Definiciones de insuficiencia renal aguda / Definitions of acute renal failure

No existe una definición universal de insuficiencia renal aguda. Por ello hemos de distinguir desde ahora dos aspectos, el concepto o definición propiamente dicha y lo que en la literatura médica los autores definen como insuficiencia renal aguda, que no es otra cosa que los límites, generalmente referidos a subrogados del filtrado glomerular, que realmente sirven para identificar las características de los enfermos estudiados en una serie. Respecto al primer punto, el concepto o definición que aparecería en un diccionario médico, las diferencias que pueden encontrarse son matices. En cuanto al segundo que atañe a la caracterización de los enfermos incluidos en un estudio, la variabilidad es amplia (tabla I). El término insuficiencia renal aguda puede sustituirse por fallo renal agudo o falla renal aguda (Latinoamérica). La utilización como sinónimo de fracaso renal agudo, gramaticalmente es incorrecta, pero su empleo puede justificarse y se ha generalizado, al menos en España1. Problemas adicionales aparecen derivados de la posición dominante de la lengua inglesa y de la afición innata del hombre a cambiar el nombre de las cosas, sustituyendo habitualmente una palabra por otra o incluso un vocablo por una frase larga, sin que exista en realidad una necesidad de cambio conceptual, ni que los nuevos nombres aporten mayor claridad al concepto original

Definitions of acute renal failure are reviewed. Four of them are discussed with higher insight. As a whole all have in common a reference to the abrupt decrease of the renal function characterised by an increment of the nitrogenous components in blood. The review stresses the fact that acute renal fialure is a syndrome and consequently, definitions of other concepts related with and/or present in the acute renal failure setting are also given. The emerging concept of the term acute kidney injury (AKI) is reviewed. Similarly reference is made to the RIFLE and SIRE classifications. The importance of use of serum creatinine and blood urea nitrogen values as well as the methods for estimating the glomerular filtration rate in this context is analysed

Efficacy and safety of Etanercept, high-dose intravenous gammaglobulin and plasmapheresis combined therapy for lupus diffuse proliferative nephritis complicating pregnancy.

We report one case of pregnancy-onset severe diffuse proliferative nephritis in a patient with systemic lupus erythematosus (SLE), who was successfully treated with a combination of anti-tumour necrosis factor (TNF)-alpha, plasmapheresis and high-dose intravenous gammaglobulin. No flares were observed either in clinical symptoms or in laboratory examinations during pregnancy or after delivery. Her autoantibodies except fluorescent anti-nuclear antibodies were negative. We suggest that a combination of anti-TNF-alpha, plasmapheresis and high-dose intravenous gammaglobulin may be a safe and effective therapy for pregnant patients suffering severe lupus nephritis.

Haemodialysis dose, extracellular volume control and arterial hypertension.

Patients with chronic renal failure on periodical dialysis frequently are hypertensive. This frequency has increased in relation to the liberalization of diet and to short dialysis with a high sodium concentration in the dialysate. Although various factors influence the pathogenesis of this type of hypertension, volume overload is the most significant. The achievement of an optimal dry weight is still one of the most difficult and important tasks of a dialysis clinic. The reduction in extracellular volume in haemodialysis implies an improvement in dialysis tolerance. The time factor is one of the principal elements in this control, but it is possible, using other elements, to improve tolerance in 4-5 h sessions and to achieve the proper dry weight associated with normotension in most patients.

The spectrum of acute renal failure in the intensive care unit compared with that seen in other settings. The Madrid Acute Renal Failure Study Group.

Acute renal failure (ARF) is at a crossroads between nephrology and intensive care medicine. However, there seems to be wide differences between the ARF observed in the intensive care unit (ICU) compared to that observed in other areas of the hospital, particularly when examining the mortality rate. Among the ICU patients the 70% mortality rate is higher to the 50% found in an overall series of studies. Recently, Druml proposed that there is a changing trend in the clinical spectrum of ARF as a convincing reason to justify these differences. According to him, we are moving from an ARF seen as a mono-organ failure to another one observed in a multiorgan dysfunction syndrome (MODS) context. Although extremely coherent, this hypothesis has not been fully confirmed in a prospective study. In fact, most authors seem to look at the problem from opposite sides of the river, either from the critical medicine or the nephrological bank. To the best of our knowledge, only one retrospective study has dealt with this topic by comparing outcome of ARF in ICU and non-ICU patients. In this article we aim to overcome this problem by reviewing the data of the prospective epidemiological ARF study carried out in Madrid using two different approaches: (1) comparing the ARF cases observed in the ICU setting with those ARF studied outside the ICU, and (2) comparing the outcome of isolated ARF with the outcome of ARF as part of a MODS in patients treated in both settings.

