Chapter 045. Azotemia and Urinary Abnormalities (Part 8)

Approach to the patient with polyuria. ATN, acute tubular necrosis; ADH, antidiuretic hormoneExcessive filtration of a poorly reabsorbed solute such as glucose, mannitol, or urea can depress reabsorption of NaCl and water in the proximal tubule and lead to enhanced excretion in the urine. Poorly controlled diabetes mellitus with glucosuria is the most common cause of a solute diuresis, leading to volume depletion and serum hypertonicity. Since the urine Na concentration is less than that of blood, more water than Na is lost, causing hypernatremia and hypertonicity. Common iatrogenic solute diuresis occurs from mannitol administration, radiocontrast media, and high-protein...
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Chapter 045. Azotemia and Urinary Abnormalities (Part 8) Chapter 045. Azotemia and Urinary Abnormalities (Part 8) Approach to the patient with polyuria. ATN, acute tubular necrosis; ADH,antidiuretic hormone Excessive filtration of a poorly reabsorbed solute such as glucose,mannitol, or urea can depress reabsorption of NaCl and water in the proximaltubule and lead to enhanced excretion in the urine. Poorly controlled diabetesmellitus with glucosuria is the most common cause of a solute diuresis, leading tovolume depletion and serum hypertonicity. Since the urine Na concentration isless than that of blood, more water than Na is lost, causing hypernatremia andhypertonicity. Common iatrogenic solute diuresis occurs from mannitoladministration, radiocontrast media, and high-protein feedings (enterally orparenterally), leading to increased urea production and excretion. Less commonly,excessive Na loss may occur from cystic renal diseases, Bartters syndrome, orduring the course of a tubulointerstitial process (such as resolving ATN). In theseso-called salt-wasting disorders, the tubule damage results in direct impairment ofNa reabsorption and indirectly reduces the responsiveness of the tubule toaldosterone. Usually, the Na losses are mild, and the obligatory urine output is A plasma vasopressin level is recommended as the best method fordistinguishing between central and nephrogenic diabetes insipidus. Alternatively,a water deprivation test plus exogenous vasopressin may also distinguish primarypolydipsia from central and nephrogenic diabetes insipidus. For a detailed discussion, see Chap. 334. Further Readings Anderson S et al: Renal and systemic manifestations of glomerular disease,in Brenner & Rectors The Kidney, 7th ed, BM Brenner (ed). Philadelphia,Saunders, 2004, pp 1927–1954 Berl T, Verbalis J: Pathophysiology of water metabolism, in Brenner &Rectors The Kidney, 7th ed, BM Brenner (ed). Philadelphia, Saunders, 2004, pp857–920 Kasiske BL, Keane WF: Laboratory assessment of renal disease:Clearance, urinalysis and renal biopsy, in Brenner & Rectors The Kidney, 7th ed,BM Brenner (ed). Philadelphia, Saunders, 2004, pp 1107–1150 Khadra MHet al: A prospective analysis of 1,930 patients with hematuria toevaluate current diagnostic practice. J Urol 163:524, 2000 [PMID: 10647670] Rodrigo E et al: Measurement of renal function in pre-ESRD patients.Kidney Int Suppl 80:11, 2002 [PMID: 11982806] Sasaki S: Nephrogenic diabetes insipidus: Update of genetic and clinicalaspects. Nephrol Dial Transplant 19:1351, 2004 [PMID: 15004257] Shrier RW et al: Acute renal failure: Definitions, diagnosis, pathogenesisand therapy. J Clin Invest 114:5, 2004