Nephrology & Urology
Archer Online USMLE Reviews
www.ccsworkshop.com
All rights reserved
Renal Failure
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Acute Vs. Chronic
Acute : Pre-Renal, Renal, Post –renal, Glomerular,
tubular, intersititial
Ind...
RENAL BIOPSY
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Indications:
Nephrotic syndrome
Glomerular disease
Unexplained renal failure
Contraindications: single ...
DEFINITION OF ARF
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PCr > 0.5mg/dL if baseline < 3.0mg/dL

PCr > 1.0 mg/dL if baseline > 3.0 mg/dL
 Urine Output :
TOTAL...
CAUSES OF NONOLIGURIC PRE
RENAL ARF
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Diuretics
Osmotic diuresis
Hypercalcemia
Protein malnourished
Post obstru...
NSAID ARF
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Form of pre renal
Occurs in states where RBF decreased and thus
prostaglandin dependent
Nonselectiv...
ACE INHIBITOR ARF
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Rapidly reversible ARF
Increase SCr > 0.5Mg/dL if < 2.0 mg/dL or increase SCr >
1.0 mg/dL ...
POST RENAL ARF
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Caused by anatomic obstruction of urine flow
Accounts for 5-10% of ARF
Patients are often as...
INTRARENAL ARF
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Renal parenchymal diseases
Glomerular
Vascular
Tubular
Interstitial
Acute tubular necrosis – most com...
Glomerular syndromes –
Nephrotic Vs Nephritic Syndromes
NEPHROTIC SYNDROME
 Urinary albumin > 3.0 – 3.5
gm/24 hours
 Hyp...
RAPIDLY PROGRESSIVE
GLOMERULONEPHRITIS
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Characterized by > 50% decrease in GFR over days to weeks
Character...
Proteinuria - Microalbuminuria
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Normal: 150 mg/day
Albumin
30 mg
Plasma proteins 60 mg
Tubular protein 60 mg
Di...
ATN
Ischemic (50%)
 Toxic:
 EXOGENOUS TOXIN ATN :
-Antibiotics, Radiocontrast, Non steroidals,
Anesthetics, Chemotherape...
RADIOCONTRAST ATN
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Risk factors: CRF especially diabetic, CHF, elderly and multiple
myeloma
ATN begins ...
ATHEROEMBOLIC ARF
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Results from cholesterol emboli to small renal
arteries and arterioles
Livedo reticularis ...
MYOGLOBINURIC ARF
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Rhabdomyolysis: trauma,alcohol, cocaine, seizures,
hypokalemia, hypophosphatemia
ECF volu...
ACUTE INTERSTITIAL
NEPHRITIS
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Fever, rash, eosinophila, eosinophiluria and
active urine sediment
Occurs 10-15...
CRYSTAL INDUCED ARF
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Uric acid
Calcium oxalate
Methotrexate
Sulfonamides
Acyclovir
Indinavir
DIAGNOSTIC MANAGEMENT
ARF
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History / Chart review
Physical exam
Urinalysis
Urine indices
Radiologic studies
Mi...
NON DIALYTIC MANAGEMENT
ARF
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Preventive measures
Fluid balance
Acid base balance
Electrolyte balance
Nutriti...
INDICATIONS FOR Emergency
DIALYSIS
REFRACTORY
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Hyperkalemia
Acidemia
Hypoxemia/ volume overload
Uremia - manifes...
Chronic Tubulo-Interstitial Diseases
Chronic issues :
 Toxins: Analgesics, Heavy metals, Chinese herbs, Lithium,
Cyclospo...
Oxalate Nephropathy
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Precipitation of calcium oxalate can cause
interstitial and intratubular crystals leading t...
Chronic Urate Nephropathy
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Related to deposition of sodium urate in the
medullary interstitium
Secondary inflamm...
Analgesic Nephropathy
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NSAID induced interstitial nephritis ( associated
with nephrotic syndrome  proteinuria)
NSAID...
Hepatorenal Syndrome
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The diagnosis of HRS iS of exclusion and depends mainly on serum creatinine level, as no spec...
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Case Studies
) A 25 y/o male comes to your office with complaints of dark red colored urine and

pain in the legs that ...
Case Study
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A 7-year-old boy is brought to the emergency department by his mother
because of "tea-colored urine" for the...
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Case studies contd…

1c) The above patient has been adequately treated but his repeat CPK after 2
days is still elevate...
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Case Study 2

Q1) A 12 y/o boy is brought to you by his mother for skin rash and complaints of intermittent
abdominal p...
UTIs
CASE STUDY
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A 76 YO DEBILITATED MALE, In extended care facility ,
develops every 6 months mild fever, frequency of mictu...
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Symptomatic complicated UTI should be
treated. Number of UTI are less than 2 in 6
mos- no need for continuous Abx...
Recurrent UTIs
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DEFINED AS 2 OR MORE EPISODES IN
PAST 6 MONTHS OR 3 OR MORE
EPISODES IN PAST ONE YEAR.
Use Bactrim...
OTHER ISSUES
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Evaluating painless hematuria elderly
Painful hematuria
Treating asymptomatic bacteriuria
Pyelonep...
Painless Hematuria

The recommended definition of microscopic hematuria is three or
more red blood cells per high-power fi...
Painless Hematuria
Risk Factors for Significant Disease in Patients with Microscopic Hematuria :
 Smoking history
 Occup...
Bladder Ca
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Most common histology is Transitional Cell ca
Routine screening in all patients for bladder ca with
...
Bladder Ca
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Do not routinely screen but however, if you find
Hematuria ( even microscopic) on routine
urinalysis that wa...
Clinical Symps/ Signs
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Hematuria
Urinary frequency or dysuria
Flank or suprapubic pain
Constitutional sy...
IMPORTANT
Refer all patients ( especially those at
high risk) presenting with unexplained
hematuria for cystoscopy, even i...
Bladder Ca - Diagnosis
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Freshly voided urine sample for cytology
Imaging of the urinary tract
Cystoscopy and exam ...
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Bladder Ca - Rx

Surgical resection for non invasive bladder ca.
Radical Cystectomy – Rx of choice for muscl...
Bladder Ca
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Post – radical cystectomy requires urinary
diversion
External diversions include conduits, usually
comp...
Complications – Urinary diversion
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Watch for the following after urinary diversion:
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Bleeding , Infection , Hern...
Painful Hematuria
UTI/ Cystitis/ Pyelonephritis
 Renal Calculi
IMAGING CHOICES:
 Computed tomography ( NON CONTRAST) is ...
Electrolytes
Hypernatremia
Hypernatremia
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Defined as serum sodium > 145 meq/L
Hospital acquired in >80% of patients
Requires defect in ...
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Isovolemic Hypernatremia : Usually hemodynaically
stable unless serum sodium > 170 meq/L
Causes:
 Hypodipsia
 Incr...
Polyuria
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? Water or solute diuresis
Water diuresis i.e. diabetes insipidus vs
polydipsia ( Uosm < 150 mOsm )

