Refeeding syndrome as described in 1507 by Antonio Benivieni in Florence.

In 1981, Weinsier and Krumdieck described death resulting from overzealous total parenteral nutrition in two chronically malnourished, but stable, patients given aggressive total parenteral nutrition. This was the birth of what is now called the refeeding syndrome, a nutrition-related disorder associated with severe electrolyte disturbances. The purpose of this work is to demonstrate that refeeding syndrome was first described medically in Florence by Antonio Benivieni in 1507 in his book On Some Hidden and Remarkable Causes of Diseases and Cures. What we now know as refeeding syndrome was described in Report No. LVII of that book. The condition occurred as a result of the famine that affected Florence in 1496. The report documents (i) death due to starvation, (ii) death due to ingestion of deteriorated/toxic foods (inevitable in times of famine when healthy food is scarce), (iii) death caused by excessive food ingestion after forced, prolonged abstinence from food in adults, (iv) the death of breast-fed children and of their starved mothers eating to satiety and (v) the more favourable clinical outcome of those admitted to hospitals. It is possible that Benivieni was inspired by the description of the deaths of starved deserters in the book The Jewish War (70 AD) by the Romano-Jewish historian Flavius Josephus. Nevertheless, Benivieni wrote the first medical account of the central clinical features of refeeding syndrome. The main, broad clinical aspects of refeeding syndrome, described by Weinsier and Krumdieck in 1981, had been documented in medical literature four centuries earlier by Benivieni.

John XXI, the Pope Philosopher and Physician-Scientist of Portuguese Origins Died of Crush Syndrome in 1277.

The aim of this work is to refer on the death due to crush syndrome in 1277 of Pope John XXI, philosopher, logician, anatomist, physician scientist, university professor of medicine at the university of Siena and author of books adopted for nearly 4 centuries in universities in the Middle Ages. The Pope died crushed by the ceiling of his office which had been built in rush to meet his need for a quiet and warm place, his need of light and nature. There he attended to his duties of governing the church, studied fine theological questions, inspected the stars, made experiments and discussed with the renowned ophthalmologists who in those days made Viterbo the center of the study on vision. Following the fall of the ceiling of his apartment, John XXI was extracted alive from among the pieces of wood and stones. However, a few days after the disaster, he died in bad conditions (miserabiliter). He experienced a typical death due to crush syndrome which was described for the first time by Antonino D'Antona, following the Messina-Reggio Calabria 1908 earthquake. He was born (c. 1210-1220) in Lisbon as Pedro Hispano (Peter of Spain). He had regular trivium and quadrivium courses at the University of Paris under Albertus Magnus, a talented naturalist. He became Master of Arts, then studied medicine out of Paris (probably Montpellier or Salerno). He wrote three treatises (On the eye (De oculo), The Treasury of Medicines for the Poor (Thesaurus Pauperum) and Little Summaries of Logic (Summulae Logicales)) which were used in the European universities from the 13th to the beginning of the 18th century. Pedro Hispano was advisor of King Alphonso III for affairs inherent to the Church, bishop of Braga and then Cardinal Bishop of Tusculum and Pope as John XXI. He was buried in the Cathedral of Viterbo, the city where he had settled the seat of the Pontiff.

Renal response to an oral protein load in patients with central diabetes insipidus before and after treatment with vasopressin.

AIM: Different factors have been hypothesized to play a role in the cascade of events associated with the protein-induced glomerular response. However, scant data are available on the possible functional effect of vasopressin (VP) on the glomerular filtration rate (GFR) in humans with central diabetes insipidus (CDI), which was the aim of the present study. METHOD: Renal function was studied under fasting conditions (baseline) and after a meat meal in 16 patients with CDI before and after treatment with desmopressin (DDAVP) and in 16 control subjects. GFR was measured by the inulin method. RESULTS: At baseline, the GFR was lower in patients with CDI. Treatment with DDAVP resulted in an insignificant increase in GFR, which was not statistically different from untreated patients. After an acute oral protein load, the GFR increased, peaking at 45 min post meal in controls, and at 135 min post meal in treated and untreated CDI patients. CONCLUSION: After a meat meal, the peak GFR response is delayed in CDI patients suggesting that VP might indirectly affect tubule-glomerular feedback.

