Do you want to buy antibiotics online without prescription? - This is pharmacy online for you!

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


Microsoft word - reglamento a la ley no. 312 de derechos de autor y conexos.docx

Decreto No. 22-2000 PRESIDENCIA DE LA REPÚBLICA DE NICARAGUA El Presidente de la República de Nicaragua. En uso de sus facultades que le confiere la Constitución Política. HA DICTADO REGLAMENTO DE LA LEY DE DERECHOS DE AUTOR Y CONEXOS1 ARTO. 1.- Objeto. El presente Decreto tiene por objeto reglamentar las disposiciones de la Ley de Derechos de Autor y Derechos C

Geographic patterns of genetic variation in brushtail possums trichosurus vulpecula and implications for pest control

1 School of Biological Sciences, Victoria University, P.O. Box 600, Wellington. Present address: Science Directorate, Department of Conservation, P.O. Box 10420, Wellington. 2 Forest Research Institute, P.O. Box 31-011, Christchurch. Present address: Advocacy and Extension Directorate, Department of Conservation, P.O. Box 10420, Wellington. GEOGRAPHIC PATTERNS OF GENETIC VARIATION INBRUSHTAIL

Copyright © 2010-2014 Medical Pdf Finder