Effect of zinc treatment on serum thyroid hormones in uremic patients under peritoneal dialysis.

In order to evaluate the effect of zinc (Zn) deficiency on thyroid abnormalities in chronic renal failure, a Zn supplement (100 mg/day, p.o.) was given for four weeks to eight uremic patients under peritoneal dialysis. Zn supplementation increased plasma levels of TSH (5.8 +/- 0.7 to 7.4 +/- 0.7 mU/l, p < 0.02), T4 (61.6 +/- 3.9 to 93.9 +/- 6.2 nmol/l, p < 0.01), T3 (1.31 +/- 0.14 to 1.70 +/- 0.18 nmol/l, p < 0.01) and Zn (7.23 +/- 0.45 to 12.27 +/- 0.76 mumol/l, p < 0.01). A close correlation was found between changes in plasma levels of Zn and changes in TSH (r = 0.82), T4 (r = 0.55) and T3 (r = 0.64), suggesting that Zn deficiency may play a role in the biosynthesis or release of hormones of the hypothalamic-pituitary-thyroid axis in chronic renal failure.

HbA1, height velocity and weight gain as indicators of metabolic control in type I diabetic children. A 5 year survey.

The purpose of this study was to evaluate the metabolic control of the type I diabetic patients seen from 1984 to 1988. We analyzed the results of HbA1, height velocity and weight gain. Results showed that from 1984 1985 a 90% of diabetics were in poor metabolic control with HbA1 > 11% (good control < 11%). For 1988 the percentage of poor controlled patients descended to 78%. On the other hand, these patients observed a significant decrease in height velocity and weight gain compared with diabetics with HbA1 < 11% (p < 0.005 and p < 0.001). In addition, diabetics in poor metabolic control were under 10 and 3 number percentiles of the weight and growth diagrams. Finally, we found a significant correlation between HbA1 and height velocity as well as HbA1 and weight gain (r = -0.77 and r = -0.79; p < 0.001 for both). Our results showed that a great percent of our patients were in poor metabolic control with a decreased height velocity and weight gain.

[Membranous nephritis after renal transplantation]. / Nefropatía membranosa después del trasplante renal.

8 cases of membranous glomerulonephritis (MG) after renal transplants (RT) are presented; one being a recurrence of the original disease and the other 7 due to a different cause of renal insufficiency. The total incidence of MG after transplantation was 1.63%; 1.39% being the incidence of MG of new cases. Only 1 patient showed decrease of renal function and in this case the MG was accompanied by chronic rejection lesions. There was no sign of neoplasias nor drugs producing MG. As far as chronic infections are concerned, only one patient showed B antigen and it was not observed during the immunofluorescent test in the biopsy. 6 patients had urological complications after the renal transplant (3 cases of urinary fistula; 2 cases of obstructive uropathy; 1 case of short ureter). 2 patients experienced the start of hemodialysis due to focal and segmentary glomerulosclerosis. The beginning of proteinuria commences between 2 and 23 months after the RT (median 13,0 +/- 7,5 moths); with a range of between 2.0 and 12.0 gr/day (median: 6.8 +/- 3,2 Z gr/day), this being nephrotic in 4 cases. Proteinuria improved 1 case, and persisted in the other patients at the same level registered previous to the diagnosis. MG is a non-frequent complication or RT and is usually benign. Patients with post-transplant urologic complications could be considered to have a higher risk of developing a MG "de novo".

Renal metabolism during four types of lactic acidosis in the dog including anoxia.

