Transcript Nephrology - Dr. Robert Bell 2010

Back to Basics
Nephrology
2010
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 130/80, (the current
target)
• 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 105115
CHRONIC KIDNEY DISEASE
• Uremic Complications:
Major:
– Pericarditis
– Encephalopathy
– Platelet dysfunction
ARF
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, gender
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
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. 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-
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
Acid-Base
Hopefully will not need this.
Normal renal response to acidosis is to
increase ammoniagenesis and more NH4
will be found in the urine
The “urine anion gap” is a way to estimate
urinary NH4
Urine anion gap = urine (Na+ + K+ – Cl-)
If positive there is decreased NH4+
production