Acute Kidney Injury in the Hospital: Who Is at Risk, What Causes It, and How It Can Be Prevented

Research-informed explainer — last updated April 12, 2026

Acute kidney injury (AKI) affects an estimated 10–15% of all hospitalized patients and more than 20% of those in intensive care units — yet most patients are unaware of their risk until it happens. Even a modest and temporary rise in creatinine during hospitalization meaningfully increases the risk of death, prolonged hospital stays, and long-term kidney damage.

This article draws on research from five nephrologists with published expertise in hospital-acquired AKI. Glenn Chertow, MD, Chief of Nephrology at Stanford University School of Medicine, published the foundational 2005 study quantifying AKI's impact on hospital mortality, length of stay, and costs, and was among the first to demonstrate AKI's independent association with mortality after cardiac surgery. Steven Coca, D.O., M.S., Director of Clinical Research in Nephrology at The Mount Sinai Hospital in New York, led two landmark meta-analyses documenting how a single AKI episode raises the risk of developing chronic kidney disease and dying in the years that follow. Sevag Demirjian, MD, Director of Critical Care Nephrology at Cleveland Clinic, has studied AKI in the context of ARDS and surgical procedures and developed prediction models for mortality in critically ill patients with AKI. Joshua Augustine, MD, Associate Professor of Medicine at Case Western Reserve University and a transplant nephrologist at Cleveland Clinic, led a landmark randomized controlled trial comparing how AKI is treated with dialysis. Meghan Sise, MD, at Massachusetts General Hospital, has conducted pivotal research on a rapidly growing cause of AKI — immune checkpoint inhibitor therapy used in cancer treatment.

What is acute kidney injury?

Acute kidney injury is defined as a sudden decrease in kidney function, typically detected through a rise in serum creatinine (a waste product normally cleared by the kidneys) or a drop in urine output. The KDIGO (Kidney Disease: Improving Global Outcomes) staging criteria define AKI as:

• Stage 1: Creatinine rise of 0.3 mg/dL or more within 48 hours, or a 50–99% increase from baseline
• Stage 2: Creatinine 2–2.9 times baseline
• Stage 3: Creatinine 3 or more times baseline, or requiring dialysis

Even Stage 1 AKI is clinically meaningful. A 2005 study by Chertow and colleagues analyzing nearly 20,000 consecutive adult admissions to an academic medical center found that even modest creatinine increases of 0.3–0.4 mg/dL were significantly associated with in-hospital death, longer length of stay, and higher costs — independent of age, illness severity, and comorbidities. Large creatinine increases were uncommon (only 1% of patients had a rise of 2 mg/dL or more), but the smaller, more common increases accounted for a substantial portion of the overall harm.

The most common causes of hospital AKI

AKI during hospitalization typically falls into three categories based on where the injury originates:

Pre-renal (reduced blood flow to the kidneys) is the most common cause and usually reversible if caught early. It results from:

• Dehydration, blood loss, or inadequate fluid intake
• Low blood pressure (septic shock, cardiogenic shock, post-surgery)
• Medications that reduce blood flow to the kidney, including NSAIDs and ACE inhibitors/ARBs in vulnerable patients

Intrinsic renal injury (direct damage to kidney tissue) includes:

• Acute tubular necrosis (ATN), the most common intrinsic cause — often from sustained low blood pressure, nephrotoxic medications (contrast dye, aminoglycoside antibiotics, vancomycin), or pigment nephropathy from muscle breakdown (rhabdomyolysis)
• Interstitial nephritis, an immune reaction to medications including antibiotics, NSAIDs, and proton pump inhibitors
• Immune checkpoint inhibitor-associated AKI (discussed below)

Post-renal (obstruction of urine flow) from enlarged prostate, kidney stones, or tumor compression is less common but treatable once identified.

AKI after cardiac surgery: a particularly high-risk setting

Among all hospital settings, cardiac surgery carries some of the highest AKI rates. Chertow and colleagues demonstrated in a 1998 study of cardiac surgery patients that acute renal failure after surgery — even when not requiring dialysis — was independently associated with a 7-fold increase in hospital mortality. This association held even after adjustment for preoperative risk factors.

Research by Coca and colleagues using biomarkers — specifically urine IL-18 and neutrophil gelatinase-associated lipocalin (NGAL) measured within 6 hours after cardiac surgery — showed that these markers could identify patients destined to develop AKI days before creatinine would rise. A 1,219-patient multicenter cohort study found that patients in the highest quintile of urine IL-18 were 6.8 times more likely to develop AKI, and those in the highest quintile of plasma NGAL were 5-fold more likely.

