Core curriculum in nephrology: disorders of sodium and water

Disorders of Sodium and Water
● Na intake controlled by Na appetite, dietary COMPOSITION OF BODY FLUIDS
● Typical Western diets contain 2 to 6 g of Na Total Body Water (TBW)
● Na elimination regulated by factors that ● Two thirds of TBW is inside cells (intracel- ● One third of TBW is outside cells (extracel- Mechanisms of Renal Na Excretion
Solute Composition of Body Water (H O)
● Na freely filtered (ϳ25 mol/d in healthy ● Ͼ99% reabsorbed; normal fractional Na ● About 65% reabsorbed along proximal tu- along distal convoluted tubule (DCT), and ● Primary energetic driving force for Na (and other solute) reabsorption is Na/K adeno- ECF and ICF are in osmotic equilibrium, at ● Na reabsorption along PT is mediated partly PHYSIOLOGY OF Na BALANCE
● H O, but not solute, removed from thin descending limb of Henle loop, increasing Background
● Definition: Na balance is difference be- tween intake (usually oral or intravenous) ● Na, but not H O, reabsorbed along thin and and excretion (usually renal, gastrointesti- thick ascending limbs of Henle loop, thereby diluting tubule fluid; along thick ascendinglimb, Na traverses an apical Na-K-2Clcotransport pathway (NKCC2) From the Department of Medicine, Division of Nephrol- ● Na, but not H O, reabsorbed along DCT, ogy and Hypertension, and the Department of Physiology predominantly via an apical Na-Cl cotrans- and Pharmacology, Oregon Health and Science University, and VA Medical Center, Portland, OR. Received September 22, 2004; accepted in revised form ● Na reabsorbed along connecting tubule and CD, largely via an apical Na channel (ENaC) Originally published online as doi:10.1053/j.ajkd.2005.03.023 Regulation of Renal Na Homeostasis
Address reprint requests to David H. Ellison, MD, Head, Division of Nephrology and Hypertension, Professor of ● Renal Na homeostasis responds to “effec- Medicine and Physiology and Pharmacology, Oregon Health and Science University, PP 262, 3314 SW US Veterans virtual volume that reflects “fullness” of Hospital Rd, Portland, OR 97239. E-mail: ellisond@ ● Na reabsorption varies inversely with arte- 2005 by the National Kidney Foundation, Inc. rial pressure, a phenomenon called “pres- 0272-6386/05/4602-0022$30.00/0doi:10.1053/j.ajkd.2005.03.023 American Journal of Kidney Diseases, Vol 46, No 2 (August), 2005: pp 356-361 ● Na reabsorption along PT regulated by peritubular protein concentration and other “physical factors”; increase in filtration along collecting duct, under typical condi- fraction (glomerular filtration rate/renal ● Proximal reabsorption is isosmotic, so rates pressure to increase, stimulating reabsorp- ● H O reabsorbed along descending limb of This link between filtration and reabsorp- loop of Henle, driven by medullary hyperto- ● Proximal Na reabsorption (largely NHE3) ● Solute, not H O, reabsorbed along ascend- ing limbs; ascending limb thus dilutes urine angiotensin II; circulating angiotensin II ● Solute, not H O, reabsorbed along DCT; levels are regulated by renin, secreted by ● H O variably reabsorbed along cortical and medullary collecting ducts, via a regulated ascending limbs of Henle loop NaCl concen- ● Na reabsorption along second half of DCT, Regulation of Renal H O Excretion
the connecting tubule and CD (collectively ● Urinary osmolality typically ranges be- termed the “aldosterone-sensitive distal nephron”), regulated by aldosterone, which ● Countercurrent multiplication generates stimulates ENaC (abundance and/or activ-ity) and NCC; aldosterone secretion regu- medullary hypertonicity in part via Na-K- Natriuretic peptides stimulate guanylyl cy- clase along CD, generating cyclic guanosine monophosphate and inhibiting apical cation channels; natriuretic peptides also increase glomerular filtration rate; atrial natriuretic ● Tubule fluid leaving loop of Henle is al- peptide secretion stimulated by atrial stretch ● Arginine vasopressin (AVP), the antidi- PHYSIOLOGY OF H O BALANCE
(usually oral or intravenous) and excretion(usually renal, gastrointestinal, perspira- ● H O intake controlled by thirst, taste, habit, and physicians; thirst regulated partly by ● Typical H O intake ranges from 1 to 5 L/d ● H O excretion regulated by factors that losses (insensible, perspiratory, and gastro- Ⅲ AVP activates V2 receptors on basolat- Ⅲ AVP stimulates adenylyl cyclase in CD Mechanisms of Renal H O Excretion
● H O freely filtered at glomerulus (ϳ150 ral deafness (resulting from defi-ciency in Cl channel ␤ subunit, 1. Nielsen S, Frokiaer J, Marples D, Kwon TH, Agre P, Knepper MA: Aquaporins in the kidney: From molecules to 2. Andreoli TE: Water: Normal balance, hyponatremia, and hypernatremia. Ren Fail 22:711-735, 2000 3. Reeves WB, Andreoli TE: Sodium chloride transport in the loop of Henle, distal convoluted tubule, and collecting duct, in Seldin DW, Giebisch G (eds): The Kidney: Physiol- ogy and Pathophysiology, chap 50. Philadelphia, PA, Lippin- cott Williams & Wilkins, 2000, pp 1333-1370 4. Blantz RC, Gabbai FB: Renin-angiotensin-aldosterone system, in DuBose T, Hamm LL (eds): Acid-Base and Electrolyte Disorders, chap 16. Philadelphia, PA, Saunders, □ Renal disease, especially interstitial Treatment
● Identify and treat underlying disease Background
● Na balance disorders are disorders of ECF ● Fludrocortisone (synthetic mineralocorti- ● Serum Na concentration may be high, low, Hypervolemia
● Occurs when Na retention is “inappropriate” Hypovolemia
Primary Na retention
● Reviewed in Core Curriculum in Nephrol- Secondary Na retention
● Congestive heart failure; secondary to inad- equate cardiac output or diastolic dysfunc- ● Cirrhosis of liver; secondary to systemic ● Nephrotic syndrome; mixed, resulting from intrinsic stimulation of renal NaCl reabsorp- Diagnosis.