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Solu...
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Hypovolemic Hypernatremia Causes

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Renal causes
 Loop diuretics
 Osmotic diuresis
Gastrointestinal causes
 Vomitin...
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Hypervolemic Hypernatremia
Causes :
Hypertonic sodium solutions
Hypertonic feedings
Ingestion of sea water...
Signs and Symptoms Hypernatremia
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Depend on rate, degree and duration
Depressed sensorium
Irritability
Foc...
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Therapy of Hypernatremia

Hemodynamic or osmolal problem?
Acute or chronic problem?
Prior losses and present loss...
CASE STUDY
Hypercalcemia
Etiology
 Clinical features : bones, moans, stones, groans
 Investigations: Ca, Phos, EKG, PTH, Urinary ca...
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Criteria for Surgery – Primary
hyperparathyroidism

Serum total calcium level >12 mg per dL (3 mmol per L) ...
Hypercalcemia – Breast Cancer
Management:
 Principal Rx : Bisphosphonates for moderate to severe
hypercalcemia ( Aridia, ...
Hyponatremia
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Classify – Hypotonic, Isotonic and Hypertonic
Classify – hypovolemic or euvolemic
Hypovol...
Hyperkalemia
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Several causes : Medication interaction is a
common one ( ACEI+Spironolactone+beta
blocker, HEPARIN), rena...
Ekg- Hyperkalemia
The following changes may be seen in hyperkalaemia
 small or absent P waves
 atrial fibrillation
 wid...
58 year old man on
haemodialysis presents with
profound weakness after a
weekend fishing trip.
The man’s K was 9.6
Next Step  IV CALCIUM CHLORIDE
( CALCIUM GLUCONATE AN
ALTERNATIVE)
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30 y/o woman evaluated in the emergency department for a 2day history of muscle weakness. An electrocardio...
Hyperkalemia - Treatment
MNEMONIC – CBIGKDrop
 Check the EKG  If EKG changes, calcium
gluconate IV
 B – BICARBONATE/ Be...
HYPOKALEMIA - EKG
The following changes may be seen in
hypokalaemia.
 small or absent T waves
 prominent U waves
 first...
Acid Base Disorders
Formulas, Case studies and
Management
Acid Base Disorders
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Metabolic Alkalosis
Respiratory Alkalosis
Metabolic Acidosis
Respiratory Acidosis
Mixed Dis...
Acid Base Disorders
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Common clinical problems
Associated with life threatening conditions
Often misdiagnosed
Dem...
Acid Base Disorders
- CARBONIC ACID - BICARBONATE
SYSTEM : H + HCO3 ↔ H2CO3 ↔ H2O +
CO2
-

HENDERSON-HASSELBACH
EQUATION :...
Acid Base Disorders
1. Factors affecting plasma Bicarbonate :
 Rate of H ion input
 Rate of H ion excretion via kidneys
...
ACIDEMIA-ALKALEMIA
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Refers to plasma acidity
Acidemia: pH < 7.36
Alkalemia: pH > 7.44

Metabolic Disorder:
- Acid-ba...
Metabolic Acidosis

Calculate Anion Gap : Na - (Cl + HCO3) - Normal 3 - 10
meq/L
Given entirely by Unmeasured anions are r...
Calculate Compensation
Compensation Metabolic Acidosis
Occurs in 12-24 hours and limit PCO2 10
mmHg :
Expected pCO2 = 1.5x...
Example
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1.
2.
3.
4.
5.
6.
7.

65 y/o man with CAD  and then
cardiogenic shock. Ph 7.26. PCo2 40 HCO310 Na+ 136 Cl- 110...
Normal Anion-Gap Metabolic Acidosis
Gastrointestinal Loss of Bicarbonate
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Diarrhea
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Urinary diversion
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Small bowel, pan...
Increased Anion Gap Acidosis
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Ketoacidosis - diabetic, alcoholic, starvation
Lactic acidosis
Uremia
Toxins - ...
Plasma Level v. Osmolality
Ethanol ÷ 4.6
Methanol ÷ 3.2
Ethylene glycol ÷ 6.2
Isopropanol ÷ 6.1
For example, a blood ethan...
Case Study

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Sam is a 35 y/o alcoholic who is brought to the ER in a comatose state. Sam’s
wife tells you that she had a...
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Ethylene Glycol Poisoning

Envelope shaped crystals

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Treatment : Consider Antidote
( Fomepizole or Ethanol )...
Increased Osmolal Gap
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Ethanol
Methanol
Ethylene Glycol
Formaldehyde
Paraldehyde
Lactic Acidosis
ESRD
Keto...
Isopropanol Ingestion
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Present with CNS depression, hypotension,
arrhytmias and gastritis
Acetest reaction posi...
Renal Tubular Acidosis
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Type 1 ( distal)
Type 2 (proximal)
Type 4 (hyporeninemic hypoaldosteronism)
Type I RTA (Distal)
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Causes: autoimmune diseases, hyperglobinemia
states and hereditary
Present with normal anion ...
Type II RTA (Proximal)
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Isolated defect or associated with generalized proximal
dysfunction i.e. Fanconi syndrom...
Type 4 RTA
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Hypoaldosteronism or aldosterone resistance
Causes: diabetes mellitus, HIV and tubulointerstitial disea...
Metabolic Alkalosis
Calculate compensation
PCO2= ( 0.7 x HCO3 ) + 21 . If measured Pco2
is more than this then there is co...
Causes of Metabolic Alkalosis
Saline responsive : ECF depleted ( contraction alkalosis ), Urine
chloride < 10 meq/L, do no...
Metabolic Alkalosis - Treatment
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Saline responsive
Normal saline to volume replete
 KCl
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Saline resistant
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In...
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Case Study
A 26 year old woman presents to the ER with generalized weakness associated with
perioral numbness. She is m...
Nephrology e tutoring2
Nephrology e tutoring2
Nephrology e tutoring2
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Nephrology e tutoring2

