Blood Pressure and Kidney Damage: What Hypertension Does to Your Kidneys and How to Stop It

When I sit with a patient and talk about high blood pressure, I often hear the same thing: "But my kidneys feel fine." That's the heart of the problem. The kidneys rarely complain until they're already in trouble. Hypertension damages them quietly, over years, with no pain and no obvious symptom, and by the time a patient notices ankle swelling, fatigue, or a new diagnosis of chronic kidney disease, a substantial fraction of the nephrons, the tiny filtering units inside each kidney, are already gone and they don't come back.

This matters because hypertension is the second leading cause of end-stage kidney disease in the United States, behind only diabetes. Among American adults with hypertension, roughly one in ten already has stage 3 or worse chronic kidney disease, and most don't know it. Globally, high systolic blood pressure is one of the top three modifiable risk factors driving kidney disease burden, alongside body weight and glucose levels. The good news is that we know exactly how to prevent and slow this damage, and the tools have never been better. Between modern blood pressure targets, the renin-angiotensin-aldosterone system blockers we've had for decades, and the newer SGLT2 inhibitors and finerenone that have transformed nephrology practice over the last five years, we can meaningfully protect a hypertensive patient's kidneys.

This article walks through what happens inside the kidney when blood pressure is chronically elevated, what tests reveal the damage early, what blood pressure targets the major trials support, and which medications actually change the trajectory. If you have high blood pressure, or you care about someone who does, this is the information I wish every patient received at the time of diagnosis.

How Hypertension Damages the Kidney

Each of your kidneys contains about a million nephrons, microscopic filtering units made up of a tuft of tiny blood vessels called a glomerulus and a long tubule that reabsorbs and secretes to fine-tune the filtered fluid into urine. The glomerulus is essentially a high-pressure sieve. Blood enters through the afferent arteriole, gets filtered across a specialized membrane, and exits through the efferent arteriole. Pressure inside the glomerulus has to be tight enough to drive filtration but not so high that the sieve breaks down.

When systemic blood pressure is chronically elevated, the kidney tries to protect itself. The afferent arteriole constricts to reduce the pressure transmitted to the glomerulus. Over years of sustained hypertension, the wall of the afferent arteriole thickens and becomes infiltrated with a glassy, eosinophilic material in a process called hyalinosis. Some arterioles scar down and effectively close, leaving the nephrons they feed to wither and die from ischemia. Other arterioles fail to constrict adequately and transmit the high pressure straight into the glomerulus, which then develops glomerular hypertension and hyperfiltration. Some nephrons starve while others are overworked, and the overall kidney loses filtering capacity in a patchy, heterogeneous pattern that pathologists call hypertensive nephrosclerosis.

The hyperfiltering glomeruli pay a price. The pressure stresses the podocytes, specialized cells that wrap around the glomerular capillaries and form the final barrier keeping protein in the blood. Stressed podocytes detach or die, and once they're gone, the filtration barrier leaks protein into the urine. This proteinuria is not just a marker of damage; it actively drives more damage. Filtered protein gets reabsorbed by the downstream tubules, and this reabsorption activates inflammatory pathways that promote scarring of the tissue between the tubules, a process called tubulointerstitial fibrosis. Animal models and clinical data agree: more proteinuria means faster progression, and interventions that lower proteinuria slow the decline.

Underneath all of this, the renin-angiotensin-aldosterone system is activated inappropriately in the hypertensive kidney. Angiotensin II constricts the efferent arteriole more than the afferent, which further raises glomerular pressure. It also promotes oxidative stress, inflammation, and fibrosis directly. This is why RAAS blockers, drugs like lisinopril, losartan, and their cousins, are so effective at protecting the kidney: they interrupt this maladaptive amplification loop.

Why Most People With Hypertensive Kidney Disease Don't Know It

The kidney has enormous reserve. A patient can lose half their nephrons and still have a normal serum creatinine, a normal estimated glomerular filtration rate, and feel completely fine. By the time creatinine rises above the upper limit of normal on a routine lab, the damage is often substantial and frequently not fully reversible. Symptoms like fatigue, leg swelling, nocturia, or loss of appetite appear even later, typically when kidney function has fallen below roughly 30 percent of normal.

This is why I screen every hypertensive patient at least once a year with two simple tests: a serum creatinine with estimated GFR, and a urine albumin-to-creatinine ratio, or UACR, on a spot urine sample. UACR is the most sensitive early marker of kidney damage in hypertension, often abnormal years before eGFR starts to fall. Patients are often surprised when I order it because their urine looks fine and they have no symptoms, but microalbuminuria is invisible to the naked eye.

