Acute kidney injury as a risk factor for chronic kidney diseases in disadvantaged populations.

Acute kidney injury (AKI) is considered to be a potential cause for developing chronic kidney disease (CKD); on the other hand, CKD predisposes to AKI. The lack of adequate epidemiological data makes it difficult to determine if AKI induces CKD in less developed countries. The etiology of AKI in rich populations, in whom sophisticated surgery, interventional radiology and oncology treatments are usually the cause of AKI, is very different from that of disadvantaged populations, where the origin of AKI is associated with endemic infections, obstetric problems, poisons, toxins and natural disasters. Any conclusions extrapolated from these two settings should be treated with caution. Moreover, people living in disadvantaged conditions are usually much younger than those in rich areas and this age factor could facilitate total recovery of renal function after AKI if treatment based on an adequate supply of water, rehydration and anti-infectious measures were provided. In the small segment of the population of less developed countries having an income per capita similar to that observed in the developed countries, the long-term outcome of AKI should also be expected to be similar. New data coming from two single centers analyzing only the long-term outcome of acute tubular necrosis (ATN) patients, with a normal or near normal renal function prior to the AKI episode, coincide in reporting a requirement for chronic dialysis among the surviving patients of 2%. If these data are confirmed, the importance of AKI as cause of CKD should be reconsidered, both in developed and less developed countries.

Long-term outcome of acute tubular necrosis: a contribution to its natural history.

As long-term outcome studies of acute renal failure (ARF) are scarce and non-homogeneous, we studied 187 consecutive acute tubular necrosis (ATN) patients without previous nephropathies, discharged alive from our hospital between October 77 and December 92 and followed-up until December 99 (range 7-22 years; median 7.2). Variables were analyzed at the time of the acute episode and during follow-up. In 2000-2001 a clinical evaluation was made in 58 of the 82 patients still alive. Ten patients were lost to follow-up and 95 died. In 59% death was related with the disease present when the ATN developed. Kaplan-Meir survival curve showed 89, 67, 50, and 40% at 1, 5, 10, and 15 years, respectively, after discharge. Survival curves were significantly better (log-rank P<0.001) among the youngest, those surviving a polytrauma, those without comorbidity and surprisingly those treated in intensive care units. The proportional Cox model showed that age (hazard ratio (HR) 1.04 per year of age; P=0.000), presence of comorbid factors (HR 4.29; P=0.006), surgical admission (HR 0.45; P=0.000), and male sex (HR 1.72; P=0.020) were the variables associated with long-term follow-up. In the evaluated patients renal function was normal in 81%. Long-term outcome after ARF depends on absence of co-morbid factors, cause of initial admission and age. Although the late mortality rate is high and related with the original disease, renal function is adequate in most patients.

[Urea distribution volume calculated by ionic dialysance]. / Cálculo del volumen de distribución de la urea mediante dialisancia iónica.

BACKGROUND: Direct dialysis quantification is considered the gold standard for determining urea distribution volume, but it is impractical for routine use. So, urea distribution volume in hemodialysis patients is usually estimated from anthropometric equations. Ionic dialysance allows to calculate the urea distribution volume dividing the Kt obtained by ionic dialysance by the Kt/V obtained by a simplified formula. The aim of the present work was to analyse the concordance between the ionic dialysance and the direct dialysis quantification methods to estimate de urea distribution volume. MATERIAL AND METHODS: In 15 hemodialysis patients (10 males and 5 females), we have estimated the urea distribution volume by the direct dialysis quantification (Vurea), by the anthropometrics equations of Watson (VWatson) and Chertow (VChertow) and by the ionic dialysance method (VDI). To obtain VDI we have used two simplified Kt/V formulas: the monocompartimental and the equilibrated Daugirdas equations (VDIm and VDIe respectively). The intermethod variability was assessed by the relative difference (absolute difference between VUrea and the other methods, divided by the mean). RESULTS: VUrea (26,2 L) was statistically different from theVDIe (30,6 L, p < 0.01), VWatson 35.2 L (p < 0.001) and VChertow (38 L, p < 0.001). VDIm was 26.3 L (p = ns). VUrea represents the 42% of the body weight for the males (range 36 to 49%) and the 33% of the body weight for the female (range 28 to 38%). The intermethod variability was high for the VDIe (21.6%), VWatson (37.4%) and VChertow (48. 1%), but it was low for the VDIm (9.9%). CONCLUSIONS: Urea distribution volume calculated by the ionic dialysance method using the monocompartimental Daugirdas Kt/V equation has an acceptable agreement with the urea distribution volume calculated by the direct dialysis quantification. Anthropometry-based equations overestimate the urea distribution volume in hemodialysis patients.