[Laws regulating transplantation should express the contemporaneity. Questions to the constitutionalist Francesco Paolo Casavola and to the philosophers Remo Bodei and Aldo Masullo about the possibility deciding the destiny of one's own organs at the time one decides on how to die and on contacts between donor families and recipients.]

Transplantation represents modernity thus the laws regulating the procedure should be continuously renovated and remodeled in order to take full advantage of progress. The debate is about Law no. 219, December 22, 2017 and on Law no. 222, April 1, 1999. The quests are a) about the possibility to modify the first so that people deciding on how they want to die, may also decide about their willingness to allow the removal of their organs for transplantation and b) the possibility for donor families and recipients to have contacts after transplantation in the case both sides agree. Questions were emailed to the constitutionalist Francesco Paolo Casavola, immediate Past President of the National Committee for Bioethics, and to the philosophers Remo Bodei and Aldo Masullo. Their answers received by September 16, support the idea a) to include in the Law no. 219, 2017 the possibility to decide not only on the modality one wants to die but also on the possibility to allow his own organs to be removed for transplantation and b) to liberalize contacts between donor families and recipients when both side agree. For both changes there is enough evidence of their feasibility-necessity. The answers related to contacts between donor families and recipients support the decision of the National Committee for Bioethics on September 27, 2018. Professor Casavola also suggests that contacts should organized and supervised by the ethical committees of the hospitals where the transplantation procedure is accomplished.

Aquaporins, vasopressin, and aging: current perspectives.

Functioning of the hypothalamic-neurohypophyseal-vasopressin axis is altered in aging, and the pathway may represent a plausible target to slow the process of aging. Arginine vasopressin, a nine-amino acid peptide that is secreted from the posterior pituitary in response to high plasma osmolality and hypotension, is central in this pathway. Vasopressin has important roles in circulatory and water homoeostasis mediated by vasopressin receptor subtypes V1a (vascular), V1b (pituitary), and V2 (vascular, renal). A dysfunction in this pathway as a result of aging can result in multiple abnormalities in several physiological systems. In addition, vasopressin plasma concentration is significantly higher in males than in females and vasopressin-mediated effects on renal and vascular targets are more pronounced in males than in females. These findings may be caused by sex differences in vasopressin secretion and action, making men more susceptible than females to diseases like hypertension, cardiovascular and chronic kidney diseases, and urolithiasis. Recently the availability of new, potent, orally active vasopressin receptor antagonists, the vaptans, has strongly increased the interest on vasopressin and its receptors as a new target for prevention of age-related diseases associated with its receptor-altered signaling. This review summarizes the recent literature in the field of vasopressin signaling in age-dependent abnormalities in kidney, cardiovascular function, and bone function.

Effects of bed-rest on urea and creatinine: correlation with changes in fat-free mass.

BACKGROUND: Bed-rest experiments are designed for investigation on catabolic effects of hypokinetic conditions and/or for microgravity simulation in on-ground aerospace research. Bed-rest effects include a reduction in fat-free mass and muscle mass. Urea and creatinine are catabolites of endogenous protein and of muscular energetic metabolism which are excreted mainly by the kidney. The study investigated on urea, creatinine, and kidney function during bed-rest. METHODS: Twenty healthy young men underwent a 7-day adaptation period (day-6 to day-0) and a 35-day bed-rest experiment (day1 to day35) during normocaloric diet. Urine were collected from day-3 to day0 (baseline) and from day1 to day35. Blood samples and anthropometrical data were collected at day0 (baseline) and bed-rest days 7, 14, 21, 28, and 35. RESULTS: Bed-rest reduced plasma volume, weight, fat-free mass, and muscle mass (P<0.001). During bed-rest there was a transient increase in plasma and urinary urea, a decrease in plasma creatinine, and no change in urinary creatinine. The overall integral of changes from day0 to day35 was on average +101.7 mg/dL for plasma urea (95%CI = +43.4/+159.9), +82.2 g/24 h for urinary urea (95%CI = +55.8/+108.7), -2.5 mg/dL for plasma creatinine (95%CI = -3.1/-1.9). Bed-rest reduced plasma cistatyn C also, which was used as mass-independent marker of glomerular filtration rate (-13.1%, P<0.05). Correlations with final reduction in fat-free mass and muscle mass were significant for the overall integral of changes in urinary urea from day0 to day35 (R = 0.706, P<0.001) and for early changes in urinary urea and plasma urea from day0 to day7 (R = 0.566, P = 0.009 and R = 0.715, P<0.001, respectively). CONCLUSIONS: Study results shows that urea is a marker of catabolic conditions secondary to hypokinetic conditions.

