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Tutorial national board 2010 Nephrology

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  • อธิบายเรื่อง ค่า Cr ที่ไม่เท่ากันในแต่ละคนขึ้นกับ Muscle Mass
  • อธิบายเรื่อง ค่า Cr ที่ไม่เท่ากันในแต่ละคนขึ้นกับ Muscle Mass
  • Transcript

    • 1. Nephrology Review February 19, 2010
    • 2. RENAL FUNCTION
      • EXCRETORY
      • REGULATORY
      • ENDOCRINE & METABOLIC
      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
    • 3. GFR
      • Inulin clearance
      • Cr clearance :
      • UcrV/Pcr = 50 mg/dl × 1500 cc = cc/min
      • 1.2 mg/dl × 1440
      • Radionucleide : iothalamate, chromium, DTPA
      • Renal blood flow : hippurate, MAG3
    • 4. Milutinovic et al. Kidney Int. 1975:8;185-190 inulin iothalamate (CCr+Curea)/2
    • 5. Na + K + Cl -
    • 6. Tubular function
      • Absorption
      • Na + , Cl - , H 2 O, HCO 3 - , glucose, Ca 2+ , PO 4 , amino acid, uric acid, protein, urea
      • Secretion
      • H + , K + , NH 4 + , organic acid-base
      • Metabolism
      • drugs, hormones (insulin, calcitriol, EPO)
    • 7. การที่มี BUN และ serum creatinine สูงเกินค่าปกติ (Normal Cr ชาย ≤ 1.5, หญิง ≤ 1.3 mg/dl) Azotemia
    • 8. Uremia กลุ่มอาการที่เกิดจากความผิดปกติของการคั่งของของเสีย สารน้ำและเกลือแร่ที่เกิดคู่กับการเสื่อมหน้าที่ของไต - nausea, vomiting - anorexia - weight loss - dyspnea - fatigue - pruritus
    • 9. Azotemia GFR ปกติ GFR ต่ำ Acute KI Chronic KD Intrinsic RF Post RF Pre RF Chronic GN Chronic TIN BUN Cr
    • 10. Normal GFR
      •  BUN
      • Protein load
      • high protein diet
      • parenteral amino acid
      • GI bleed
      • hypercatabolism
      • BUN  > 30
      • uric  > 2
      • K  > 1 – 2
      • PO 4  > 1
      • Drugs : steroid, tetracycline
      •  Cr
      • Muscle injury
      • trauma, rhabdomyolysis
      • Inhibit secretion
      • cimethidine, trimethoprim
      • Interfere assay
      • ketone, cefoxitin, methanol
    • 11. Decrease GFR
      • Normal BUN
      • Low protein diet
      • Advance chronic liver disease
      • Normal Cr
      • Low muscle mass
      • Advance chronic liver disease
    • 12. Acute Renal Failure (ARF)  Acute Kidney Injury (AKI)
      • Prerenal
      • Renal
      • Post renal
    • 13. Definition of Acute kidney injury OR 2004 Level of dysfunciton Outcome
    • 14.  
    • 15. 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
    • 16. 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
    • 17.  
    • 18. 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
    • 19. Renal causes
      • ATN : ischemic, nephrotoxic
      • AIN : allergy (drugs-betalactam), tumor (lymphoma), infection, rejection
      • Vessels : renal artery or vein thrombosis
      • Microvascular :
      • HUS, TTP
      • RPGN
      • scleroderma
      • drugs (CSA, amphoB, radiocontrast) malignant HT pregnancy related hyperviscosity (MM)
    • 20. 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
    • 21. Pre-renal VS Renal
      • Index Pre-renal Renal
      • Urine sp.gr. >1.018 < 1.012
      • Urine Osm > 500 < 350
      • BUN / Cr ratio > 20 < 10
      • U Na (mEq/l) < 10 > 20
      • FE Na (%) < 1 > 1
      • RFI < 1 > 1
      • U / P Cr > 40 < 20
      = UNa  PCr  100 PNa  UCr FE Na (%) RFI
    • 22. Na + K + Cl - Medullary ischemia Intermediate syndrome Urine Na low Urine spgr low
    • 23. Risk of aminoglycosides nephrotoxic
      • Dose frequency : once daily better
      • Cationic amino group (NH3 + ) :
      • neomycin - worst, streptomycin – least
      • Duration (>1 wk)
      • Renal ischemia, other nephrotoxic
      • Hypokalemia
      • Liver diseases
      • Earliest lesion : ↑ lysosomal myeloid bodies
    • 24. Amphotericin B
      • Renal vasoconstriction & tubular injury
      • Renal complication
      • distal RTA type I (back leak)
      • nephrogenic DI
      • hypomagnesemia
      • Dose & cumulative dose dependent
      • Rx : hydration, liposome? (phospholipid vesicles)
    • 25. Cisplatin
      • Tubular injury (low Cl, reactive hydroxyl radical)
      • Hypomagnesemia
      • Rx : hydration
      • Cyclosporin
      • Renal vasoconstriction
      • Hyperkalemia , met acidosis : Cl shunt
    • 26. Radiocontrast nephropathy
      • Azotemia within 48 hours after exposure
      • High risk : CKD (esp. DM ) with eGFR < 60 mL/min/1.73 m 2 , high contrast volume > 100 mL
      • Prevention
      • nonionic & isoosmolar contrast media
      • correct prerenal : effective volume
      • NSS 1-1.5 ml/kg/hr 3-12 hr before & 12-24 hr after contrast exposure
      • drug : N-acetyl cysteine before & after 24 hrs
    • 27. Acute renal failure
      • Prerenal : volume depletion, heart failure
      • Hx : volume loss, PND, CAD, orthopnea
      • PE : JVP, S3 gallop, crepitation
      • Renal : Drugs (ACEI, NSAID, radiocontrast, antibiotics)
        • RAS : Hx – DM, age, hyperlipidemia, claudication, CAD, stroke
        • PE : peripheral pulse, abdominal bruit
      • Postrenal :
      • common pathway : BPH, CA cervix
      • DM  neurogenic bladder
      • bilat ureteric obstruction
      • single kidney
      • Hx : dysuria, pass stone, hesitancy, urine flow&volume
      • PE : full bladder, bimanual palpation
    • 28. Investigation
      • U/S : obstruction, kidney size,
      • doppler, MRA – RAS, renogram (Cr > 3 – 4 can not be interpreted)
      • Electrolyte acid base, Ca, P
      • Glom dis : urine sediments, UPCR, 24h urine proteins, serum albumin, lipid
      • Underlying Dis and complication !