  1. 1. Nephrology & Urology Archer Online USMLE Reviews www.ccsworkshop.com All rights reserved
  2. 2. Renal Failure       Acute Vs. Chronic Acute : Pre-Renal, Renal, Post –renal, Glomerular, tubular, intersititial Indicators : BUN/CREA, FeNA, Urine Spgravity, serum Sodium, serum osmolality, urine output. Chronic – stages  elective hemodialysis Stage V, Emergent hemodialysis indications Acute tubular necrosis : toxic, pigment induced, Ischemic Evaluating renal function : urinalysis - ? Protein, ?rbc , ? Wbc, ? Casts , ? Crystals, ? Bacteria, ? Nitrite, ? Cytology , ? Leucoesterase, - Creatinine clearance, Renal ultrasound, Renal biopsy
  3. 3. RENAL BIOPSY   Indications: Nephrotic syndrome Glomerular disease Unexplained renal failure Contraindications: single kidney, bleeding, severe hypertension. obesity and uncooperative patient
  4. 4. DEFINITION OF ARF  PCr > 0.5mg/dL if baseline < 3.0mg/dL PCr > 1.0 mg/dL if baseline > 3.0 mg/dL  Urine Output : TOTAL ANURIA 0 cc ANURIA < 100 cc OLIGURIA 100-400 cc NON OLIGURIA 400-1000cc POLYURIA > 1000cc 
  5. 5. CAUSES OF NONOLIGURIC PRE RENAL ARF       Diuretics Osmotic diuresis Hypercalcemia Protein malnourished Post obstructive diuresis Diabetes Insipidus
  6. 6. NSAID ARF       Form of pre renal Occurs in states where RBF decreased and thus prostaglandin dependent Nonselective and selective NSAID’s inhibit compensatory afferent arteriolar vasodilation Volume contraction, CHF, cirrhosis, CKD, vascular disease and elderly – increases risk. COX-2 inhibitors have similar effect Allergic interstitial nephritis can also occur
  7. 7. ACE INHIBITOR ARF       Rapidly reversible ARF Increase SCr > 0.5Mg/dL if < 2.0 mg/dL or increase SCr > 1.0 mg/dL if > 2.0 mg/dL Bilateral renal artery stenosis, unilateral stenosis in solitary kidney, small vessel disease and decreased RBF: CHF, cirrhosis, decreased ECF Inhibition of A-II efferent arteriole vasoconstriction leads to decrease PGC and GFR Age, diuretics, diabetes, NSAID’s, cyclosporine and CKD are risk factors ARB’s pose similar risk
  8. 8. POST RENAL ARF       Caused by anatomic obstruction of urine flow Accounts for 5-10% of ARF Patients are often asymptomatic and thus should always be considered Ultrasound useful, but can have 10-20% false negatives Patients are often oligo-anuric, but any pattern of urine output may occur Intraureteric obstruction, Extraureteric obstruction, Urethral obstruction
  9. 9. INTRARENAL ARF   Renal parenchymal diseases Glomerular Vascular Tubular Interstitial Acute tubular necrosis – most common
  10. 10. Glomerular syndromes – Nephrotic Vs Nephritic Syndromes NEPHROTIC SYNDROME  Urinary albumin > 3.0 – 3.5 gm/24 hours  Hypoalbimunemia  Edema  Hyperlipidemia  Lipiduria FSGN ( HIV), MGN( SLE, hepb, Cancer – solid tumors ), Minimal ( children), MPGN ( HepC) FSGN – Rx High dose steroids, cyclosporine MGN – Methylprednisolone pulse, cyclosporin Others : DM, Malignancy, vasulitis, amyloidosis   Nephritic Syndrome Hematuria/ RBC Casts  Oliguria  Hypertension  Decreased GFR  Proteinuria +/ Focal glomerulonephritis    IgA nephropathy Focal SLE ( Type III )  Diffuse glomerulonephritis   Post infectious Diffuse SLE ( Type IV )  IgA nephropathy : most common presentation asymptomatic microhematuria with mild proteinuria
  11. 11. RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS        Characterized by > 50% decrease in GFR over days to weeks Characterized pathologically by crescent formation and clinically by progression to ESRD in untreated patients within weeks Related to the degree of crescent formation Present with active urine sediment, hypertension and oliguric ARF Nephrologic emergency Classification of RPGN:  Type 1: Anti GBM  Type 2: Immune complex  Type 3: Pauci-immune ( p-ANCA ) Early evaluation and biopsy
  12. 12. Proteinuria - Microalbuminuria      Normal: 150 mg/day Albumin 30 mg Plasma proteins 60 mg Tubular protein 60 mg Dipstick test detects (-) charge Does not detect light chains Function of urine concentration Total Protein : creatinine ratio estimates 24 hour urine collection  Microalbuminuria   Albumin excretion rate > 15 ugm/min = 30 mg/day Predictor of early diabetic nephropathy and CVD Urine albumin: urine creatinine < 0.03 Positive in exercise, fever, stress, CHF Repeat urinalysis in 3-6 months if u think its transient proteinuria ACE Inhibitor *****     
  13. 13. ATN Ischemic (50%)  Toxic:  EXOGENOUS TOXIN ATN : -Antibiotics, Radiocontrast, Non steroidals, Anesthetics, Chemotherapeutics, Heavy metals/ solvents  ENDOGENOUS TOXIN ATN : Pigment Nephropathy  Myoglobin, Hemoglobin Crystal Nephropathy  Uric acid , Calcium, Oxalate 
  14. 14. RADIOCONTRAST ATN          Risk factors: CRF especially diabetic, CHF, elderly and multiple myeloma ATN begins abruptly and SCr peaks in 3-5 days Usually reversible, but some have prolonged renal damage Usually nonoliguric, but oliguria can be seen and FE Na decreased Prevention : Consider non contrast study if high risk D/C NSAID’s, ACE inhibitors. ARB’s etc Ensure optimal volume status and RBF  0.9% saline @ 1cc/kg/hr for 6 hours prior  D W + 3 amps NaHCO3 @ 3.5 cc/kg/hr for 1 hour and 5 then 1 cc/kg/hour for 6 hours after N-acetylcysteine 600mg bid pre and day of study Minimize amount of contrast and consider iso-osmolar agent - nonionic and/or isosmolar contrast are less nephrotoxic
  15. 15. ATHEROEMBOLIC ARF      Results from cholesterol emboli to small renal arteries and arterioles Livedo reticularis – A clue!!! Aortic surgery, trauma, angiography, fibrinolytic therapy or spontaneously Eosinophilia, eosinophiluria, leukocytosis and complement activation Retinal, peripheral and abdominal vessels
  16. 16. MYOGLOBINURIC ARF       Rhabdomyolysis: trauma,alcohol, cocaine, seizures, hypokalemia, hypophosphatemia ECF volume depletion Heme (+) urine without RBC’s, hyperkalemia, hyperuricemia, hyperphosphatemia and hypocalcemia Decreased FE Na ECF volume repletion, ?mannitol, and ?alkaline diuresis Hypercalcemia during recovery
