Acidose metabólica: um importante fator na etiologia da desnutrição em pacientes renais crônicos / Metabolic acidosis: an important factor in the etiology of malnutrition in chronic renal patients / La acidosis metabólica: un factor importante en la etiología de la malnutrición en los pacientes renales crónicos

A Insuficiência Renal Crônica (IRC) constitui sério problema de saúde em todo o mundo, com incidência crescente e elevada morbimortalidade, sendo que a desnutrição protéico-energética (DPE) é um importante fator que contribui para o agravamento desse quadro nosológico. Existem muitas causas que predispõem os pacientes renais crônicos à desnutrição, recentemente o papel da acidose metabólica tem sido bem-enfatizado. Desse modo, o objetivo desta revisão foi descrever os mecanismos pelos quais a acidose metabólica contribui para o catabolismo protéico nos pacientes IRC, bem como avaliar os efeitos da utilização de bicarbonato de sódio na correção da acidose e consequentemente, na redução da prevalência de desnutrição. Relatos da literatura mostram que a acidemia persistente aumenta a degradação protéica e a oxidação de aminoácidos, resultando em balanço nitrogenado negativo. Além disto, a acidose metabólica pode ocasionar resistência á insulina, supressão do hormônio do crescimento e da vitamina D, elevação do nível circulante de glicocorticóides e reduzida sensibilidade do paratormônio ao cálcio. Por outro lado, há uma escassez de estudos no que se refere aos efeitos nutricionais da correção da acidose metabólica. No entanto, as evidências encontradas demonstram que a monitoração do bicarbonato sérico e a manutenção dos seus níveis em valores superiores a 22 mmol/L (correção da acidose metabólica) deveriam ser o objetivo na conduta de pacientes renais crônicos, na tentativa de minimizar os efeitos deletéricos sobre o estado nutricional.

The Chronic Renal Failure (CRF) is a serious health problem worldwide, with increasing incidence and high mortality, and the protein-energy malnutrition (EPD) is an important contributing factor to the aggravation of this nosological. There are many causes that predispose CRF patients with malnutrition, recently the role of metabolic acidosis has been well-emphasized. Thus, the purpose of this review was to describe the mechanisms by which acidosis contributes to the protein catabolism in patients IRC, as well as evaluating the effects of using sodium bicarbonate in correcting acidosis and consequently in reducing the prevalence of malnutrition. Medical reports show that the persistent acidemia increases protein degradation and amino acid oxidation, resulting in negative nitrogen balance. Moreover, metabolic acidosis can lead to insulin resistance, suppression of growth hormone and vitamin D, elevated circulating level of glucocorticoids and reduced sensitivity of parathyroid calcium. On the other hand, there is a paucity of studies regarding the effects of nutritional correction of metabolic acidosis. However, the evidence found shows that monitoring of serum bicarbonate levels and maintenance of its values in excess of 22 mmol/L (correction of metabolic acidosis) should be the goal in treating patients with chronic renal failure in an attempt to minimize the deleterious effects on nutritional status.

La insuficiencia renal crónica (IRC) es un grave problema de salud en todo el mundo, con una incidencia y elevada mortalidad y la malnutrición proteico-energética (EPD) es un factor importante que contribuye a la agravación de esta nosológica. Hay muchas causas que predisponen a los pacientes con IRC con la desnutrición, recientemente el papel de la acidosis metabólica ha sido así-subrayó. Así, el objetivo de esta revisión fue describir los mecanismos por los que la acidosis contribuye al catabolismo proteico en los pacientes con IRC, así como la evaluación de los efectos de sodio con bicarbonato en corregir la acidosis y en consecuencia en la reducción de la prevalencia de la desnutrición. Los informes médicos muestran que la acidemia persistente aumento de la degradación de proteínas y la oxidación de aminoácidos, lo que resulta en balance negativo de nitrógeno. Por otra parte, la acidosis metabólica puede llevar a la resistencia a la insulina, la supresión de la hormona del crecimiento y la vitamina D, elevado nivel de circulación de los glucocorticoides y sensibilidad reducida de calcio paratiroides. Por otro lado, hay una escasez de estudios sobre los efectos de la corrección de la acidosis metabólica nutricional. Sin embargo, la evidencia encontrada muestra que la vigilancia de los niveles séricos de bicarbonato y el mantenimiento de sus valores por encima de 22 mmol/L (corrección de la acidosis metabólica) debería ser el objetivo en el tratamiento de pacientes con insuficiencia renal crónica en un intento de minimizar los efectos nocivos sobre el estado nutricional.

