Embarazo en hemodiálisis crónica: experiencia de un hospital universitario / Pregnancy during chronic hemodialysis. A series of cases

Background: Pregnancies in women with end stage renal failure are uncommon. However, correction of anemia and improvement in dialysis techniques increases the rate of successful pregnancies. Aim: To describe a 16 years' experience treating pregnant women on hemodialysis and to analyze maternal-fetal outcomes. Materials and Methods: Observational study of a dialysis center historical cohort in a university hospital, between 2001 and 2016. Results: Thirteen pregnancies were found in 11 women aged 23 to 32 years, 77% on dialysis prior to pregnancy. Residual diuresis was 1,300 [625-1,575] mL in 24 hrs. The baseline hemoglobin was 9.0 [7.6-9.9] g/dL and 92% of patients did not use contraception. The pre-dialysis blood urea nitrogen was 34 [29-36] mg /dL. An ultrasound to confirm pregnancy was done in all. At 23 [14-25] weeks of pregnancy, dialysis hours were increased, reaching 24 [19.5-24.0] hours per week. The most common complications were severe arterial hypertension (54%), severe anemia (46%), polyhydramnios (31%) and severe intrauterine growth retardation (IUGR) (23%). The median time of pregnancy at delivery was 34 [29-34] weeks. Neonatal median hospitalization length was 4 [4-32] days, with 18% of neonatal deaths. Conclusions: Pregnancies in dialysis are no longer exceptional. Despite better maternal and fetal outcomes, morbidity and mortality remains higher than in the normal population, which makes multidisciplinary management essential.

Hipoxemia espuria por hiperleucocitosis: Reporte de un caso y revisión de la literatura / Spurious hypoxemia due to hyperleukocytosis: Report of one case

Background: Arterial gasometry is considered the gold standard for establishing a diagnosis of respiratory failure of any etiology. However, there are some circumstances in which it loses specificity, making necessary to consider other tests such as pulse oximetry to adequately determine hypoxemia. We report a 67 years old patient with sudden hypoacusia, right hemiparesis and polypnea. His laboratory exams on admission, showed extreme hypoxemia in several readings, without correlation to the patient's clinical condition nor the pulse oximetry, and a leukocytosis of 800.000 cells x ml, with many immature cells. Chronic myeloid leukemia was diagnosed and treatment with hydroxyurea was initiated, achieving normalization in the arterial gases in accordance with the fall of the white cell count. Interpretation of laboratory findings according to the general clinical context of the patient allowed to suspect a spurious hypoxemia, saving the patient from unnecessary and risky interventions.

Rol de Klotho y FGF23 en la regulación del fosfato y calcio plasmático / Klothos role and FGF23 in the regulation of phosphate and plasmatic calcium

Recently, two proteins have been discovered, named Klotho and FGF23, which are involved in several physiologic phenomena. One of the most relevant is the reduction of phosphatemia and the increase of phosphaturia. This effect is mainly caused by the activation of the membrane receptor FGFR1 by a joined action of Klotho and FGF23 (called Klotho/FGF23 pathway). It has been proved that Klotho/FGF23 suppresses production and secretion of parathyroid hormone (PTH) in parathyroid gland, reduces active vitamin D levels by inhibition of 1α-hydroxylase synthesis and increased expression of 24-hydroxylase in the kidney. It is also described that FGF23 expression is promoted by active vitamin D and plasmatic phosphate. Because of that, it has been proposed the existence of a bone-kidney-parathyroid endocrine axis, which regulates serum phosphate levels. Although it has not been studied yet, it is likely that Klotho and FGF23 also have a role in regulation of serum calcium levels, due to the effects of Klotho/FGF23 over key calcium regulators. The discovery of Klotho/FGF23 axis has expanded our knowledge concerning the endocrine mechanisms of the calcium-phosphate metabolism, and it might also help in the development of new clinical approaches and treatments of calcium and phosphate disorders.

