemia hasta aproximadamente el final del estadio IIIb de su enfermedad (tasa de filtrado glomerular: 30 ml/min/1,73 m²), donde, merced al progresivo incremento de la excreción fraccional de fósforo, estimulado en parte por el ascenso sérico de la parathormona, la excreción fraccional de fósforo puede pasar de un 9 ± 05 %, en personas sanas, a un 25 ± 0,9 % en pacientes insuficientes renales crónicos estadio III, hasta un 40 ± 09 % en nefrópatas crónicos estadío V 3,4 .Sin embargo, suele ocurrir en estadios avanzados de insuficiencia renal crónica (estadios IV y V) que, pese a que sigue aumentando la excreción fraccional de fósforo en orina, su magnitud no alcanza para evitar que, a tales niveles de reducción de filtrado glomerular (tasa de filtrado glomerular ˂ 30 ml/min/ 1.73 m²), no se produzca hiperfosfatemia. Resulta entonces que, dada la escasa dializancia del fósforo, poder incrementar farmacológicamente la excreción tubular de fósforo a fin de combatir la hiperfosfatemia sería de suma utilidad no solo en la enfermedad renal crónica avanzada (estadios IV y V), sino además en el paciente en diálisis crónica con significativa diuresis residual.…”