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Nephrology Review February 19, 2010
RENAL FUNCTION ,[object Object],[object Object],[object Object],END PRODUCTS DRUGS TOXINS FLUID ELECTROLYTES OSMOLARITY ACID-BASE RENIN ERYTHROPOIETIN 1,25(OH) 2 VIT.D3 Briggs JP, Schnermann JB. Primer on KIDNEY DISEASES. 2nd ed. 1998
GFR ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Milutinovic et al. Kidney Int. 1975:8;185-190 inulin iothalamate (CCr+Curea)/2
Na + K + Cl -
Tubular function ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
การที่มี  BUN  และ  serum creatinine  สูงเกินค่าปกติ   (Normal Cr  ชาย  ≤   1.5,  หญิง   ≤   1.3 mg/dl)  Azotemia
Uremia กลุ่มอาการที่เกิดจากความผิดปกติของการคั่งของของเสีย สารน้ำและเกลือแร่ที่เกิดคู่กับการเสื่อมหน้าที่ของไต - nausea, vomiting - anorexia - weight loss - dyspnea - fatigue - pruritus
Azotemia GFR   ปกติ GFR   ต่ำ Acute KI Chronic KD Intrinsic RF Post RF Pre RF Chronic GN Chronic TIN BUN  Cr
Normal GFR ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Decrease GFR ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Acute Renal Failure (ARF)  Acute Kidney Injury (AKI) ,[object Object],[object Object],[object Object]
Definition of Acute kidney injury OR 2004 Level of  dysfunciton Outcome
 
Acute Kidney Injury Within 48 hours  serum Cr > 0.3 mg/dL  serum Cr > 50% (1.5 fold) More than 6 hours  urine output < 0.5 ml/kg/hr  Adequate fluid resuscitation
AKIN classification   Baseline serum Cr (48 hr)   urine output Stage 1 (R)  >0.3 mg/dL or   1.5-2 fold  <0.5 mL/kg/hr >6 hr Stage 2 (I)  2-3 fold  <0.5 mL/kg/hr >12 hr Stage 3 (F)  >3 fold or  <0.3 mL/kg/hr >24 hr  >0.5 mg/dL if Cr > 4 mg/dL)  anuria for 12 hr RRT No GFR criteria
 
