Single and combination immunotherapy with chemotherapy and the risk of AKI in patients with solid cancer.

BACKGROUND AND OBJECTIVES: Acute kidney injury (AKI) has emerged as an important toxicity among patients with advanced cancer treated with immune checkpoint inhibitors. The aim of this study was to describe the incidence, risk factors and mortality of AKI in patients receiving immune checkpoint inhibitors alone or in combination with another form of immunotherapy or chemotherapy. DESIGN, SETTING AND PARTICIPANTS: We included all patients who received immune checkpoint inhibitors alone or in combination with another form of immunotherapy or chemotherapy at AC Camargo Cancer Center from January 2015 to December 2019. AKI was defined as a ≥ 1.5 fold increase in creatinine from baseline within 12 months of immune checkpoint inhibitor initiation. We assessed the association between baseline demographics, comorbidities, medications and risk of AKI using a competing risk model, considering death as a competing event. RESULTS: We included 614 patients in the analysis. The mean age was 58.4 ± 13.5 years, and the mean baseline creatinine was 0.8 ± 0.18 mg/dL. AKI occurred in 144 (23.5%) of the patients. The most frequent AKI etiologies were multifactorial (10.1%), hemodynamic (8.8%) and possibly immunotherapy-related (3.6%). The likelihood of AKI was greater in patients with genitourinary cancer (sHR 2.47 95% CI 1.34-4.55 p < 0.01), with a prior AKI history (sHR 2.1 95% CI 1.30-3.39 p < 0.01) and taking antibiotics (sHR 2.85 95% CI 1.54-5.27 p < 0.01). CONCLUSIONS: In this study, genitourinary cancer, previous AKI and antibiotics use were associated with a higher likelihood of developing AKI.

Hypercalcemic crisis as a presentation of primary hyperparathyroidism / Crisis hipercalcémica como presentación de hiperpara-tiroidismo primario

Abstract Hyperparathyroidism-induced hypercalcemic crisis (HIHC) is an unusual state of marked progressive pri mary hyperparathyroidism (PHPT). Patients have severe hypercalcemia and may have severe symptoms such as kidney failure, acute pancreatitis, and mental changes. PHPT is due to the presence of a single gland adenoma/ disease in 80 to 85%; parathyroid carcinoma is reported in <1%. Among patients with adenoma, atypical parathy roid tumor can be found infrequently. Parathyroidectomy is the only curative approach for PHPT. In this report we present three cases of HIHC due to giant parathyroid adenomas (GPAs), one of them with histopathological characteristics of an atypical parathyroid tumor, with satisfactory evolution after parathyroidectomy.

Resumen La crisis hipercalcémica inducida por hiperparatiroi dismo (HIHC) es un estado inusual de hiperparatiroidis mo primario progresivo y marcado (HPTP). Los pacientes tienen hipercalcemia grave y pueden tener síntomas graves como insuficiencia renal, pancreatitis aguda y cambios mentales. El HPTP se debe a la presencia de un adenoma/enfermedad de una sola glándula en 80 a 85%; el carcinoma de paratiroides se informa en <1%. Entre los pacientes con adenoma, el tumor paratiroideo atípico se puede encontrar con baja frecuencia. La paratiroidec tomía es el único abordaje curativo del HPTP. En este reporte presentamos tres casos de HIHC por adenomas paratiroideos gigantes (APGs), uno de ellos con características histopatológicas de tumor paratiroideo atípico, con evolución satisfactoria luego de paratiroidectomía.

Hypercalcemic crisis as a presentation of primary hyperparathyroidism.

Hyperparathyroidism-induced hypercalcemic crisis (HIHC) is an unusual state of marked progressive primary hyperparathyroidism (PHPT). Patients have severe hypercalcemia and may have severe symptoms such as kidney failure, acute pancreatitis, and mental changes. PHPT is due to the presence of a single gland adenoma/ disease in 80 to 85%; parathyroid carcinoma is reported in <1%. Among patients with adenoma, atypical parathyroid tumor can be found infrequently. Parathyroidectomy is the only curative approach for PHPT. In this report we present three cases of HIHC due to giant parathyroid adenomas (GPAs), one of them with histopathological characteristics of an atypical parathyroid tumor, with satisfactory evolution after parathyroidectomy.