The present study was undertaken to evaluate the metabolic response of the kidney to lactic acidosis. Four types of lactic acidosis were induced in the dog: infusion of lactic acid, infusion of lactic acid with phenformin, administration of phenformin alone, and hypoxia by breathing 95% nitrogen. In all groups of animals, the same degree of acidosis was observed with plasma bicarbonate ranging from 12.8 to 14.9 mM. Plasma lactate concentration ranged from 3.0 to 8.1 mumol/mL. Renal ammoniagenesis failed to be influenced by lactic acidosis. As a matter of fact, it fell during anoxia. The extraction of glutamine by the kidney rose except during anoxia where it fell. The renal production of alanine rose during the infusion of lactic acid with and without phenformin. This coincided with the extraction of glutamine. The renal extraction of lactate rose in all forms of acidosis as well as the production of pyruvate. In the renal cortical tissue, the concentration of malate, pyruvate, and lactate rose. Alanine also rose except during anoxia. An important fall in cytosolic redox potential (NAD+/NADH lactate dehydrogenase) was observed, as well as a fall in mitochondrial redox (NAD+/NADH beta-hydroxybutyrate dehydrogenase). Lactate also accumulated in the liver and in the muscle. We propose that the kidney is unable to respond to lactic acidosis in terms of ammonia production and that this phenomenon is explained by transamination of pyruvate and glutamate into alanine and also by the observed fall in cytosolic redox potential. It is likely that renal gluconeogenesis is also inhibited and this is reflected by the rise in the concentration of malate in the kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

The metabolic response of the kidney to acute sodium lactate alkalosis.

In vivo studies were performed in the dog to verify if sodium lactate had an important effect on the metabolism of glutamine by the kidney. The animals were infused with 0.6 M sodium lactate to induce acute metabolic alkalosis with plasma bicarbonate of 29.7 mM. During these experiments, it was demonstrated that the renal uptake of glutamine increased by 46%, while the renal production of ammonia was unchanged. The renal production of alanine rose from 6.0 to 16.8 mumol/min. Plasma concentration of lactate increased from 1.3 to 19.2 mM, while that of pyruvate increased from 0.075 to 0.454 mM. In the renal tissue, alpha-ketoglutarate, malate, oxaloacetate, lactate, pyruvate, citrate, and alanine increased significantly. Similar changes were found in the liver and skeletal muscle. The observed changes are best described by transamination of pyruvate and glutamate under the influence of alanine aminotransferase (GPT). It can be calculated that this reaction was responsible for 76% of the production of ammonia from glutamine, the latter being necessary to provide glutamate for the synthesis of alanine. Dogs infused with 0.3 M sodium bicarbonate instead of sodium lactate with the same degree of acute metabolic alkalosis, showed a depression of 40% in the renal uptake of glutamine with a 38% decrease in renal ammoniagenesis and a 20% fall in the production of alanine. The present studies demonstrate that the production of ammonia from glutamine is not necessarily related to changes in acid-base balance, but may be associated with biochemical alterations related to the synthesis of alanine by the kidney.

Leucopenia, hypoxia and complement activation in haemodialysis. Three unrelated phenomena.

Acute, transient leucopenia occurs in uraemic patients during the first minutes of haemodialysis, haemofiltration and ultrafiltration, and this leucopenia depends on the membrane used: maximal with cuprophan, less marked using cellulose acetate in haemofiltration and minimal with polyacrylonitrile. Complement activation was noted in all dialysis procedures except ultrafiltration. However, no correlation was found between the intensity of the complement activation and the degree of leucopenia. Significant hypoxia only appeared in haemodialysis using an acetate bath even with the polyacrylonitrile membrane. Sequential ultrafiltration-dialysis studies clearly demonstrate that leucopenia and hypoxia are unrelated effects of haemodialysis. Leucopenia depends on the membrane used and hypoxia may be related to the use of an acetate dialysate. In addition, the presence of dialysis fluid was necessary for membrane-induced complement activation suggesting an important influence of the dialysate on membrane biocompatibility.

[Therapeutic guides in hypertonic dehydration (author's transl)]. / Pautas terapéuticas en la deshidratación hipertónica.

Physiopathology of hypertonic dehydration is revised. The bases of treatment are discussed; they are based on: 1. Basal requirements of fluids. 2. Slow correction of deficit. 3. Replacement of maintaining losses. Total fluids support will carry to rehydration in 2 or 3 days. In the most severe cases peritoneal dialysis is associated. The indications, technique and realization of peritoneal dialysis during hypertonic dehydration are discussed.