Decreased circulatory volume Activation of central baroreceptors Norepinephrine Vasopressin Angiotensin II PGE2 / PGI2 Nitric oxide Autoregulation (MAP > 70) Vasoconstriction Mesangial contraction Reduced renal blood flow & GFR Prerenal
Renal causes ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Functional & Physiologic change Loss of cell polarity Loss Cell-cell, cell matrix interaction Tight junction  defect ↑  Distal Na delivery Tubular obstruction Back leak Renal vasoconstriction ↓ GFR Tubuloglomerular feedback Brush border detachment
Pre-renal VS Renal ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],=  UNa  PCr    100   PNa  UCr FE Na (%) RFI
Na + K + Cl - Medullary ischemia Intermediate syndrome Urine Na low Urine spgr low
Risk of aminoglycosides nephrotoxic  ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Amphotericin B ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Cisplatin ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Radiocontrast nephropathy ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Acute renal failure ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Investigation ,[object Object],[object Object],[object Object],[object Object],[object Object]
Management ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
CAUSES OF ANEMIA IN CRF ,[object Object],[object Object],[object Object],[object Object],[object Object],Schrier RW, Gottschalk CW. Diseases of the kidney. 6th ed. Vol.III, 1996. Fe   ,  Folate , B1, B6, B12 Mild hemolysis :  ↓ Na-K-ATPase activity sensitive to oxidants ,  dialysis Factors?, PTH, Al
RENAL OSTEODYSTROPHY ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Hypocalcemia Hyperphosphatemia Low vitamin D Bone resistance
Comprehensive strategy ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Med Clin N Am 89 (2005) 489–509
RENAL Na +  REABSORPTION HCO 3 - HCO 3 -  + H 2 O+CO 2 CA H +  +HCO 3 - CA Na + glucose PO 4 AA Carbonic anhydrase inhibitor H + Na + 3 HCO 3 - Na + 3Na + 2K + 3Na + 2K + 3HCO 3 - Na +
TAL of Henle Loop diuretics
DISTAL TUBULE Thiazide
CORTICAL COLLECTING TUBULE Na + K + H + spironolactone Amiloride
POLYURIA
DEFINITION ,[object Object],[object Object],[object Object],[object Object],[object Object]
What is urine? ,[object Object],[object Object]
   GFR    salt excretion    H 2 O excretion
Polyuria ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Central DI ,[object Object],[object Object],[object Object]
Nephrogenic DI ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Water reabsorption V2 Medullary Hypertonicity
Approach ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Approach ,[object Object],[object Object],[object Object],[object Object]
Approach ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
CAUSES ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Water diuresis ,[object Object],[object Object],[object Object],[object Object],[object Object]
Gestational DI ,[object Object],[object Object],[object Object],[object Object]
Primary polydipsia ,[object Object],[object Object],[object Object],[object Object],[object Object]
Water deprivation test ,[object Object],[object Object],[object Object],[object Object]
ADH stimulation Central Nephrogenic Partial Complete
Water Deprivation Test ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Solute diuresis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Solute diuresis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],} > 250 mmol/L
Fluid therapy
hypotonic isotonic colloid ICF 2/3 ECF 1/3 II 3/4 IV 1/4 TBW  - male : 60%BW, Female 50%BW Elder - male : 50%BW, Female 45%BW Children  : 60%BW
HYPERTONIC SALINE ,[object Object],[object Object],[object Object],[object Object],[object Object],! Benefit in head injured patients ! Arch Surg 1993;128
Bunn F, Trivedi D, Ashraf S. Colloid solutions for fluid resuscitation.  Cochrane Database of Systematic Reviews 2008, Issue 1. Art. No.: CD001319. DOI: 10.1002/14651858.CD001319.pub2. There is no evidence that one colloid solution is  more effective or safe than any others  (albumin, PPF, dextran, HES, gelatin) There is no evidence from RCTs that resuscitation  with colloids reduces the risk of death, compared  to resuscitation with crystalloids,in patients with  trauma, burns or following surgery. Perel P, Roberts I. Colloids versus crystalloids for fluid resuscitation in critically ill patients.  Cochrane Database of Systematic Reviews 2007, Issue 4. Art. No.: CD000567. DOI: 10.1002/14651858.CD000567.pub3.
Fluid therapy ,[object Object],[object Object],[object Object],[object Object],[object Object]
SUMMARY ,[object Object],[object Object],[object Object],[object Object],[object Object]
Water balance
Hyponatremia  ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],No corrected formula for any serum glucose level
Management hyponatremia ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
 
Potassium
K BALANCE ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
50 – 55 mEq/kg 3,000 – 4,000 mEq 65 mEq (2%) Red cell 250 mEq Muscle 2,635 mEq Liver 250 mEq  Bone 300 mEq ICF ECF II IV K 160mEq/l K 4mEq/l 5-10 mEq 5-10 mEq 50-100 mEq 90-95  mEq
 
100% 25% 10% 25% 20% ,[object Object],[object Object],[object Object]
HYPOKALEMIA
DEFINITION ,[object Object]
DIAGNOSIS ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
SIGNS & SYMPTOMS ,[object Object],[object Object],[object Object],[object Object],[object Object]
ST depress, Peak P, PR prolong Widening QRS
CAUSES ,[object Object],[object Object],[object Object],[object Object]
Hypokalemia [acid-base, ECF volume, hypertension, urine K + ] Metabolic acidosis urine K +   low    high (urine Na+ > 100 mEq/day) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Metabolic alkalosis urine K +   low    high (urine Na +  > 100 mEq/day) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],normotension   hypertension ,[object Object],[object Object],Normal acid-base ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Urine pH < 5.5    diarrhea   > 5.5    urine net charge   -ve    diarrhea   +ve    RTA
Hypokalemia, Hypertension, Metabolic alkalosis, renal K +  loss (screening test) [plasma renin activity (PRAng/ml/hr), plasma aldosterone concentration (PAC,ng/dl)] ↑  PRA   ↓ PRA (<1)  ↓ PRA  ↑  PAC   ↑ PAC ( > 9)     ↓ PAC  PAC/PRA ~10   > 50   24 hr urine aldosterone >14    g   < 20 exclude ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Algorithm ,[object Object],[object Object],[object Object],[object Object],[object Object]
TTKG ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Treatment ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],+
Treatment ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
HYPERKALEMIA
DIAGNOSIS ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Flat P Prolong PR AV block Widening QRS Sine-wave
CAUSES ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
DIAGNOSIS ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
TREATMENT ,[object Object],[object Object],[object Object],[object Object],[object Object]
TREATMENT ,[object Object],[object Object],[object Object],[object Object]
SPECIFIC TREATMENT ,[object Object],[object Object],[object Object]
 