Understanding Your UACR Number

The UACR measures how many milligrams of albumin are being lost in the urine per gram of urinary creatinine. It corrects for how concentrated the urine is, so a random sample gives a reliable number. The international KDIGO guidelines classify UACR into three bands.

Normal to mildly increased is less than 30 mg per gram. Moderately increased, what we used to call microalbuminuria, is 30 to 300 mg per gram. Severely increased, formerly macroalbuminuria, is 300 mg per gram or higher. The cutoffs are a bit arbitrary, because albuminuria predicts cardiovascular and kidney risk on a continuous scale, even within the normal range. A UACR of 28 carries slightly more risk than a UACR of 8, even though both are called normal.

I prefer to order a first-morning-void sample when possible, because orthostatic changes and exercise can raise albumin excretion transiently. If the first UACR is elevated at 30 or higher, I confirm with a repeat measurement before making a diagnosis, because a single abnormal value can reflect a urinary tract infection, heavy exercise, or menstrual contamination rather than true kidney disease. Two of three samples above 30 over several weeks confirms persistent albuminuria.

Moderately or severely increased UACR changes everything about how I treat hypertension. It means the kidney is already leaking, and it shifts the priority toward drugs that reduce intraglomerular pressure and proteinuria, not just systemic pressure.

How Low Should Blood Pressure Go in Someone With Kidney Damage?

The question of the right blood pressure target in patients with CKD has been debated for two decades. The short answer from the current evidence is that lower is better for cardiovascular outcomes, with a ceiling of around 120 systolic for most patients, but the benefit on kidney outcomes specifically is more modest than many assume.

The SPRINT trial, published in 2015, enrolled over 9,000 patients with hypertension at elevated cardiovascular risk, of whom 28 percent had an eGFR below 60. It compared an intensive systolic blood pressure target of less than 120 with a standard target of less than 140, using standardized automated office measurement. Intensive control reduced major cardiovascular events by 25 percent and all-cause mortality by 27 percent, with the CKD subgroup benefiting similarly. The trial was stopped early because the signal was so strong. A follow-up analysis of the CKD subgroup, sometimes called SPRINT-CKD, confirmed the cardiovascular benefit but did not show a meaningful reduction in kidney failure. That's an important nuance: intensive BP control in CKD saves lives and reduces strokes and heart attacks, but does not clearly slow the rate of kidney decline.

The earlier Intensive Blood-Pressure Control in Hypertensive CKD trial from 2010 had suggested that very aggressive BP lowering might delay kidney failure specifically in patients with baseline proteinuria, and that signal still informs my practice. Patients with both hypertension and substantial proteinuria are the ones for whom a more aggressive BP target seems to pay off on the kidney side.

The ACCORD-BP trial, which tested intensive blood pressure control in patients with type 2 diabetes, showed a reduction in stroke but did not hit its primary composite cardiovascular endpoint. That trial excluded patients with serum creatinine above 1.5, so its direct relevance to advanced CKD is limited. The STEP trial in Chinese adults aged 60 to 80 compared intensive treatment (systolic 110 to less than 130) with standard treatment (systolic 130 to less than 150) and showed a 26 percent reduction in cardiovascular events with fewer adverse effects from low pressure than SPRINT found, perhaps because the intensive target was less aggressive.

Current guidelines synthesize all of this differently. KDIGO recommends a systolic BP under 120 mmHg for most adults with CKD, measured with standardized office technique. The 2025 ACC/AHA guideline for the general adult CKD population recommends a treatment goal under 130 mmHg, balancing benefit against the adverse effects seen at more intensive targets. The American Diabetes Association's 2026 standards recommend under 130/80 for patients with diabetes and CKD, with consideration of under 120 systolic when it's safely achievable.

In my own practice, I target a systolic BP under 130 for most hypertensive patients with CKD, and I push toward under 120 when the patient has significant albuminuria, tolerates the intensity well, and has no orthostatic symptoms. For frail elderly patients or those prone to falls, I'm comfortable staying between 130 and 140 if that's where they feel well. The emphasis is not hitting a number on one visit but sustained control over years, using medications and lifestyle that the patient can actually live with.