  17. 17. ACUTE INTERSTITIAL NEPHRITIS      Fever, rash, eosinophila, eosinophiluria and active urine sediment Occurs 10-15 days after exposure to usually new medication NSAID induced associated with nephrotic syndrome ? Renal biopsy Rx: Stop the agent and ?steroids
  18. 18. CRYSTAL INDUCED ARF       Uric acid Calcium oxalate Methotrexate Sulfonamides Acyclovir Indinavir
  19. 19. DIAGNOSTIC MANAGEMENT ARF       History / Chart review Physical exam Urinalysis Urine indices Radiologic studies Miscellaneous studies
  20. 20. NON DIALYTIC MANAGEMENT ARF        Preventive measures Fluid balance Acid base balance Electrolyte balance Nutritional balance Drug management Management of uremia
  21. 21. INDICATIONS FOR Emergency DIALYSIS REFRACTORY      Hyperkalemia Acidemia Hypoxemia/ volume overload Uremia - manifestations ? Prophylactic when BUN > 60-100 mg/dL
  22. 22. Chronic Tubulo-Interstitial Diseases Chronic issues :  Toxins: Analgesics, Heavy metals, Chinese herbs, Lithium, Cyclosporine, Radiation, Cisplatin  Hematologic diseases: Myeloma  Immunologic: Sjogren’s syndrome, Transplant rejection  Infection: Bacterial pyelonephritis, Tuberculosis, Sarcoid  Anatomic: Obstruction, Reflux  Metabolic disorders: Gout, Oxalosis, Hypercalcemia, Hypokalemia, Cystinosis  Hereditary: ADPKD, MCD  Vascular : Nephrosclerosis, Ischemic nephropathy, Atheroembolic disease  Acute cases : check urine eosinophil count, peripheral eosinophilia
  23. 23. Oxalate Nephropathy     Precipitation of calcium oxalate can cause interstitial and intratubular crystals leading to inflammation and fibrosis Primary hyperoxaluria leads to ESRD Ethylene glycol, methoxyflurane, excessive intake ascorbic acid Increase intestinal absorption: Ileal bypass, short bowel syndrome and Crohn’s disease
  24. 24. Chronic Urate Nephropathy     Related to deposition of sodium urate in the medullary interstitium Secondary inflammation and interstitial fibrosis and CRF Hypertension, bland urinalysis and hyperuricenia Associated with tophaceous gout or an increase in uric acid out of proportion to degree of CRF
  25. 25. Analgesic Nephropathy   NSAID induced interstitial nephritis ( associated with nephrotic syndrome  proteinuria) NSAID induced vasomotor renal insufficiency
  26. 26. Hepatorenal Syndrome    The diagnosis of HRS iS of exclusion and depends mainly on serum creatinine level, as no specific tests establish the diagnosis of HRS. Serum creatinine level is a poor marker of renal function in patients with cirrhosis. But no other reliable noninvasive markers exist for monitoring renal function in these patients. Diagnosis of HRS depends on the presence of a reduced GFR in the absence of other causes of renal failure in patients with chronic liver disease.    Major criteria (All major criteria are required to diagnose HRS .)  Low GFR, indicated by a serum creatinine level higher than 1.5 mg/dL or 24-hour creatinine clearance lower than 40 mL/min  Absence of shock, ongoing bacterial infection and fluid losses, and current treatment with nephrotoxic medications  No sustained improvement in renal function (decrease in serum creatinine to <1.5 mg/dL or increase in creatinine clearance to >40 mL/min) after diuretic withdrawal and expansion of plasma volume with 1.5 L of plasma expander  Proteinuria less than 500 mg/d and no ultrasonographic evidence of obstructive uropathy or intrinsic parenchymal disease Additional criteria (Additional criteria are not necessary for the diagnosis but provide supportive evidence.)  Urine volume less than 500 mL/d  Urine sodium level less than 10 mEq/L  Urine osmolality greater than plasma osmolality , Urine red blood cell count of less than 50 per high-power field & Serum sodium concentration greater than 130 mEq/L Urinary indices are not considered major criteria because a subset of patients with HRS may have high urine sodium levels and low urine osmolality (similar to acute tubular necrosis [ATN]), while other patients with cirrhosis and ATN may have low urine sodium levels and high urine osmolality.
  27. 27.  Case Studies ) A 25 y/o male comes to your office with complaints of dark red colored urine and pain in the legs that started this morning. He has been working out at the local gym excessively for the past three days. He does consume alcohol on weekends but reports having involved in a binge drinking episode that included 10 beers yesterday. On physical examination, he weighs 70kg and he has some tenderness in his calf muscles which he attributes to the excessive squats he performed yesterday. Urine dipstick reveals large blood. If this patient develops acute renal failure , the most likely mechanism would be: A) Interstitial nephritis due to pigment B) Glomerulonephritis C) Acute Tubular necrosis due to pigment deposition D) Acute Tubular Necrosis due to Ischemia E) Alcohol related direct toxic injury 1b) Lab studies revealed normal electrolytes and normal creatinine but a CPK of 50,000. His Urine output has been at 70 ml/hr for the past 6 hours. Your first step in the management to prevent development of patient's Acute Renal Faliure : A) Intravenos Fluids B) Furosemide C) Calcium Gluconate D) No treatment because serum creatinine is normal D) Sodium Bicarbonate
  28. 28. Case Study  A 7-year-old boy is brought to the emergency department by his mother because of "tea-colored urine" for the last several days. He has also had some nausea and vomiting, and his eyes appear swollen when he wakes up in the morning. The eye swelling tends to resolve over the course of the day. He is generally very healthy and there is no family history of any chronic diseases. His temperature is 36.7 C (98.0 F), blood pressure is 130/90 mm Hg, pulse is 96/min, and respiratory rate is 16/min. Physical examination is unremarkable. A urinalysis shows red cell casts. At this time the most appropriate study to confirm your diagnosis is A. antinuclear antibody B. antistreptolysin O antibody C. renal biopsy D. renal ultrasound E. urine culture