La crisis hipercalcémica inducida por hiperparatiroidismo (HIHC) es un estado inusual de hiperparatiroidismo primario progresivo y marcado (HPTP). Los pacientes tienen hipercalcemia grave y pueden tener síntomas graves como insuficiencia renal, pancreatitis aguda y cambios mentales. El HPTP se debe a la presencia de un adenoma/enfermedad de una sola glándula en 80 a 85%; el carcinoma de paratiroides se informa en <1%. Entre los pacientes con adenoma, el tumor paratiroideo atípico se puede encontrar con baja frecuencia. La paratiroidectomía es el único abordaje curativo del HPTP. En este reporte presentamos tres casos de HIHC por adenomas paratiroideos gigantes (APGs), uno de ellos con características histopatológicas de tumor paratiroideo atípico, con evolución satisfactoria luego de paratiroidectomía.

Kinin B1 Receptor Antagonism Prevents Acute Kidney Injury to Chronic Kidney Disease Transition in Renal Ischemia-Reperfusion by Increasing the M2 Macrophages Population in C57BL6J Mice.

BACKGROUND: Chronic kidney disease (CKD) is a multifactorial, world public health problem that often develops as a consequence of acute kidney injury (AKI) and inflammation. Strategies are constantly sought to avoid and mitigate the irreversibility of this disease. One of these strategies is to decrease the inflammation features of AKI and, consequently, the transition to CKD. METHODS: C57Bl6J mice were anesthetized, and surgery was performed to induce unilateral ischemia/reperfusion as a model of AKI to CKD transition. For acute studies, the animals received the Kinin B1 receptor (B1R) antagonist before the surgery, and for the chronic model, the animals received one additional dose after the surgery. In addition, B1R genetically deficient mice were also challenged with ischemia/reperfusion. RESULTS: The absence and antagonism of B1R improved the kidney function following AKI and prevented CKD transition, as evidenced by the preserved renal function and prevention of fibrosis. The protective effect of B1R antagonism or deficiency was associated with increased levels of macrophage type 2 markers in the kidney. CONCLUSIONS: The B1R is pivotal to the evolution of AKI to CKD, and its antagonism shows potential as a therapeutic tool in the prevention of CKD following AKI.

Amazonia Phytotherapy Reduces Ischemia and Reperfusion Injury in the Kidneys.

Acute kidney injury (AKI) is defined as a sudden decrease in kidney function. Phytomedicines have shown positive effects in the treatment of AKI worldwide. The aim of this study was to evaluate the effect of Abuta grandifolia on the renal function of rats submitted to AKI. A phytochemical study of the plant was performed through liquid chromatography coupled with mass spectrometry (CL-EM) and DPPH and ABTS antioxidant tests. Renal function tests were performed in 20 male adult Wistar rats weighing from 250 to 300 g distributed in the following groups: SHAM (submitted to laparotomy with simulation of renal ischemia); ABUTA (animals that received 400 mg/kg of AG, orally-VO, once a day, for 5 days, with simulation of renal ischemia); I/N (animals submitted to laparotomy for clamping of bilateral renal pedicles for 30 min, followed by reperfusion); ABUTA + I/R (animals that received AG-400 mg/kg, 1× per day, VO, for 5 days, submitted to renal ischemia after treatment with herbal medicine). The results suggest that the consumption of Abuta grandifolia promoted renoprotection, preventing the reduction of renal function induced by ischemia, oxidizing activity, and deleterious effects on the renal tissue, confirmed by the decrease of oxidative metabolites and increase of antioxidants in the animals' organisms.

The relationship between chikungunya virus and the kidneys: A scoping review.