RAAS Blockade: The First-Line Kidney Protector

The first medication I reach for in a hypertensive patient with any degree of albuminuria is an ACE inhibitor or an angiotensin receptor blocker. These drugs reduce intraglomerular pressure by preferentially dilating the efferent arteriole, which takes the load off the glomerulus and substantially reduces proteinuria. They also block angiotensin II's direct pro-fibrotic effects in the kidney tissue. The benefit on kidney outcomes is large and reproducible.

A network meta-analysis of 119 randomized trials with over 64,000 patients showed that ACE inhibitors reduced the risk of kidney failure by 39 percent compared with placebo and 35 percent compared with active controls. ARBs reduced kidney failure by 30 percent versus placebo and 25 percent versus active controls. The benefit extends into advanced CKD, including patients with eGFR below 30, where RAAS blockers reduce progression to dialysis by roughly 40 percent. ACE inhibitors may have a slight edge over ARBs for both kidney and cardiovascular outcomes, though most cardiologists and nephrologists consider them interchangeable in practice.

A few practical points matter when starting these drugs. First, uptitrate to the maximum tolerated dose. A low dose of lisinopril is better than nothing, but the trials showing kidney protection used full doses, and partial dosing gives partial benefit. Second, expect a small bump in creatinine and a corresponding dip in eGFR of up to 30 percent within the first two weeks of starting or uptitrating. This is not kidney injury; it reflects the intended reduction in intraglomerular pressure. I do not stop the medication for this expected change unless potassium rises above the acceptable range or the creatinine rise is substantially larger than 30 percent, which can indicate renal artery stenosis. Third, I monitor potassium and creatinine at two to four weeks after any dose change and periodically thereafter. Fourth, I continue RAAS blockers even if eGFR has fallen into a range below where we would have started them initially; there is no eGFR threshold for stopping. Finally, I never combine an ACE inhibitor with an ARB. Dual RAAS blockade increases adverse effects without adding benefit and is explicitly recommended against by the ACC.

SGLT2 Inhibitors: The New Standard of Kidney Care

The second drug class I now layer on top of RAAS blockade in most hypertensive patients with CKD is the SGLT2 inhibitor. Originally developed as diabetes drugs, these medications turned out to have profound kidney and cardiovascular protective effects that are independent of their glucose-lowering action. In the last five years, they have moved from novel to standard of care in CKD.

Three landmark trials established the evidence base. CREDENCE, which enrolled patients with type 2 diabetes and albuminuric CKD, tested canagliflozin and showed a 30 percent reduction in the primary kidney composite of kidney failure, doubling of creatinine, or renal or cardiovascular death. DAPA-CKD tested dapagliflozin in patients with CKD regardless of whether they had diabetes and showed a 39 percent reduction in the composite of kidney disease progression, sustained eGFR decline, or death. EMPA-KIDNEY extended the evidence to a much broader CKD population, including patients without diabetes and without albuminuria, and showed a 28 percent reduction in kidney disease progression or cardiovascular death. A meta-analysis pooling 13 trials with over 90,000 patients confirmed a 37 percent reduction in kidney disease progression, a 23 percent reduction in acute kidney injury, and a 23 percent reduction in cardiovascular death or heart failure hospitalization, with benefits consistent across every eGFR category down to below 30.

I initiate an SGLT2 inhibitor in any hypertensive patient with CKD and an eGFR of 20 or higher, whether or not they have diabetes. The benefit is independent of glycemic control, and I will start the drug even in a patient whose hemoglobin A1c is already at goal. I expect a small reversible dip in eGFR in the first weeks, similar to what happens with RAAS blockade, and I do not stop the drug for this. I continue it if the eGFR later falls below 20, because the benefit persists. Combining SGLT2 inhibitors with ACE inhibitors or ARBs is not only safe but probably reduces the risk of hyperkalemia, which is a nice additional benefit for patients on dual therapy.

Finerenone and the Role of Aldosterone Blockade

The third drug I consider in selected patients is finerenone, a nonsteroidal mineralocorticoid receptor antagonist. Aldosterone, like angiotensin II, contributes to kidney inflammation and fibrosis, and blocking its receptor in the kidney slows disease progression. The older steroidal mineralocorticoid antagonists spironolactone and eplerenone also block this pathway, but finerenone has structural differences that reduce hormonal side effects like gynecomastia and has a more favorable safety profile for long-term kidney use.

