↑ 2–3×rising incidence over two decades: age, comorbidity, detection
Frame it this way
In a 20-bed ICU, roughly 11 patients will have AKI today and 2–3 will need dialysis before discharge.
Hoste EAJ et al. Intensive Care Med 2015;41:1411 (AKI-EPI) · Susantitaphong P et al. Clin J Am Soc Nephrol 2013;8:1482 · Koyner Ch 6
AKI is a driver of poor outcomes, not just a marker
In hospital
Mortality rises stepwise with KDIGO stage
AKI needing KRT: 90-day mortality ≈ 45–50%
More ventilator days, more fluid overload, more infection
Distant organ injury
Lung: capillary leak, impaired fluid clearance
Heart: arrhythmia, myocardial depression
Brain: uremic encephalopathy, delirium
After discharge
New/progressive CKD (pooled HR ≈ 8.8)
ESKD (HR ≈ 3.1), death (HR ≈ 2.6)
Excess risk persists in "recovered" patients
Coca SG et al. Kidney Int 2009;76:893 · See EJ et al. Kidney Int 2019;95:160 · Koyner Ch 6, 51
“AKI is a clinical syndrome defined by laboratory and urine-output criteria — not a single disease with a single cause. The criteria tell you that the kidney is injured; they never tell you why.”
— The mental frame for every ICU consult
02
Definitions & staging
Twenty years of consensus criteria — powerful, standardised, and built on two imperfect signals.
Koyner Ch 5 · KDIGO 2012 · Levey Kidney Int 2020
Two decades of consensus criteria
Year
System
Key innovation
Legacy problem
2004
RIFLE
First consensus: Risk · Injury · Failure · Loss · ESKD; introduced urine output
Needed a baseline creatinine
2007
AKIN
Added the 48-h absolute rise ≥0.3 mg/dL; 3 stages; no eGFR criterion
Over-called small fluctuations
2012
KDIGO
Merged both: 48-h absolute or 7-day relative rise — still the standard
Creatinine and urine output are both indirect
2017–21
ADQI / KDIGO nomenclature
Added AKD, transient vs persistent AKI, sub-phenotypes
Not yet in most EHR alerts
Bellomo R et al. Crit Care 2004 · Mehta RL et al. Crit Care 2007 · KDIGO AKI Work Group, Kidney Int Suppl 2012 · Chawla LS et al. Nat Rev Nephrol 2017
KDIGO staging — the language of the ICU
Stage
Serum creatinine
Urine output
1
1.5–1.9× baseline (within 7 d) or ≥0.3 mg/dL rise within 48 h
<0.5 mL/kg/h × 6–12 h
2
2.0–2.9× baseline
<0.5 mL/kg/h × ≥12 h
3
≥3.0× baseline, or rise to ≥4.0 mg/dL, or start of KRT, or eGFR <35 mL/min/1.73 m² (age <18 y)
<0.3 mL/kg/h × ≥24 h or anuria ≥12 h
Key point
Either criterion can stage, and the higher of the two wins. Document both — and document the baseline you used.
KDIGO AKI Work Group, Kidney Int Suppl 2012;2:19–36
Staging in practice: a worked example
Bedside numbers
Weight 70 kgBaseline Cr 0.9Day 1 Cr 1.3Day 2 Cr 2.1UO 190 mL / 12 h
Cr
2.1 ÷ 0.9 = 2.3× baseline → creatinine stage 2
UO
190 mL ÷ 70 kg ÷ 12 h = 0.23 mL/kg/h for 12 h → urine-output stage 2 (needs ≥24 h for stage 3)
→
Final: KDIGO stage 2 AKI, both axes concordant — and already 48 h into the injury
Three habits that prevent errors
Use ideal or adjusted body weight in the obese — actual weight falsely reassures
Read UO in blocks (6/12/24 h), never a single hour
State the baseline explicitly in the note: "baseline Cr 0.9 from clinic, 4 months ago"
KDIGO 2012 · Koyner Ch 5
Urine output: powerful, but easy to get wrong
Why it earns its place
Detects injury hours to days earlier than creatinine
Oliguria alone (normal Cr) still predicts mortality and KRT
Free, continuous, already being measured
Why it fails
Diuretics uncouple flow from function — UO looks "fine"
Needs a catheter and honest hourly charting
Obesity: mL/kg/h on actual weight under-calls oliguria
Non-oliguric ATN is common — normal UO never excludes AKI
Common pitfall
"Creatinine is fine" does not rule out AKI when the urine-output criterion is met — and a patient on a furosemide infusion can be anuric-in-truth while charting 60 mL/h.
KDIGO 2012 · Kellum JA et al. J Am Soc Nephrol 2015;26:2231 · Koyner Ch 5
The baseline creatinine problem
KDIGO needs a baseline. In the ICU it is often unknown — and the choice changes the stage, which changes the decisions.