Intracellular K +  shift ,[object Object],[object Object],[object Object]
Remove K + ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
TREATMENT   mechanism   onset  peak Ca  antagonist   1-5 min   HD  remove   15 min PD  remove   2 h Kay exalate  remove   1-6 h NaHCO 3  shift   unreliable Insulin  shift   1 0 - 2 0 min   1-2 h B2 agonist  shift   1 0 - 20  min   1-2 h
ADJUNCTIVE TREATMENT ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Acid-Base Disorders
DEFINITION ,[object Object],[object Object],[object Object],[object Object],[object Object],Clinical &  Arterial blood gas
PCO 2 H + , HCO 3 - HCO 3 - /CO 2 Albumin Bone Proteins PO 4 Buffers
 
REMEMBER ,[object Object],[object Object],[object Object],[object Object],PCO 2 H + , HCO 3 -
Normal  meat-based  Diet ,[object Object],[object Object]
KIDNEYS ,[object Object],[object Object],[object Object],[object Object]
COMPENSATORY RESPONSE [ACIDOSIS] ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
COMPENSATORY RESPONSE [ALKALOSIS] ,[object Object],[object Object],[object Object],[object Object],[object Object]
 
ASSESSMENT OF ACID-BASE DISORDER ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Hypoventilation
Hyperventilation
Causes of  metabolic acidosis
H + X -   -> H + X -   ->   CO 2  + NaX   ->  Kidney   ->   + HCO 3 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],H +  : TA,  NH 4 + NaX
[object Object],[object Object],[object Object],SERUM ANION GAP ( Albumin , phosphate, sulphate, organic anion) – (K + , Mg 2+ , Ca 2+ ) = 12 HA   H +   +  A - 1 g/dL = 2.5 - 3 mEq/L
H + X -   -> H + X -   ->   CO 2  + NaX   ->  Kidney   -> H + X -   + Na HCO 3 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Wide anion gap Normal anion gap
H + X -   -> H + X -   ->   CO 2  + NaX   ->  Kidney   -> H + X -   + Na HCO 3 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Wide anion gap Normal anion gap Poor tissue perfusion     serum lactate > 5 mmol/l DKA, alcolhol     serum ketone Methanol, ethylene glycol     serum osmolol gap > 25  Urine NH 4 +     urine net charge    (Na +  + K + ) - Cl -
Mixed wide & normal gap acidosis ,[object Object],[object Object],[object Object],[object Object],[object Object]
TREATMENT ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
CAUSES OF METABOLIC ALKALOSIS (Generation) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Renal HCO 3 -   reabsorption Serum  HCO 3 -   (mEq/l) HCO 3 -   reabsorption 25   50 Volume depletion K +  depletion
Assessment ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
CAUSES OF METABOLIC ALKALOSIS (Generation) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Volume depletion, ↓ urine Cl - Hypertension, ↑ urine Cl - Volume depletion, ↓ urine Cl -
CAUSES OF METABOLIC ALKALOSIS ,[object Object],[object Object],[object Object],[object Object],Treatment
TREATMENT ,[object Object],[object Object],[object Object],[object Object]
Approach to Patients with Glomerular Diseases Suchai Sritippayawan Division of Nephrology , Internal Medicine, Siriraj Hospital, Mahidol University
Structure
pore fenestration charge Slit pore
Pathogenesis
JOURNAL OF NEPHROLOGY Vol .  11 No .  4  -  1998  /  177-182
 