The evidence for finerenone comes from the FIDELIO-DKD and FIGARO-DKD trials, pooled into the FIDELITY analysis of over 13,000 patients with type 2 diabetes, CKD with eGFR of 25 or higher, and albuminuria despite optimized RAAS blockade. FIDELITY showed a 23 percent reduction in the composite kidney outcome of kidney failure, sustained eGFR decline of at least 57 percent, or renal death. Cardiovascular outcomes improved by 14 percent, and end-stage kidney disease specifically was reduced by 20 percent.

I consider finerenone for a patient who has type 2 diabetes, has eGFR of 25 or higher, and still has albuminuria above 30 mg per gram despite being on a maximally tolerated ACE inhibitor or ARB plus an SGLT2 inhibitor. The main safety issue is hyperkalemia, so I require a baseline potassium of 4.8 or below before starting, check potassium at one month, and monitor periodically thereafter. In the trials, hyperkalemia requiring discontinuation occurred in about 1.7 percent of patients on finerenone versus 0.6 percent on placebo. The risk is real but manageable with monitoring, and combining finerenone with an SGLT2 inhibitor appears to reduce the hyperkalemia risk compared with using finerenone alone.

What a Typical Treatment Plan Looks Like

When I see a new patient with hypertension and some degree of albuminuria or reduced eGFR, I layer therapies in a predictable order. I start with an ACE inhibitor or ARB, uptitrated to the maximum tolerated dose. If the blood pressure is still above target, I add a long-acting calcium channel blocker like amlodipine, which provides additional BP lowering without blunting the kidney-protective effect of the RAAS blocker. If a third drug is needed, I typically use a thiazide-like diuretic such as chlorthalidone, which has slightly better evidence than hydrochlorothiazide for preventing cardiovascular events.

Once blood pressure is reasonably controlled, I add an SGLT2 inhibitor regardless of whether the patient has diabetes. In patients with type 2 diabetes and persistent albuminuria despite these steps, I layer in finerenone next. I generally avoid combining more than one RAAS blocker, so if a patient is on an ACE inhibitor and starting finerenone, I don't add spironolactone to the regimen.

Alongside the medications, we talk about sodium restriction. The data support aiming for under 2,300 mg of sodium per day, with larger BP reductions as intake drops further. I encourage the DASH dietary pattern, with its emphasis on vegetables, fruits, whole grains, lean protein, and low-fat dairy. I advise at least 150 minutes of moderate aerobic activity per week, weight loss when the patient is overweight, smoking cessation, and moderation of alcohol. For patients with type 2 diabetes, I target an individualized HbA1c, typically under 7, while being mindful of hypoglycemia in older or frail patients.

Statin therapy is part of the package for most patients with CKD, because the cardiovascular risk is disproportionately high even at moderate eGFR. Current guidelines recommend statin therapy for patients with CKD who are 50 years or older and for younger patients with additional cardiovascular risk factors.

When to Involve a Nephrologist

Most hypertensive patients with CKD can be managed well in primary care or in a cardiology office like mine, with periodic communication with a nephrologist if needed. I refer for specialist input when eGFR falls below 30, when CKD is progressing rapidly, defined as an eGFR decline of more than 5 per year, when UACR exceeds 300 mg per gram and is not responding to layered therapy, when blood pressure remains uncontrolled despite three or more antihypertensive agents including a diuretic, or when hematuria or other unusual features suggest a diagnosis beyond routine hypertensive nephrosclerosis.

The nephrologist adds value in several ways: evaluating for reversible causes of kidney disease, making decisions about renal replacement therapy planning when eGFR approaches 15, managing the complications of advanced CKD such as anemia and mineral bone disorder, and handling the complexity of drug dosing in severe kidney impairment. An early referral is often more useful than a late one, because advance planning smooths the eventual transition if the patient approaches the need for dialysis or transplant.

Why This Matters for Anyone With High Blood Pressure

If there is a single takeaway from the last decade of evidence in this space, it is this: blood pressure control protects kidneys, and the tools that protect kidneys also protect hearts. The RAAS blockers, the SGLT2 inhibitors, and now finerenone all reduce cardiovascular events in parallel with their kidney benefits. When I treat a patient's hypertension properly, with the right targets and the right medication stack, I am lowering their risk of stroke, heart attack, heart failure, kidney failure, and premature death simultaneously.