  29. 29.  Case studies contd… 1c) The above patient has been adequately treated but his repeat CPK after 2 days is still elevated at 48,000. He complains of increasing pain in his left leg and some tingling and pricking sensations. On examination his left leg was mildly swollen and there was pain on passive stretching of the leg muscles. Dorsalis pedis and posterior tibial pulses are intact. The most likely diagnosis at this time: A) Deep Vein Thrombosis B) Cellulitis C) Compartment Syndrome D) Edema due to renal failure E) Congestive Heart Failure 1d) The immediate course of treatment in this condition would be : A) Anticoagulation with Heparin B) Antibiotics C) Emergency Fasciotomy D) Loop diuretics E) Elevation of the leg
  30. 30.  Case Study 2 Q1) A 12 y/o boy is brought to you by his mother for skin rash and complaints of intermittent abdominal pain, joint pains for past 2 days. He did have an upper respiratory infection about 2 days ago. On physical exam, his vitals are normal. Abdomen is benign with out any tenderness or rigidity. However, you notice patchy purple discolorations on his extremities and the back. Lab studies are obtained that revealed WBC: 6.6 , HGB: 15.3 , MCV: 88 , Platelets: 290,000 ( normal 180k to 400k) BUN: 11 , Creatinine : 0.6 ( normal) , Anti streptolysin O titer : negative Streptozyme : negative ,Urine dipstick : normal without any blood Urinalysis : normal/ no rbcs/ no protein  The mother is very anxious and asks about the long term prognosis of her son. Your response : A) Reassure the mother that boys disorder is self limiting and does not require any follow up B) Tell her the boy needs to be admitted and treated vigorously to prevent renal failure C) Tell her that renal failure develops 100% of such cases and hence needs very cautious follow up D) Tell her that 50% of such cases progress to end stage renal disease. E) Tell her that the boy requires follow up monthly urinalysis for at least 3 months in order to make sure there is no heamaturia/ renal dysfunction. If the boy presented with Renal failure in the above case, the most likely underlying pathology would be : A) IgA mediated vasculitis B) Post streptococcal glomerulonephritis C) Anti GBM disease D) Acute tubular necrosis E) Interstitial Nephritis.
  31. 31. UTIs
  32. 32. CASE STUDY  A 76 YO DEBILITATED MALE, In extended care facility , develops every 6 months mild fever, frequency of micturation with urinary incontinence. USUALLY E.COLI count is >100,000. What is the appropriate treatment? A. CYSTOSCOPY and IVP B. Continuous low dose antibiotics C. Catheterize and irrigate the Bladder daily D. Treat only the acute episode of infection E. No need of treatment as this is colonization
  33. 33.    Symptomatic complicated UTI should be treated. Number of UTI are less than 2 in 6 mos- no need for continuous Abx. His Symptoms are associated with UTI and are not persistent. So just treat the acute episode REMEMBER THE INDICATIONS FOR TREATING “ASYMPTOMATIC “ BACTERIURIA.
  34. 34. Recurrent UTIs    DEFINED AS 2 OR MORE EPISODES IN PAST 6 MONTHS OR 3 OR MORE EPISODES IN PAST ONE YEAR. Use Bactrim DS post sexual activity for women with hx of recurrent UTIs related to sexual activity. Use daily bactrim for people withj no relation to sex activity.
  35. 35. OTHER ISSUES      Evaluating painless hematuria elderly Painful hematuria Treating asymptomatic bacteriuria Pyelonephritis – pyonephric abscess When to admit and when to order imaging studies in pyelonephritis?
  36. 36. Painless Hematuria The recommended definition of microscopic hematuria is three or more red blood cells per high-power field on microscopic evaluation of urinary sediment from two of three properly collected urinalysis specimens.  Always confirm on repeat testing  If Red cell casts/ dysmorphic RBCs or Renal function is compromised/ new onset HTN, combined with mild proteinuria  consider glomerulonephritis.  Recurrent painless Hematuria  consider IgA nephropathy  Other causes : 1. Consider strongly CA.Bladder in the elderly and in smokers 2. R/O benign causes like BPH ( Ask for symptoms of BPH) 3. R/O Prostate Ca in the elderly and in those with family history DO NOT NEGLECT POSSIBILITY OF BLADDER CA IN PTS WITH HEMATURIA 
  37. 37. Painless Hematuria Risk Factors for Significant Disease in Patients with Microscopic Hematuria :  Smoking history  Occupational exposure to chemicals or dyes (benzenes or aromatic amines)  History of gross hematuria  Age >40 years  History of urologic disorder or disease  History of irritative voiding symptoms  History of urinary tract infection  Analgesic abuse  History of pelvic irradiation The presence of significant proteinuria, red cell casts or renal insufficiency, or a predominance of dysmorphic red blood cells in the urine should prompt an evaluation for renal parenchymal disease or referral to a nephrologist.
  38. 38. Bladder Ca     Most common histology is Transitional Cell ca Routine screening in all patients for bladder ca with either urinalysis or cytology is not recommended Screening for bladder cancer in high risk individuals ( those exposed to dyes/ leather, smokers) is controversial  no clear recommendations. High risk History : Smoking history, Occupational exposure to dyes, rubber, or leather, previous exposure to Cyclophosphamide
  39. 39. Bladder Ca  Do not routinely screen but however, if you find Hematuria ( even microscopic) on routine urinalysis that was done for another purpose  do not neglect this finding. ABNORMAL LAB always need to be addressed  pursue further w/u for this hematuria ( BPH, Ca.Bladder, ca.prostate, cystitis, r/o glomerulonephritis)  Remember Micro-HEMATURIA is the most common manifestation of bladder cancer.
  40. 40. Clinical Symps/ Signs          Hematuria Urinary frequency or dysuria Flank or suprapubic pain Constitutional symptoms, such as weight loss Weight loss Adenopathy Palpable suprapubic mass Organomegaly BLADDER CA CAN BE TOTALLY ASYMPTOMATIC
  41. 41. IMPORTANT Refer all patients ( especially those at high risk) presenting with unexplained hematuria for cystoscopy, even if their hematuria is intermittent, and regardless of the findings on history and physical exam.
