Back to BasicsBack to BasicsNephrologyNephrology

20102010

Major issues in Nephrology, Electrolytes, Acid-base disturbances

CKD

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

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

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 105-115

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

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

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.

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

• If cannot control these by other means:HyperkalemiaPulmonary edemaAcidosisUremia

• (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

Dialysis: Who Needs It?

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 =

[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

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:

0

200

400

600

800

1000

30 60 90 120

GFR

Cre

at

(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:

• 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

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

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

Proteinuria

Proteinuria

• Albumin vs. other protein– Dipstick tests albumin

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

PROTEINURIA

• Microalbuminuria: less than dipstick albumin

• Can use albumin to creatinine ratio on random urine sample… best done with morning urine sample

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

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

• “MUDPILES”:– Methanol– Uremia– Diabetic/alcoholic

ketosis

– Paraldehyde– Isopropyl alcohol– Lactic acid– Ethylene glycol– Salicylate

Increased anion Gap acidosis:

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