Back to Basics Nephrology 2012 Major issues in Nephrology, Electrolytes, Acid-base disturbances.

Back to BasicsBack to BasicsNephrologyNephrology

20122012

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 100-110

CHRONIC KIDNEY DISEASE

• Uremic Complications:

Major:– Pericarditis– Encephalopathy– Platelet dysfunction

ARF

Question 1

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, sex

• Labs now calculate this for anyone who has a serum creatinine checked

• Use serum creatinine, age, sex

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

Question 2

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

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

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

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