Early referral to nephrological care improves long-term survival and hospitalization after dialysis initiation, independent of optimal dialysis start - a call for harmonization of reimbursement policies.

Early treatment of kidney disease can slow disease progression and reduce the increased risk of mortality associated with end-stage kidney disease. However, uncertainty exists whether early referral (ER) to nephrological care per se or an optimal dialysis start impacts patient outcome after dialysis initiation. We determined the effect of ER and suboptimal dialysis start on the 3-year mortality and hospitalizations after dialysis initiation. Between January 2015 and July 2018, 349 patients with ≥1 month of follow-up started dialysis at nine Romanian dialysis clinics. After excluding patients with COVID-19 during follow-up, 254 patients (97 ER and 157 late referral) were included in this retrospective study. The observational period was truncated at 3 years, death, or loss to follow-up. Clinical and laboratory data were retrieved from the quality database of the nephrological care providers. Patients were followed for a median (25-75%) of 36 (16-36) months. At dialysis start, ER patients had higher hemoglobin, phosphate, and albumin levels and started dialysis less often via a central dialysis catheter (p < 0.001 for each). Logistic regression analysis demonstrated an independent lower risk for frequent hospitalizations for ER patients (odds ratio 0.22 (95% confidence interval 0.1-0.485), p < 0.001), and Cox regression analysis revealed an improved survival (hazard ratio 0.540 (95% confidence interval 0.325-0.899), p = 0.02), both independent of optimal dialysis start. In conclusion, early referral to nephrological care was associated with improved survival and lower hospitalization rates during the three years after dialysis initiation, independent of optimal dialysis start. These results strongly support the reimbursement of nephrological care before dialysis initiation.

[Lipid profile and alteration of body composition in growth hormone deficient adults]. / Perfil lipídico e composição corporal na deficiência do hormônio de crescimento em adultos.

BACKGROUND: The growth hormone deficiency (GHD) syndrome in adults and the increased associated cardiovascular risk have been extensively studied in recent years. Abnormal body composition with excess of visceral adiposity and adverse lipid profile are important features of this syndrome. Abnormal lipid profile has been described with increased levels of total cholesterol (C), LDL-cholesterol (LDL-C), triglycerides, decreased levels of HDL-cholesterol (HDL-C) and apolipoproteins abnormalities. METHODS: Lipid profile and the amount of visceral adipose tissue were studied in 31 GHD adults compared with a control group of healthy subjects matched for age, gender and body mass index (BMI). Visceral adipose tissue was evaluated by abdominal computed tomography and anthropometric measurements--BMI (kg/m2) and waist circumference (cm). The lipid profile was studied by measurement of C, LDL-C, HDL-C, triglycerides, apolipoproteins A and B, and Lipoprotein (a). RESULTS: The GHD adults showed increased visceral adipose tissue (156.66 +/- 72.72 vs. 113.51 +/- 32.97 cm2, p = 0.049), higher levels of triglycerides (158.58 +/- 80.29 vs. 97.17 +/- 12.37 mg/dl; p = 0.007) and lower HDL- cholesterol (45.41 +/- 13.30 vs. 55.34 +/- 14.31 mg/dl; p = 0.002). There were no differences in others aspects of lipid profile and anthropometric measurements. CONCLUSION: Growth Hormone Deficient adults showed increased visceral adipose tissue, higher levels of triglycerides and lower HDL- cholesterol levels.

Glucose metabolism and visceral fat in GH deficient adults: 1 year of GH replacement.

The aim of the current study is to evaluate the effects of 12-month growth hormone (GH) replacement on glucose metabolism and visceral fat in 24 adults with GH deficiency (11 men, 13 women, age 41+/-1.9 year, BMI 27+/-1.2 kg/m2. Glucose metabolism was measured in the fasting state by the homeostatic model assessment (HOMA) insulin resistance index and during a standard oral glucose tolerance test (OGTT). Data were analyzed by HOMA and the insulin sensitivity index (ISI)-composite derived from the OGTT. Visceral fat was evaluated by CT scan. GH-deficient adults had increased visceral fat (P=0.029) with lower fasting glucose levels (P=0.004) than the control group on baseline evaluation. GH replacement induced deterioration in glucose metabolism, with progressive increment in fasting insulin levels at 6 and 12 months (P=0.024) and in 2-h-OGTT insulin levels at 3, 6 and 12 months (P=0.001). Plasma glucose levels did not change during the study. There was a deterioration in insulin sensitivity index observed by an increase in HOMA-IR (P=0.049) and a reduction in the ISI-composite (P=0.028), both at 12 months of replacement. Visceral fat and waist-to-hip-ratio (WHR) reduced not only at month 6 but also at month 12 (P=0.0001 and 0.023, respectively). In conclusion, 12 months of GH replacement seem to impair glucose homeostasis, despite favorable alterations in body composition.

