Functional Profile of the Isolated Uremic Nephron

Fine, Leon G.; Schlöndorff, Detlef; Trizna, Walter; Gilbert, Richard; Bricker, Neal S.

doi:10.1172/jci109072

Cited by 68 publications

(9 citation statements)

References 26 publications

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“…However, there is evidence that the epithelium of the collecting ducts from experimental animals with chronic renal failure does not respond appropriately to vasopressin 32. Post-obstructive diuresis is due to osmotic diuresis, to a large extent 33.…”

Section: Osmolality In Renal Medullamentioning

confidence: 99%

The renal concentrating mechanism and the clinical consequences of its loss

2012

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The integrity of the renal concentrating mechanism is maintained by the anatomical and functional arrangements of the renal transport mechanisms for solute (sodium, potassium, urea, etc) and water and by the function of the regulatory hormone for renal concentration, vasopressin. The discovery of aquaporins (water channels) in the cell membranes of the renal tubular epithelial cells has elucidated the mechanisms of renal actions of vasopressin. Loss of the concentrating mechanism results in uncontrolled polyuria with low urine osmolality and, if the patient is unable to consume (appropriately) large volumes of water, hypernatremia with dire neurological consequences. Loss of concentrating mechanism can be the consequence of defective secretion of vasopressin from the posterior pituitary gland (congenital or acquired central diabetes insipidus) or poor response of the target organ to vasopressin (congenital or nephrogenic diabetes insipidus). The differentiation between the three major states producing polyuria with low urine osmolality (central diabetes insipidus, nephrogenic diabetes insipidus and primary polydipsia) is done by a standardized water deprivation test. Proper diagnosis is essential for the management, which differs between these three conditions.

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Section: Osmolality In Renal Medullamentioning

confidence: 99%

The renal concentrating mechanism and the clinical consequences of its loss

2012

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“…Using the same concentration gradient, the hydro-osmotic response to vasopressin was markedly blunted in cortical collecting tubules obtained from uremic rabbits whether bathed in normal or uremic media 32 (Fig 4). The cellular mechanism responsible for this blunted response was investigated.…”

Section: Pathophysiology Of Impaired Concentrating and Diluting Abilimentioning

confidence: 92%

“…A post–cyclic adenosine monophosphate (cAMP) generation defect also was postulated because the hydraulic conductivity of these tubules failed to increase when exposed to the analogue 8-bromocyclic AMP. 32 These studies were complemented by experiments in cultured inner medullary collecting tubules cells. 33 Cells obtained from the inner medulla of 5/6 nephrectomized rats as a model of chronic kidney failure uniquely failed to generate cAMP in response to vasopressin.…”

Section: Pathophysiology Of Impaired Concentrating and Diluting Abilimentioning

confidence: 99%

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Dysnatremias in Patients With Kidney Disease

Combs

Berl

2014

American Journal of Kidney Diseases

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Dysnatremias are among the most common electrolyte disorders in clinical medicine. Recent studies have shown that individuals with chronic kidney disease also are afflicted by these electrolyte disorders. Furthermore, their presence imparts an increased risk of mortality. In this review, we discuss studies in experimental animals and in humans that have attempted to establish the mechanisms responsible for limiting urinary dilution and urinary concentration in progressive kidney disease. The clinical implications of these disorders in water excretion are discussed in the setting of optimal water intake as kidney disease progresses. This review emphasizes the management of patients with chronic kidney disease who have marked abnormalities in serum sodium concentrations and gives specific recommendations for modifications in renal replacement therapy prescription in hyponatremic patients with end-stage renal disease.

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“…In experimental glomerulonephritis, an increased renal excretion of potassium has been clearly demonstrated independent of distal flow (Simon et al 1988). When isolated uraemic cortical collecting tubules from control and nephrectomized rabbits are perfused at identical flow rates, potassium secretion is significantly increased in the latter group (Fine et al 1979).…”

Section: A Renal Adaptation In Potassium Excretionmentioning

confidence: 99%