Cerebral salt wasting is characterized by inappropriate natriuresis and volume contraction with associated cerebral pathology. It is distinct from the syndrome of inappropriate antidiuretic hormone secretion, which is characterized by inappropriate retention of free water. We report a patient with a porencephalic cyst who developed cerebral salt wasting. His initial treatment was supplementation of water and salt, which did not improve natriuresis or volume contraction. Fludrocortisone administration effectively managed the cerebral salt wasting.
Adolescent ; Fludrocortisone/*therapeutic use ; Humans ; Hyponatremia/*drug therapy ; Male ; Natriuresis/physiology ; Sodium Chloride/therapeutic use

Although the obstruction is potentially reversible with treatment, marked and sometimes prolonged diuresis and natriuresis associated with an impaired ability to concentrate the urine may follow relief of the obstruction. Various factors contributing to the postobstructive diuresis and natriuresis have been suggested, including decreases of tubular sodium reabsorption, retention of urea and expansion of extracellular fluid volume. Tubular damage as a consequence of obstruction may occur one or more nephron segments and may result in decreased reabsorption of filtrate. The discovery of aquaporin (AQP) membrane water channels and sodium (co)transporters and channels provided insight, at the molecular level, into the fundamental physiology and pathophysiology of water and sodium balance. In addition, recent studies have shown that the kidney per se is also a site of production and release of atrial natriuretic peptide (ANP). The locally synthesized ANP may act in a paracrine manner to increase the urinary excretion of sodium and water. In this context, an altered regulation of ANP in the kidney may result in an altered urinary excretion. The combined interactions of multiple independent mechanisms are thought to be involved in the pathogenesis of postobstructive diuresis and natriuresis. We examined the changes of AQP water channels, sodium (co)transporters and natriuretic peptide system in obstructed kidneys. The expression of AQP water channels and sodium transporters was decreased in the obstructed kidneys, which may at least in part account for the urinary concentration defect associated with postobstructive diuresis and natriuresis. In addition, the postobstructive natriuresis was associated with an enhanced renal expression of ANP mRNA and an increased urinary excretion of ANP. The plasma dendroaspis natriuretic peptide (DNP) level was increased following an experimental ureteral obstruction. The urinary excretion of DNP was increased along with the postobstructive diuresis. An enhanced activity of DNP system may in part play a role in mediating the postobstructive diuresis
Animals ; Aquaporins* ; Atrial Natriuretic Factor ; Diuresis* ; Elapidae ; Extracellular Fluid ; Kidney* ; Membranes ; Natriuresis ; Natriuretic Peptides ; Negotiating ; Nephrons ; Physiology ; Plasma ; Rats* ; RNA, Messenger ; Sodium* ; Urea ; Ureteral Obstruction

OBJECTIVETo investigate the effect of AT₁ receptor on the changes of tyrosine hydroxylase-immunoreactivity (TH-IR) in rostral ventrolateral medulla (RVLM) induced by brain cholinergic stimuli in rats.

METHODSMale SD rats were randomly divided into 4 groups: NS + CBC group, Los + CBC group, Los + NS group and NS + NS group. AT₁ was blocked by pretreatment of 20 μg losartan in Los + CBC and Los + NS groups; intracerebroventricular injection of 0.5 μg carbachol was used for cholinergic stimuli in NS + CBC and Los + CBC groups; normal saline (NS) was used for control. The output amount of natrium in kidney, glomerular filtration rate (GFR) and renal plasma flow (PRF) were observed. The changes of TH-IR in the RVLM were observed by immunohistochemistry.

RESULTIn NS + CBC group carbachol induced potent natriuresis, after pretreatment of losartan the natriuretic effect was partially inhibited in Los + CBC group. Both the number and optical density of TH-IR positive neurons in NS + CBC group were markedly increased than those in NS + NS group (P < 0.05); while those in Los + CBC group were significantly lower than those in NS+CBC group (P < 0.05). Intracerebroventricular injection of carbachol and losartan had no effect on GFR and RPF(P > 0.05).

CONCLUSIONThe results suggest that cholinergic stimuli can induce potent natriuresis and increase the activity of adrenergic neurons in the RVLM; the above effects can be down regulated by blockade of brain AT₁ receptor.

Animals ; Carbachol ; administration & dosage ; pharmacology ; Drug Antagonism ; Glomerular Filtration Rate ; drug effects ; Losartan ; pharmacology ; Male ; Medulla Oblongata ; drug effects ; metabolism ; Natriuresis ; drug effects ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1 ; physiology ; Tyrosine 3-Monooxygenase ; metabolism