Several atypical forms of chikungunya fever (CHIK) have been described, including neurological, cardiac and renal involvement. These forms may be related to high morbidity and mortality rates. This scoping review based on the PubMed, Scopus, and WOS databases aims to identify and summarise all the available evidence regarding the clinical and histopathological presentations and risk factors associated with kidney injury related to CHIK, as well as the clinical impact. Thus, a total of 54 papers were selected from 1606 initial references after applying the defined inclusion criteria. Data on the association between kidney injury and CHIK are scarce, with studies only conducted in the acute phase of the disease, lacking further characterisation. Kidney injury incidence in hospitalised patients using the Kidney Disease Improving Global Outcomes criteria varies from 21% to 45%, being higher among patients with atypical and severe manifestations. Although acute kidney injury does not seem to be related to viraemia, it may be related to higher mortality. Few studies have described the renal histopathological changes in the acute phase of CHIK, with prevalent findings of acute interstitial nephritis with mononuclear infiltrate, glomerular congestion and nephrosclerosis. Only one study assessed the kidney function of patients in the subacute and chronic phases of CHIK. Additionally, individuals with comorbidities, including chronic kidney disease, may be among those with a greater risk of presenting worse outcomes when affected by CHIK. The results described herein may contribute to better understand the relationship between the kidneys and chikungunya virus.

Acute kidney injury and renal replacement therapy: terminology standardization / Injúria renal aguda e métodos de suporte: padronização da nomenclatura

Abstract The Department of Acute Kidney Injury (IRA) of the Brazilian Society of Nephrology prepared this document for the purpose of standardizing AKI terminology and dialysis modalities in the Portuguese language for Brazil. Several terms with similar meanings have been used in AKI and its dialysis modalities, causing confusion and disparities among patients, nephrologists, health institutions, private care companies, insurance companies and government entities. These disparities can impact medical care, hospital organization and care, as well as the funding and reimbursement of AKI-related procedures. Thus, consensual nomenclature and definitions were developed, including the definitions of AKI, acute kidney disease (AKD) and chronic kidney disease (CKD). Additionally, we addressed all dialysis modalities and extracorporeal procedures related to AKI, currently approved and available in the country. The Brazilian Society of Nephrology hopes that this Consensus can standardize the terminology and provide technical support to all involved in AKI care in Brazil.

Resumo O Departamento de Injúria Renal Aguda (IRA) da Sociedade Brasileira de Nefrologia elaborou o presente documento para fins de padronização da terminologia em IRA e modalidades dialíticas na língua portuguesa para o Brasil. Diversos termos com significados semelhantes têm sido empregados em IRA e suas modalidades dialíticas, causando confusão e disparidades entre pacientes, nefrologistas, instituições de saúde, empresas privadas de assistência, seguradoras e entidades governamentais. Essas disparidades podem impactar a assistência médica, a organização e o atendimento hospitalares, assim como o financiamento e reembolso dos procedimentos relacionados com a IRA. Assim, nomenclatura e definições consensuais foram elaboradas, incluindo-se as definições de IRA, doença renal aguda (DRA) e doença renal crônica (DRC). Adicionalmente, todas as modalidades dialíticas e os procedimentos extracorpóreos relacionados a IRA, atualmente aprovados e disponíveis no país, foram abordados. A Sociedade Brasileira de Nefrologia espera que este Consenso possa padronizar a nomenclatura e prover suporte técnico para todos os atores envolvidos na assistência à IRA no Brasil.

Immunosuppression as a trigger for hyperinflammatory syndrome due to Strongyloides stercolaris in membranous nephropathy. / Inmunosupresión como desencadenante de un síndrome de hiperinfestación por Strongyloides stercolaris en la nefropatía membranosa.

The relationship between parasites and glomerulonephritis (GN) is well documented in certain parasitoses, but not in cases of Strongyloides stercolaris (S. stercolaris) where there are few cases described being the majority GN of minimal changes. We report a case of hyperinfestation by S. stercolaris in a patient affected by a membranous GN treated with oral corticosteroids with fatal outcome for the patient. This case provides a double teaching: first about a rare association of strongyloid and membranous GN and second about the importance of establishing a diagnosis of suspected and appropriate treatment for certain infections or diseases with little clinical expression before starting any immunosuppressive treatment.

Metabolomic and biochemical characterization of a new model of the transition of acute kidney injury to chronic kidney disease induced by folic acid.

