Stage III CKD

Yesterday we reviewed stage III chronic kidney disease. So today I will review the main points I make as I discuss this condition.

Above chart taken from – Chronic renal failure and its progression

1. I focus on stage III because that is the generalist's responsibility. We have around 7-8 million Americans with stage III CKD. We do not have enough nephrologists to see all these patients.
2. Most patients with stage III die prior to progressing to stage IV or V. They mostly die of CAD – thus we should always remember to address coronary artery disease prevention aggressively in these patients.
3. We generally classify patients using eGFR (estimated GFR.) We use 1 or 2 formulas – Cockcroft-Gault or MDRD. These formulas assume average muscle mass for demographics. They do not work accurately for those with excess muscle mass (e.g., NFL football players), decreased muscle mass (muscular dystrophies, major amputations, cord injury patients) or when the patient's creatinine is not stable (in acute renal failure with a changing creatinine one cannot estimate or measure GFR.)
4. I suspect in the future we will estimate GFR using a combination of serum creatinine and serum cystatin C measurements – combined eGFR estimation.
5. Our main goal for stage I and II extends to stage III – delay progression of disease. We know that decreasing urine protein delays progression of disease. Currently we use ACE-I & ARBs (the combination is better than either alone) to maximize this decrease. I have seen some research studies starting on newer approaches to decrease proteinuria and thus delay progression. We also try to maximize blood pressure control as this additionally delays progression.
6. We generally estimate progression with the graph of 1/creatinine versus time. Studies of progression often use the slope of this line as an outcome parameter.
7. Recent research suggests that we may soon divide stage III into IIIa (eGFR 45-60) and IIIb (eGFR 30-45.)  Most of the metabolic consequences of decreased GFR do not occur until IIIb or IV.
8. I generally focus on 3 consequences – anemia, mineral metabolism and normal gap acidosis.
9. Anemia – some IIIb patients will develop anemia. I currently believe that all patients with Hgb < 10 and CKD deserve erythropoietin and some between 10 and 11 (especially if they also have CHF.)  The goal of therapy in 2008 is a Hgb of 11.5. (New anemia guidelines) Remember that most patients will also need iron supplementation, usually IV with iron sucrose.
10. Mineral metabolism – many IIIb patients develop secondary hyperparathyroidism. The hyperPTH is traditionally taught to be related to hypocalcemia from decreased vitamin D metabolism and from the increased phosphate levels from decreased excretion. Currently the phosphotonin FGF 23 has received much attention as a contributor to these problems.
11. We should regularly measure calcium, phosphate and PTH levels in CKD patients.  We can start treating hypocalcemia and/or hyperphosphatemia with calcium (calcium carbonate or gluconate or citrate.)  We can add vitamin D. If we cannot control the calcium or phosphate with this approach alone, I refer the patient to nephrology. They will probably start sevelamer – a phosphate binder.
12. If the patient develops a normal gap acidosis – start sodium citrate at about 0.5 cc/kg. I spent about 5 minutes discussing this issue – if the readership is interested I can do another entry on this problem alone.
13. If the patient will need dialysis in less than 1 year or one stage IV is reached – consider preparation for end stage management.  If the patient has the characteristics of a good transplant candidate – refer to a transplant center.  If the patient will need hemodialysis, establish an AV fistula and allow it to mature prior to needing it.

I hope this summary gives some of the flavor of our discussion.  Clearly this is incomplete – my standard CKD talk takes almost an hour.