Living Donor Risks

Why GFR is Not Enough

The current paradigm of Chronic Kidney Disease (CKD) is based on eGFR, or measure of renal function, alone. The kidney’s job, however, is not only to discard what the body doesn’t need, but to keep what it does.

Enter protein.

Under normal circumstances, protein molecules are too large to pass through the nephrons, the actual filter part of the kidney. Sometimes however, the glomerules can leak, allowing protein molecules to sneak through. Microalbumin or albumin is a type of protein that can be detected by a urine test and is usually the first signal of glomeruli damage.

Why is this important to living kidney donors? Because albuminuria is the hallmark of hyperfiltration damage, and hyperfiltration is what an LKDs remaining kidney does to compensate for the loss of 50% of the body’s nephrons.

Hemmelgard et. al. analyzed how proteinuria (level of protein in urine) correlated with morality (death), myocardial infarction (heart attack), end-stage renal disease, and doubling of Serum Creatinine (harbinger of kidney malfunction) in folks with different levels of GFR.

Why this study is good: it examined nearly a million people residing Alberta, and thereby covered by government provided health insurance.

Limitations: 85% of Alberta is white, and less than 1% is black.

The researchers found that participants with heavier proteinuria had markedly increased adjusted rates of all four measured adverse effects.

– The adjusted mortality risk was two-fold higher for those with heavy proteinuria (>300 mg/g) and a GFR > 60, compared to a GFR of 45-59.9 and normal proteinuria.

– 60-90 GFR is considered ‘mildly reduced’, but “among the 597,870 participants, a graded increased in the adjusted rate of all-cause mortality was seen with rates of 2.2, 4.3, and 5.1 per 1000 person years among participants with no, mild, or heavy proteinuria, respectively.”

Similar outcomes were seen for heart attack, initiation of renal replacement therapy (dialysis; done upon diagnosis of ESRD), or doubling of serum creatinine.

Here’s their big conclusion:

In fact, patients with heavy proteinuria but without overtly abnormal eGFR appeared to have worse clinical outcomes than those with moderately reduced eGFR but without proteinuria. .

Similarly, a patient with an eGFR of 80 mL/min/1.73 m2 and 3 + proteinuria on dipstick reading (or ACR of 400 mg/g) would be assigned to stage 1 CKD under the current system—even though his or her age-adjusted risks of death and the need for renal replacement therapy would be approximately 2 and 10 times higher, respectively, than an otherwise similar patient with an eGFR of 50 mL/min/ 1.73 m2 but no evidence of proteinuria (stage 3 disease).

What does this mean? That a simple measure of renal function (GFR) is not enough to ensure our long-term kidney health and well-being. We must be aware of our protein levels and how we can control them too.

And don’t let any doctor talk you out of it.

Hemmelgarn BR, Manns BJ, Lloyd A, James MT, Klarenbach S, Quinn RR, Wiebe N, Tonelli M, & Alberta Kidney Disease Network (2010). Relation between kidney function, proteinuria, and adverse outcomes. JAMA : the journal of the American Medical Association, 303 (5), 423-9 PMID: 20124537

One reply on “Why GFR is Not Enough”

knowledge is one of the best ways to protect ourselves and help live better. thank you steve,lovingly donated kidney to my brother tom

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