BACKGROUND: Renal diseases represent a major public health problem. The demonstration that maladaptive repair of acute kidney injury (AKI) can lead to the development of chronic kidney disease (CKD) and end-stage renal disease has generated interest in studying the pathophysiological pathways involved. Animal models of AKI-CKD transition represent important tools to study this pathology. We hypothesized that the administration of multiple doses of folic acid (FA) would lead to a progressive loss of renal function that could be characterized through biochemical parameters, histological classification and nuclear magnetic resonance (NMR) profiling. METHODS: Wistar rats were divided into groups: the control group received a daily intraperitoneal (I.P.) injection of double-distilled water, the experimental group received a daily I.P. injection of FA (250 mg kg body weight-1). Disease was classified according to blood urea nitrogen level: mild (40-80 mg dL-1), moderate (100-200 mg dL-1) and severe (>200 mg dL-1). We analyzed through biochemical parameters, histological classification and NMR profiling. RESULTS: Biochemical markers, pro-inflammatory cytokines and kidney injury biomarkers differed significantly (P < 0.05) between control and experimental groups. Histology revealed that as damage progressed, the degree of tubular injury increased, and the inflammatory infiltrate was more evident. NMR metabolomics and chemometrics revealed differences in urinary metabolites associated with CKD progression. The main physiological pathways affected were those involved in energy production and amino-acid metabolism, together with organic osmolytes. These data suggest that multiple administrations of FA induce a reproducible model of the induction of CKD. This model could help to evaluate new strategies for nephroprotection that could be applied in the clinic.

Diagnostic performance of salivary urea nitrogen dipstick to detect and monitor acute kidney disease in patients with malaria.

BACKGROUND: Acute kidney injury (AKI) is a common complication of malaria. In low resource settings, a lack of diagnostic tools and delayed treatment of malaria associated AKI lead to significant morbidity and mortality. The aim of this study was to assess the diagnostic performance of salivary urea nitrogen (SUN) dipstick to detect and monitor kidney disease [KD = AKI or acute kidney disease (AKD) without AKI] in malaria patients in Angola. METHODS: Patients 11-50 years old admitted with malaria at the Josina Machel (Maria-Pia) Hospital, Luanda, Angola, between 2nd March and 10th May 2016 were enrolled in this study. All participants had serum creatinine (sCr), blood urea nitrogen (BUN) and SUN dipstick tested at the time of recruitment and daily for up to 4 days. AKD without AKI refers to acute renal impairment which do not fulfilled the main criteria for AKI (increases in the baseline serum creatinine and/or decreases in urine output) according defined by the kidney disease improving global outcomes (KDIGO) guideline. RESULTS: Eight-six patients were admitted with malaria diagnosis (mean age 21.5 ± 9.4 years, 71% male) and 27 (32%) were diagnosed with KD. The mean (± SD) sCr and BUN of the KD group at admission (day 0) were 5.38 (± 5.42) and 99.4 (± 61.9) mg/dL, respectively. Three (3.5%) patients underwent haemodialysis and eight (9.3%) died within the first 4 days of hospital admission [5 (62.5%) with KD; 3 (37.5%) without kidney disease; p = 0.047]. The SUN threshold for KD diagnosis was tested pad #5 (SUN > 54 mg/dL). At this threshold, the SUN dipstick had a sensitivity of 67% and specificity of 98% to diagnose KD. The area under the receiver operating characteristics curve (ROC) for KD diagnosis on admission was 0.88 (95% CI 0.79-0.96). The SUN dipstick was most accurate at higher levels of BUN. CONCLUSION: The SUN dipstick had reasonable sensitivity and excellent specificity when used to diagnose KD in a cohort of patients with malaria in a resource-limited setting. Given the severity of presenting illness and kidney injury, the SUN dipstick diagnostic threshold was high (test pad #5). SUN may be used to detect AKI in patients with malaria in low resources settings, thus facilitating earlier access to adequate treatment, which may improve survival.

