RESUMEN Introducción: Se ha estudiado la tinción inmunohistoquímica de Ki-67, CD68 y Bcl-2 en glomerulonefritis. Objetivo: Evaluar estas características de tinción inmunohistoquímica, el inicio de la hemodiálisis y la tasa de mortalidad a los 60 meses en la glomerulonefritis crescéntica. Material y métodos: En este estudio retrospectivo, los pacientes, con diagnóstico previo de glomerulonefritis crescéntica se dividieron en dos grupos: Hemodiálisis iniciada y no iniciada.La puntuación de tinción Ki-67, CD68 y Bcl-2 de las muestras de biopsia de riñón se definió del siguiente modo: por debajo del 5% "0", 5-10% "+1", 11-20% "+2", más del 20% "+3".Se compararon los siguientes datos en los pacientes: demografía, resultados de laboratorio, de iniciación de la hemodiálisis y la mortalidad obtenida de los registros médicos y las puntuaciones de tinción inmunohistoquímica entre los grupos.La Tasa de filtrado glomerular estimada(TFGe) fue evaluada a los 0, 6 y 12 meses,excepto en los pacientes en hemodiálisis en curso. Resultados: Un total de 56 pacientes fueron diagnosticados con glomerulonefritis crescéntica. La glomerulonefritis crescénticapauciinmune(58,9%) fue la etiología más común. Se inició hemodiálisis en 36 pacientes.La edad media, los niveles basales de creatinina, urea y proteína C reactiva fueron significativamente más altos, y los niveles de hemoglobina y proteinuria fueron significativamente más bajos en el grupo de Hemodiálisis Iniciada. Las puntuaciones de tinción inmunohistoquímica no fueron significativas entre los grupos. En el grupo de Hemodiálisis Iniciada 8,33% de los pacientes recuperó función renal y salió de diálisis. La tasa de mortalidad en el grupo de Hemodiálisis no Iniciada fue del 10,0% y en el grupo que inicio HD del 44%. Cuando combinamos los pacientes Hemodiálisis no Iniciada y los pacientes recuperados de hemodiálisis la mediana de TGFe en la línea de base, 6º y 12º mes fue 32,9, 43,9 y 58,0 mL/minuto/1,73m2, respectivamente (p<0,016). Conclusión: El inicio de la hemodiálisis se asoció con una alta mortalidad. El grado de tinción inmunohistoquímica fue similar en ambos grupos. El incremento de la TFGe se documentó en el primer año en pacientes distintos de los que aún estaban en hemodiálisis.

ABSTRACT Introduction: Immunohistochemical staining of Ki-67, CD68 and Bcl-2 have been studied in glomerulonephritis. We aimed to assess these immunohistochemical staining features, hemodialysis initiation and 60 month mortality ratesin crescentic glomerulonephritis. Methods: In this retrospective study, patients, with a previous diagnosisof crescentic glomerulonephritis weredivided into two groups: Hemodialysis Initiated and Not Initiated groups. Kidney biopsy specimens’Ki-67, CD68 and Bcl-2 staining scores were defined as below 5% "0", 5-10% "+1", 11-20% "+2", over 20% "+3". Patients demographic, laboratory data, status ofhemodialysis initiation, and mortality wereobtained from medical records and immunohistochemical staining scores were compared between groups. Estimated glomerular filtration rates (eGFR) were assessed at 0, 6, and 12 months, except patients’ ongoing hemodialysis. Results: A total of 56 patients were diagnosed as crescentic glomerulonephritis. Pauci-immune crescentic glomerulonephritis (58.9%) was the most common etiology. Hemodialysis was initiated in 36 patients. Mean age, baseline creatinine, urea, C-reactive protein levels were significantly higher and, hemoglobin and proteinuria levels were significantly lower in the Hemodialysis Initiated group. Immunohistochemical staining scores were not significantlydifferentbetween groups. In Hemodialysis Initiated group, 8.33% of patients were recovered from hemodialysis. Mortality rates were 44,4% and 10% in patients in the group of hemodialysis initiated and not initiated group respectively. When we combine the hemodialysis not initiated patients and patients recovered from hemodialysis;median eGFR atbaseline, 6th and 12th month were32.9, 43.9, and 58.0 mL/min/1.73m2, respectively (p=0.016). Conclusion: Hemodialysis initiation was associated with high mortality. Degree of immunohistochemical staining was similar in both groups. Increment in eGFR was documented in first year in patients, other than the ones on still on hemodialysis.

