scholarly journals THE CONTROL OF THE RENAL EXCRETION OF WATER

1942 ◽  
Vol 76 (4) ◽  
pp. 387-399 ◽  
Author(s):  
James A. Shannon

1. The administration of the posterior pituitary antidiuretic hormone by constant intravenous infusion has been used to examine the two characteristic actions of the hormone; namely, the facilitation of the active renal tubular reabsorption of water distally in the nephron and the inhibition of the renal tubular reabsorption of sodium proximally. 2. Experimental evidence was obtained which indicates that variations in the excretion of water and electrolyte involve the integration of these two actions with obscure variables which are discemible in the experimental data but are not subject to definition at this time. 3. Graded antidiuresis in the animal with diabetes insipidus, when normally hydrated, was only obtained in the range of 0.001 to 0.005 unit (pressor) per hour. This range of hormone administration was also found to be physiologically active in the normal animals. These observations together with others permit the placing of the normal rate of liberation of the antidiuretic hormone in a10 to 15 kilo dog in the range of 0.001 to 0.005 unit per hour.

1964 ◽  
Vol 45 (1) ◽  
pp. 151-160 ◽  
Author(s):  
Bent Nielsen

ABSTRACT The effect of injection of physiological doses of commercial preparations of lysine- or arginine-vasopressin on the renal excretion of magnesium and calcium was studied in 20 hydrated normal subjects. In the majority of the experiments the injections were followed by a rise in the rate of excretion of magnesium as well as of calcium. In 3 subjects endogenously induced antidiuresis produced similar effects. In 1 case no changes were revealed during antidiuresis. The most probable explanation of these results would seem to be that the antidiuretic hormone exerts an inhibitory effect on the renal tubular reabsorption of magnesium and calcium.


1956 ◽  
Vol 187 (3) ◽  
pp. 529-535 ◽  
Author(s):  
Gerhard Giebisch ◽  
Martha B. MacLeod ◽  
Frederic Kavaler

Radioiodide and creatinine clearances were measured simultaneously in dogs. Osmotic diuresis was induced by loading with mannitol, sodium salts of various anions such as chloride, bromide, iodide, nitrate and ferrocyanide, and by the administration of mercurial diuretics. Results of these experiments are compared with those obtained during water diuresis. No evidence for active tubular reabsorption of radioiodide could be observed. Renal tubular reabsorption of I131 was found to be chiefly determined by the degree of tubular water reabsorption and hence the transtubular diffusion gradient of radioiodide. Nonspecific effects of other anions in the tubular urine may modify passive tubular reabsorption: anions less readily reabsorbed displace I131 from the urine and depress its renal clearance. Indirect evidence suggests that about 95% of filtered radioiodide is reabsorbed at a tubular site proximal to that of final water reabsorption.


1973 ◽  
Vol 44 (2) ◽  
pp. 99-111 ◽  
Author(s):  
Frances T. Lester ◽  
D. C. Cusworth

1. The renal handling of lysine was studied during the intravenous infusion of a lysine load given in such a way that the plasma lysine concentration was constantly increasing. Theoretical renal thresholds, and maximum rates of renal tubular reabsorption of lysine, have been determined in three normal adults, five homozygous cystinuric patients, and three persons, two ‘completely’ and the third ‘incompletely’ recessive, heterozygotes for cystinuria. All the cystinuric patients were found to have thresholds at less than 1 mg of lysine/100 ml of plasma; the thresholds of all three heterozygotes fell within the same range as those of the three normal persons, that is, at values only two to three times the fasting plasma lysine concentration. 2. Not only was the lysine load shown to greatly increase the excretion of cystine, arginine and ornithine in the normal and heterozygous persons, but it was also shown to increase the already high clearance of these three amino acids in three of the homozygous cystinuric patients. 3. It was shown that a water diuresis alone will not cause increased excretion of any amino acids except taurine.


2011 ◽  
Vol 164 (5) ◽  
pp. 839-847 ◽  
Author(s):  
Andrea Trombetti ◽  
Laura Richert ◽  
Karine Hadaya ◽  
Jean-Daniel Graf ◽  
François R Herrmann ◽  
...  