The flip side is that neglecting hypertension, or settling for imperfect control because the patient feels fine, quietly accelerates damage in every vascular bed in the body. Kidney disease that shows up late in life is rarely bad luck; it is usually the cumulative product of decades of unchecked pressure acting on susceptible tissue. The patient who starts on lisinopril at age 45 and stays on it for twenty years has often avoided a cascade of problems that the patient who waits until age 60 cannot fully reverse.

If you are reading this and your blood pressure has been running above 130/80, or you have been told you have borderline creatinine or a little protein in your urine, please take it seriously. Get a home blood pressure monitor, take readings in the morning and evening for two weeks, and bring the average to your physician. Ask for a UACR if you have not had one. If you are already on a medication, ask whether your dose is at the maximum tolerated, whether an SGLT2 inhibitor is appropriate, and whether your UACR has been followed over time. Kidney disease moves slowly, and that is actually good news: with the current tools, we can almost always change the trajectory if we start early enough.

Frequently Asked Questions

Can high blood pressure damage my kidneys even if my creatinine is normal?

Yes. The kidneys have tremendous reserve, and damage often shows up in the urine as albumin long before creatinine rises. A normal creatinine with an elevated UACR tells me the filtration barrier is leaking even though the overall eGFR has not yet dropped. This is the stage where treatment is most effective, because we can often halt or reverse the albuminuria and prevent the eGFR from declining in the future.

What does it mean if my UACR is 50?

A UACR of 50 milligrams per gram falls into the moderately increased category, what we used to call microalbuminuria. It means your kidneys are leaking protein. I would confirm it with a repeat first-morning sample, because single samples can be falsely elevated by infection, recent exercise, or menstrual contamination. If two or three samples over several weeks confirm the finding, that is persistent albuminuria, and it warrants treatment with an ACE inhibitor or ARB and probably an SGLT2 inhibitor, plus tighter blood pressure control.

Will my kidney function improve if I get my blood pressure under control?

It depends on where you are starting. If you have albuminuria but still-normal eGFR, good blood pressure control combined with an ACE inhibitor or ARB and an SGLT2 inhibitor can reduce the albumin leak and prevent progression, often for decades. If you have already lost substantial nephrons and your eGFR is below 45, we are usually aiming to slow further decline rather than fully reverse it. Either way, the effort pays off. Even slowing progression by a few percent per year translates into many added years of dialysis-free life.

Why did my doctor tell me not to worry about a small rise in creatinine after starting lisinopril?

Because a small rise in creatinine after starting an ACE inhibitor is expected and is not kidney injury. These drugs reduce the pressure inside the glomerulus on purpose, which mildly reduces instantaneous filtration and raises creatinine by a few points. The long-term effect is protective. I worry only if the rise exceeds 30 percent or if the potassium also climbs; otherwise, the medication is doing exactly what it should.

Should I take an SGLT2 inhibitor if I don't have diabetes?

Often yes. The DAPA-CKD and EMPA-KIDNEY trials specifically enrolled patients with CKD regardless of diabetes status and showed similar kidney and cardiovascular benefit whether or not diabetes was present. If you have hypertension plus CKD, particularly with any albuminuria, an SGLT2 inhibitor is worth a serious conversation with your physician. The main considerations are eGFR at initiation, which should be 20 or higher, and the small risks of volume depletion and genital mycotic infections.

Is it safer to aim for under 130 or under 120 systolic when I have CKD?

Both targets have evidence, and the right answer depends on the patient. Under 120 gives slightly more cardiovascular protection in selected patients but comes with a higher rate of syncope, acute kidney injury, and electrolyte problems. Under 130 is a reasonable target for most patients with CKD. For a younger, fit patient with significant albuminuria, I often push for under 120 if they tolerate it. For an 80-year-old with falls and frailty, I may accept 135 to 140 to keep them safe and functional. This is a conversation worth having with your physician rather than a number to chase in isolation.

Do I need to see a nephrologist, or can my primary care doctor or cardiologist manage this?

For most patients with hypertension and early CKD, your primary care physician or a cardiologist can manage therapy effectively, especially if they are using the modern stack of ACE inhibitor or ARB, SGLT2 inhibitor, and appropriate lifestyle measures. I involve a nephrologist when eGFR falls below 30, when CKD is progressing quickly, when blood pressure is uncontrolled on three or more agents, or when a diagnosis beyond routine hypertensive nephrosclerosis is suspected. Early specialist input helps when things get complex; routine management does not require it.

How often should my kidney function be checked?