  42. 42. Bladder Ca - Diagnosis     Freshly voided urine sample for cytology Imaging of the urinary tract Cystoscopy and exam under anesthesia with biopsies Additional diagnostic evaluations, based on findings from the cystoscopy and pathologic evaluation of the tumor, to assess the upper urinary tract or to look for metastatic disease  lfts, ivp, cxr, ct scan of abd/pelvis, bone scan.
  43. 43.       Bladder Ca - Rx Surgical resection for non invasive bladder ca. Radical Cystectomy – Rx of choice for muscle-invasive bladder ca. Adjuvant Intravesical therapy with BCG/ mitomycin-c for  Cis, T1 tumors, tumor > 5cm size. Adjuvant chemotherapy on case-by case basis  gemcitabine+cisplatin or methotrexate Local side effects of BCG include: Cystitis (90% of patients) , Hematuria (30%) , Contracted bladder , Ureteral obstruction, Inflammation (prostatitis, epididymitis, epididymoorchitis) Systemic side effects of BCG, which should resolve in 48 hours, include: Flu-like symptoms , Arthralgias , Rash
  44. 44. Bladder Ca    Post – radical cystectomy requires urinary diversion External diversions include conduits, usually composed of a section of bowel (ileum or colon). Internal conduits include those that require a stoma to empty the reservoir (Kock pouch and Indiana pouch) and orthotopic replacements (e.g., Le Bag, Mainz pouch,
  45. 45. Complications – Urinary diversion  Watch for the following after urinary diversion:    Bleeding , Infection , Hernias , Necrosis , Reflux, Incontinence , Obstruction of conduit, upper tract, or intestines and Recurrent cancer Monitor for bacteremia, treat patients with Proteus or Pseudomonas sp., and observe patients with other organisms if they are asymptomatic. Monitor closely:  Vitamin B12 levels , Acid/base status , Electrolyte levels and Bone mineralization
  46. 46. Painful Hematuria UTI/ Cystitis/ Pyelonephritis  Renal Calculi IMAGING CHOICES:  Computed tomography ( NON CONTRAST) is the best imaging modality for the evaluation of urinary stones, renal and perirenal infections, and associated complications  Ultrasound : Excellent for detection and characterization of renal cysts (Limitations in detection of small solid lesions (<3 cm))  Also, used for stones eval in pregnancy. 
  47. 47. Electrolytes
  48. 48. Hypernatremia
  49. 49. Hypernatremia       Defined as serum sodium > 145 meq/L Hospital acquired in >80% of patients Requires defect in renal concentrating ability and defect in thirst mechanism Normal patients do not become hypernatremic Hypernatremia occurs in very young and very old with a defect in thirst Isovolemic, Hypovolemic & Hypervolemic
  50. 50.   Isovolemic Hypernatremia : Usually hemodynaically stable unless serum sodium > 170 meq/L Causes:  Hypodipsia  Increases insensible losses  Nephrogenic diabetes insipidus – congenital, acquired  CRF, Hypokalemia, Hypercalcemia, Sickle cell disease Amyloidosis, Obstruction, Alcohol, Lithium, Demeclocycline, Glyburide, Amphotericin   Essential hypernatremia Central Diabetes Insipidus : Granulomas, Histiocytosis, Infections, CVA, Postpartum necrosis, Pregnancy, Head traumaPost hypophysectomy, Suprasellar masses, Intrasellar masses
  51. 51. Polyuria   ? Water or solute diuresis Water diuresis i.e. diabetes insipidus vs polydipsia ( Uosm < 150 mOsm )  Solute diuresis i.e. electrolyte vs non electrolyte ( Uosm 300 - 400 mOsm )  Diagnostics: Urinalysis, urine osmolality, and urine electrolytes
  52. 52.  Hypovolemic Hypernatremia Causes  Renal causes  Loop diuretics  Osmotic diuresis Gastrointestinal causes  Vomiting / nasogastric drainage  Diarrhea / cathartics Water loss into cells  Exercise / seizures Cuteaneous causes  Burns / excessive sweating   
  53. 53.        Hypervolemic Hypernatremia Causes : Hypertonic sodium solutions Hypertonic feedings Ingestion of sea water Hypertonic dialysis Primary aldosteronism Cushing’s syndrome
  54. 54. Signs and Symptoms Hypernatremia         Depend on rate, degree and duration Depressed sensorium Irritability Focal neurologic deficits / seizures Muscle spasms Nausea/vomiting Thirst / fever Volume depletion / hyperglycemia
  55. 55.     Therapy of Hypernatremia Hemodynamic or osmolal problem? Acute or chronic problem? Prior losses and present losses? Rate of correction?  Acute: 1-1.5 meq/L/hour reduction  Chronic: 0.5 meq/L/hour reduction or 50% within first 24hours - WHICH FLUID ?    Isovolemic  water: PO or intravenous  Water deficit = 0.6 (BW ) x (P /140 -1) Kg na Hypovolemic – unstable pt????  Correct volume problem i.e. normal saline  Correct osmolal problem Hypervolemic  Salt removal with loop diuretics and free water
  56. 56. CASE STUDY
  57. 57. Hypercalcemia Etiology  Clinical features : bones, moans, stones, groans  Investigations: Ca, Phos, EKG, PTH, Urinary calcium excretion ( R/o familial hypocalciuric hypercalcemia)  Management:  Criteria for surgery in primary hyperparathyroidism  Sestamibi scan only if surgery is planned/indicated  Hypercalcemic crisis management – ivf + lasix after volume repletion only  Indications for corticosteroids : are useful for treating hypercalcemia caused by vitamin D toxicity, certain malignancies (eg, multiple myeloma, lymphoma), sarcoidosis, and other granulomatous diseases  Cinacalcet (Sensipar) -- Directly lowers parathyroid hormone (PTH) levels by increasing sensitivity of calcium sensing receptor on chief cell of parathyroid gland to extracellular calcium. Also results in concomitant serum calcium decrease  Indicated for hypercalcemia with parathyroid carcinoma. Do not lower Calcium too much  Serum calcium reduction may cause lowered seizure threshold, paresthesia, myalgia, cramping, and tetany; 
  58. 58.        Criteria for Surgery – Primary hyperparathyroidism Serum total calcium level >12 mg per dL (3 mmol per L) at any time Hyperparathyroid crisis (discrete episode of life-threatening hypercalcemia) Marked hypercalciuria (urinary calcium excretion more than 400 mg per day) Nephrolithiasis Impaired renal function Osteitis fibrosa cystica Reduced cortical bone density (measure with dual x-ray absorptiometry or similar technique)     Bone mass more than two standard deviations below age-matched controls (Z score less than 2) Classic neuromuscular symptoms Proximal muscle weakness and atrophy, hyperreflexia, and gait disturbance Age younger than 50