    • 29. Management
      • Rx causes
      • Stop harmful drugs
      • Nutrition
      • Volume status & urine output
      • Electrolytes
      • Acid base
      • Dialysis
    • 30.  
    • 31.  
    • 32. CAUSES OF ANEMIA IN CRF
      • ↓ Erythropoietin production
      • ↓ Erythrocyte survival
      • Marrow inhibitors
      • Malnutrition
      • Blood loss
      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
    • 33. RENAL OSTEODYSTROPHY
      • High turnover
      • Hyperparathyroidism
      • Low turnover
      • Osteomalacia
      • Adynamic bone
      • Mixed
      Hypocalcemia Hyperphosphatemia Low vitamin D Bone resistance
    • 34. Comprehensive strategy
      • Intervention Goal
      • ACEI or ARB or Both proteinuria < 0.5 g/d
      • ↓ GFR < 2 mL/min/y
      • Blood pressure <130/80 proteinuria < 1g/d
      • <125/75 proteinuria > 1g/d
      • Dietary protein restriction 0.6 – 0.8 g/kg/d
      • Glycemic control in DM HbA1c < 7.0%
      • Lipid lowering Rx LDL < 100 mg/dL
      • EPO Rx Hb > 11-12 g/dL
      • Na restriction 3 – 5 g/d
      • Ca × P product 55
      • iPTH 150-300
      • Smoking cessation, weight control, avoid nephrotoxins
      Med Clin N Am 89 (2005) 489–509
    • 35. 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 +
    • 36. TAL of Henle Loop diuretics
    • 37. DISTAL TUBULE Thiazide
    • 38. CORTICAL COLLECTING TUBULE Na + K + H + spironolactone Amiloride
    • 39. POLYURIA
    • 40. DEFINITION
      • Urine volume
      • > 3 L/day,
      • > 2 cc/min,
      • > 30 cc/kg/day
      • Inappropriate urine output
    • 41. What is urine?
      • Clearance of H 2 O + Clearance of solute
      • (CH 2 O + Csolute)
    • 42.  GFR  salt excretion  H 2 O excretion
    • 43. Polyuria
      •  CH 2 O  water diuresis
      • Diabetes insipidus :
      • central or nephrogenic
      • Polydipsia
      •  Csolute  solute diuresis
      • salt losing
      •  salt loading (intake or GFR)
    • 44. Central DI
      • Sudden onset
      • Trauma, pituitary surgery, tumor, hypoxic encephalopathy
      • 50%  idiopathic
    • 45. Nephrogenic DI
      • Abnormality of V2 receptor, aquaporin 2, medullary hypertonicity
      • Reduce maximal conscentrating ability : common (elderly, renal diseases)  can not produce polyuria
      • True polyuria
      • X-linked (V2 receptor)
      • Li (20%)
      • hypercalcemia
      • Hypokalemia, amyloidosis, Sjogren
    • 46. Water reabsorption V2 Medullary Hypertonicity
    • 47. Approach
      • History
      • Nocturia : DI
      • Psychogenic disorders : polydipsia
      • Onset : acute – central DI
      • ATN : diuretic phase, postobstructive
      • IV load : solute diuresis
      • Drugs : Li–NDI, diuretics, dopamine – solute diuresis
      • Pregnancy :  GFR, DI
      • Intracranial lesion : surgery, pituitary-DI;
      • SAH-cerebral salt losing
      • Thirst : cool water – central DI
    • 48. Approach
      • Physical examination :
      • ECF depletion : salt losing
      • CNS lesion : bitemporal hemianopia
      • subarachnoid hemorrhage
    • 49. Approach
      • Hx : brain lesion, drugs, electrolytes, intake, ATN
      • Volume status
      • Lab :
      • serum Na +
      • low  polydipsia
      • high  DI
      • urine osmolality
      • < 150 :  CH 2 O
      • > 300 :  Csolute
      • 150 – 300 : mixed
    • 50. CAUSES
      • 1 patient : > 1 lesions
      •  CH 2 O
      •  Csolute
      •  CH 2 O +  Csolute
      •  CH 2 O +  Csolute
      •  CH 2 O +  Csolute
    • 51. Water diuresis
      • DI
      • central
      • nephrogenic
      • gestational DI
      • Primary polydipsia
    • 52. Gestational DI
      • Vasopressinase from placenta
      • (cystine aminopeptidase)
      • Resist to AVP
      • Respond to dDAVP
    • 53. Primary polydipsia
      • Anxious, middle-aged women
      • Psychiatric illness, phenothiazine
      • (dry mouth)
      • Hypothalamic lesion (thirst center, dipsogenic DI) : infiltrative lesion (granoloma)
      • Serum Na < 137
    • 54. Water deprivation test
      • ADH stimulation
      • ADH response
      • (5 u of aq vasopressin SC
      • or 10 ug of dDAVP nasal insufflation)
    • 55. ADH stimulation Central Nephrogenic Partial Complete
    • 56. Water Deprivation Test
      • Urine vol, urine osmolality, BW q 1 hr
      • Plasma osmolality and Na q 2 hr
      • End point :
      • serum osmolality > 295 mOsm/kg
      •  urine osmolality < 30 mOsm/kg 2 times
      • body weight 3 – 5%
    • 57.  