Every hypertensive patient should have an eGFR and UACR at least yearly. If you have established CKD, frequency increases with severity. Stage 3a CKD with low albuminuria can be followed twice a year; stage 3b or worse, or moderate to severe albuminuria, typically needs quarterly labs. When you start or adjust an ACE inhibitor, ARB, SGLT2 inhibitor, or finerenone, a potassium and creatinine at two to four weeks confirms the medication is safe at the new dose.

Does how much salt I eat really matter if I am already on blood pressure medication?

Yes, and possibly more than when you are not on medication. Dietary sodium blunts the effectiveness of almost every antihypertensive drug. A patient who stays on a high-sodium diet often ends up needing a larger dose or an additional medication to reach target, whereas moderating sodium to around 2,300 mg per day, and ideally closer to 1,500, allows lower doses, better blood pressure control, and reduced proteinuria. The DASH eating pattern combined with sodium restriction can lower systolic pressure by 8 to 11 mmHg independent of medication, which is larger than what most individual drugs achieve.

References

1. Erviti J, Saiz LC, Leache L, et al. Blood Pressure Targets for Hypertension in People With Chronic Renal Disease. Cochrane Database Syst Rev. 2024.

2. Arendshorst WJ, Vendrov AE, Kumar N, Ganesh SK, Madamanchi NR. Oxidative Stress in Kidney Injury and Hypertension. Antioxidants (Basel). 2024.

3. Meyrier A. Nephrosclerosis: Update on a Centenarian. Nephrol Dial Transplant. 2015;30(11):1833-1841.

4. Remuzzi G, Bertani T. Pathophysiology of Progressive Nephropathies. N Engl J Med. 1998;339(20):1448-1456.

5. Kohagura K, Zamami R, Oshiro N, Shinzato Y, Uesugi N. Heterogeneous Afferent Arteriolopathy: A Key Concept for Understanding Blood Pressure-Dependent Renal Damage. Hypertens Res. 2024.

6. Zeng X, Zeng Q, Zhou L, Zhu H, Luo J. Prevalence of Chronic Kidney Disease Among US Adults With Hypertension, 1999 to 2018. Hypertension. 2023.

7. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024.

8. American Diabetes Association Professional Practice Committee. 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes-2026. Diabetes Care. 2026.

9. SPRINT Research Group. A Randomized Trial of Intensive versus Standard Blood-Pressure Control. N Engl J Med. 2015;373(22):2103-2116.

10. Cushman WC, Evans GW, Byington RP, et al. Effects of intensive blood-pressure control in type 2 diabetes mellitus (ACCORD-BP). N Engl J Med. 2010;362(17):1575-1585.

11. Zhang W, Zhang S, Deng Y, et al. Trial of Intensive Blood-Pressure Control in Older Patients with Hypertension (STEP). N Engl J Med. 2021;385(14):1268-1279.

12. Appel LJ, Wright JT Jr, Greene T, et al. Intensive Blood-Pressure Control in Hypertensive Chronic Kidney Disease. N Engl J Med. 2010;363(10):918-929.

13. Perkovic V, Jardine MJ, Neal B, et al. Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy (CREDENCE). N Engl J Med. 2019;380(24):2295-2306.

14. Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al. Dapagliflozin in Patients with Chronic Kidney Disease (DAPA-CKD). N Engl J Med. 2020;383(15):1436-1446.

15. The EMPA-KIDNEY Collaborative Group. Empagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2023;388(2):117-127.

16. Bakris GL, Agarwal R, Anker SD, et al. Effect of Finerenone on Chronic Kidney Disease Outcomes in Type 2 Diabetes (FIDELIO-DKD). N Engl J Med. 2020;383(23):2219-2229.

17. Pitt B, Filippatos G, Agarwal R, et al. Cardiovascular Events with Finerenone in Kidney Disease and Type 2 Diabetes (FIGARO-DKD). N Engl J Med. 2021;385(24):2252-2263.

18. Agarwal R, Filippatos G, Pitt B, et al. Cardiovascular and kidney outcomes with finerenone in patients with type 2 diabetes and chronic kidney disease: the FIDELITY pooled analysis. Eur Heart J. 2022;43(6):474-484.

19. Goodbred AJ, Langan RC. Chronic Kidney Disease: Prevention, Diagnosis, and Treatment. Am Fam Physician. 2023.

20. Hao XM, Liu Y, Hailaiti D, et al. Mechanisms of Inflammation Modulation by Different Immune Cells in Hypertensive Nephropathy. Front Immunol. 2023.