Back to Basics Nephrology 2010
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Transcript of Back to Basics Nephrology 2010
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Back to BasicsBack to BasicsNephrologyNephrology
20102010
Major issues in Nephrology, Electrolytes, Acid-base disturbances
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CKD
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K/DOQI Classification of Chronic K/DOQI Classification of Chronic Kidney DiseaseKidney Disease
StageStage GFR GFR ((≥≥3mo)3mo) Description Description
(ml/min/1.73m(ml/min/1.73m22))
1 1 90 90 Damage with normal Damage with normal GFRGFR
22 60-90 60-90 Mild Mild GFR GFR
33 30-59 30-59 Moderate Moderate GFR GFR
44 15-29 15-29 Severely Severely GFR GFR
5 5 <15 <15 Kidney FailureKidney Failure
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In this K/DOQI staging, “kidney damage” means:
• Persistent proteinuriaPersistent proteinuria
• Persistent glomerular hematuriaPersistent glomerular hematuria
• Structural abnormality:Structural abnormality:– such as PCKD, reflux nephropathysuch as PCKD, reflux nephropathy
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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
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CHRONIC KIDNEY DISEASE
• Common causes of CKD:• Diabetic nephropathy
• Vascular disease
• GN
• PKD
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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
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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
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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
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CHRONIC KIDNEY DISEASE
• Treatment of the consequences of decreased GFR:– Anemia:
• Erythropoetin current target Hb 105-115
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CHRONIC KIDNEY DISEASE
• Uremic Complications:
Major:– Pericarditis– Encephalopathy– Platelet dysfunction
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ARF
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ARF
• Pre renal and ATN most common causes (quoted at 70% of cases of ARF)
• DDx:– Pre Renal– Intra Renal– Post Renal
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U Na U Osm Fe Na
• Pre-Renal
• ATN
Urine: Pre-Renal vs. RenalAssessment of Function
Fe Na =U/P NaU/P Cr X 100
> 500 < 1%
> 40 < 350 > 2%
< 20
• Pigmented granular casts found in up to 70% of cases of ATN
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Fe Urea
• Pre-Renal
• ATN
Urine: Pre-Renal vs. RenalAssessment of Function
Fe Urea = U/P UrU/P Cr X 100
> 55
< 35
• FeUrea might be useful to Dx pre renal ARF in those who received diuretics…but not all studies support its use.
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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
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• If cannot control these by other means:HyperkalemiaPulmonary edemaAcidosisUremia
• (GFR < 10-15% for CRF)
Dialysis: Who Needs It?
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• Hemodialysis is also used for intoxications with:– ASA– Li– Alcohols: i.e. methanol, ethylene glycol– Sometimes theophylline
Dialysis: Who Needs It?
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Na+
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Hyponatremia
• Pseudo: – If total osmolality is high: hyperglycemia/
mannitol– If total osmolality is normal, could be due to
very high serum lipoprotein or protein
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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
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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
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Hyponatremia
• Treatment:– Hypovolemic:
• Replace volume
– Decreased effective volume:• Improve cardiac output if possible• Water restrict
– SIADH:• Water restrict
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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
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Potassium
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Hyperkalemia
• Real or Not:– Hemolysis of sample– Very high WBC, PLT– Prolonged tourniquet time
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Hyperkalemia
• Shift of K from cells:– Insulin lack– High plasma osmolality– Acidosis– Beta blockers in massive doses
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Hyperkalemia
• Increased total body K:– Decreased GFR plus:
• High diet K• KCl supplements• ACEI/ARB• K sparing diuretics
– Decreased Tubular K secretion
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TTKG• Requirements:
– Urine osmolality > 300– Urine Na+ > 25– Reasonable GFR
• TTKG =
[urine K[urine K++ (urine osmol/serum osmol)] (urine osmol/serum osmol)]
serum Kserum K++
<7, esp < 5 = hypoaldosteronism<7, esp < 5 = hypoaldosteronism
U/P K+/U/P Osm
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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
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GFR
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ASSESSMENT OF GFR:
0
200
400
600
800
1000
30 60 90 120
GFR
Cre
at
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(140-age) x Kg x1.2 Creat
(x .85 for women)
ASSESSMENT OF GFR:
• Cockroft-Gault Cockroft-Gault estimated Creatinine estimated Creatinine clearanceclearance
UCr x V PCr
Need a Steady State for these to be valid
Creatinine clearance formula:
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• Labs now calculate this for anyone who has a serum creatinine checked
• Use serum creatinine, age, gender
• Labs now calculate this for anyone who has a serum creatinine checked
• Use serum creatinine, age, gender
MDRD eGFRMDRD eGFR
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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 isthe exponential. The value obtained must be multiplied by 0.762 if the patient is female or by 1.180 if the patient is black.
