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Silent decline in T2D: why early kidney and heart risk checks can change long-term outcomes

In type 2 diabetes (T2D), kidney and cardiovascular complications often progress without symptoms until later stages, when fewer treatment options remain. Early risk stratification using estimated glomerular filtration rate (eGFR) and urinary albumin-to-creatinine ratio (UACR) offers significant prognostic value—predicting acute kidney injury, hospitalization for heart failure, and cardiovascular death years before clinical signs emerge.

Timing is key. In patients with preserved kidney function (eGFR ≥60 mL/min/1.73 m²), early intervention has been associated with a reduction of nearly 40% in acute kidney injury. This benefit declines substantially once eGFR falls below 45.

Mechanistic studies show that reducing intraglomerular pressure, improving natriuresis, and attenuating inflammatory signaling through modulation of proximal tubular sodium–glucose transport can slow chronic kidney disease (CKD) progression and reduce cardiovascular risk—even in people without diabetes. These findings highlight the need to tailor treatment not only to HbA1c, but also to kidney and heart health.

Early incorporation of eGFR and UACR testing in T2D management enables timely, targeted treatment—helping to alter disease trajectory and improve long-term outcomes.

What prompts you to escalate therapy or involve specialists early? How do you communicate the rationale for going ‘beyond glucose’ to patients?

  • 2w
    worsening slgl2ow decline of gf2 and proteinuria greater than 30 I add sgl2 and sometimes kerendia to patients who have diabetes typ2 and nondiabetic with great success
  • 1mo
    I see this a lot where sugars look controlled, but kidney and CV risk progresses in the background. I usually escalate therapy based on risk markers and trends, not A1c alone. Worsening albuminuria, a slow eGFR decline, or added HF risk will push me to act early.

    With patients, I talk about it as "organ protection" rather than "sugar control". I explain that diabetes affects the kidneys and heart years before symptoms show up, and these tests help us prevent damage instead of reacting to it later. Once they understand the goal is staying off dialysis and out of the hospital, most are open to going “beyond glucose.”
  • 1mo
    A urinary albumin-to-creatinine ratio (UACR) above 30 mg/g is a primary indicator of kidney damage, even if estimated glomerular filtration rate (eGFR) is still in the normal range Is UACR rising?
    • Is eGFR stable or declining?
    • Is HbA1c controlled but organ risk increasing?

    Escalation
    • RAAS blockade optimized?
    • Kidney- and heart-protective therapy initiated when appropriate?
    • BP and volume status reviewed?
    • Medication nephrotoxicity check (NSAIDs, contrast exposure