    • 58. Solute diuresis
      • Electrolytes
      • Diuretics : furosemide, dopamine
      • Diuretic ATN,
      • postobstructive
      • Solute load :
      • ↑ GFR – pregnancy
      • ↑ intake parenteral
      • cerebral salt wasting (subarachnoid hemorrhage)
      • Salt losing  NO!
      • Non-electrolytes
      • Mannitol
      • Hyperglycemia
      • Urea
    • 59. Solute diuresis
      • Electrolytes
      • 2(U[Na+K]) > 0.6
      • Uosm
      • Nonelectrolytes
      • Urea
      • Glucose
      • mannitol
      } > 250 mmol/L
    • 60. Fluid therapy
    • 61. 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
    • 62. HYPERTONIC SALINE
      • ↑ Intravascular volume > volume infused
      • (prehospital use !)
      • ↓ endothelial cell swelling
      • ↑ cardiac output
      • ↓ peripheral vascular resistance
      ! Benefit in head injured patients ! Arch Surg 1993;128
    • 63. 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.
    • 64. Fluid therapy
      • Side effects : coagulopathy (dextran)
      • anaphylaxis (gelatin)
      • Goals : ↑ O 2 delivery & microcirculation
      • Hb 7 - 9 g/dl
      • Monitoring : clinical , CVP, PCWP, echocardiography, gastric tonometry, laser doppler flowmetry
    • 65. SUMMARY
      • Control loss or bleeding
      • Prehospital hypertonic fluid therapy benefit in head injury
      • Colloids are not better than crystalloids.
      • Human albumin is not better than synthetic colloids
      • Fluid warming
    • 66. Water balance
    • 67. Hyponatremia
      • Water retention + Na loss
      • Why water is retained?
      • severe impair GFR?
      • low solute excretion?
      • ADH effect?
      • volume depletion
      • SIADH (CNS, lung, drugs, malignancy)
      • severe stress, pain
      • hypothyroidism, adrenal insuff
      No corrected formula for any serum glucose level
    • 68. Management hyponatremia
      • Acute or chronic : symptoms
      • Chronic or mild : 8 – 12 mEq/day
      • Acute or severe :
      • convulsion, coma, brain herniation
      • 2 mEq/hr 2 – 3 hr
      • Complication of Rx
      • Central pontine myelinolysis or
      • osmotic demyelination syndrome
    • 69.  
    • 70.  
    • 71.  
    • 72. Potassium
    • 73. K BALANCE
      • Intake : 40 – 120 mEq/day
      • Distribution :
      • intracellular anabolism : glucose, insulin, folic, B12
      • cell membrane factor : Na +- K +- ATPase, insulin, adrenergic receptor (  -out,  2- in)
      • extracellular factor : acidosis-out, alkalosis-in
      • GI : secretion - upper 5 – 15 mEq/L
      • lower 90 mEq/L
      • Renal excretion
      • K depletion  renal K ~ 5-25 mEq/day
    • 74. 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
    • 75.  