RESUMO INTRODUÇÃO: Em pacientes com doença renal crônica (DRC), toxinas urêmicas e hipervolemia contribuem para aumentar o risco cardiovascular. Nosso objetivo foi determinar o estado de hidratação em pacientes com DRC iniciando hemodiálise (HD) e avaliar os efeitos da correção da hipervolemia sobre o sistema cardiovascular. MÉTODOS: Foram incluídos 52 pacientes que haviam acabado de iniciar HD. Antes do início da sessão, foram determinados o diâmetro e o volume atrial esquerdo, a velocidade de onda de pulso (VOP) e o índice de amplificação sistólica (“augmentation index”, AI). Além disso, realizamos análise da composição corporal por bioimpedância elétrica (BIA) e mensuramos os níveis plasmáticos de peptídeo natriurético tipo B. Os mesmos procedimentos foram repetidos após os pacientes alcançarem o “peso seco”. RESULTADOS: O peso corporal dos pacientes foi reduzido, em média, em 4,38 kg. Na BIA, todos os parâmetros, exceto o índice de gordura corporal, foram significativamente reduzidos após a hemodiálise. Antes da HD, a VOP se correlacionou positivamente com idade e razão cardiotorácica (RCT), e negativamente com a massa magra e a água intracelular. Ao final da hemodiálise, a VOP se correlacionou positivamente com idade, RCTe pressão de pulso central, correlacionando-se negativamente com a Lean Tissue Index (LTI). CONCLUSÃO: A hemodiálise melhora a VOP por meio da redução da volemia. O controle da hipervolemia via ultrafiltração pode reduzir a mortalidade cardiovascular por meio da redução da rigidez arterial.

SUMMARY AIM: Uremic toxins and excess fluid contributes to increased cardiovascular (CV) risk. We aimed to determine the body fluid status in patients who are just starting hemodialysis (HD) and to determine the effects of excess fluid removed by HD on the CV system. METHODS: A total of 52 patients with chronic kidney disease (CKD) who had just started HD were included. Before the HD, the left atrial diameter was measured, the volumes were calculated, the pulse wave velocity (PWV) and the augmentation index (AIx) were measured, the bioimpedance analysis (BIA) was performed, the blood was taken for brain natriuretic peptide (BNP). When patients reached their dry weight with HD, the same measurements were repeated. RESULTS: Measurements were made to determine the volume status, and all parameters except the fat tissue index decreased significantly after HD. With the removal of fluid by HD, there was an average weight reduction of 4.38 kilograms. Positive correlations between PWV and age and cardiothoracic ratio (CTR) before HD were determined. Negative correlations were found between PWV and lean tissue mass (LTM) and intracellular water (ICW) before HD. At the end of the last HD, PWV was positively correlated with age, CTR, central pulse pressure Correlation between pulse wave velocity and LTI was negative CONCLUSIONS: HD significantly improves PWV in patients reaching dry weight. Reduction of fluid excess by ultrafiltration in HD patients may reduce CV mortality by reducing arterial stiffness.