Tratamiento de pacientes pediátricos con diagnóstico de desnutrición grave de acuerdo a resultados de estudio metabólico renal / Treatment of paediatric patients with diagnosis of serious malnutrition of agreement to results of metabolic renal study

El objetivo del presente estudio fue realizar pruebas metabólicas renales a niños desnutridos graves hospitalizados, las cuales sirvieron de guía en el tratamiento de estos pacientes. La investigación fue de tipo experimental (terapéutica), se evaluaron 176 pacientes entre febrero 2002-2004. Edad entre 6 meses y 5 años, desnutrición grave primaria, ambos sexos, con acidosis metabólica, hipercloremia y anión gap urinario positivo. A los 85 restantes se les realizó estudio metabólico inicial resultando 30 con acidosis metabólica hiperclorémica y anión gap urinario positivo. A estos se les realizó prueba de sobrecarga con bicarbonato al 5 porciento y se dividieron en dos grupos: los primeros 15 tratados de acuerdo a los resultados del estudio, y los segundo 15 que recibío el tratamiento convencional. Resultados: El grupo de edad mas frecuente fueron los lactantes con distribución similar para ambos sexos. La acidosis metabólica se observó en 35,2 por ciento de la muestra evaluada. 40 por ciento luego de la prueba de sobrecarga en bicarbonato al 5 porciento resultó con acidosis tubular renal distal, con incidencia significativa (p<0.0001). 66.7 por ciento presentó hipercalciuria: 50 por ciento hiperuricosuria y 40 por ciento ambas alteraciones. La diferencia del promedio de peso entre el ingreso y egreso fue estadísticamente significativa en ambos grupos. La diferencia del valor medio de la albúmina sérica el egreso entre los pacientes tratados según resultados y tratamiento convencional fue significativa (p<0.05). El valor medio de los días de hospitalización fue de 17.3 días en los tratados y 20.4 en los no tratados, con un ahorro de 624.175,80 bolivares por cada paciente. Discusión y Conclución: La acidosis metabólica es frecuente en la desnutrición infantil grave, la cual, de acuerdo a los resultados observados obedece a una disfunción tubular renal distal.

Metabolic assessment in patients with urinary lithiasis

INTRODUCTION: Metabolic investigation in patients with urinary lithiasis is very important for preventing recurrence of disease. The objective of this work was to diagnose and to determine the prevalence of metabolic disorders, to assess the quality of the water consumed and volume of diuresis as potential risk factors for this pathology. PATIENTS AND METHODS: We studied 182 patients older than 12 years. We included patients with history and/or imaging tests confirming at least 2 stones, with creatinine clearance > 60 mL/min and negative urine culture. The protocol consisted in the collection of 2, 24-hour urine samples, for dosing Ca, P, uric acid, Na, K, Mg, Ox and Ci, glycemia and serum levels of Ca, P, Uric acid, Na, K, Cl, Mg, U and Cr, urinary pH and urinary acidification test. RESULTS: 158 patients fulfilled the inclusion criteria. Among these, 151 (95.5 percent) presented metabolic changes, with 94 (62.2 percent) presenting isolated metabolic change and 57 (37.8 percent) had mixed changes. The main disorders detected were hypercalciuria (74 percent), hypocitraturia (37.3 percent), hyperoxaluria (24.1 percent), hypomagnesuria (21 percent), hyperuricosuria (20.2 percent), primary hyperparathyroidism (1.8 percent) secondary hyperparathyroidism (0.6 percent) and renal tubular acidosis (0.6). CONCLUSION: Metabolic change was diagnosed in 95.5 percent of patients. These results warrant the metabolic study and follow-up in patients with recurrent lithiasis in order to decrease the recurrence rate through specific treatments, modification in alimentary and behavioral habits.

Study of urinary acidification in patients with idiopathic hypocitraturia

Hypocitraturia (HCit) is one of the most remarkable features of renal tubular acidosis, but an acidification defect is not seen in the majority of hypocitraturic patients, whose disease is denoted idiopathic hypocitraturia. In order to assess the integrity of urinary acidification mechanisms in hypocitraturic idiopathic calcium stone formers, we studied two groups of patients, hypocitraturic (HCit, N = 21, 39.5 + or - 11.5 years, 11 females and 10 males) and normocitraturic (NCit, N = 23, 40.2 + or - 11.7 years, 16 females and 7 males) subjects, during a short ammonium chloride loading test lasting 8 h. During the baseline period HCit patients showed significantly higher levels of titratable acid (TA). After the administration of ammonium chloride, mean urinary pH (3rd to 8th hour) and TA and ammonium excretion did not differ significantly between groups. Conversely, during the first hour mean urinary pH was lower and TA and ammonium excretion was higher in HCit. The enhanced TA excretion by HCit during the baseline period and during the first hour suggests that the phosphate buffer mechanism is activated. The earlier response in ammonium excretion by HCit further supports other evidence that acidification mechanisms react promptly. The present results suggest that in the course of lithiasic disease, hypocitraturia coexists with subtle changes in the excretion of hydrogen ions in basal situations