Asociación de insuficiencia renal aguda con mortalidad y complicaciones en pacientes hospitalizados con cirrosis hepática / Association of acute renal failure with mortality and complications in hospitalized patients with liver cirrhosis

Resumen ANTECEDENTES: la insuficiencia renal aguda es una de las complicaciones más severas de la cirrosis y conlleva un pronóstico ominoso. Los estudios que han utilizado definiciones más actuales de daño renal agudo, como AKIN (Acute Kidney Injury Network) o RIFLE (The Risk, Injury, Failure, Loss and End-stage kidney disease criteria) se enfocan en pacientes admitidos en unidades de cuidados intensivos y no pueden generalizarse a otros pacientes hospitalizados. El Club Internacional de Ascitis (ICA por sus siglas en inglés) recientemente adoptó una definición dinámica de insuficiencia renal crónica en pacientes con cirrosis, definiéndola como el incremento de la creatinina sérica mayor o igual de 0.3 mg/dL en las últimas 48 horas o un incremento de más de 50% de la creatinina basal conocida ocurrida en los últimos siete días, estadificándose de acuerdo con los incrementos de la creatinina. OBJETIVO: evaluar la repercusión de la severidad de la insuficiencia renal aguda de acuerdo con la clasificación del Club Internacional de Ascitis en la mortalidad de los pacientes con cirrosis hepática hospitalizados, así como conocer los principales desencadenantes de insuficiencia renal aguda en pacientes con cirrosis hepática hospitalizados, los patrones de recuperación o progresión de la misma. PACIENTES Y MÉTODO: estudio transversal, observacional, no aleatorizado y multicéntrico, en el que se utilizó la definición de insuficiencia renal aguda propuesta por el Club Internacional de Ascitis. Los pacientes se captaron en un lapso de cuatro meses, del 1 de abril al 31 de julio de 2015, en el Hospital General Ticomán y en el Hospital General de Ecatepec; se solicitó consentimiento informado de los pacientes o en caso pertinente, del familiar responsable del mismo. Se excluyeron los pacientes menores de 18 años, sujetos con insuficiencia hepática aguda y los pacientes con enfermedad renal crónica. RESULTADOS: se incluyeron 45 pacientes con cirrosis hepática, de los que 36 eran hombres, con edad promedio de 46.2 años. La causa de la cirrosis hepática fue por alcohol en 40 pacientes (89%), viral en 3 (7%) y mixta en 2 (4%); la estadificación de insuficiencia renal aguda inicial fue: estadio 1: 36 (80%), estadio 2: 8 (18%) y estadio 3: 1 (2%). Ocurrieron siete defunciones (15.5%); de éstas, todos los pacientes estaban en la categoría C de la clasificación Child-Pugh, con insuficiencia renal aguda en estadio inicial 1; en 6 (13%) pacientes con progresión a estadio 3 y en estadio inicial 2; en 1 (2%) paciente con progresión a estadio 3. La severidad de la cirrosis en la escala MELD (Model for End-Stage Liver Disease) fue de 31.07±8.44 puntos en los pacientes que fallecieron versus 22.98±9.64 puntos (p=1.21) en los supervivientes. El puntaje de Child-Pugh en el grupo de pacientes fallecidos fue de 14.29±0.9 vs 0.29±2.31 en los supervivientes (p=0.001). CONCLUSIONES: la mortalidad en pacientes con cirrosis hepática e insuficiencia renal aguda fue más frecuente en pacientes con progresión al estadio de insuficiencia renal aguda y en sujetos con mayor severidad de la cirrosis hepática, valorada por Child-Pugh o por la escala MELD. Se requieren estudios de cohorte en nuestra población para validar la reciente clasificación del Club Internacional de Ascitis de la insuficiencia renal aguda en cirrosis y para determinar los factores asociados con incremento en la mortalidad en este grupo de pacientes.