    • 76. 100% 25% 10% 25% 20%
      • Flow
      • Aldosterone
      • serum K +
    • 77. HYPOKALEMIA
    • 78. DEFINITION
      • Serum K + < 3.5 mEq/L
    • 79. DIAGNOSIS
      • CLINICAL SIGNS & SYMPTOMS (rate of  )
      • proximal muscle weakness
      • arrhythmia
      • SERUM K + < 3.5 mEq/L
      • Exclude : spurious hypokalemia
      • WC > 100,000/mm 3
    • 80. SIGNS & SYMPTOMS
      • CARDIAC CONDUCTION DEFECTS
      • ISCHEMIA
      • HEART FAILURE
      • LVH
      • DIGITALIS
    • 81. ST depress, Peak P, PR prolong Widening QRS
    • 82. CAUSES
      • Decrease intake
      • Shift
      • Extrarenal loss
      • Renal loss
    • 83. Hypokalemia [acid-base, ECF volume, hypertension, urine K + ] Metabolic acidosis urine K + low high (urine Na+ > 100 mEq/day)
      • Lower GI loss
      • diarrhea
      • laxative abuse
      • villous adenoma
      • Renal loss
      • RTA
      • DKA
      • acetazolamide
      Metabolic alkalosis urine K + low high (urine Na + > 100 mEq/day)
      • loss gastric secretion (late)
      • (urine pH<5.5, low urine Cl - )
      • remote diuretic use
      • (thiazide, loop diuretics)
      • laxative abuse
      • loss gastric secretion (early)
      • (urine pH>7, low urine Cl - )
      • recent diuretic use
      • (thiazide, loop diuretics)
      • Bartter’s syndrome
      • Gitelman’s syndrome
      • Mg 2+ depletion
      normotension hypertension
      • mineralocorticoid
      • excess or effects
      Normal acid-base
      • Intracellular shift
      • insulin
      • β -agonist
      • ↑ extracellular pH
      • thyrotoxicosis
      • periodic paralysis
      • ↑ cell production
      • intoxication
      • other drugs (see text)
      Urine pH < 5.5  diarrhea > 5.5  urine net charge -ve  diarrhea +ve  RTA
    • 84. 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
      • Secondary hyperaldosteronism
      • renovascular hypertension
      • diuretic use
      • renin producing tumor
      • malignant hypertension
      • coarctation of the aorta
      • Primary hyperaldosteronism
      • GRA
      • Mineralocorticoid-like effects
      • exogenous (licorice, see text)
      • congenital adrenal hyperplasia
      • DOC-producing tumor
      • cushing’s syndrome
      • 11-HSD deficiency
      • altered aldosterone metabolism
      • Liddle’s syndrome
      • Confirmatory test
      • NaCl loading test
      • Fludrocortisone suppression
      • test
    • 85. Algorithm
      • History : diarrhea,
      • diuretic uses, vomiting, drugs
      • ECF volume : JVP
      • Blood pressure : hypertension or orthostatic hypotension
      • 24 hr urine K or TTKG
    • 86. TTKG
      • Urine Osm CCT = Urine K + CCT
      • Urine Osm Urine K +
      • TTKG = Urine K + CCT
      • plasma K +
      • = Urine K +  plasma Osm
      • plasma K +  urine Osm
      • K + depletion : TTKG < 2
      • Hyperkalemia : TTKG > 9
    • 87. Treatment
      • Evaluation : EKG and weakness
      • Emergency : arrhythmia, respiratory failure, paralysis
      • IV KCl (1 cc : K + and Cl - 2 mEq)
      • 40 – 60 mEq/ IV 1 L without glucose
      • rate <10 – 20 mEq/hr
      • 40 – 60 mEq/day
      • Oral : KCl (general) > Kcitrate (RTA)
      • Check serum K + q 60 mEq iv replacement
      • Causes : Mg 2+ depletion
      +
    • 88. Treatment
      • IV K +
      • 15%KCl (1cc = K + 2 mEq) ,
      • 8.7%K 2 HPO 4 (1cc = K + 1 mEq)
      • Oral K +
      • KCl : elixir (15 cc  20 mEq)
      • tablet (wax matrix, microencapsulated)
      • Kcitrate (15 cc  10 mEq)
    • 89. HYPERKALEMIA
    • 90. DIAGNOSIS
      • CLINICAL SIGNS & SYMPTOMS
      • proximal muscle weakness
      • arrhythmia
      • SERUM K + > 5.0 mEq/L
      • Exclude : spurious hyperkalemia
      • WC > 100,000/mm 3
      • Plt > 1,000,000/mm 3
      • Hemolysis
      • Clenching
    • 91. Flat P Prolong PR AV block Widening QRS Sine-wave
    • 92. CAUSES
      • K + load
      • Shift
      • Decrease renal K + excretion
      • Decrease distal flow
      • Decrease aldosterone effect
      • Cell defect
    • 93. DIAGNOSIS
      • Rule out factitious hyperkalemia
      • K + load
      • Cause of shift
      • Decrease renal K + excretion
      • advanced renal failure
      • decrease aldosterone effect : drugs
    • 94. TREATMENT
      • Emergency
      • Abnormal EKG
      • Serum K + > 6.5 (or acute > 6.0)
      • Severe paralysis, respiratory failure
      • EKG monitoring
    • 95. TREATMENT
      • SPECIFIC
      • ADJUNCTIVE
      • CAUSE
      • PREVENTION
    • 96. SPECIFIC TREATMENT
      • Antagonize membrane effect
      • Decrease K + level
      • Remove K + from the body
    • 97.  
    • 98. Intracellular K + shift
      • Insulin : most effective and reliable
      • Beta2 agonist : modest, tachycardia (IV)
      • HCO 3 - : ineffective in advanced renal failure, use in metabolic acidosis cases
    • 99. Remove K +
      • Hemodialysis : most rapid
      • Anion exchange resin + laxative
      • Kayexalate : Na polystylene sulfonate
      • 0.6 – 0.7 mEq K + /1 g resin
      • 15 g + 70%sorbitol 50 ml q 6 hr
      • Complication
      • intestinal necrosis
      • Na + overload
    • 100. 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
    • 101. ADJUNCTIVE TREATMENT
      • Restrict K + 2 g/day
      • Stop risk factors
      • Diuretics : increase ECF
      • Fludrocortisone : decrease ICF
      • Long term kayexalate with meal
      • Avoid fasting without glucose
    • 102. Acid-Base Disorders
    • 103. DEFINITION
      • Acidemia --- Euphemia --- Alkalemia
      • (-emia  pH of blood)
      • Acidosis  Alkalosis OR Mixed
      • (-osis : pathologic process causing acid or alkali accumulation)
      • Metabolic OR Respiratory OR Mixed
      Clinical & Arterial blood gas
    • 104. PCO 2 H + , HCO 3 - HCO 3 - /CO 2 Albumin Bone Proteins PO 4 Buffers
    • 105.  
