Abstract
Urine volume normally is closely matched to the dietary intake of water and is largely independent of the intake of solute over the range encountered in normal diets. Water balance in the face of varying intake is achieved by renal regulation of urine volume through the operation of the concentrating and diluting mechanism: Extrarenal fluid losses via the skin and lungs, and in stool, occur, but they are relatively constant and do not contribute to the pathophysiology of polyuric states. Although urine volume is regulated independently of solute excretion in most circumstances, the two are related at the extremes: very low rates of solute excretion may impair the ability to maintain water balance and result in dilutional hyponatremia, while extremely high rates of solute excretion may obligate urinary water excretion and lead to negative water balance and hypernatremia. This circumstance of solute diuresis is one of the polyuric syndromes and will be discussed more fully below.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Simpson JB, Epstein AN, Camardo JS Jr: Localization of receptors for the dipsogenic action of angiotensin II in the subfornical organ of rats. J Comp Physiol Psychol 92:768, 1978.
Caverson MM, Ciriello J: Effects of stimulation of afferent renal nerves on plasma levels of vasopressin. Am J Physiol 252:R801, 1987.
Hall DA, Varney DM: Effect of vasopressin on electrical potential differences and chloride transport in mouse medullary thick ascending limb of Henle. J Clin Invest 66:792, 1980.
Forrest JN Jr, Cox M, Hong C, et al.: Superiority of demyclo-cycline over lithium in the treatment of chronic syndrome of inappropriate secretion of antidiuretic hormone. N Engl J Med 298:173, 1978.
Beck TR, Hassid A, Dunn MJ: The effect of arginine vasopressin and its analogs on the synthesis of prostaglandin E2 by rat renal medullary interstitial cells in culture. J Pharmacol Exp Ther 215:15, 1980.
Gross PA, Schrier RW, Anderson RJ: Prostaglandins and water metabolism: A review with emphasis on in vivo studies. Kidney Int 19:839, 1981.
Miller M, Dalakos T, Moses AM, et al.: Recognition of partial defects in antidiuretic hormone secretion. Ann Int Med 73:721, 1970.
Moses AM, Notman DD: Diabetes insipidus and syndrome of inappropriate antidiuretic hormone secretion. Adv Int Med 27:73, 1982.
Coggins CH, Leaf A: Diabetes insipidus. Am J Med 42:807, 1967.
Robinson MG, Kaplan SA: Inheritance of vasopressin resistant (‘nephrogenic’) diabetes insipidus. Am J Dis Child 99:164, 1960.
Silverstein E, Tobian L: Pitressin-resistant diabetes insipidus with massive hydronephrosis. Am J Med 30:819, 1961.
Carter RD, Goodman AD: Nephrogenic diabetes insipidus accompanied by massive dilation of the kidneys, ureters and bladder. J Urol 89:366, 1963.
Fichman MP, Brooker G: Deficient renal cyclic adenosine 3′, 5′-monophosphate production in nephrogenic diabetes insipi-duc. J Clin Endocrinol Metab 35:35, 1972.
Shearn MA, Tu W: Nephrogenic diabetes insipidus and other defects of renal tubular function in Sjogren’s syndrome. Am J Med 39:312, 1965.
Carone FA, Epstein FH: Nephrogenic diabetes insipidus caused by amyloid disease: Evidence in man of role of collecting ducts in concentrating urine. Am J Med 29:539, 1960.
Smithline N, Kassirer J, Cohen JJ: Light-chain nephropathy, tubular dysfunction and light-chain proteinuria. N Engl J Med 294:71, 1976.
Holliday MA, Egar TJ, Morris CR, et al.: Vasopress in resistant hyposthenuria in chronic renal disease. Am J Med 42:378, 1967.
Earley LE: Extreme polyuria in obstructive uropathy: Report of a case of ‘water-losing nephritis’ in an infant with discussion of polyuria. N Engl J Med 255:600, 1956.
Levitt MF, Hausser AD, Levy MS, et al.: The renal concentrating defect in sickle cell disease. Am J Med 29:611, 1960.
Buckalew VM Jr, Someren A: Renal manifestations of sickle cell disease. Arch Intern Med 133:660, 1974.
Tannen RL, Regal EM, Dunn MJ, et al.: Vasopressin-resistant hyposthenuria in advance chronic renal disease. N Engl J Med 280:1135, 1969.
Miller PD, Krebs RA, Neal BJ, et al.: Polyuric prerenal failure. Arch Int Med 140:907, 1980.
Singer I, Forrest JN: Drug-induced states of nephrogenic diabetes insipidus. Kidney Int 10:82, 1976.
Singer I, Rotenberg D, Puschett JB: Lithium-induced nephrogenic diabetes insipidus: In vivo and in vitro studies. J Clin Invest 51:1081, 1972.
Myers JB, Morgan TO, Carney SL, et al.: Effects of lithium on the kidney. Kidney Int. 18:601, 1980.
Singer I, Rotenberg D: Demeclocycline-induced nephrogenic diabetes insipidus. Ann Intern Med 79:679, 1973.
