Diabetes is the leading cause of kidney failure in the United States. About one in three people with diabetes develops kidney disease.
It is also the kidney disease we are best equipped to slow. Four drug classes change the trajectory. Most patients who should be on them are on none of them.
Ask what you are taking, and ask why not
Here is the stack that protects a diabetic kidney. Check yourself against it.
An ACE inhibitor or an ARB. The foundation, and the one most often absent. It reduces proteinuria and protects the kidney beyond its effect on blood pressure. Many patients with albuminuria have never been started on one at all.
And of those who are started, a large share are stopped — because the creatinine rose modestly in the first weeks. That rise is expected. It reflects a change in pressure inside the glomerulus, not injury. A rise up to roughly thirty percent is not a reason to stop the drug, and stopping it hands back the protection it was providing.
An SGLT2 inhibitor. The most important development in nephrology in a generation. It slows progression substantially in diabetic kidney disease, independent of any effect on blood sugar. If you have diabetes with albuminuria and no contraindication, you should be on one. Most are not.
Finerenone. A non-steroidal mineralocorticoid antagonist added on top of the ACE inhibitor or ARB. It reduces kidney and cardiovascular events. Uptake has been poor.
A GLP-1 receptor agonist, increasingly supported for kidney protection in its own right.
These are additive, not alternatives. A patient on the full stack is on a different curve than a patient on one drug, and the gap between what exists and what is prescribed is the single largest missed opportunity in diabetic kidney disease.
Board-certified nephrology at Remix Medical in Houston. Call (713) 597-5131 or book online.
The test that finds it early
The first sign is albumin in the urine, appearing years before creatinine rises and long before you feel anything. A urine albumin-to-creatinine ratio catches it. A creatinine alone does not.
Annual albumin screening is standard of care in diabetes and is skipped constantly. Finding albuminuria early is what makes the drug stack worth starting.
How it develops
Years of elevated blood sugar damage the glomeruli — the filtering units. They thicken, scar, and begin leaking protein into the urine that should have stayed in the blood.
Blood pressure control matters as much as glucose control and possibly more. Glucose control matters most early, and less once substantial damage is established.
What we watch for
Diabetic kidney disease rarely arrives alone. Retinopathy nearly always accompanies it — if you have kidney disease and diabetes but a normal eye exam, the diagnosis deserves questioning, because something else may be happening.
We also watch for the things that mimic it. Sudden heavy proteinuria, blood in the urine, or a rapid creatinine rise are not the pattern of diabetic nephropathy. Those findings prompt a search for a different disease, sometimes with a biopsy.
The trajectory is not fixed
Patients hear a diagnosis of diabetic kidney disease and assume dialysis is coming. For many it is not, and for many others it is decades away.
The rate of decline is what matters, and the rate is modifiable. Somebody with albuminuria who starts an SGLT2 inhibitor, gets their blood pressure to target, and stays off NSAIDs is on a different curve than they were.
If you have diabetes and albuminuria, and you are not on an ACE inhibitor or ARB plus an SGLT2 inhibitor, ask why. There is usually no good answer.
Call (713) 597-5131 or book online.