    • 106. REMEMBER
      • Metabolic Acidosis/Alkalosis =
      • disturbances of blood bicarbonate
      • Respiratory Acidosis/Alkalosis =
      • disturbances of PaCO 2
      PCO 2 H + , HCO 3 -
    • 107. Normal meat-based Diet
      • Carbohydrate and fat metabolism will generate 20,000 mEq of acid/day in the form of CO 2 excreted by the lungs
      • Protein catabolism produces 1 mEq/kg (50-60 mEq/day) of inorganic acids (like sulfuric, phosphoric, or hydrochloric acids) which must be excreted by the kidney
    • 108. KIDNEYS
      • Regulate acid-base by the following mechanisms:
      • Reabsorption of filtered HCO 3 ¯
      • Formation of titrable acid
      • Excretion of NH 4 + in the urine
    • 109. COMPENSATORY RESPONSE [ACIDOSIS]
      • Respiratory acidosis
      • acute : ↑ PCO 2 10 mmHg  ↑ HCO 3 - 1 mmol/L
      • chronic : ↑ PCO 2 10 mmHg  ↑ HCO 3 - 4 mmol/L
      • ( kidney 3 – 5 days, HCO 3 - > 15 mmol/L )
      • Metabolic acidosis (1hr  12 – 24 hr)
      • PCO 2 = 1.5  [HCO 3 - ] + 8 + 2 mmHg
      • ∆ PCO 2 = 1.2∆[HCO 3 - ]
    • 110. COMPENSATORY RESPONSE [ALKALOSIS]
      • Respiratory alkalosis
      • acute : ↓ PCO 2 10 mmHg  ↓ HCO 3 - 2 mmol/L
      • chronic : ↓ PCO 2 10 mmHg  ↓ HCO 3 - 5 mmol/L
      • Metabolic alkalosis
      • ∆ PCO 2 = 0.7∆[HCO 3 - ]
    • 111.  
    • 112. ASSESSMENT OF ACID-BASE DISORDER
      • Clinical (history & physical exam)
      • correct diagnosis
      • Extracellular
      • acute or chronic (pH out of normal range?),
      • primary problem (metabolic or respiratory)
      • pH  PCO 2 , HCO 3 -
      • Compensation
      • mixed acid-base disorder ??
    • 113. Hypoventilation
    • 114. Hyperventilation
    • 115. Causes of metabolic acidosis
    • 116. H + X - -> H + X - -> CO 2 + NaX -> Kidney -> + HCO 3
      • ↑ H + PRODUCTION
      • lactic acidosis
      • ketoacidosis
      • toxic substances
      • renal failure
      • HCO 3 - loss
      • diarrhea
      • proximal RTA
      • ↓ RENAL H + EXCRETION
      • (HCO3 regeneration)
      • renal failure
      • distal RTA
      H + : TA, NH 4 + NaX
    • 117.
      • Measured ⊕ + Unmeasured ⊕ = Measured ⊖ + Unmeasured ⊖
      • Measured ⊕ - Measured ⊖ = Unmeasured ⊖ - Unmeasured ⊕
      • (Na + ) – (Cl- + HCO 3 - ) = Unmeasured ⊖ - Unmeasured ⊕
      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
    • 118. H + X - -> H + X - -> CO 2 + NaX -> Kidney -> H + X - + Na HCO 3
      • ↑ H + PRODUCTION
      • lactic acidosis
      • ketoacidosis
      • toxic substances
      • renal failure
      • HCO3- loss
      • diarrhea
      • proximal RTA
      • ↓ RENAL H + EXCRETION
      • renal failure
      • distal RTA
      Wide anion gap Normal anion gap
    • 119. H + X - -> H + X - -> CO 2 + NaX -> Kidney -> H + X - + Na HCO 3
      • ↑ H + PRODUCTION
      • lactic acidosis
      • ketoacidosis
      • toxic substances
      • renal failure
      • HCO3- loss
      • diarrhea
      • proximal RTA
      • ↓ RENAL H + EXCRETION
      • renal failure
      • distal RTA
      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 -
    • 120. Mixed wide & normal gap acidosis
      • Wide anion gap
      • ↑ anion gap = ↓HCO 3 -
      • ∆ anion gap/∆HCO 3 - = 1
      • ∆ anion gap/∆HCO 3 - < 1
      • mixed normal and wide anion gap
    • 121. TREATMENT
      • CAUSES
      • ALKALI THERAPY
      • chronic loss : RTA
      • pH < 7.15
      • Bicarbonate deficit (mEq) =
      • LBWx0.5x(Desired HCO 3 ¯ –actual HCO 3 ¯ )
    • 122. CAUSES OF METABOLIC ALKALOSIS (Generation)
      • H + LOSS
      • GI (gastric content) :
      • vomiting, gastric outlet obstruction
      • Diuretics
      • kidney (aldosterone)
      • hyperaldosteronism
      • Intracellular shift (hypokalemia)
      • HCO 3 - gain
      • intake, bone apatite
      • CONTRACTION ALKALOSIS
      • ECF volume contraction
    • 123. Renal HCO 3 - reabsorption Serum HCO 3 - (mEq/l) HCO 3 - reabsorption 25 50 Volume depletion K + depletion
    • 124. Assessment
      • Blood pressure :
      • hypertension  aldosteronism