  59. 59. Hypercalcemia – Breast Cancer Management:  Principal Rx : Bisphosphonates for moderate to severe hypercalcemia ( Aridia, Zolendronic acid) ( and also prevent osteoporosis) ( esply pts on Aromatase inhibitors are even prone to osteoporosis)   Manage hypercalcemic crises as in all other cases ( IV Fluids and only after complete hydration, then furosemide)
  60. 60. Hyponatremia          Classify – Hypotonic, Isotonic and Hypertonic Classify – hypovolemic or euvolemic Hypovolemic Hyponatremia – Diarrhea, Vomiting, early excess diuresis Euvolemic Hyponatremia  SIADH Isotonic Hyponatremia  Pseudohyponatremia ( Hyperglycemia, Hypertriglyceridemia, does not occur with uremia) Rx  Correct volume and then osmolal problem Volume problem  Isotonic saline always !!!!!!!!!! Asymptomatic  fluid restriction CNS symptoms  3% Saline
  61. 61. Hyperkalemia  Several causes : Medication interaction is a common one ( ACEI+Spironolactone+beta blocker, HEPARIN), renal failure, Addisons disease, Rhabdomyolysis, Metabolic acidosis, Hyperglycemic states.  Effects : arrhythmias, Can lead to tall tented twaves on EKG
  62. 62. Ekg- Hyperkalemia The following changes may be seen in hyperkalaemia  small or absent P waves  atrial fibrillation  wide QRS  shortened or absent ST segment  wide, tall and tented T waves  ventricular fibrillation
  63. 63. 58 year old man on haemodialysis presents with profound weakness after a weekend fishing trip.
  64. 64. The man’s K was 9.6 Next Step  IV CALCIUM CHLORIDE ( CALCIUM GLUCONATE AN ALTERNATIVE)
  65. 65.        30 y/o woman evaluated in the emergency department for a 2day history of muscle weakness. An electrocardiogram taken in the emergency department is shown. Which of the following is the best immediate treatment option? ( A ) Hemodialysis ( B ) 50% glucose, 50 mL, intravenously ( C ) Calcium gluconate, 10 mL ( D ) Sodium polystyrene sulfonate (Kayexalate), 50 g, in sorbitol, rectally ( E ) Peritoneal dialysis
  66. 66. Hyperkalemia - Treatment MNEMONIC – CBIGKDrop  Check the EKG  If EKG changes, calcium gluconate IV  B – BICARBONATE/ Beta agonists  I – INSULIN  G – DEXTROSE  K – KAYEXALATE If total body potassium is an issue  D – Hemodialysis for refractory Hyperkalemia
  67. 67. HYPOKALEMIA - EKG The following changes may be seen in hypokalaemia.  small or absent T waves  prominent U waves  first or second degree AV block  slight depression of the ST segment
  68. 68. Acid Base Disorders Formulas, Case studies and Management
  69. 69. Acid Base Disorders      Metabolic Alkalosis Respiratory Alkalosis Metabolic Acidosis Respiratory Acidosis Mixed Disorders
  70. 70. Acid Base Disorders      Common clinical problems Associated with life threatening conditions Often misdiagnosed Demands an understanding of physiology and pathophysiology pH is a major determinant of enzymatic reactions – Acedemia denatures the enzymes, decreases threshold for ventricular fibrillation and increases respiratory drive. Alkalemia suppresses respiratory drive, can cause myocardial ischemia, coronary vasospasm etc
  71. 71. Acid Base Disorders - CARBONIC ACID - BICARBONATE SYSTEM : H + HCO3 ↔ H2CO3 ↔ H2O + CO2 - HENDERSON-HASSELBACH EQUATION : pH = pKa + log HCO3 / H2CO3 PLASMA ACIDITY : determined by : Balance between concentration of plasma bicarbonate and pCO2 Measured as pH or H ion concentration -
  72. 72. Acid Base Disorders 1. Factors affecting plasma Bicarbonate :  Rate of H ion input  Rate of H ion excretion via kidneys  Rate of H ion or bicarbonate loss via GI tract  Availability of non bicarbonate buffers  Volume of distribution of bicarbonate 2. Factors affecting pCO2  Rate of CO2 excretion via alveolar ventilation  Rate of CO2 production
  73. 73. ACIDEMIA-ALKALEMIA    Refers to plasma acidity Acidemia: pH < 7.36 Alkalemia: pH > 7.44 Metabolic Disorder: - Acid-base disorder caused by primary change in plasma bicarbonate - Plasma bicarbonate = 24-28 meq/L  Respiratory Disorder - Acid-base disorder caused by primary change in pCO2 pCO2 = 36 - 44 mmHg  Compensatory Mechanisms :  Appropriate proportional physiologic responses which tend to restore pH toward, but not to normal Terms “over” and “under” compensation should be avoided – INSTEAD USE “ MIXED “ DISORDER!!!
  74. 74. Metabolic Acidosis Calculate Anion Gap : Na - (Cl + HCO3) - Normal 3 - 10 meq/L Given entirely by Unmeasured anions are related to (-) charge on albumin  One gram albumin = 2.5 meq/L anion i.e. Albumin of 4 gm/L, baseline anion gap would be 10 meq/L which is Normal. Correct Gap for Albumin!!!  If albumin is 2gm%, the baseline anion gap should be 5 in which case 10 should be assumed as increased Anion gap.  Delta Gap : Delta AG / Delta HCO3: 1:1 = Anion gap acidosis >1 = Anion gap acidosis plus metabolic alkalosis < 1 = Increased Anion gap acidosis plus normal anion gap acidosis  Classify Metabolic Acidosis – Increased Gap - Normal Anion gap 
  75. 75. Calculate Compensation Compensation Metabolic Acidosis Occurs in 12-24 hours and limit PCO2 10 mmHg : Expected pCO2 = 1.5x HCO3 + 8 +/- 2 pCO2 = last 2 digits pH pCO2 = HCO3 + 15  If measured Pco2 is less than expected pco2 as calculated by this equation – suspect a primary respiratory alkalosis. If it is more than expected suspect primary respiratory acidosis. This is how you diagnose mixed disorders!!! 
  76. 76. Example  1. 2. 3. 4. 5. 6. 7. 65 y/o man with CAD  and then cardiogenic shock. Ph 7.26. PCo2 40 HCO310 Na+ 136 Cl- 110 Albumin 2.0 What's the Anion Gap? Corrected Anion Gap ? {gap + 2.5(measured albumin)} Delta Anion Gap? Delta Hco3-? ( 24 – bicarb) Delta Gap? Adequately Compensated or mixed ? Name the disorder ?