  • 1mo
    If I see a significant increase in microalbuminuria over a year's time, or continued decline of eGFR without response to SGLT-2 inhibitors or ACE/ARB (which I initiate early in my diabetics), I proceed to referral to nephrology. I discuss the importance of yearly urine microalbumin screening and frequent screening of eGFR to my diabetics as well as a routine part of their care. I discuss with them how diabetes is one of the top 2 reasons why patients end up on dialysis (and this is preventable if caught early) as well as how diabetes can also affect other organs (peripheral nerves, heart, eyes), and screen appropriately for developing issues with these organ systems as well.
  • 1mo
    Often if we have microalbuminuria that doesn't respond to ACE/ARB or SGLT-2 inhibitor I will refer to specialist. Certainly if GFR is already dipping in that setting. I talk to patients about how diabetes affects every organ and we need to monitor each organ on a regular basis (microalbumin, eye checks, etc).
  • 1mo
    MIcroalbuminuria, declining GFR and new onset retinopathy prompt me to start an SGLT-2 agent or add on finerenone. If not already on an a GLP-1 agent, I would add one on as well. Should none of these measures slow a decline in renal function, I will then refer to nephrology.
  • 1mo
    Needs to monitor renal function/proteinuria and HGA1c. I usually start pt on SLGT2 once there is evidence of proteinuria. Some patients are on GLP1 as well for diabetes.
    I usually refer pts to Nephrologist stage 4 or 3b if it is rapid deterioration or worsening proteinuria. It is very important to avoid nephrotic drugs and any nephrotic drugs
  • 1mo
    i feel that it is very important to add UACR to lab screening to determine renal issues early. eGFR is so often done, but less so with UACR. So adding UACR and help detect patients early and start ACE/ARB therapy and SGLT2 to slow renal loss.
  • 1mo
    Worsening eGFR or proteinuria despite glucose control and SGLT2/ACE or ARB control. I explained that patients don't die of high sugar. They die of heart disease, which is directly related to kidney disease.
  • 2mo
    Worsening proteinuria, elevation in blood pressure will prompt further management
  • 2mo
    when nephropathy worsens or hypertension is not controlled, it's time to think of adding Kerendia to a regimen of sglt2i in order to improve the outcomes hoping to slow down the decline in eGFR and /or reduce the nephropathy albuminuria level
  • 2mo
    If the GFR or proteinuria are worsening, despite SGLT2 med, I refer
  • 2mo
    I routinely order eGFR and UACR in all my high risk patients; Along with SOC, I start SGLT2 inhibitors such as Jardiance or Farxiga along with Kerendia early. I refer to Nephrologists if it's CKD3b or higher or macroalbuminuria. Benefits of SGLT2 inhibitors in preserving renal function and decreasing adverse cardiovascular outcomes are explained to the patients before starting therapy.
  • 2mo
    I refer pts to nephrology when they have nephrotic range proteinuria and they are in stage 4 CPK or unable to tolerate ACEI and SgLt-2i or simply requesting a specialist referral
  • 2mo
    I consult with nephrologists when gfr is going down despite ace/arb and sglt2 or uacr is high.
  • 2mo
    THE KIDNEY IS THEFIRST ORGAN THAT THE HEART PUMPS INTO. IF THERE IS A LOT OF RESISTANCE DUE KIDNEY DISEASE TH HEART WILL START TO FAI. IN REVERSE IF HEART FAILURE ALREADY EXISTS THE KIDNEY CANNOT BE PRIMED TO DO FILTRATION AND IT WILL START TO FAIL.
  • 2mo
    Referral for increasing creatinine or macroalbuminuria despite max med therapy.
  • 3mo
    I don't have time to explain all these ins and outs. I just add an SGLt right away
  • 3mo
    I will usually consult Nephrology once UACR is greater than 300 or GFR is below 45 because may of effect of GFR on ACE and ARB and Metformin. Discussion with patients regarding the multi-organ effect of diabetes
  • 3mo
    usually, the first thing i the positive urine microalbumin. Also, of there a reduction in the baseline GFR. Usually discuss the multiple conditions (renal cv etc) as multiple processes with a common origin. Usually refer to Nephrology once a patient enters stage 2.
  • 3mo
    I screen for kidney disease routinely and use sglt 2 inhibitors and Arbs to reduce renal disease and improve cardiac protection. I explain to patients that these meds reduce their risk of many diabetes complications including heart disease and kidney failure.
  • 3mo
    Once microalbuminuria is present, all Type 2 DM spatients should be on ACEI or AEB’ s coupled with proven track record SGLT2i . Generic Farxiga ( dapaglifozin) is mow available also. This class should now be like the statins are for elevated LDL cholesterol
  • 3mo
    I check eGFR and UaCR in all my patients with DM; HTN; obesity; CHF; smokers. In patients with CKD and/or micro/macroalbuminuria I start SGLT2 and Kerendia ( only in Type 2 Diabetics ) to preserve kidney function and to decrease cardiovascular morbidity and mortality, I refer patients with CKD 4 /5 to Nephrologists. I explain the close relationship between CKD and albuminuria to cardiovascular mortality to my patients before starting these meds; Ozempic is another fine option for this class of patients.
  • 3mo
    I review complications of type 2 diabetes and glycemic goals with all my patients at every visit. If I see a decline in EGFR or new proteinuria, I review CKD and it's complications and the need of starting SGLT-2 or GLP-1 therapy. If proteinuria is significant or pts have fast decline in EGFR, I refer these pts to nephrology
  • 3mo
    All patients with type 2 diabetes should attempt to be on an sglt2 inhibitor
  • 3mo
    SGLT-2 Inhibitors have opened up a whole new chapter in the understaning and perspective of Cardio-Renal -Metabolic pathway and interconnection and has gone beyond the Control of diabetes and role of the primary care physicians have become more important in the early detection and prevent the progression of this axis of pathogenesis and UACR is the corner stone of this paradigm . So it is imperative to screen pts with Diabetes , HTN , CVD for microalbuminuria and if its there to start the SGLT-2 Inh along with other risk factor modification pts need to be educated about like managing their other CVD risk factors and need to be explained that glucose /Hba1c levels are just tip of the iceberg and there is lot more going on in the kidneys with microlbuminura that predisposes them for increased risk for CVD and there is really no need to refer to a specialist for this as it falls very much in the domain of the PCP as these meds are very well tolerated and easy to monitor

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