      • Volume status : ECF volume loss
      • H + , GI loss, Diuretics
      • Lab : Urine Cl - (not urine Na + ) :
      • ECF volume status
    • 125. CAUSES OF METABOLIC ALKALOSIS (Generation)
      • H + LOSS
      • GI (gastric content) :
      • vomiting, gastric outlet obstruction
      • Diuretics
      • kidney (aldosterone)
      • hyperaldosteronism
      • Intracellular shift (hypokalemia)
      • HCO 3 - gain
      • intake, bone apatite
      • CONTRACTION ALKALOSIS
      • ECF volume contraction
      Volume depletion, ↓ urine Cl - Hypertension, ↑ urine Cl - Volume depletion, ↓ urine Cl -
    • 126. CAUSES OF METABOLIC ALKALOSIS
      • Generation factors
      • Maintenance factor
      • ECF volume (Cl - ) depletion
      • hypokalemia
      Treatment
    • 127. TREATMENT
      • CAUSES (generation factors)
      • Maintenance factors
          • Cl - depletion
          • K + depletion
    • 128. Approach to Patients with Glomerular Diseases Suchai Sritippayawan Division of Nephrology , Internal Medicine, Siriraj Hospital, Mahidol University
    • 129. Structure
    • 130. pore fenestration charge Slit pore
    • 131. Pathogenesis
    • 132. JOURNAL OF NEPHROLOGY Vol . 11 No . 4 - 1998 / 177-182
    • 133.  
    • 134. Structure Proliferation Expansion Endocap-proliferation Thinkening : spike, double contour Necrosis Leucocytic infiltration Extracap-proliferation (crescent) vasculitis
    • 135. Mesangial : IgMN, IgAN, lupus Subepithelial : membranous Subendothelial : lupus Intra GBM : lupus, MPGN I
    • 136. Brenner : Brenner and Rector's The Kidney, 8th ed. Copyright © 2007 Saunders, An Imprint of Elsevier
    • 137. Clinical features
      • Proteinuria
      •  GFR
      • Nephritis
      • Edema
      • Hypertension
      • Foamy urine
      • Hematuria
      • Lipiduria
      • Oliguria
      • Kidney failure
    • 138. Clinical syndromes
      • Asymptomatic : hematuria, proteinuria
      • Nephrotic
      • Nephritis
      • Nephrotic-nephritic
      • Rapidly progressive glomerulonephritis (RPGN)
      • Chronic kidney failure
    • 139. Asymtomatic hematuria
      • RC > 3/HD, glomerular RC
      • No nephrotic, nephritic, HT, edema, azotemia, oliguria
      • If no proteinuria (< 2 g/day) 
      • <10% from glomerular disease
      • Proteinuria < 1 g, serum Cr < 1.5 mg/dL  IgA or thin BM nephropathy
    • 140. >70% of RC are glomerular RC Proteinuria > 1 g/day or 2+ Indetermine 30–70% Nonglom. <30% acanthocyte ring
    • 141. Proteinuria
      • Normal : < 200 mg/day of total protein
      • Microalbuminuria : 30 – 300 mg/day
      • Overt proteinuria : > 300 mg/day
      • Albustix : 20 – 300 mg/dL  abuminuria
      • turbidometry  total protein
      • if –ve albustix but +ve turbidometry
      •  low MW proteinuria
      • Urine protein or albumin/Cr ratio (UPCR)
      •  24 h urine protein
    • 142. Types of proteinuria (pathophysiology)
      • Glomerular : glomerulonephritis
      • Tubular : tubulointerstitial dis, drugs, toxin
      • Overflow :  protein production (MM)
      • Tissue : urinary tract inflammation, tumor
    • 143. Asymptomatic proteinuria
      • Transient or orthostatic proteinuria  good prognosis
      • diagnosis : separate urine collection
      • Persistent proteinuria
      • if no underlying dis and active urine sediment or azotemia  yearly follow up (proteinuria, BP and kidney function)
    • 144. Nephrotic syndrome
      • Proteinuria > 3 g/1.73 m 2 /day
      • Edema
      • Hypoalbuminemia
      • Hyperlipidemia & lipiduria
      • Hypertension
      • Kidney failure
      • Complications
      • Thromboembolism
      • Hyperlipidemia & Atherosclerosis
      • Infections
      • Malnutrition
    • 145.  
    • 146. Nephrotic syndrome
      • Most common :
      • 1 o  IgMN, MCD, membranous GN
      • 2 o  DM, amyloidosis
    • 147.  
    • 148. Nephritic syndrome
      • Hematuria :
      • microscopic hematuria
      • macroscopic : IgAN
      • Postinfectious
      • ANCA-GN Hereditary nephritis
      • Hypertension
      • Kidney failure
    • 149.  
