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Chronic kidney disease (CKD) is a frequent complication of type 2 diabetes (T2D) that affects about 40% of T2D patients. T2D disproportionately affects Black and Hispanic Amercians. New kidney-focused treatments offer hope to the millions of people with CKD associated with T2D. So why are fewer than half of at-risk patients adequately tested for CKD?

Part of the reason for inadequate testing could be low awareness of CKD, resulting in a lack of timely identification and diagnosis. Health disparities have also played a role, with underrepresented minorities having increased risk of T2D and CKD — Hispanics are approximately 1.5 times as likely to be diagnosed with diabetes than non-Hispanic whites and experience end-stage kidney disease (ESKD) at 1.4 times the rate of non-Hispanic whites. Blacks are 2 times as likely to be diagnosed with diabetes than Caucasians and experience ESKD at 3 times the rate of Caucasians. Race has also been historically considered a variable in rendering a laboratory diagnosis of CKD. Detecting CKD before symptoms appear gives room for kidney-protecting treatments that can slow CKD progression and reduce the risk of cardiovascular complications.

Diabetes is a leading cause of CKD

T2D affects over 10% of people in the U.S., primarily those over the age of 45. Up to 40% of patients with T2D develop CKD, which causes progressive and irreversible damage to the kidney and reduces its ability to filter waste. The prevalence of CKD has increased proportionally with elevated prevalence of diabetes, making diabetes-associated CKD the single largest contributor to ESKD, accounting for 39% of ESKD cases. CKD also greatly increases the risk of cardiovascular complications, with the risk of cardiovascular death increasing as CKD progresses. In fact, patients with stage 3 CKD are over 10 times more likely to die than progress to kidney failure.

“Patients and providers may not be aware of how common chronic kidney disease is with type 2 diabetes or that controlling blood sugar or A1C levels isn’t enough to prevent irreversible kidney damage. Fortunately, new therapies are available to protect the kidneys and reduce associated renal and cardiovascular complications.”

Amit Sharma, U.S. Vice President Cardiovascular & Renal, Medical Affairs at Bayer Pharmaceuticals

An intervention to slow CKD progression in patients with CKD associated with T2D

Controlling blood glucose and blood pressure are the top priorities in patients with CKD associated with T2D; however, controlling these alone does not stop the progression of kidney disease. KERENDIA, a nonsteroidal mineralocorticoid receptor antagonist (MRA), works by blocking overactivation of the mineralocorticoid receptor (MR). MR overactivation is thought to contribute to fibrosis and inflammation. Fibrosis and inflammation can contribute to permanent structural kidney damage. KERENDIA is the first and only nonsteroidal MRA indicated to reduce the risk of sustained eGFR decline, ESKD, nonfatal myocardial infarction, hospitalization for heart failure, and cardiovascular death in adult patients with CKD associated with T2D.

KERENDIA is contraindicated in patients who are receiving concomitant treatment with strong CYP3A4 inhibitors and in patients with adrenal insufficiency. The KERENDIA label contains a Warning and Precaution that KERENDIA can cause hyperkalemia. For more information, see “Important Safety Information” at the end of the article.

A wake-up call for CKD testing

Early detection of CKD is critical to detect CKD before severe damage has occurred. CKD progression in patients with CKD associated with T2D can be slowed with interventions like KERENDIA. Testing for CKD is done using two tests: a blood test for estimated glomerular filtration rate (eGFR) and a urine test for urinary albumin-to-creatinine ratio (uACR). A joint study by the National Kidney Foundation and LabCorp found that fewer than 20% of at-risk patients are adequately tested according to guideline recommendations; nearly 90% of patients have their eGFR levels tested, but only 21% of at-risk patients receive uACR testing. It is important to use both measurements, as uACR can detect kidney damage that may be missed using only eGFR. A recent analysis using linked laboratory and claims data by NCQA, Duke University, and CMS showed that only 49% of Medicare Advantage beneficiaries whose lab results identified stage 3 CKD carried the proper diagnosis code.

“Nine out of 10 patients with chronic kidney disease in the United States don’t even know they have it. It is so important to test at-risk patients early, before extensive damage is done, so that kidney-protecting treatments like KERENDIA can be used in appropriate patients.”

Michael Devoy, Chief Medical Officer and Head of Medical Affairs and Pharmacovigilance at Bayer Pharmaceuticals

Race-free approach to estimate GFR

The National Kidney Foundation and American Society of Nephrology in September 2021 issued new guidelines where race is no longer considered a factor in determining eGFR from blood creatinine levels. These new guidelines also recommend increased use of cystatin C as a confirmatory measure of kidney function to enhance the accuracy of blood-based tests for CKD.

To keep all the tools in the treatment toolbox available, early detection of CKD in patients with T2D — through screening using both eGFR and uACR — is of utmost importance. To find out more about KERENDIA as an option for treating chronic kidney disease associated with type 2 diabetes in patients with lab-detected CKD, visit




  • Concomitant use with strong CYP3A4 inhibitors
  • Patients with adrenal insufficiency


  • Hyperkalemia: KERENDIA can cause hyperkalemia. The risk for developing hyperkalemia increases with decreasing kidney function and is greater in patients with higher baseline potassium levels or other risk factors for hyperkalemia. Measure serum potassium and eGFR in all patients before initiation of treatment with KERENDIA and dose accordingly. Do not initiate KERENDIA if serum potassium is > 5.0 mEq/L.

Measure serum potassium periodically during treatment with KERENDIA and adjust dose accordingly. More frequent monitoring may be necessary for patients at risk for hyperkalemia, including those on concomitant medications that impair potassium excretion or increase serum potassium.


Adverse reactions reported in ≥ 1% of patients on KERENDIA and more frequently than placebo: hyperkalemia (18.3% vs. 9%), hypotension (4.8% vs. 3.4%), and hyponatremia (1.4% vs. 0.7%).


  • Strong CYP3A4 Inhibitors: Concomitant use of KERENDIA with strong CYP3A4 inhibitors is contraindicated. Avoid concomitant intake of grapefruit or grapefruit juice.
  • Moderate and Weak CYP3A4 Inhibitors: Monitor serum potassium during drug initiation or dosage adjustment of either KERENDIA or the moderate or weak CYP3A4 inhibitor and adjust KERENDIA dosage as appropriate.
  • Strong and Moderate CYP3A4 Inducers: Avoid concomitant use of KERENDIA with strong or moderate CYP3A4 inducers.


  • Lactation: Avoid breastfeeding during treatment with KERENDIA and for 1 day after treatment.
  • Hepatic Impairment: Avoid use of KERENDIA in patients with severe hepatic impairment (Child Pugh C) and consider additional serum potassium monitoring with moderate hepatic impairment (Child Pugh B).

Please read the Prescribing Information for KERENDIA.