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renal physiology

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Huang Ying

on 11 October 2012

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Transcript of renal physiology

BUN & Creatine Renal Physiology & Pathology Urea and creatinine are nitrogenous end products of metabolism. Urea is the primary metabolite derived from dietary protein and tissue protein turnover. Blood Urea Nitrogen metabolism BUN:Cr Ratio
>20:1 Prerenal (before thekidney)
BUN reabsorption is increased. BUN is disproportionately elevated relative to creatinine in serum. Dehydration is suspected.
10-20:1 Normal or Postrenal (after the kidney)
Normal range. Can also be postrenal disease. BUN reabsorption is within normal limits.
<10:1 Intrarenal (within kidney)
Renal damage causes reduced reabsorption of BUN, therefore lowering the BUN:Cr ratio. BCR Creatinine is the product of muscle creatine catabolism Creatinine The normal range of urea nitrogen in blood or serum is 5 to 20 mg/dl, or 1.8 to 7.1 mmol urea per liter. The range is wide because of normal variations due to protein intake, endogenous protein catabolism, state of hydration, hepatic urea synthesis, and renal urea excretion. A BUN of 15 mg/dl would represent significantly impaired function for a woman in the thirtieth week of gestation. Her higher glomerular filtration rate (GFR), expanded extracellular fluid volume, and anabolism in the developing fetus contribute to her relatively low BUN of 5 to 7 mg/dl. In contrast, the rugged rancher who eats in excess of 125 g protein each day may have a normal BUN of 20 mg/dl. The normal serum creatinine (sCr) varies with the subject's body muscle mass and with the technique used to measure it. For the adult male, the normal range is 0.6 to 1.2 mg/dl, or 53 to 106 mol/L by the kinetic or enzymatic method, and 0.8 to 1.5 mg/dl, or 70 to 133 mol/L by the older manual Jaffé reaction. For the adult female, with her generally lower muscle mass, the normal range is 0.5 to 1.1 mg/dl, or 44 to 97 mol/L by the enzymatic method. Acute Renal Failure IF Mr. Wang's BUN and Creatinine are abnormal.... Classification and major cause Prerenal ARF
1.Hypovolemia
A.Increased extracellular fluid losses: Hemorrhage
B.Gastrointestinal fluid loss : vomiting, diarrhea, enterocutaneous fistula
C.Renal fluid loss: Diuretics, osmotic diuresis, hypoadrenalism, nephrogenic diabetes insipidus
D.Extravascular sequestration: burns, pancreatitis, severe hypoalbuminemia
E.Decreased intake : dyhydration, altered mental status
2.Altered renal hemodynamics resulting in hypoperfusion
Intrinsic ARF
Postrenal ARF Clinical Features Volume depletion(absolute/postural hypotension, low jugular venous pressure, dry mucus membranes) or decreased effective circulatory volume( e.g. heart failure or liver disease) Serum Studies High BUN/CR ratio(20) is suggestive but not diagnostic

80/4.5=17.8 Urine Studies Hyaline casts yes
FENa<1% FENa=0.703
UNa<10mmol/L UNa=10
SG<1.018 SG=1.028 FeNa=(UNa*PCr/PNa*UCr)*100%
=(10*4.5/80*80)*100%
=0.703% Reference: FeNa fractional excretion of sodium Hosten AO. BUN and Creatinine. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 193. Available from: http://www.ncbi.nlm.nih.gov/books/NBK305/Bun-to-creatinine ratio. (n.d.).
Retrieved from http://en.wikipedia.org/wiki/BUN-to-creatinine_ratio
Kroll, M. (1987). Mechanism of interference with the jaffé reaction for creatinine. Clinical Chemistry, 33(7), 1129-1132. Retrieved from http://www.clinchem.org/content/33/7/1129.long
Harrison's principles of internal medicine 17th edition it can distingushing prerenal ARF from ischemic or nephrotoxic intrinsic renal ARF.
Sodium is reabsorbed avidly from glomerular filtrate in patients with prerenal ARF, in an attempt to restore intravascular volume.

FeNa<1%(frequently<0.1%)
High FeNa......ishemic ATN Etiology and Pathophysiology Hypovolemia
arterial and cardiac baroreceptors
activation of the sympathetic nervous system, RAAS,
release of arginine vasopressin
in an attempt to preserve cardiac and cerebral perfusion pressure
salt loss through sweat glands is inhibited
thirst and salt appetite are stimulated
Renal salt and water retention also occur. Conclusion Mr. Wang has a prerenal acute renal failure because of keeping vomiting which caused hypovolemia.
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