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 isthe 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)
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)
MDRD eGFRMDRD eGFR
Do NOT memorize this formula
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Limitations of GFR estimates:Limitations of GFR estimates: Not reliable for:Not reliable for:
• extremes of weight or different body extremes of weight or different body composition such as post composition such as post amputation, paraplegiaamputation, paraplegia
• acute changes in GFRacute changes in GFR
• use in pregnancy use in pregnancy
• eGFR greater than 60ml/min/1.73meGFR greater than 60ml/min/1.73m22
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Proteinuria
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Proteinuria
• Albumin vs. other protein– Dipstick tests albumin
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PROTEINURIA
• Quantitative:
– 24 hour collection24 hour collection
– ACR: random albumin to creatinine ACR: random albumin to creatinine ratioratio
– PCR: random protein to creatinine PCR: random protein to creatinine ratioratio
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PROTEINURIA
• Microalbuminuria: less than dipstick albumin
• Can use albumin to creatinine ratio on random urine sample… best done with morning urine sample
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Random Random UrineUrine
24h 24h UrineUrine
Random Random UrineUrine
24h Urine24h Urine
ACRACR
(g/mol)(g/mol)
AlbuminAlbumin
(mg/24h)(mg/24h)
PCRPCR
(g/mol)(g/mol)
ProteinProtein
(mg/24h)(mg/24h)
NormalNormal MM
FF
<2.0<2.0
<2.8<2.8
<30<30 <20<20 <200<200
Micro-Micro-albuminuriaalbuminuria
MM
FF
2.0-302.0-30
2.8-302.8-30
30-30030-300
Macro-Macro-albuminuriaalbuminuria
>30>30 >300>300
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Nephrotic Syndrome
• Definition:– > 3 g proteinuria per day– Edema– Hypoalbuminemia– Hyperlipidemia and lipiduria are also
usually present
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Nephrotic Syndrome
• Causes:– Secondary: DM, lupus– Primary:
• Minimal change disease• FSGS• Membranous nephropathy
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Nephrotic Syndrome
• Complications:– Edema– Hyperlipidemia– Thrombosis…with membranous GN and
very low serum albumin
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Nephrotic Syndrome
• Treatment:– Treat cause if possible– Treat edema, lipids– Try to decrease proteinuria
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Hematuria
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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
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Hematuria
• Other investigation:– Imaging of kidneys– Serum creatinine– Age over 40-50 rule out urologic
bleeding, i.e. referral for cystoscopy
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Hematuria
• For glomerular hematuria without proteinuria DDx includes:– IgA nephropathy
– Thin GBM disease
– Hereditary nephritis
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Ca++, PO4, Mg++
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Ca++ and PO4--
Decreased GFR and increased PO4
Decreased Ca
1 OH of 25-OHD3
Increased PTH
Renal osteodystrophy
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Magnesium
• Hypomagnesemia:– GI loss/lack of dietary Mg– Renal loss:
• Diuretics• Toxins esp cisplatin
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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-
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Acid-Base
• Approach to:– Resp or metabolic
– Compensated or not
– If metabolic: anion gap or not
– Anion gap = Na - (Cl + HCO3)
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Acid-Base
• “MUDPILES”:– Methanol– Uremia– Diabetic/alcoholic
ketosis
– Paraldehyde– Isopropyl alcohol– Lactic acid– Ethylene glycol– Salicylate
Increased anion Gap acidosis:
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Acid-Base
Metabolic acidosis with normal serum anion gap can be due to:
1) GI losses of HCO3
2) Renal tubular acidosis
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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