Abstract BACKGROUND: Acute renal failure is one of the most severe complications of cirrhosis and entails a bad prognosis. The studies that had used most current definitions of acute kidney injury such as AKIN (Acute Kidney Injury Network) or RIFLE (The Risk, Injury, Failure, Loss and End-stage kidney disease criteria) has focused in patients admitted to the critical care units, and thus they can not be generalized to other hospitalized patients. Recently, the International Club of Ascites (ICA) adopted a dynamic definition of acute kidney failure in patient with cirrhosis, defined like increase of the creatinine level ≥0.3 mg/dL in the last 48 h; or a increase ≥50% from the basal creatinine in the last seven days, staged according the increase of creatinine. OBJECTIVES: To evaluate the impact of acute kidney injury severity according to the classification of the International Club of Ascites in the mortality of hospitalized patients with liver cirrhosis. To know the main triggers of acute kidney failure in hospitalized patients with liver cirrhosis, and to know the patterns of recovery and progression of renal failure. PATIENTS AND METHOD: A transversal, observational, no-randomized multicentric study designed. We used the definition of acute kidney failure proposed for the ICA. Patients were included from the General Hospital Ticoman and the General Hospital of Ecatepec in Mexico, in a four-month-period, from 1st April to 31st July of 2015; informed consent was obtained from the patients or in the pertinent case from the responsible familiar. Patients with less than 18 years old, with acute liver failure or chronic renal failure were excluded. RESULTS: They were included 45 patients with liver cirrhosis, 36 men, with a mean age of 46.2 years old. The etiology of the liver cirrhosis was alcohol in 40 patients (89%), viral in 3 (7%) and mixed in 2 (4%). The stage of acute liver failure was stage 1: 36 (80%), stage 2: 8 (18%) and stage 3: 1 (2%). Seven deaths occurred (15.5%), from there all the patients were classified in the C stage of the Child-Pugh Classification; death occurred with acute renal failure in initial stage 1; in 6 (13%) with progression to the stage 3 and in initial stage 2 in 1 (2%) with progression to stage 3. The severity of cirrhosis accord to the MELD classification was 31.07±8.44 points in the mortality cases, compared with 22.9±9.64 points (p=1.21) in the survivals. Child-Pugh score in the cases of death was 14.29±.9 vs 0.29±2.31 in survivals (p=0.001). CONCLUSION: Mortality in patients with liver cirrhosis and acute kidney failure was more frequent in patients with progression of the acute kidney failure, and in those with a more severe liver damage in the MELD or Child-Pugh scores. There are necessary cohort studies for the validation of the recent classification of the International Club of Ascites for Acute kidney failure in cirrhosis, and to determine the factors associated to the increase of mortality in this group of patients.

Role of Pharmacogenomics in Kidney Disease and Injury.

There has been considerable excitement in the kidney community surrounding the research findings on the genetic contributions to kidney diseases. However, positive outcomes of personalized therapeutic interventions can be circumvented by unpredictable pharmacokinetics of prescribed drugs. Furthermore, unpredictable drug disposition can result in toxicities such as kidney injury. Patient covariates, disease covariates, and pharmacogenetics all contribute to variability in drug disposition. Further treatment personalization and avoidance of drug- and biologic- induced kidney injury will require extensive knowledge and expertise in renal clinical pharmacology. The current review will focus on the pharmacogenetics of drugs and biologics used in the treatment of glomerular kidney diseases and drugs implicated in inducing kidney injury phenotypes.

Cistatina C como prueba de rutina para evaluar la función renal en pacientes pediátricos / Cystatin C as a routine test to evaluate kidney function in pediatric patients / Cistatina C como um teste de rotina para avaliar a funþÒo renal em pacientes pediátricos

