Download Nephrology - Dr. Robert Bell 2013

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Nephrology
2013
Major issues in Nephrology, Electrolytes,
Acid-base disturbances
CKD
K/DOQI Classification of Chronic
Kidney Disease
Stage
GFR (≥3mo)
Description
(ml/min/1.73m2)
1
2
3
4
5
90
60-90
30-59
15-29
<15
Damage with normal GFR
Mild  GFR
Moderate  GFR
Severely  GFR
Kidney Failure
In this K/DOQI staging,
“kidney damage” means:
• Persistent proteinuria
• Persistent glomerular hematuria
• Structural abnormality:
– such as PCKD, reflux nephropathy
CHRONIC KIDNEY DISEASE
• Diagnosis:
• Acute vs. chronic:
–Small kidneys on U/S or
unenhanced imaging mean CKD
–Diabetic CKD may still have normal
sized kidneys
CHRONIC KIDNEY DISEASE
• Common causes of CKD:
• Diabetic nephropathy
• Vascular disease
• GN
• PKD
CHRONIC KIDNEY DISEASE
• Causes of CKD:
• Best to divide as proteinuric or
non-proteinuric CKD
• Proteinuric is much more likely
to have deterioration in GFR and
higher cardiovascular morbidity
and mortality
CHRONIC KIDNEY DISEASE
• Treatment
• Delay progression:
• Treat underlying disease i.e. good glucose
control for DM
• BP control to 140/90, (the current
target); 130/80 for diabetics
• ACEI or ARB has extra benefit for
proteinuric CKD
• Lower protein diet…maybe
CHRONIC KIDNEY DISEASE
• Treatment of the consequences
of decreased GFR:
– PO4:
• decrease dietary intake
• PO4 binders such as CaCO3
– Hypocalcemia:
• CaCO3, 1,25 OH D3
CHRONIC KIDNEY DISEASE
• Treatment of the consequences
of decreased GFR:
– Anemia:
• Erythropoetin current target Hb 95105
CHRONIC KIDNEY DISEASE
• Uremic Complications:
Major:
– Pericarditis
– Encephalopathy
– Platelet dysfunction
ARF
Click here in slide show mode
Question 1
Urine values compatible with pre-renal failure:
A)
B)
C)
D)
Osm < 300 mosm/L
RBC casts
Na+ < 20 mmol/L
Fex Na+ > 2%
ARF
• Pre renal and ATN most common
causes (quoted at 70% of cases of ARF)
• DDx:
– Pre Renal
– Intra Renal
– Post Renal
Urine: Pre-Renal vs. Renal
Assessment of Function
U Na
• Pre-Renal < 20
> 40
• ATN
U Osm
> 500
< 350
Fe Na
< 1%
> 2%
U/P
Na
Fe Na =
X 100
U/P Cr
• Pigmented granular casts found in
up to 70% of cases of ATN
Urine: Pre-Renal vs. Renal
Assessment of Function
Fe Urea
• Pre-Renal < 35
Fe Urea = U/P Ur X 100
U/P
Cr
>
55
• ATN
• FeUrea might be useful to Dx pre renal
ARF in those who received diuretics…but
not all studies support its use.
ARF
• Investigations:
– Pre Renal: Urine tests as noted and
responds to volume
– Intra-Renal: look for GN, interstitial
nephritis as well as ATN
– Post Renal: Imaging showing bilateral
hydronephrosis is highly specific for
obstruction causing ARF
Dialysis: Who Needs It?
• If cannot control these by other means:
Hyperkalemia
Pulmonary edema
Acidosis
Uremia
• (GFR < 10-15% for CRF)
Dialysis: Who Needs It?
• Hemodialysis is also used for
intoxications with:
–
–
–
–
ASA
Li
Alcohols: i.e. methanol, ethylene glycol
Sometimes theophylline
+
Na
Hyponatremia
• Pseudo:
– If total osmolality is high: hyperglycemia/
mannitol
– If total osmolality is normal, could be due to
very high serum lipoprotein or protein
Hyponatremia
• Volume status:
– Hypovolemic: high ADH despite low
plasma osmolality
– High total volume: CHF/ cirrhosis have
decreased effective circulating volume
and high ADH despite low plasma
osmolality
Hyponatremia
• Volume status:
– If volume status appears normal:
• If urine osmolality is low: normal response
to too much water intake…”psychogenic
polydipsia”
• If urine osmolality is high: inappropriate
ADH
Hyponatremia
• Treatment:
– Hypovolemic:
• Replace volume
– Decreased effective volume:
• Improve cardiac output if possible
• Water restrict
– SIADH:
• Water restrict
Hyponatremia
• Treatment:
– Rate of correction of Na:
• Not more than 10 mmol in first 24 h and not
more than 18 mmol over first 48 h of
treatment
• Or Central Pontine Myelinosis may occur
Potassium
Hyperkalemia
• Real or Not:
– Hemolysis of sample
– Very high WBC, PLT
– Prolonged tourniquet time
Hyperkalemia
• Shift of K from cells:
– Insulin lack
– High plasma osmolality
– Acidosis
– Beta blockers in massive doses
Hyperkalemia
• Increased total body K:
– Decreased GFR plus:
•
•
•
•
High diet K
KCl supplements
ACEI/ARB
K sparing diuretics
– Decreased Tubular K secretion
TTKG?