A decrease in aquaporin 2 excretion is associated with bed rest induced high calciuria.

BACKGROUND: Exposure to microgravity or immobilization results in alterations of renal function, fluid redistribution and bone loss, which couples to a rise of urinary calcium excretion. We recently demonstrated that high calcium delivery to the collecting duct reduces local Aquaporin-2 (AQP2) mediated water reabsorption under vasopressin action, thus limiting the maximal urinary concentration and reducing calcium saturation. To investigate renal water balance adaptation during bed rest, a model to mimic the effects of microgravity on earth, the effect of changes in urinary calcium on urinary AQP2 excretion were assessed. METHODS: Ten healthy men (aged 21-28 years) participated in the experiment. Study design included 7 days of adaptation and 35 days of continuous bed rest (days -6 to 0 and 1 to 35, respectively) under controlled diet. Food records and 24-hour urine samples were collected daily from day -3 to 35. Changes in blood hematocrit were used as an indirect index of plasma volume changes. AQP2 excretion was measured by ELISA. RESULTS: Bed rest induced bone demineralization and a transient increase in urinary calcium followed by transient decrease in AQP2 excretion, which can reduce the urine concentrating ability causing plasma volume reduction. The return of calciuria to baseline was followed by a recovery of AQP2 excretion, which allows for a partial restoration of plasma volume. CONCLUSIONS: These results further support the view that urinary calcium can modulate the vasopressin-dependent urine concentration through a down-regulation of AQP2 expression/trafficking. This mechanism could have a key role in the prevention of urine super-saturation due to hypercalciuria.

Protein intake and kidney function in the middle-age population: contrast between cross-sectional and longitudinal data.

BACKGROUND: Protein intake is considered a determinant of glomerular filtration rate (GFR). Urinary urea is an objective marker of protein intake. The population-based study investigated, cross-sectionally and longitudinally, the association of protein intake with GFR, indexed by estimated GFR (eGFR). METHODS: Data were collected on overnight urinary urea, serum creatinine (S-cr), eGFR and other variables in 1522 men and women aged 45-64 years who participated in the Gubbio study (baseline). S-Cr, eGFR and other variables were re-assessed in 1144 of the 1425 survivors after 12-year follow-up. RESULTS: At baseline, mean ± SD was 84.0 ± 11.4 mL/min × 1.73 m(2) for eGFR calculated by CKD-Epi equation and 1.34 ± 0.57 g/day per kg of ideal weight for protein intake assessed by measurements of overnight urine excretion of urea nitrogen. Cross-sectional analyses of baseline data indicated a positive correlation of protein intake with eGFR (R = 0.180, P < 0.001). In multi-variable regression, 1 g/day higher protein intake related to 4.7 mL/min × 1.73 m(2) higher eGFR [95% confidence interval (CI) = 3.7/5.7]. At follow-up, mean ± SD of 12-year eGFR change was -11.6 ± 9.0 mL/min × 1.73 m(2). Baseline protein intake correlated with more negative eGFR change (R = -0.251, P < 0.001). In multi-variable regression, 1 g/day higher protein intake related to -4.1 mL/min × 1.73 m(2) more negative eGFR change (95% CI = -5.1/-3.1) and to 1.78 risk for incidence of eGFR < 60 mL/min × 1.73 m(2) (95% CI = 1.15/2.78). CONCLUSIONS: In middle-aged adults, high protein intake is associated cross-sectionally with higher GFR but longitudinally with greater GFR decline over time.