Summary Objective: Arterial stiffness refers to arterial wall rigidity, particularly developing in central vessels. Arterial stiffness increases in early stage chronic kidney disease (CKD), and it is a strong predictor of cardiovascular and all cause mortality. Vitamin D has beneficial effects on blood pressure, vascular endothelial function and arterial stiffness. 25-hydroxyvitamin D (25(OH)D) deficiency is quite common worldwide and in the CKD population. We aimed to evaluate the prevalence of 25(OH)D deficiency and its relation with arterial stiffness in CKD. Method: Our study included 101 patients (51 male, 50 female), with stages 3B-5 CKD not on dialysis. A single-cuff arteriograph device (Mobil-O-Graph) was used to evaluate arterial stiffness parameters of pulse wave velocity (PWV) and augmentation index (Alx@75). The patients were divided into two groups: group I vitamin D non-deficient [25(OH)D > 15 ng/mL] and group II vitamin D deficient [25(OH)D ≤ 15 ng/mL]. Results: Overall, the mean 25(OH)D level was 14.1±7.9 ng/mL and 70 patients (69.4%) were vitamin D deficient. The mean Alx@75 value was significantly higher in group II (28.6±10.8% vs. 23.3±13.5%, p=0.038). PWV was higher in group II, but the difference was not significant. Group II exhibited significantly lower serum albumin (p<0.001), hemoglobin (p=0.005), calcium (p=0.041) and estimated glomerular filtration rate (eGFR) (p=0.041), but significantly higher 24-hour proteinuria (p=0.011) and more females (p=0.006). Vitamin D was negatively correlated with Alx@75 augmentation pressure, parathyroid hormone, proteinuria and body mass index, and positively correlated with albumin, hemoglobin, eGFR, calcium and transferrin. 25(OH)D was independently associated with Alx@75 (beta=-0.469, p=0.001) and albumin (beta=0.447, p=0.002). Conclusion: In CKD patients 25(OH)D deficiency was common, particularly in females. Level of 25(OH)D was independently associated with Alx@75.

Summary Acute kidney injury is an important cause of mortality and morbidity today and can occur due to several reasons. As time, geographic regions, and living conditions change, various etiological agents arise with nephrotoxic effects. Awareness of such nephrotoxic effects has been raised with the increasing frequency of addictive substance use, especially among young people in society.

Hypertension (HT) represents a major public health problem affecting many individuals worldwide. It is well known to be an important risk factor for the development of cerebrovascular and cardiovascular diseases. Classifying hypertension as 'primary' or 'secondary' depends on the underlying mechanism. In 5 to 10% of hypertensive patients, HT develops 'secondary' to a separate mechanism that has been encountered with increasing frequency in the tertiary refferral centers. The frequent causes of secondary hypertension include renal parenchymal disease, renal artery stenosis, primary hyperaldosteronism, phaeochromocytoma and Cushing's syndrome. Polyarteritis nodosa (PAN) can involve any organ and in varying degrees. Here we present a young hypertensive patient diagnosed as PAN with the angiographic findings of multiple microaneurysms involving celiac, renal and superior mesenteric arteries and associated with a rarely seen neurological entity-PRES syndrome.

La hipertensión es uno de los principales problemas de salud pública, que afecta a muchas personas en todo el mundo. Se sabe que es un importante factor de riesgo para el desarrollo de enfermedades cerebrovasculares y cardiovasculares. Su clasificación como "primaria" o "secundaria" depende del proceso subyacente. En el 5-10% de los pacientes hipertensos, se trata de un problema "secundario" a otro proceso de creciente frecuencia en los centros de atención terciaria. Las causas más frecuentes de la hipertensión secundaria son: enfermedades del parénquima renal, estenosis de la arteria renal, hiperaldosteronismo primario, feocromocitoma y el síndrome de Cushing. La poliarteritis nodosa puede afectar a cualquier órgano y en diferentes grados. A continuación presentamos a un paciente joven hipertenso al que se le ha diagnosticado poliarteritis nodosa, cuya angiografía muestra múltiples microaneurismas que afectan al tronco celíaco, a la arteria renal y a la arteria mesentérica superior, asociada a un síndrome de encefalopatía posterior reversible de entidad neurológica poco visto.