Perfil lipídico e composição corporal na deficiência do hormônio de crescimento em adultos / Lipid profile and alteration of body composition in growth hormone deficient adults

OBJETIVO: A síndrome da deficiência de hormônio de crescimento (DGH) no adulto e o conseqüente aumento no risco cardiovascular têm sido bastante estudados nos últimos anos. De grande relevância clínica são as alterações na composição corporal com aumento do tecido adiposo visceral e perfil lipídico adverso. MÉTODOS: Estudou-se o perfil lipídico e o tecido adiposo visceral de 31 adultos com DGH comparado com um grupo controle de indivíduos saudáveis pareados por idade, sexo e índice de massa corporal (IMC). A avaliação da gordura visceral foi feita por tomografia computadorizada de abdome e por medidas antropométricas, através do IMC (Kg/m²) e da medida da cintura (cm). A avaliação do perfil lipídico foi obtida através de dosagens laboratoriais de colesterol (CT), triglicerídeos (TG), HDL, LDL, apolipoproteínas A e B e lipoproteína (a). RESULTADOS: Foi observado aumento do tecido adiposo visceral nos pacientes DGH (156,66 ± 72,72 vs. 113,51 ± 32,97 cm²; p-valor = 0,049), além de aumento nos níveis de TG (158,80 ± 80,29 vs. 97,17 ± 12,37 mg/dl; p-valor = 0,007) e diminuição nos níveis de HDL (45,41 ± 13,30 vs. 55,34 ± 14,31 mg/dl; p-valor = 0,002). Não houve diferença entre os demais parâmetros do perfil lipídico e nas medidas antropométricas. CONCLUSÃO: Adultos deficientes de GH apresentam aumento da adiposidade visceral e aumento das concentrações de TG com diminuição das concentrações de HDL.

Avaliação do metabolismo glicídicoe da gordura visceral em adultos deficientes de hormônio de crescimento / Evaluation of glucose metabolism and visceral adiposity in growth hormone deficient adults

A síndrome da deficiência de hormõnio de crescimento (DGH) no adulto e o conseqüente aumento no risco cardiovascular têm sido bastante estudados nos últimos anos. Com o objetivo de avaliar as alterações na composição corporal e a presença de resistência à insulina em adultos com DGH, estudamos 27 pacientes comparados a 27 indivíduos saudáveis pareados por idade, sexo e índice de massa corporal, através de tomografia computadorizada de abdomen para medida da gordura visceral e teste de tolerância oral à glicose (TTOG), com curva de glicose e insulina e estimativa da resistência à insulina pelo Homeostasis Model Assessment (HOMA). Observamos, nos pacientes, aumento do tecido adiposo visceral (p= 0,008) sem aumento da freqüência de alterações no TTOG. As glicemias e insulinemias basais e após 2 horas de sobrecarga oral de glicose e as áreas sob as curvas de glicose e insulina foram semelhantes ao grupo controle (p> 0,05). Não houve diferença na sensibilidade à insulina pelo método HOMA (p= 0,989). Houve correlação positiva significativa da medida de gordura visceral nos pacientes com as dosagens de glicemia (r= 0,583; p= 0,001) e insulina (r= 0,728; p= 0,001) após sobrecarga de glicose e as áreas sob a curvas de glicose (r= 0,403; p= 0,040) e insulina (r= 0,713; p= 0,001), porém sem correlação significativa nos controles (r< 0,40; p> 0,05). Em conclusão, não houve alteração significativa no metabolismo glicídico, apesar do aumento da adiposidade visceral observada em adultos DGH.