    • 150. Rapidly progressive GN (RPGN)
      • Clinical diagnosis
      • loss of kidney function >50% within weeks to months
      • Pathological diagnosis
      • crestcent > 50%
      • Causes : immune complex GN
      • antiGBM GN
      • Pauci-immune GN (ANCA)
    • 151. Telescopic urine sediment
    • 152. How to approach?
    • 153.
      • Primary or secondary???
      • clinical features of
      • Hypertension
      • Nephritis
      • kidney function
    • 154. Secondary glomerular diseases
    • 155. Secondary glomerular diseases
      • Metabolic diseases : DM (most common)
      • Autoimmune diseases : SLE, small vessel vasculitis
      • Ig deposition diseases
      • Infections : postinfectious GN
      • Drugs : NSAID, gold, D-penicillamine
      • Malignancy : solid or hematologic
      • Others : cirrhosis
    • 156. Secondary glomerular diseases
      • Nephrotic
      • Diabetic nephropathy
      • Ig deposition disease
      • Preeclampsia
      • Lupus nephritis V
      • Nephritis
      • Postinfectious GN
      • lupus nephritis III, IV
      • Mixed cryoglobulinemia
      • ANCA related GN
      • AntiGBM GN
      • HUS, TTP
    • 157. Metabolic disorders
      • DM Diabetic nehropathy (Nephrotic)
      • Hyperthyroidism membranous GN
    • 158. Diabetic nephropathy
      • Type 1
      • 5 – 10 y : microalbuminemia
      • 13 – 20 y : overt proteinuria
      • then :  GFR 1 ml/min/month
      • >90% have retinopathy
      • control : blood sugar
      • BP (130/80 mmHg), ACEI, protein diet, lipid
    • 159. Diabetic nephropathy
      • Type 2
      • duration : variable (HT, atherosclerosis)
      • 50 – 80% have retinopathy
      • control : blood sugar
      • BP (130/80 mmHg), ARB, protein diet, lipid
    • 160. DM & glomerular diseases
      • Diabetic nephropathy
      • Hypertensive nephropathy
      • Other primary or secondary glomerular diseases
      • no retinopathy
      • hematuria
      • rapid  serum Cr
      • acute onset
      • very low serum albumin (< 2 g/dL)
    • 161. Collagen vascular diseases autoimmune disease
      • SLE lupus nehritis (nehritic, nephrotic)
      • RA membranous GN, amyloidosis
      • Polymyositis membranous GN
      • AS IgAN
      • Psoriasis IgAN
    • 162. Ig deposition diseases
      • Amyloidosis
      • Light chain deposition diseases
      • Heavy chain deposition diseases
      • Associated with plasma cell dyscrasia
      • Investigation :
      • CBC, serum immunoelectrophoresis
      • serum free light chains :  , 
      • biopsy : skin, rectal, abdominal fat pad, kidney, liver
    • 163. Infections
      • Viral
      • HBV membranous GN
      • HCV mixed cryoglobulinemia
      • HIV collapsing FSGS
      • Bacteria postinfectious GN
      • syphilis (2 nd , congenital)
      • Fungus
      • Parasite : malaria, schistosomiasis
      • (membranous GN)
    • 164. Drugs
      • NSAID : minimal change disease
      • Gold, d-penicillamin : membranous
    • 165. Malignancy
      • Hematologic :
      • non Hodgin  membranous
      • Hodgin  minimal change dis
      • Solid tumor
      • membranous nephropathy
    • 166. Others
      • Cirrhosis  IgA nephropathy
    • 167. Primary glomerular diseases
    • 168. Primary glomerular diseases
      • Nephrotic
      • IgM nephropathy
      • Minimal change dis
      • FSGS (or IgM with sclesrosis)
      • Membranous GN
      • MPGN type1
      • Fibrillary GN
      • Nephritis
      • IgA nephropathy
      • MPGN type2
      • Hereditary nephritis
      • Alport syndrome
      • TBM dis
    • 169. Investigations
      • Diagnosis of glomerular diseases
      • blood pressure
      • GFR
      • urine protein excretion
      • 24h > 2 g/day, UPCR > 2
      • urine sediment :
      • oval fat body
      • glomerular red cell
      • cast – fatty, red cell, cellular
      • systemic or extrarenal manifestations
      • kidney biopsy
    • 170. Kidney biopsy
      • Indication
      • Diagnosis
      • Prognosis
      • Method
      • Light microsope study : morphology
      • Immunofluorescence study : Ig, C3, C4
      • Electron microscope study : deposition & ultrastructure
    • 171. Individual investigations
      • ANA, antiDNA  lupus nephritis
      • Complement  inflammatory related
      • ANCA, CXR  pauci-immune : WG, CS, micro.PAN
      • antiGBM, CXR  antiGBM dis
      • RF, cyroglobulin  mixed cryoglob GN
      • ASO, antiDNAase  postinfectious
      • HBsAg, antiHCV  hepatitis related NS
      • antiHIV  HIVAN
      • VDRL  2 nd syphilis, congenital
      • CBC, electrophoresis  IgDD
    • 172. Managements
    • 173. Managements
      • Primary or secondary
      • Nephrotic syndrome
      • most common causes : minimal change disease
      • try predinolone 1 mg/kg/day
      • (check infection : CXR, stool exam, fever)
      • if response : continue 1 mg/kg/day for 1 month and reduced 5 – 10 mg/month
      • if not response (16 wks) :
      • refer for kidney biopsy
      • ACEI or ARB  reduce proteinuria
    • 174. Managements
      • Nephrotic syndrome
      • most common causes : minimal change disease
      • cyclophosphamide 1mg/kg/day for 1 month may benefit in
      • Steroid dependent (can not stop steroid or relapse within 2 wks after stop steroid)
      • frequent relapse ( > 2 times/6 m)
      • steroid side effects
    • 175. Managements
      • Nephritis
      • treatment depends on etiology
      • recommend kidney biopsy in
      • urine protein > 1-2 g/day
      • hypertension
      •  GFR
    • 176. IgA nephropathy
      • Asymptomatic hematuria  RPGN
      • Factors associated with progressive disease (Siriraj experiencea)
      • serum Cr > 1.5 mg/dL
      • proteinuria > 1 g/day
      • Rx with prednisolone 1 mg/kg/day as minimal change disease (Siriraj experience)
    • 177. Lupus nephritis : Siriraj experience
      • ANA +ve 90%, antiDNA +ve 67%
      • Classification
      • class I 0.6%
      • class II 17.9%
      • class III 9.9%
      • class IV 58.6%
      • class V 12.9%
      • Edema, hypertension, nephrotic, nephritis,  GFR
    • 178. Lupus nephritis treatment
      • Class II
      • oral prednisolone 0.5 mg/kg/day
      • Class IV
      • oral prednisolone 1 mg/kg/day plus cyclophosphamide or mycophinolate mofetil
      • Class V
      • steroid plus cytotoxic drugs
    • 179.  
