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Chronic Renal Failure

1. CRF - irreversible kidney dysfx.with azotemia >3 months.

2. Azotemia - BUN >28mg/dL & Cr>1.5mg/dL

3. ESRD (GFR <5%) - uremia requiring transplantation or dialysis

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Etiology

1. Episodes of ARF (usually ATN) often lead to CRF

2. Over time, combinations of acute renal insults are additive and lead to CRF

3. The definition of CRF requires that at least 3 months of renal failure have occurred

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Risk Factor

1. Diabetes: most common cause ESRD.

2. HTN.

3. Medications.

4. Pregnancy.

5. Black men have a 3.5-4 fold increased risk of CRF compared with white men.

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Treatment

• Pre-Dialysis Treatment

1. Maintain normal electrolytes

a. k, ca, po4 are major electrolytes affected in CRF

b. ACEI may be acceptable in many pts with cr >3.0mg/dL

c. ACEI may slow the progression of diabetic & non-diabetic pt.

d. or D/c other renal toxins (including NSAIDS)

e. Diuretics (eg. furosemide) may help maintain k in normal range

f. Renal diet including high calcium and low phosphate

2. Protein intake to < 0.6 gm/kg body wt.

Equations used to evaluate RF

• Cockcroft-Gult (suitable in patient with stable kidney function).

• Jelliffe (GFR in adults).• MDRD (evaluate the effect of dietary protein restriction & BP

control on the progression of kidney function).• Schwartz (GFR in children).

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Limitations of the use of cr

• Affected by muscle mass.• Affected by diet (meat).• Affected by liver disease (over estimate).• Remain normal in initial stages of kidney disease.• Lab differences.

• So we should use other markers to evaluate kidney function as proteinuria.

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Advantages of MDRD

• It is derived from Modification of Diet in Renal Disease study.• It may provide a better estimate based on the fact that the

equation was derived using GFR measured directly in urinary clearance of radio labeled marker (125 I-Iothalamate).

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MDRD Equation

• Estimated GFR(ml/min/1.72m2)= 70 * (SrCr) -0.999 *(age) -0.176 * (BUN) -0.170 * (Alb) 0.318 * (0.762 F) * (1.18 if African)

• Abbreviated version:

• Estimated GFR(ml/min/1.72m2) =186* (SrCr) -1.154 *(age) -0.203

* (0.742 F) * (1.21 if African)

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Schwartz Equation

• CL cr (ml/min) = (K * length in cm)/SrCr

• K= 0.45 (infants 1-52 wks)• K= 0.55 (child 1-13 yrs)• K= 0.7 (adolescence male)• K=0.55 (adolescence female)

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24-hour urine collection

• Incomplete urine collection.

• Diurnal variation in GFR.

• Variation in Cr excretion.

• However it is suitable for population with variation in dietary intake of cr source as vegetarians, or pt with poor muscle mass (malnourished , amputees).

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When to use proteinuria?

• Pt how r at risk of KD should have an additional assessment by prot excretion.

• Prot is not normally filtered by the glomerulas unless there is damage.

• It is considered as an early marker for KD since it may proceed elevation in SrCr.

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Classification

• Microalbuminuria: defined as albumin excretion rate of 20-200 Mg/min or 30-300 mg/24hr.

• Proteinuria (or albuminuria): total prot exc rate>200 Mg/min or >300 mg/24hrs.

• Albumin is better used than total prot since it is an early indicator of G damage.

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Methods for quantification of albumin

• 24 hr urine collection (can take only over night).

• Spot urine sample for measurement of albumin/Cr ratio (correct for hydration status, better use early morning sample).

• Dipstick test (pt with a +ve dipstick test should be further evaluated by quantitative assessment of Alb/Cr ratio to confirm albuminuria).

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Factors associated with proteinuria

• High protein meal.

• Vigorous exercise.

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The pt has proteinuria if

• According to NKF Kidney Disease Quality initiative (K/DOQI) persistent proteinuria at least 2 +ve quantitative tests separated by 1-2wks.

• ADA microalbuminurea 2 +ve out of three quantitative measurements separated by 3-6 m.

• Microalbuminuria alb/cr 30 – 300 Mg/mg, any thing over albuminuria.

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Other test to confirm kidney dysfunction

• Biopsy.

• Urinalysis.

• Radiographic procedure.

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Recommendations

•Assessment of kidney function (SrCr, BUN, urinary protein) should be done annually.

•Primary prevention is the best treatment goal in patient with diabetes including tight glycemic and blood pressure control.

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Recommendations

ADA recommend the use of:

•ACEI for all patient with type 1 DM, and patient with type 2 without protein urea;

•ACEI or ARBs in patient with type 2 DM and microalbumin urea;

•ARBs in patient with type 2 DM and macroalbumin urea.

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Recommendations

• Some data indicate protein restriction to 0.8-1 g/kg/d can result in stable kidney function.

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Case Study

• M.R is a 32 years, African American female. (wt=63kg,ht=5’8’’)

• CC: – one week N, V, Malaise.

• HPI: – Type 1diabetes mellitus since15 years (noncompliant)– Peptic ulcer for the past 6 months

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PE

• BP=155/102 mmHg• Mild pulmonary congestion• 2+pedal edema

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Labs

Na 143 mEq/l H

K 5.3 mEq/l H

Cl 106 mEq/l SH

SrCr 2.9mg/dl H

BUN 63mg/dl H

GLU 220mg/dl H

ph 7.6mg/dl H

Mg 2.8mg/dl H

Uric Acid 8.8mg/dl H

Hgb 8.7g/dl L

Albumin 700mg/day H

Urineanalysis 4+proteinturia

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• WHAT IS THE CAUSE ADNANCED KIDNEY DISEASE?

• WHAT IS THE SIGNIFICANCE ALBUMINURIA?

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Factors affecting progression of kidney disease

• Male & genetics.• Hi Bp.• Hi glucose & Hgb A1c.• Hi cholesterol.• Advanced age.• Smoking.• Hi protein intake.• Insulin deficiency & keton bodies.• Advanced glycosylation end products (AGEs) that form in

hyperglycemia cause of end organ damage.

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Testing

• Annual in pt DM I>5yrs.

• Annual in pt DM II starting from diagnosis.

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Management

• Intensive glucose control

• Antihypertensive therapy

• Dietary protein restriction(0.6-0.8g/kg/day)

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Intensive glucose control

• DCCT fasting glu 70-120 mg/dl pp glu < 180 mg/dl.• DM I, Intensive insulin V conventional , Monitoring after 6.5

yr follow up.• <39% in risk of microalbuminuria, < 54% in albuminuria.• Risk of hypoglycemia , ADA 90-130 mg/dl, pp <180 mg/dl,

Hgb A1C< 7%.• DM II insulin or POHG V dietary therapy, over 10yrs, reduce

microvascular complications.

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Antihypertensive therapy

• Systemic HTN occure in pt DM I & MicroAU.• 1/3 pt DM II at time of diagnosis.• Nephropathy can cause inc vascular resistance or inc plasma

volume soooooo HTN• DM + HTN------ VC + inc SVR from ATII.• So ACEI or ARBs are the preferred agents even with normal

BP.• Goal BP <130/80 mmHg.• Diuretics in DM + edema.

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