Cálculo del volumen de distribución de la urea mediante dialisancia iónica / Urea distribution volume calculated by ionic dialysance

Introducción: En la práctica clínical el volumen de distribución de la urea sesuele calcular por fórmulas antropométricas, pero el método más seguro es mediantela cuantificación de la urea eliminada en la sesión de diálisis, lo que implicala recogida del dializado y la determinación de la concentración plasmáticade urea tras haberse alcanzado el equilibrio postdiálisis. La dialisancia iónica permitecalcular el volumen de distribución de la urea dividiendo el Kt obtenido pordialisancia iónica por el Kt/V proporcionado por las fórmulas simplificadas.El objetivo del presente trabajo ha consistido en estudiar la concordancia entrelos diversos métodos para calcular el volumen de distribución de la urea.Material y métodos: En 15 enfermos (10 varones y 5 mujeres) hemos calculadoel volumen de distribución de la urea mediante la cuantificación de la ureaeliminada (VUrea) y lo hemos comparado con el obtenido por dos fórmulas antropométricas(Watson y Chertow) y por la dialisancia iónica (VDI). Para obtenerel VDI se utilizaron las ecuaciones de Daugirdas para los modelos monocompartimentaly equilibrado. Se consideraron pues dos VDI (VDIm y VDIe respectivamente)según la ecuación de Daugirdas empleada. Para estudiar la concordanciahemos utilizado la diferencia relativa (diferencia absoluta entre cada método y elVUrea dividido por la media aritmética).Resultados: El VUrea fue de 26,2 L que representa el 42% del peso en varones(con un amplio rango entre 36 y 49%) y un 33% en mujeres (rango 28-38%). El volumen de distribución de la urea con los otros métodos fue: Watson35,2 L (p < 0,001), Chertow 38 L (p < 0,001), VDIe 30,6 L (p < 0,01) y VDIm26,3 L (p = ns). La diferencia relativa del VUrea con las fórmulas antropométricasy con el VDIe fue muy alta (Watson: 37,4%, Chertow: 48,1%, VDIe 21,6%),obteniéndose una concordancia aceptable con el VDIm (9,9%).Conclusiones: El volumen de distribución de la urea calculado por dialisanciaiónica y la ecuación de Kt/V monocompartimental de Daugirdas, tiene una concordanciaclínicamente aceptable con el obtenido mediante la recogida del dializado.Los métodos antropométricos proporcionan unos valores mucho más elevados,con diferencias que son inaceptables desde el punto de vista clínico

Background: Direct dialysis quantification is considered the gold standard fordetermining urea distribution volume, but it is impractical for routine use. So, ureadistribution volume in hemodialysis patients is usually estimated from anthropometricequations. Ionic dialysance allows to calculate the urea distribution volumedividing the Kt obtained by ionic dialysance by the Kt/V obtained by a simplifiedformula. The aim of the present work was to analyse the concordancebetween the ionic dialysance and the direct dialysis quantification methods to estimatede urea distribution volume.Material and methods: In 15 hemodialysis patients (10 males and 5 females),we have estimated the urea distribution volume by the direct dialysis quantification(Vurea), by the anthropometrics equations of Watson (VWatson) and Chertow(VChertow) and by the ionic dialysance method (VDI). To obtain VDI wehave used two simplified Kt/V formulas: the monocompartimental and the equilibratedDaugirdas equations (VDIm and VDIe respectively). The intermethod variabilitywas assessed by the relative difference (absolute difference between VUreaand the other methods, divided by the mean).Results: VUrea (26,2 L) was statistically different from theVDIe (30,6 L, p <0.01), VWatson 35.2 L (p < 0.001) and VChertow (38 L, p < 0.001). VDIm was26.3 L (p = ns). VUrea represents the 42% of the body weight for the males(range 36 to 49%) and the 33% of the body weight for the female (range 28 to38%). The intermethod variability was high for the VDIe (21.6%), VWatson(37.4%) and VChertow (48.1%), but it was low for the VDIm (9.9%).Conclusions: Urea distribution volume calculated by the ionic dialysance methodusing the monocompartimental Daugirdas Kt/V equation has an acceptableagreement with the urea distribution volume calculated by the direct dialysis quantification.Anthropometry-based equations overestimate the urea distribution volumein hemodialysis patients

Cytomegalovirus infection after renal transplantation: selective prophylaxis and treatment.