Mannitius A, Levitin H, Epstein FH: On the mechanism of impairment of renal concentrating ability in hypercalcemia. J Clin Invest 39:693, 1960.
Zeffren JL, Heinemann HO: Reversible defect in renal concentrating mechanism in patients with hypercalcemia. Am J Med 33:54, 1962.
Back N, Sigh H, Reed E, et al.: Pathogenic role of cyclic AMP in the impairment of urinary concentrating ability in acute hypercalcemia. J Clin Invest 54:1049, 1974.
Manitius A, Levitin H, Beck D, et al.: On the mechanism of impairment of renal concentrating ability in potassium deficiencies. J Clin Invest 39:684, 1960.
Berl T, Aisenbrey GA, Linas SL: Renal concentrating defect in the hypokalemic rat is prostaglandin independent. Am J Physiol 238:F37, 1980.
Berl T, Linas S, Ainsenbrey G, et al.: On the mechanism of polyuria in potassium depletion. The role of polydipsia. J Clin Invest 60:620, 1977.
Levi M, Peterson L, Berl T: Mechanism of concentrating defect in hypercalcemia. Role of polydipsia and prostaglandins. Kidney Int 23:489, 1983.
Barlow ED, De Wardener HE: Compulsive water drinking. Q J Med 28:235, 1959.
Dubovsky SL, Grabon S, Berl T, et al.: Syndrome of inappropriate secretion of antidiuretic hormone with exacerbated psychosis. Ann Int Med 79:551, 1973.
Gennari FJ, Kassirer JP: Osmotic diuresis. N Engl J Med 291:714, 1974.
Kosmas ME: Evaluation of a new antidiuretic agent, desmopressin acetate (DDAVP). JAMA 240:1896, 1978.
Ziai F, Waller R, Rosenthal IM: Treatment of central diabetes insipidus in adults and children with desmopressin. Arch Intern Med 138:1382, 1978.
Earley LE, Orloff J: The mechanism of antidiuresis associated with the administration of hydrochlorothiazide to patients with vasopressin-resistant diabetes insipidus. J Clin Invest 41:1988, 1962.
Moses AM, Numann P, Miller M: Mechanism of chlorpropa-mide-induced antidiuresis in man. Evidence for release of ADH and enhancement of peripheral action. Metabolism 22:59, 1973.
Froyshov I, Haugen HN: Chlorpropamide treatment in diabetes insipidus. Acta Med Scand 183:397, 1968.
Zusman RM, Keiser HR, Handler JS: Inhibition of vasopres-sin-stimulated prostaglandin E biosynthesis by chlorpropamide in the toad urinary bladder. Mechanism of enhancement of vasopressin-stimulated water flow. J Clin Invest 60:1348, 1977.
Fichman MP, Speckart P, Zia P, et al.: Antidiuretic response to prostaglandin inhibition in primary and nephrogenic diabetes insipidus. Clin Res 23:505A, 1977.
Wales JK: Treatment of diabetes insipidus with carba-mazepine. Lancet 2:948, 1975.
Rado JP: Combination of carbamazepine and chlorpropamide in the treatment of ‘hyporesponders’ pituitary diabetes insipidus. J Clin Endocrinol Metab 38:1, 1974.
Usberti M, Dechaux M, Guillot M, et al.: Renal prostaglandin E2 in nephrogenic diabetes insipidus. Effects of inhibition of prostaglandin synthesis by indomethacin. J Pediat 97:476, 1980.
Delaney V, dePertuz Y, Nixon D, et al.: Indomethacin in streptozocin-induced nephrogenic diabetes insipidus. Am J Kidney Dis 9:79, 1987.
Bucht G, Wahlin A: Renal concentrating capacity in long-term lithium treatment and after withdrawal of lithium. Acta Med Scand 207:309, 1980.
Kennedy RM, Earley LE: Profound hyponatremia resulting from a thiazide induced decrease in urinary diluting capacity in a patient with primary polydipsia. N Engl J Med 282:1185, 1970.
Vaughan ED Jr, Gillenwater JY: Diagnosis, characterization and management of post-obstructive diuresis. J Urol 109:286, 1973.
Feig PV: Hypernatremic and hypertonic syndromes. Med Clin North Am 65:271, 1981.
Moran SM, Jamison RL: The variable hyponatremia response to hyperglycemia. West J Med 142:49, 1985.
Katz MA: Hyperglycemia-induced hyponatremia. Calculation of expected serum sodium depression. N Engl J Med 289:843, 1973.
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1991 Kluwer Academic Publishers
About this chapter
Cite this chapter
Muldowney, W.P., Humphreys, M.H. (1991). Polyuric Syndromes. In: Suki, W.N., Massry, S.G. (eds) Therapy of Renal Diseases and Related Disorders. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0689-4_2
Download citation
DOI: https://doi.org/10.1007/978-1-4613-0689-4_2
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4612-8027-9
Online ISBN: 978-1-4613-0689-4
eBook Packages: Springer Book Archive