AKI in ARDS and critical illness

Critically ill patients — particularly those with acute respiratory distress syndrome (ARDS) — face compounded risks. Research by Demirjian and colleagues identified the factors most strongly associated with AKI among ARDS patients: high-pressure ventilation, systemic inflammation, and hemodynamic instability each compound the risk. Demirjian also developed a mortality prediction model specifically for critically ill patients with AKI, finding that factors including the need for vasopressors, pre-existing CKD, and degree of creatinine elevation can stratify 60-day mortality risk — a tool with real implications for ICU decision-making.

The growing threat: checkpoint inhibitor-associated AKI

One of the fastest-growing causes of drug-induced AKI is the class of cancer immunotherapy drugs called immune checkpoint inhibitors (ICIs), including pembrolizumab, nivolumab, and ipilimumab. These drugs unleash the immune system against tumors, but can also trigger immune-mediated kidney injury.

Research by Sise and colleagues at Massachusetts General Hospital has defined this emerging pattern. A 2020 multicenter study in the Journal of the American Society of Nephrology found that ICI-associated AKI typically presents as acute tubulointerstitial nephritis, occurs at a median of 14 weeks after starting treatment, and responds well to corticosteroids in most patients — provided it is identified early. A companion study found that approximately 2–5% of patients receiving ICIs develop AKI. Critically, ICI-associated AKI often presents without the eosinophilia or rash that might signal drug-induced nephritis in other contexts, making awareness and kidney function monitoring essential in all cancer patients receiving these drugs.

How severe AKI is treated with dialysis

When AKI is severe enough to require kidney replacement therapy, clinicians must decide between intermittent hemodialysis (sessions several times per week) and continuous renal replacement therapy (CRRT), which runs 24 hours per day at lower flow rates. A randomized controlled trial by Augustine and colleagues published in the American Journal of Kidney Diseases compared these approaches in patients with acute renal failure, finding that while outcomes were similar overall, intermittent dialysis was associated with earlier kidney recovery — an important consideration when the goal is maximizing the chance the kidneys will regain function.

A larger subsequent trial — the ATN study, published in the NEJM with Chertow as a lead investigator — randomized 1,124 critically ill patients with AKI and found that more intensive renal support (higher dose dialysis) did not improve survival or kidney recovery compared to a standard dose. This finding reshaped how ICUs approach AKI dialysis intensity, shifting attention toward optimizing other modifiable factors rather than simply escalating dialysis frequency.

The long shadow: AKI and long-term kidney health

Perhaps the most clinically underappreciated aspect of hospital AKI is its long-term consequences. Research by Coca and colleagues synthesized the evidence in two influential meta-analyses. The 2009 analysis in the American Journal of Kidney Diseases, covering more than 5,000 AKI patients, found that survivors had a 2-fold increased risk of death in follow-up compared to matched patients who did not have AKI. The 2011 meta-analysis in Kidney International, covering 13 studies, found that AKI survivors were 8.8 times more likely to develop CKD, 3.1 times more likely to develop end-stage renal disease, and 2.0 times more likely to die during follow-up.

The clinical imperative is clear: AKI should not be considered a resolved problem at hospital discharge. Patients who experienced AKI during hospitalization should have their kidney function checked within 90 days of discharge and be monitored for CKD development.

Prevention: what patients and clinicians can do

For patients at high risk (pre-existing CKD, diabetes, heart failure, advanced age, or undergoing major surgery):

• Inform all providers about pre-existing kidney disease before any procedure involving contrast dye or general anesthesia
• Ensure adequate hydration, particularly when taking nephrotoxic medications or undergoing bowel prep
• Ask your care team whether any medications should be held temporarily during illness or hospitalization
• For cancer patients: ask your oncologist whether your checkpoint inhibitor requires baseline and ongoing kidney function monitoring

Questions to ask your doctor

• Did I experience any AKI during my recent hospitalization, and what was my creatinine trend?
• Do I need follow-up kidney function testing after discharge, and when?
• Should any of my regular medications be adjusted given my kidney function now?
• Am I at elevated risk for AKI before my upcoming procedure, and what can be done to reduce that risk?
• If I am receiving a checkpoint inhibitor, how often will my kidney function be checked?

The bottom line

Acute kidney injury during hospitalization is more common and more consequential than most patients realize. Even modest creatinine rises carry real mortality risk, and a single AKI episode increases long-term risk of chronic kidney disease and death for years afterward. Patients who are at high risk — particularly those with existing CKD, cardiac surgery planned, or cancer immunotherapy underway — should discuss kidney monitoring with their care team before and after hospitalization.