Numerosos estudios han demostrado que los niveles plasmáticos de cistatina C tienen más exactitud que los de creatinina en la estimación de la tasa de filtración glomerular (eTFG). Sin embargo, no se utiliza como prueba rutinaria en el diagnóstico de patologías renales pediátricas. El objetivo de este estudio fue comparar la TFG para cistatina C en pacientes pediátricos mexicanos con y sin exposición a factores de riesgo para presentar Insuficiencia Renal Aguda (IRA) y corroborar las ventajas de emplear este marcador en el diagnóstico oportuno de patologías renales en relación con la creatinina. Se analizaron 106 muestras para estimar la TFG. Se cuantificó la concentración de creatinina y cistatina C, sustituyendo los valores en las fórmulas MDRD v-4 y Filler y Lepage, respectivamente. Se compararon las concentraciones tanto de creatinina como de cistatina entre los grupos de estudio por medio de U de Mann Whitney. Asimismo, se evaluó la correlación entre estos dos metabolitos divididos por presencia o no de factores de riesgo para presentar la enfermedad renal. Se observó una correlación entre las concentraciones de creatinina y cistatina C sérica, tanto en el grupo de pacientes sin factores de riesgo para IRA (r=0,936, p<0,001) como en los que sí presentaron factores de riesgo para IRA (r=0,952, p<0,001). El grupo con factores de riesgo mostró concentraciones mayores tanto de cistatina como de creatinina, así como de eTFG para ambos metabolitos. La cistatina C muestra una buena correlación con la creatinina. Por otro lado, la cistatina alterada identificó a un mayor número de pacientes con factores de riesgo para IRA, por lo cual se propone su uso como prueba de escrutinio en pacientes pediátricos.(AU)

Numerous studies have shown that plasma levels of cystatin C are more accurate than creatinine estimating the Glomerular Filtration Rate (eGFR), however they are not used as a routine test in the diagnosis of pediatric renal pathologies. The aim of this study was to determine GFR for cystatin C in Mexican pediatric patients exposed to risk factors of Acute Kidney Disease (AKD) compared to children without risk factors for AKD and corroborate the advantages of using this marker in the early diagnosis of kidney diseases in relation to creatinine. A total of 106 samples were analyzed to estimate the GFR. Creatinine and cystatin C concentration were quantified by substituting the values in the MDRD v-4 and Filler and Lepage formulas respectively. The concentrations of both creatinine and cystatin between the study groups were compared by Mann Whitney. Likewise, the correlation between these two metabolites divided by presence or absence of risk factors present in renal disease was assessed. A correlation between creatinine and serum cystatin C concentrations was observed in both groups of patients without risk factors of AKD (r=0.936, p<0.001) and in those who presented risk factors of AKD (r=0.952 , p<0.001). The risk factor group showed higher concentrations of cystatin and creatinine as well as eTFG for both metabolites. Cystatin C shows a good correlation with creatinine. Furthermore, altered cystatin identified a greater number of patients with risk factors of AKD and it is proposed as a screening test in pediatric patients.(AU)

Numerosos estudos tÛm demonstrado que os níveis plasmáticos de cistatina C sÒo mais exatos do que a creatinina para calcular a taxa de filtraþÒo glomerular (TFG). No entanto, nÒo é usado como teste de rotina no diagnóstico de patologias renais pediátricas. O objetivo deste estudo foi comparar a TFG para cistatina C em pacientes pediátricos mexicanos expostos ou nÒo a fatores de risco para apresentar InsuficiÛncia Renal Aguda (IRA) e comprovar as vantagens da utilizaþÒo deste marcador no diagnóstico oportuno de doenþas renais em relaþÒo O creatinina. 106 amostras foram analisadas para estimar a TFG. Foi quantificada a concentraþÒo em creatinina e cistatina C, substituindo os valores nas fórmulas MDRD v-4 e Filler e Lepage respectivamente. As concentraþ§es tanto de creatinina quanto de cistatina foram comparadas entre os grupos de estudo através do U de Mann Whitney. Do mesmo modo, foi avaliada a correlaþÒo entre estes dois metabólitos divididos por presenþa ou ausÛncia de fatores de risco para apresentar a doenþa renal. Foi observada uma correlaþÒo entre as concentraþ§es de creatinina e cistatina C sérica tanto no grupo de pacientes sem fatores de risco para IRA (r=0,936, p<0,001) quanto naqueles que sim apresentavam fatores de risco para IRA (r=0,952, p<0,001). O grupo com fatores de risco apresentou concentraþ§es mais elevadas tanto de cistatina como de creatinina, bem como de ETFG para ambos os metabólitos. A Cistatina C mostra uma boa correlaþÒo com a creatinina. Além disso, a cistatina alterada identificou maior número de pacientes com fatores de risco para IRA, pelo qual se prop§e sua utilizaþÒo como teste de triagem em pacientes pediátricos.(AU)