  77. 77. Normal Anion-Gap Metabolic Acidosis Gastrointestinal Loss of Bicarbonate  Diarrhea  Urinary diversion  Small bowel, pancreatic, or bile drainage ( fistulas, surgical drains )  Cholestiramine Renal Loss of Bicarbonate ( or Bicarbonate equivalent )  Renal tubular acidosis  Recovery phase of Ketoacidosis  Renal Insufficiency  Acidifying Substances- HCl, NH4Cl, Arginine HCl, Lysine HCl, Sulfur To differentiate calculate Urinary Anion Gap = Urine (Na + k) – (cl-). Normal is from +10 to -10. If UAG > +10  Renal loss. If UAG < -10 or more negative  GI Causes
  78. 78. Increased Anion Gap Acidosis       Ketoacidosis - diabetic, alcoholic, starvation Lactic acidosis Uremia Toxins - Ethylene glycol, methanol, salicylate, paraldehyde Osmolar Gap = Measured Osmolarity – Calculated Osmolarity Calculated Serumosm = 2(Na) + Glucose/18 +BUN/2.8 ( + ethylalcohol/4.5)
  79. 79. Plasma Level v. Osmolality Ethanol ÷ 4.6 Methanol ÷ 3.2 Ethylene glycol ÷ 6.2 Isopropanol ÷ 6.1 For example, a blood ethanol level of 100mg/dL would increase plasma osmolality 100/4.6 or 22 mOsm/L
  80. 80. Case Study  Sam is a 35 y/o alcoholic who is brought to the ER in a comatose state. Sam’s wife tells you that she had an argument in the evening about 5 hrs ago over Sam’s alcohol habits. Sam apparently got mad over the discussion, drove his car and returned an hour ago in a very intoxicated state. Wife called the EMS and rushed him to the ER. On examination Sam is disoriented and hallucinating , Pulse 120 Tm 99, RR 26 BP 126/76. The rest of the physical exam is normal except for stuporos state and alcohol smell. Lab studies revealed Na 130 k 3.4 cl- 95 Hco3 16, Glucose 90 Creatinine 1.6 BUN 45. Blood Ethylalcohol level was 180. Serum osmolarity was 360mg%. ABGs revealed 7.28, Pco2 28, Po2 76 Sao2 93. The next best step in management ?  A) Endotracheal intubation in view of severe acidosis B) Hemodialysis because this is an acute renal failure causing acidosis C) Fomepizole because of suspicion of ethylene glycol intoxication D) Supportive treatment for now because this is an ethylalcohol induced lactic acidosis E) Bicarbonate drip to reverse the acidosis because this is renal tubular acidosis    
  81. 81.  Ethylene Glycol Poisoning Envelope shaped crystals     Treatment : Consider Antidote ( Fomepizole or Ethanol ) if Level > 20mg% or if you suspect ethylene glycol intake with 2 or more – a) arterial ph < 7.3, Hco3 <20, osmolar gap>10, calcium oxalate crystals in urine. Antidote blocks Alcohol dehydrogenase and prevents the Glycolic acid formation. In case of methanol, toxic meatbolite is formic acid Ethylene glycol found in antifreeze and de-icer Toxicity results at doses >1.0 ml/kg  Ethylene glycol causes CNS depression , converts to Glycolic Acid (metabolite) effects  Metabolic Mcido &Renal Failure  Oxalic acid (metabolite) effects  Calcium oxalate crystal deposition    C/F: Confusion, Ataxia, Slurred speech ,Hallucination, Tetany Seizures (Hypocalcemia) Hypertension Tachycardia
  82. 82. Increased Osmolal Gap         Ethanol Methanol Ethylene Glycol Formaldehyde Paraldehyde Lactic Acidosis ESRD Ketoacidosis      Mannitol Isopropyl alcohol Hyperlipidemia Hyperproteinemia Diethyl ether
  83. 83. Isopropanol Ingestion      Present with CNS depression, hypotension, arrhytmias and gastritis Acetest reaction positive Increased osmolal gap No metabolic acidosis Anion gap normal
  84. 84. Renal Tubular Acidosis    Type 1 ( distal) Type 2 (proximal) Type 4 (hyporeninemic hypoaldosteronism)
  85. 85. Type I RTA (Distal)    Causes: autoimmune diseases, hyperglobinemia states and hereditary Present with normal anion gap acidosis, urine pH >5.5, hypokalemia, hypercalciuria, nephrocalcinosis and stones Treatment: alkali i.e. K citrate
  86. 86. Type II RTA (Proximal)      Isolated defect or associated with generalized proximal dysfunction i.e. Fanconi syndrome Failure to reclaim filtered bicarbonate Increase FEHCO3 Urine pH > 5.5, but may be < 5.5 once HCO3 < 16 meq/L Causes:     Multiple myeloma Acetozolamide Ifosfamide Lead, cadmium, copper
  87. 87. Type 4 RTA    Hypoaldosteronism or aldosterone resistance Causes: diabetes mellitus, HIV and tubulointerstitial disease Present with hyperkalemia, normal anion gap acidosis and normal urine pH
  88. 88. Metabolic Alkalosis Calculate compensation PCO2= ( 0.7 x HCO3 ) + 21 . If measured Pco2 is more than this then there is concomitant respiratory acidosis. If less than this then concomitant respiratory akalosis. Delta Gap to r/o mixed disorder – metabolic acidosis + metabolic alkalosis if delta gap >1 
  89. 89. Causes of Metabolic Alkalosis Saline responsive : ECF depleted ( contraction alkalosis ), Urine chloride < 10 meq/L, do not go by urine sodium in assessing volume status Gastrointestinal Loss eg : Surreptious vomiting, NG tube suctions,Villous adenoma, Chloride diarrhea, Diuretics (late),Post hypercapnea  Saline resistant : Saline Resistant Metabolic Alkalosis , Increased mineralocorticoid effect,Urine Cl > 20 meq/L  Hypertensive causes:Primary aldosteronismCushing’s syndrome, 11 or 17 hydroxylase deficiency, Licorice / carbenoxolone, Liddle’s syndrome, Steroids  Normotensive causes: Bartter’s syndrome ( thiazide), Gitelman’s syndrome ( like loop diuretic), Diuretics (present), Severe potassium depletion, Severe magnesium depletion 
  90. 90. Metabolic Alkalosis - Treatment  Saline responsive Normal saline to volume replete  KCl   Saline resistant   Inhibit or remove excess mineralocorticoid effect Miscellaneous Acetazolamide, HCl, NH4Cl  Hemodialysis 
  91. 91.  Case Study A 26 year old woman presents to the ER with generalized weakness associated with perioral numbness. She is moderately built and looks slightly depressed. On physical exam, she has mild pallor. She denies use of any medications. BP 120/88 mmHg and physical exam is normal. Lab data: Cr 1.2mg/dL, BUN 15mg/dLNa 136 , K 2.8 , Cl 88 , HCO3 38. Urine Na 45 meq/L, Urine K 35 meq/L, Urine Cl 8 meq/L, Urine specific gravity 1.010, Urine pH 7 The most likely diagnosis is : A) Laxative Abuse B) Surreptious vomiting C) Licorice abuse D) Malabsorption Syndrome E) Hyporeninemic Hypoaldosteronism Treatment : A) IV normal saline B) Spronolactone C) Amiloride D) Psychiatry consult E) Reassurance because this is self limiting

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