We have reviewed our experience in selective cytomegalovirus (CMV) infection prophylaxis and treatment in our renal transplant population. Between 1996 and 2001, 263 cadaveric renal transplant recipients had at least 6 months follow up. Immunosuppression was based on cyclosporine Neoral (n=108) or tacrolimus (n=155). CMV infection prophylaxis (oral acyclovir or gancyclovir at half usual doses) was only prescribed in recipients receiving a CMV positive ve kidney and in recipients treated with OKT3. CMV infection was diagnosed by a positive pp65 antigenemia upon appearance of CMV-related symptoms, leading to specific treatment (IV ganciclovir) only if symptoms were intense or there was visceral involvement. Thus, no preemptive treatment or programmed or periodic antigenemia was performed in any case. Nineteen episodes of symptomatic CMV infection were diagnosed (prevalence 7.2%). The frequency was similar for all immunosuppressive regimens. Only 9 of 19 (47%) of patients were given IV ganciclovir; the others were not treated. All patients survived without apparent complications, relapses, or recurrences. No oral gancyclovir was delivered after IV treatment. Our CMV prophylaxis protocol was limited to high-risk patients, using lower gancyclovir dosages than those usually advocated. It does not include programmed or scheduled search for CMV antigenemia in asymptomatic renal transplant patients. Despite these factors, our CMV infection rate and severity were similar to those reported with more aggressive protocols, with extended prophylaxis, preemptive therapy, or intense surveillance.

A low incidence of new-onset insulin-dependent diabetes mellitus using tacrolimus in kidney recipients in Europe.

Employing tacrolimus (Tac) for routine immunosuppression in renal transplantation (RT), produced an incidence of new-onset, insulin-treated, diabetes mellitus (newDM) as high as 20%. More recently, several large multicenter kidney studies using Tac as the primary immunosuppressant have been reported in Europe. Between 1997 and 2001, we performed 155 RTs using Tac (0.2 mg/k/per day, targeting whole blood trough levels <15 ng/mL) with a rapid steroid taper. The acute rejection rate was 13%, and 89% of grafts are still functioning. Only 5 Tac-treated patients not previously requiring insulin needed insulin therapy for > or =30 days (3.2%). Eight separate studies employing Tac in at least one arm (N=2728) have been reported between 1997 and 2002. Tac was combined with azathioprine or MMF, and/or steroids. The incidence of new DM at study end ranged from 2.3% to 8.3%. The only trial with >6% incidence was the first one, using an initial dose of 0.3 mg/kg per day. The most recent studies utilized an initial dose of 0.2 mg/kg per day, targeting whole blood trough levels of <15 ng/mL and a steroid taper, with newDM at <6%. On the basis of these data, we confirm in that the use of Tac as a first-line immunosuppressant in renal transplant patients affords protection against acute rejection with a low level of newDM. The tendency to employ lower oral doses of Tac, lower blood target levels, and a reduced steroid dose appear to minimize glucose disturbances in RT.

Funciones del facultativo especialista de área de Nefrología y su importancia en el sistema sanitario / The functions of the comunity nephrologist and its importance in health care system

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Treatment of secondary hyperparathyroidism in hemodialyzed patients with high-dose calcium carbonate without vitamin D3 supplements.

BACKGROUND: Vitamin D compounds are usually indicated for the treatment of secondary hyperparathyroidism in dialysis patients. The possibility to induce a reversal of hyperparathyroidism with calcium supplementation alone is controversial. The present study was conducted to assess if oral calcium carbonate may constitute a therapeutic option for the control of hyperparathyroidism in patients with high PTH concentrations at the beginning of the treatment with chronic hemodialysis. METHODS: Thirty-one patients with end-stage renal failure with an intact PTH concentration above 250 pg/ml at the beginning of chronic hemodialysis therapy were treated with high doses of calcium carbonate; no patient received either aluminium-containing binders or vitamin D compounds. To minimize hypercalcemia, a calcium dialysate concentration of 2.5 mEq/l was used in all patients. The goal of the study was to reduce the intact PTH concentration to 250 pg/ml with oral calcium carbonate supplements alone. RESULTS: Throughout the first year on hemodialysis treatment, the intact PTH concentration decreased from 538 +/- 256 to 251 +/- 218 pg/ml (p < 0.001). By the end of the study, the therapeutic objective was achieved in 22 patients (71%) ('responder' group). The remaining 9 patients were classified as the 'treatment failure' group. The basal intact PTH concentration was not different between both groups (508 +/- 235 vs. 612 +/- 303 pg/ml, respectively, p = n.s.), but 5 'treatment failure' patients admitted to take a dose of calcium carbonate lower than that prescribed. There were 40 episodes of hyperphosphatemia (11% of all measurements) in 7 of 31 patients, 5 of them belonged to the noncompliance 'treatment failure' patients. Only 15 episodes (4% of all measurements) of transient hypercalcemia (range 11.1 - 11.9 mg/dl) were detected in 8 patients. CONCLUSIONS: Secondary hyperparathyroidism in hemodialysis patients can often be reverted by oral calcium carbonate alone. But a good adherence to treatment is absolutely necessary.