● Physical examination (edema, ascites, jugu- lar pressure, pulmonary crackles, S , oth- ● Laboratory (brain natriuretic peptide 1. Ellison DH: Diuretic therapy and resistance in conges- tive heart failure. Cardiology 96:132-143, 2001 Treatment
2. Ellison DH: Salt-wasting disorders, in DuBose T, Hamm LL (eds): Acid-Base and Electrolyte Disorders, chap 18. Philadelphia, PA, Saunders, 2002, pp 311-333 ● Restrict Na intake (keep intake Ͻ100 3. Hebert SC: Bartter syndrome. Curr Opin Nephrol 4. Okusa MD, Ellison DH: Physiology and pathophysiol- ogy of diuretic action, in Seldin DW, Giebisch G (eds): The Kidney: Physiology and Pathophysiology, chap 103. Phila- Ⅲ Loop diuretics usually first line for delphia, PA, Lippincott Williams & Wilkins, 2000, pp2877-2922 5. Meneton P, Oh YS, Warnock DG: Genetic renal tubular disorders of renal ion channels and transporters. Semin 6. Palmer BF, Alpern RJ, Seldin DW: Physiology and pathophysiology of sodium retention, in Seldin DW, Gie- bisch G (eds): The Kidney: Physiology and Pathophysiol- ogy, chap 54. Philadelphia, PA, Lippincott Williams & 7. Schrier RW, Gurevich AK, Cadnapaphornchai MA: Pathogenesis and management of sodium and water reten- tion in cardiac failure and cirrhosis. Semin Nephrol 21:157- 8. Warnock DG, Textor SC: Hypertension [Core Curricu- lum in Nephrology]. Am J Kidney Dis 44:369-375, 2004 DISORDERS OF H O BALANCE
Ⅲ CD diuretics (spironolactone, eplerenone, Background
● Are manifested by changes in serum osmo- ● Are classified on the basis of ECF volume Hyponatremia
Factitious (normotonic) hyponatremia
● Results from laboratory artifact (high con- Ⅲ Proximal tubule diuretics (carbonic anhy- Hypertonic hyponatremia
free H O from cells ([Na] declines by ϳ1.6 Hypotonic hyponatremia
Dilutional. Urine is dilute (Ͻ100 mOsm/kg
Ⅲ Combine diuretic classes if resistance ● H O intake exceeds dilutional capacity (“psychogenic polydipsia,” requires as much as 12 L/d in normals); treatment is to reduceH O intake ● Dilutional capacity limited by low solute intake (“beer drinkers potomania”); treat- ment is to reduce intake and increase solute Hypovolemic. Urine is concentrated:
● Urine [Na] is usually Ͻ20 mEq/L, except with diuretic drugs and salt wasting, where it is inappropriately elevated; urine [Cl] appropriately (eg, sweat or gastrointesti- nal); losses replaced with hypotonic fluids, ● Diagnosis: by history, physical examination Hypervolemic. Urine concentrated, Na often
(orthostatic hypotension, low jugular ve- ● AVP secreted because “effective arterial blood volume” reduced (ECF volume defi- laboratory (high hematocrit and serum pro- cits, when severe, overcome AVP inhibition ● Causes include congestive heart failure, Euvolemic. Urine is concentrated; urine [Na]
cirrhosis, nephrotic syndrome, kidney fail- ● Syndrome of inappropriate ADH secretion ● Treatment includes oral H O restriction ● Angiotensin-converting enzyme inhibitors ● Aquaretics (V2 receptor antagonists, cur- rently investigational drugs) may be useful ● Hypothyroidism or glucocorticoid insuffi- ● Diagnosis: by history, absence of signs of Hypernatremia
volume depletion or overload, and labora- Hypervolemic
Aggressiveness of treatment depends onseverity, chronicity, and symptoms ● Usually only when it occurs with other Ⅲ “Rapid” treatment for symptomatic and to increase no more than 12 mEq/L infirst 24 h H O loss
Ⅲ ϾOsmotic diuresis (osmotic diuresis, post- ● H O deprivation test for hypernatremia associated with dilute urine (restrict H O Ⅲ Diabetes insipidus (dilute urine, urine Na consecutive urine osmolalities within 10%; patient for signs of excess volume deple- Ⅲ Response to exogenous vasopressin de- ● Plasma vasopressin levels correlated with plasma and urinary osmolality often needed Treatment
● Hypovolemic hypernatremia, with saline History; history of exertion, fever, thirst, ● Deficit Ϸ current body H O ϫ (actual Physical examination: signs of EABV deple- ● Aim to correct at Ͻ0.5 mEq/L/h and usu- ● Note that ongoing free H O excretion both 1. Andreoli TE: Water: Normal balance, hyponatremia, and hypernatremia. Ren Fail 22:711-735, 2000 2. Palmer BF, Gates JR, Lader M: Causes and manage- ment of hyponatremia. Ann Pharmacother 37:1694-1702, 3. Adrogue HJ, Madias NE: Hypernatremia. N Engl J Med If this value has negative sign, it represents 4. Adrogue HJ, Madias NE: Hyponatremia. N Engl J Med


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