Effect of thyroparathyroidectomy on urinary acidification in diabetic rats

In previous studies we have shown stimulation of renal acid excretion in the proximal tubules of rats with diabetes of short duration, with no important alterations in glomerular hemodynamics; on the other hand, in thyroparathyroidectomized rats (TPTX model), a significant decrease in renal acid excretion, glomerular filtration rate (GFR) and renal plasma flow (RPF) was detected. Since important changes in the parathyroid hormone-vitamin D-Ca axis are observed in the diabetic state, the present study was undertaken to investigate the renal repercussions of thyroparathyroidectomy in rats previously made diabetic by streptozotocin (45 mg/kg). Four to 6 days after the induction of diabetes (DM), a group of rats were thyroparathyroidectomized (DM + TPTX). Renal functional parameters were evaluated by measuring the inulin and sodium para-aminohippurate clearance on the tenth day. The decrease in the GFR and RPF observed in TPTX was not reversed by diabetes since the same alterations were observed in DM + TPTX. Net acid (NA) excretion was unchanged in DM (6.19 ± 0.54), decreased in TPTX (3.76 ± 0.25) and returned to normal levels in DM + TPTX (5.54 ± 0.72) when compared to the control group (6.34 ± 0.14 µmol min-1 kg-1). The results suggest that PTH plays an important vasodilator role regarding glomerular hemodynamics, since in its absence the impairment in GFR and RPF was not reversed by the diabetic state. However, with respect to acid excretion, the presence of diabetes was able to overcome the negative stimulus represented by TPTX

Effect of metabolic acidosis on renal tubular sodium handling in rats as determined by lithium clearance

Systemic metabolic acidosis is known to cause a decrease in salt and water reabsorption by the kidney. We have used renal lithium clearance to investigate the effect of chronic, NH4Cl-induced metabolic acidosis on the renal handling of Na+ in male Wistar-Hannover rats (200-250 g). Chronic acidosis (pH 7.16 ñ 0.13) caused a sustained increase in renal fractional Na+ excretion (267.9 ñ 36.4 per cent), accompanied by an increase in fractional proximal (113.3 ñ 3.6 per cent) and post-proximal (179.7 ñ 20.2 per cent) Na+ and urinary K+ (163.4 ñ 5.6 per cent) excretion when compared to control and pair-fed rats. These differences occurred in spite of an unchanged creatinine clearance and Na+ filtered load. A lower final body weight was observed in the acidotic (232 ñ 4.6 g) and pair-fed (225 ñ 3.6 g) rats compared to the controls (258 ñ 3.7 g). In contrast, there was a significant increase in the kidney weights of acidotic rats (1.73 ñ 0.05 g) compared to the other experimental groups (control, 1.46 ñ 0.05 g; pair-fed, 1.4 ñ 0.05 g). We suggest that altered renal Na+ and K+ handling in acidotic rats may result from a reciprocal relationship between the level of metabolism in renal tubules and ion transport.

Metabolic acidosis and urinary acidification defect during the course of hemorrhagic fever with renal syndrome

To evaluate urinary acidification defect and its contribution to metabolic acidosis (MA) during hemorrhagic fever with renal syndrome (HFRS), we serially analyzed acid-base balance and urinary acidification indices in 10 HFRS patients. Data of the patients were compared with those of 8 normal volunteers (NC). MA was observed in 6 of 8 patients in the oliguric phase, 5 of 7 in the early diuretic phase, 8 of 10 in the late diuretic phase and 2 of 9 in the convalescent phase. HFRS patients with MA had a higher plasma anion gap in the oliguric and early diuretic phases than NC and a higher plasma Cl/Na ratio in the late diuretic phase than NC. As compared with acid-loaded NC, HFRS patients had a higher urine pH in the oliguric, early diuretic and late diuretic phases, a higher urine anion gap (UAG) in the oliguric and early diuretic phases and a lower urinary NH4+ excretory rate in the oliguric, early diuretic and late diuretic phases. Overt distal acidification defect was observed in 6 of 8 patients in the oliguric phase, 3 of 7 in the early diuretic phase, 5 of 10 in the late diuretic phase and none of 9 in the convalescent phase. None of the convalescent patients had latent acidification defect. In conclusion, urinary acidification defect is marked in the oliguric and diuretic phases of severe HFRS and may play a role in the development of a high anion gap (AG) metabolic acidosis in the earlier phase and hyperchloremic MA in the later phase, but rapidly recovers in the convalescent phase.