BackgroundWe examined the hypothesis that high FGF-23 levels early after transplantation contribute to the onset of hypophosphatemia, independently of parathyroid hormone (PTH) and other factors regulating phosphate metabolism.MethodsWe measured serum phosphate levels (sPi), renal tubular reabsorption of Pi (TmPi/GFR), estimated GFR (eGFR), intact PTH (iPTH), calcitriol, intact (int) and C-terminal (Cter) FGF-23, dietary Pi intake and cumulative doses of glucocorticoids in 69 patients 12 days (95% confidence interval, 10–13) after renal transplantation.ResultsHypophosphatemia was observed in 43 (62%) of the patients 12 days after transplantation. Compared with non-hypophosphatemic subjects, their post-transplantation levels of intact and CterFGF-23 were higher (195 (108–288) vs 48 (40–64) ng/l, P<0.002 for intFGF-23; 205 (116–384) vs 81 (55–124) U/ml, P<0.002, for CterFGF-23). In all subjects, Cter and intFGF-23 correlated inversely with sPi (r=−0.35, P<0.003; −0.35, P<0.003, respectively), and TmPi/GFR (r=−0.50, P<0.001; −0.54, P<0.001, respectively). In multivariate models, sPi and TmPi/GFR were independently associated with FGF-23, iPTH and eGFR. Pre-transplant iPTH levels were significantly higher in patients developing hypophosphatemia after renal transplantation. Pre-transplant levels of FGF-23 were not associated with sPi at the time of transplantation.ConclusionIn addition to PTH, elevated FGF-23 may contribute to hypophosphatemia during the early post-renal transplant period.


1965 ◽  
Vol 208 (6) ◽  
pp. 1165-1170 ◽  
Author(s):  
W. Joseph Rahill ◽  
Mackenzie Walser

Simultaneous clearances of inulin, calcium, and either Be7, Ba140, or Ra226, given by constant infusion, were measured in salt-depleted dogs or dogs undergoing mild saline, mannitol, or sulfate diuresis. Urine-to-plasma ratios of all three cations less than 0.5 were noted, suggesting that all can be actively reabsorbed. Clearances of barium and radium were correlated with calcium clearance, but the clearance of beryllium was unpredictable. Protein binding of beryllium was shown to be of the same order of magnitude as other alkaline earths when errors due to adsorption of Be7 onto containers were minimized. Protein binding of barium averaged 54%. The excreted-to-filtered ratio for barium was a constant power (.54) of the ratio for calcium. The data do not exclude the possibility that these cations are reabsorbed by a common transport mechanism with calcium.


2019 ◽  
Vol 8 (2) ◽  
pp. 99-104
Author(s):  
Bona Akhmad Fithrah ◽  
Marsudi Rasman ◽  
Siti Chasnak Saleh

Cedera otak traumatika adalah salah satu penyebab kematian dan kesakitan tersering pada kelompok masyarakat muda. Hasil akhir dari cedera kepala berat dapat menyebabkan gangguan kognitif, perilaku, psikologi dan sosial. Salah satu konsekuensi dari cedera kepala berat adalah terjadinya disfungsi hormonal baik dari hipofise anterior maupun posterior. Angka kejadian disfungsi hormonal ini sekitar 20-50%. Salah satu yang paling menantang dan sering terjadi adalah diabetes insipidus (DI) dan Syndrome inappropriate antidiuretic hormone (SIADH). Angka kejadian diabetes insipidus pasca cedera kepala diduga sebesar 1-2,9% dengan berbagai tingkatannya. Pada beberapa kasus bersifat sementara tapi beberapa kasus terjadi bersifat menetap. Pada laporan kasus ini akan dibawakan sebuah kasus diabetes insipidus pasca cedera kepala berat. Pasien mengalami cedera kepala berat, hingga dilakukan decompressive craniectomi dan trakeostomi. Untuk perawatan lanjutan pasien dirujuk ke Jakarta. Saat menjalani terapi lanjutan ini pasien terdiagnosis diabetes insipidus Pada kasus ini diabetes insipidus tidak timbul langsung setelah cedera kepala tetapi baru timbul lebih kurang satu bulan setelah cedera kepala. Diabetes insipidus dikelola dengan menggunakan desmopressin spray dan oral disamping mengganti cairan yang hilang. Pada kasus ini desmopressin sempat di stop sebelum akhirnya diberikan terus menerus dan pasien diterapi sebagai diabetes insipidus yang menetap. Managing Central Diabetes Insipidus in Post Severe Head Injury PatientAbstractTraumatic brain injury is the cause of mortality and morbidity in society mostly in male-young generation. The last outcome of traumatic brain injury might be deficit in cognitive, behavioral, psychological and social. the consequences of traumatic brain injury might be hormonal disfunction from anterior and posterior pituitary. The incidence around 20-50%. The most challenging problem is diabetes insipidus (DI) and syndrome of inappropriate antidiuretic hormone (SIADH). The incident of post traumatic diabetes insipidus around 1-2,9% with several degree. In certain case its only occurred transiently but some report it could be permanent. In this case report will find one case post traumatic diabetes insipidus. This pasien had severe traumatic brain injury and underwent decompressive craniectomy and tracheostomy. For further therapy patient was referred to Jakarta. In this further treatment patient diagnosed with diabetes insipidus. Diabetes insipidus doesn’t occurred since the first day of injury but occurred almost one month after. Diabetes insipidus managed with desmopressin spray and oral beside replace water loss. For a few days desmopressin stop but diabetes insipidus occurred again so desmopressin given daily both spray and oral and the patient had therapy as diabetes insipidus permanent. 


Sign in / Sign up

Export Citation Format

Share Document