• Requirements:
– Urine osmolality > 300
– Urine Na+ > 25
– Reasonable GFR
• TTKG = U/P K+/U/P Osm
[urine K+  (urine osmol/serum osmol)]
serum K+
<7, esp < 5 = hypoaldosteronism
Hyperkalemia
• Treatment
– IV Ca
– Temporarily shift K into cells:
• Insulin and glucose
• Beta 2 agonists (not as reliable as insulin)
• HCO3 if acidosis present
– Remove K
GFR
ASSESSMENT OF GFR:
1000
Creat
800
600
400
200
0
30
60
90
GFR
120
ASSESSMENT OF GFR:
Creatinine clearance formula:
• Cockroft-Gault
estimated Creatinine
clearance
UCr x V
PCr
(140-age) x Kg x1.2
Creat
(x .85 for women)
Need a Steady State for these to be valid
MDRD eGFR
• Labs now calculate this for anyone
who has a serum creatinine checked
• Use serum creatinine, age, sex
MDRD eGFR
GFR, in mL/min per 1.73 m2 =
(170 x (PCr [mg/dL])exp[-0.999]) x (Age exp[-0.176]) x
((Surea [mg/dL])exp[-0.170]) x ((Albumin [g/dL])exp[+0.318])
where SUrea is the serum urea nitrogen concentration; and exp is
the exponential. The value obtained must be multiplied by 0.762 if
the patient is female or by 1.180 if the patient is black.
Simplified:
GFR, in mL/min per 1.73 m2 =
186.3 x ((serum creatinine) exp[-1.154]) x (Age exp[-0.203])
x (0.742 if female) x (1.21 if African American)
Do NOT memorize this formula
Limitations of GFR estimates:
Not reliable for:
• extremes of weight or different body
composition such as post
amputation, paraplegia
• acute changes in GFR
• use in pregnancy
• eGFR greater than 60ml/min/1.73m2
Proteinuria
Proteinuria
• Albumin vs. other protein
– Dipstick tests albumin
PROTEINURIA
• Quantitative:
– 24 hour collection
– ACR: random albumin to creatinine
ratio
– PCR: random protein to creatinine
ratio
PROTEINURIA
• Microalbuminuria: less than dipstick
albumin
• Can use albumin to creatinine ratio
on random urine sample… best done
with morning urine sample
Normal
Random
Urine
ACR
(g/mol)
24h
Urine
Albumin
(mg/24h)
Random 24h Urine
Urine
PCR
Protein
(g/mol) (mg/24h)
M <2.0
F <2.8
<30
<20
MicroM 2.0-30
albuminuria F 2.8-30
30-300
Macroalbuminuria
>300
>30
<200
Question 2
The definition of nephrotic syndrome includes:
:
A)Hypolipidemia
B)Lipiduria
C)24 hr protein ≥2g
D)hypertension
Nephrotic Syndrome
• Definition:
– > 3 g proteinuria per day
– Edema
– Hypoalbuminemia
– Hyperlipidemia and lipiduria are also
usually present
Nephrotic Syndrome
• Causes:
– Secondary: DM, lupus
– Primary:
• Minimal change disease
• FSGS
• Membranous nephropathy
Nephrotic Syndrome
• Complications:
– Edema
– Hyperlipidemia
– Thrombosis…with membranous GN and
very low serum albumin
Nephrotic Syndrome
• Treatment:
– Treat cause if possible
– Treat edema, lipids
– Try to decrease proteinuria
Hematuria
Hematuria
• Significance: ≥3 RBC's per hpf
• DDx: Is it glomerular or not?
• Glomerular:
– RBC casts
– Dysmorphic RBCs in urine
– Coinciding albuminuria may
indicate glomerular disease
Hematuria
• Other investigation:
– Imaging of kidneys
– Serum creatinine
– Age over 40-50 rule out urologic
bleeding, i.e. urine cytology and referral
for cystoscopy
Hematuria
• For glomerular hematuria without
proteinuria DDx includes:
– IgA nephropathy
– Thin GBM disease
– Hereditary nephritis
Ca++, PO4, Mg++
Ca++ and PO4-
Decreased GFR and increased PO4

Decreased Ca
 1 OH of 25-OHD3
 Increased PTH
 Renal osteodystrophy
Magnesium
• Hypomagnesemia:
– GI loss/lack of dietary Mg
– Renal loss:
• Diuretics
• Toxins esp cisplatin
Hypophosphatemia
• Shift
• Decreased total body PO4
– GI loss/decreased intake
– Renal loss
• Fanconi Syndrome?
– Very rare renal tubular loss of:
• PO4, amino acids, glucose, HCO3-
Question 3
Most likely cause of Na 140 Cl 110 HCO3 10
:
A)
B)
C)
D)
RTA
serum albumin 20
resp alkalosis
ketoacidosis
Acid-Base
• Approach to:
– Resp or metabolic
– Compensated or not
– If metabolic: anion gap or not
– Anion gap = Na - (Cl + HCO3)
Acid-Base
Increased anion Gap acidosis:
• “MUDPILES”:
– Methanol
– Uremia
– Diabetic/alcoholic
ketosis
– Paraldehyde
– Isopropyl alcohol
– Lactic acid
– Ethylene glycol
– Salicylate
Acid-Base
Metabolic acidosis with normal
serum anion gap can be due to:
1) GI losses of HCO3
2) Renal tubular acidosis
Renal Tubular Acidosis
Hopefully will not need this.
Normal renal response to acidosis is to increase
ammoniagenesis and more NH4 will be found in
the urine
For those with close to normal GFR, the “urine
anion gap” is a way to estimate urinary NH4
Urine anion gap = urine (Na+ + K+ – Cl-)
If it is positive there is decreased NH4+ production
and likely a renal component to the acidosis
AKI