    • 180. PREGNANCY & KIDNEY DISEASE
    • 181. NORMAL PHYSIOLOGY
      • Systemic hemodynamics
      •  blood volume
      •  peripheral vascular resistance
      • Onset : early preg. Peak : 2nd trim.
      • BP  10 mmHg  105/60 mmHg
      • Cardiac output  30 – 50%
      • PLASMA  30 – 40%
      • water :  6 – 8 litrs
      • Na+ :  900 – 1,000 mEq
      • RC :  250 – 450 ml (24-26wk)
      • Nitric oxide
      • relaxin (ovarian hormone)
      • HCG
    • 182. RENAL FUNCTIONS
      •  GFR & RPF 40 – 50%
      • Onset : 1 m, Peak : end of 1st trim.
      •  20 – 30% : 3rd trim. Normal : PPT 3 m
      • Serum Cr 0.4 – 0.5 ( < 0.8) mg/dl
    • 183. ELECTROLYTES & ACID-BASE
      • Chronic respiratory alkalosis
      •  RC center : progesterone
      • Hyponatremia (  5 mEql)
      • relaxin (by HCG)
      • normal 1 – 2 m PPT
      • Polyuria
      • vasopressinase (   4 : placenta),  GFR
      • impair secretory reserve or renal response
      • normal : 2 – 3 wk PPT
      • dDAVP - sensitive
      Sheehan’s Nephrogenic DI Acute fatty liver (central DI)
    • 184. HYPERTENSION
      • PREECLAMSIA
      • CHRONIC HYPERTENSION
      • GESTATIONAL HYPERTENSION
      • RENAL DISEASES
    • 185. DEFINITION
      • > 140/90 mmHg
      • mild & moderate
      • (140-169/90-109)
      • severe : DBP > 110 mmHg
    • 186. DIFFERENTIAL DIAGNOSIS
      • Preeclapmsia RD&CHT GHT
      • Onset > 20 wk < 20 wk 3 rd trim
      • Proteinuria + -/+ -
      • Sediment - -/+ -
      • Serum uric >4  -
      • Urine Ca <100 >200 >200
      Gradual onset HT Proteinuria edema
    • 187. ACUTE RENAL FAILURE
      • EARLY PREGNANCY
      • Prerenal : hyperemesis gravidarum
      • ATN : septic abortion
    • 188. 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    
    • 189. ACUTE RENAL FAILURE
      • RENAL CORTICAL NECROSIS
      • abruptio placenta, placenta previa, amniotic fluid embolism, prolong intrauterine fetal death
      • URINARY TRACT OBSTRUCTION
      • ACUTE PYELONEPHRITIS
    • 190. PREGNANCY  RENAL DIS.
      • Cr < 1.5 : same outcome
      • Cr > 1.5
      • Renal failure :  40%, 1/3 irreversible, 10% -ESRD
      • Proteinuria : ½ 
      • HT : ¼ 
      • Lupus nephritis : active if remission < 6 m
    • 191.
      • Azotemia
      • Pretermature 6 times
      • HYPERTENSION
      • fetal death, preterm labour,
      • IUGR, LBW
      RENAL DIS.  PREGNANCY
    • 192. TERMINATION OF PREGNANCY
      • Serum Cr > 1.4 or GFR < 70 ml/min
      • Uncontrolled HT
      • Severe nephrotic or nephritis
    • 193. TREATMENT
      • Benefit ? : restrict activity, admission
      • AntiHT drugs in mild – moderate HT :
      • ↓ risk of severe HT
      • preeclampsia, fetal death, SGA
      • Acute severe HT
      • IV labetalol, oral nifedipine are better than IV hydralazine
    • 194. ANTIHYPERTENSIVE
      • Methy DOPA or labetalol 
      • Hydralazine 
      • Ca ch blocker 
      • Beta blocker ?
      • Diuretic ?
      • ACEI ×