Structure Proliferation Expansion  Endocap-proliferation Thinkening : spike, double contour Necrosis Leucocytic infiltration  Extracap-proliferation  (crescent)  vasculitis
Mesangial : IgMN, IgAN, lupus Subepithelial : membranous Subendothelial : lupus Intra GBM : lupus, MPGN I
Brenner :  Brenner and Rector's The Kidney,  8th ed. Copyright ©  2007 Saunders, An Imprint of Elsevier
Clinical features ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Clinical syndromes ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Asymtomatic hematuria  ,[object Object],[object Object],[object Object],[object Object],[object Object]
>70% of RC are glomerular RC Proteinuria > 1 g/day   or 2+ Indetermine 30–70% Nonglom. <30% acanthocyte ring
Proteinuria ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Types of proteinuria (pathophysiology) ,[object Object],[object Object],[object Object],[object Object]
Asymptomatic proteinuria ,[object Object],[object Object],[object Object],[object Object]
Nephrotic syndrome ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Nephrotic syndrome ,[object Object],[object Object],[object Object]
 
Nephritic syndrome ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Rapidly progressive GN (RPGN) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Telescopic urine sediment
How to approach?
[object Object],[object Object],[object Object],[object Object],[object Object]
Secondary  glomerular diseases
Secondary  glomerular diseases ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Secondary  glomerular diseases ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Metabolic disorders ,[object Object],[object Object]
Diabetic nephropathy ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Diabetic nephropathy ,[object Object],[object Object],[object Object],[object Object],[object Object]
DM & glomerular diseases ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Collagen vascular diseases autoimmune disease ,[object Object],[object Object],[object Object],[object Object],[object Object]
Ig deposition diseases ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Infections  ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Drugs ,[object Object],[object Object]
Malignancy  ,[object Object],[object Object],[object Object],[object Object],[object Object]
Others  ,[object Object]
Primary  glomerular diseases
Primary glomerular diseases ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Investigations ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Kidney biopsy ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Individual investigations ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Managements
Managements ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Managements ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Managements ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
IgA nephropathy ,[object Object],[object Object],[object Object],[object Object],[object Object]
Lupus nephritis   :  Siriraj experience ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Lupus nephritis treatment ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
PREGNANCY  &  KIDNEY DISEASE
NORMAL PHYSIOLOGY ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
RENAL FUNCTIONS ,[object Object],[object Object],[object Object],[object Object]
ELECTROLYTES & ACID-BASE ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Sheehan’s Nephrogenic DI Acute fatty liver (central DI)
HYPERTENSION ,[object Object],[object Object],[object Object],[object Object]
DEFINITION ,[object Object],[object Object],[object Object],[object Object]
DIFFERENTIAL DIAGNOSIS ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Gradual onset HT Proteinuria edema
ACUTE RENAL FAILURE ,[object Object],[object Object],[object Object]
  HELLP  acute fatty live HUS,TTP Onset > 20 wk      < 20 wk < 48 hr PPT      > 48 hr PPT Plt        Coag   DIC DIC   normal Liver dysfn          normal  hypoglycemia Renal failure  mild              
ACUTE RENAL FAILURE ,[object Object],[object Object],[object Object],[object Object]
PREGNANCY    RENAL DIS. ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],RENAL DIS.    PREGNANCY
TERMINATION OF PREGNANCY ,[object Object],[object Object],[object Object]
TREATMENT ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
ANTIHYPERTENSIVE ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]

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Tutorial national board 2010 Nephrology

Hinweis der Redaktion

  1. อธิบายเรื่อง ค่า Cr ที่ไม่เท่ากันในแต่ละคนขึ้นกับ Muscle Mass
  2. อธิบายเรื่อง ค่า Cr ที่ไม่เท่ากันในแต่ละคนขึ้นกับ Muscle Mass