Función y disfunción endotelial / Endothelial function and dysfunction

El endotelio es el principal regulador de la homeostasis vascular, modula el balance vasoconstricción/vasodilatación, inhibe la proliferación/migración de células musculares de la pared vascular (VSMC), y también modula la hemostasia. La disfunción endotelial es un evento que precede los cambios morfológicos característicos de la aterogénesis y contribuye al desarrollo de complicaciones de la placa ateroesclerótica. Además, la evidencia disponible indica que el desarrollo de disfunción endotelial participa en el daño cardiovascular en condiciones que abarcan desde procesos fisiológicos como el envejecimiento, hasta procesos fisiopatológicos diversos como hipertensión arterial, insuficiencia cardíaca, insuficiencia renal, diabetes mellitus, coagulación intravascular, preeclampsia, enfermedades inflamatorias y la apnea del sueño(1, 2). El objetivo del presente artículo es revisar brevemente la función endotelial, definir disfunción endotelial en un contexto amplio y presentar los mecanismos generales que conducen a disfunción endotelial en relación a las enfermedades cardiovasculares más prevalentes.

The endothelium is the main regulator for vascular homeostasis. The functions of the endothelium include regulation of the balance between vasoconstriction and vasodilation, inhibition of proliferation and migration of smooth muscle cells (VSMC) from the vascular wall and modulation of hemostasis. Endothelial dysfunction precedes the morphological changes characteristic of atherogenesis and contributes to the development atherosclerotic plaques. Also, current evidence indicates that the development of endothelial dysfunction is associated with cardiovascular damage in several physiological conditions such as arterial hypertension, heart and renal failure, diabetes mellitus, intravascular coagulation, preeclampsia, inflammatory disease and sleep apnea (1,2). The purpose of this article is to provide a brief review of endothelial dysfunction, broadly define endothelial dysfunction, and to present general mechanisms that are correlated with endothelial dysfunction in most prevalent cardiovascular diseases.

La insulinoterapia intensificada más antineuríticos es superior a antineurítico puro en neuropatía diabética dolorosa / Intensified insulin therapy plus antineuritic medication is more effective than antineuritics alone in painful diabetic neuropathy

Background: The basis of the treatment of painful diabetic neuropathy is the use of drugs that block the transmission of pain (antineuritics) and a good metabolic control of underlying disease. Aim: To describe the outcomes of 17 type-2 diabetics with painful neuropathy, treated between 1988 and 2005 with symptomatic therapy plus intensified insulin. Material and methods: Review of medical records of 17 type-2 diabetic patients, aged 63±11 years and a duration of diabetes of 15±8 years. All patients received intensified insulin therapy with 0.35 units/kg of NPH insulin (2/3 before breakfast and 1/3 evening meal), plus capillary glucose measurements and regular insulin (with sliding-scale centered in ~0.1 units/kg) before the 3 main meals. All patients were also treated with gabapentin, nortriptyline or clomipramine. Pain was assessed using a visual analog score of 10 points. Results: After 1 year, glycosilated hemoglobin decreased from 10.0±1.4 percent to 7.7±1.2 percent (p~=0.003). Pain decreased from 10 to 5.1±3.3 at one month, 2.3±3.2 at six months, and 3.1±3.6 at 1 year (p <0.01). There was a direct statistical correlation between the reduction of HbA1C and pain decline (r =0.736; p =0.037). Pain scores were lower than those reported elsewhere for Pregabalin (n =76; p =0.05), Lamotrigine (n =27; p <0.0005), Topiramate (n =208; p <0.005), and Gabapentin (n =84; p <0.025). The lack of difference to Sodium Valproate (n =21; p =0.07) had borderline significance. Conclusions: The addition of intensified insulin therapy to the symptomatic treatment of painful neuropathy in type-2 diabetics, significantly enhanced the reduction of pain. The lowering of glycosilated hemoglobin was a significant predictor of success in pain reduction.