Best
Stable outpatient value 7–365 days before admission
Acceptable
Lowest inpatient creatinine during this admission
Last resort
Back-calculate assuming eGFR 75 mL/min/1.73 m² (MDRD) — systematically over-diagnoses AKI in CKD
Never
Admission creatinine in a patient who arrived already injured
Why it matters
A patient with true baseline Cr 1.8 (CKD 3b) back-calculated to 0.9 is instantly mislabelled stage 2 — triggering nephrotoxin stops, imaging and sometimes a dialysis conversation that was never needed.
KDIGO 2012 · Siew ED et al. Kidney Int 2010;77:536 · Koyner Ch 5
Creatinine is a lagging, diluted, muscle-dependent signal
Lag
Creatinine rises only after GFR has already fallen substantially, and takes 24–72 h to reach a new steady state. Early injury looks normal.
Dilution
Aggressive resuscitation expands total body water and dilutes creatinine — the same kidney looks "better" after 5 L of fluid.
Production
Sarcopenia, liver failure, immobility and sepsis all lower creatinine generation. A "normal" 0.6 mg/dL in an ICU patient may mean GFR 40.
Kinetic eGFR
Uses the rate of change of creatinine rather than a steady-state value — estimates real-time GFR during rapidly changing injury.
Cystatin C
Independent of muscle mass; the combined creatinine–cystatin C CKD-EPI 2021 equation is the most accurate and is race-free. Confounded by steroids and thyroid disease.
Chen S. J Am Soc Nephrol 2013;24:877 · Inker LA et al. N Engl J Med 2021;385:1737 · Koyner Ch 5, 16 (biomarkers in Lecture 4)
AKI is not a one-off event: the continuum
0–48 H
Transient AKIReverses within 48 h — usually haemodynamic
→
2–7 D
Persistent AKICriteria still met beyond 48 h — worse outcomes
→
7–90 D
AKDAcute kidney disease — recovery or progression is decided here
→
>90 D
CKDResidual damage — lifelong follow-up
Key point
Every AKI consult is also a referral for future kidney care. The AKD window (7–90 days) is where nephrology follow-up actually changes trajectories — and it is the window most often dropped at discharge.
Chawla LS et al. Nat Rev Nephrol 2017;13:241 (ADQI 16) · Levey AS et al. Kidney Int 2020;97:1117 · Koyner Ch 51
Sub-phenotypes: not all "stage 2" is the same patient
Transient / rapidly reversing
Resolves ≤48–72 h after perfusion is restored
Usually haemodynamic or volume-responsive
Mortality close to no-AKI patients
Persistent
Criteria met >48 h despite correction of haemodynamics
Structural injury; biomarker-positive
Independently predicts KRT, non-recovery and death
Renal angina
Combine risk (sepsis, transplant, ventilation, pressors) with early injury signs (fluid overload, small Cr change) to decide who deserves a biomarker or a closer look — the "chest pain" analogy for the kidney.
Why you should care
Trial enrolment, biomarker use and KRT-timing decisions all now hinge on this distinction. "Will it reverse?" is a more useful question than "what stage?"
Chawla LS et al. Nat Rev Nephrol 2017 (ADQI 16) · Goldstein SL, Chawla LS. Clin J Am Soc Nephrol 2010;5:943 · Koyner Ch 5, 7
03
Etiologies
The three-compartment framework still works — as long as you remember ICU patients rarely have only one cause.
Koyner Ch 5, 8–9 · Ronco Ch 11–16
The classic framework: three compartments
Prerenal ~30%
Hypoperfusion without structural injury — responds to restoring perfusion, by definition only diagnosable in retrospect.
Intrinsic ~60%
Damage to tubules, interstitium, glomeruli or vessels — the ICU majority, and mostly acute tubular injury.
Postrenal <10%
Obstruction — small in numbers, large in consequences if missed, and the only fully reversible cause.
Common pitfall
ICU AKI is usually multifactorial: sepsis plus hypovolemia plus nephrotoxins plus raised intra-abdominal pressure. Naming one cause and stopping the search is the commonest consult error.
Koyner Ch 5 · Uchino S et al. JAMA 2005;294:813 (BEST Kidney: sepsis in ~50% of severe ICU AKI)
Prerenal AKI — the reversible one
Mechanisms
True hypovolemia: haemorrhage, GI losses, burns, diuresis
Low cardiac output: cardiogenic shock, tamponade, PE
Venous congestion: right heart failure, raised IAP, fluid overload
Signatures (before diuretics)
BUN/Cr >20:1, FeNa <1%, FeUrea <35%
UOsm >500 mOsm/kg, urine Na <20 mEq/L
Bland sediment, hyaline casts only
Creatinine falls within 24–72 h of correcting the insult
Key point
Prerenal and ATN are the two ends of one spectrum, not two diseases. Prolonged or repeated hypoperfusion converts one into the other — and the transition has no laboratory marker.
Koyner Ch 5 · Ronco Ch 18
Sepsis-associated AKI: the model that broke the model
Septic AKI is not simply renal ischaemia. Renal blood flow is often normal or increased, and biopsies show remarkably little necrosis.
Microcirculatory failure — heterogeneous peritubular flow despite adequate global flow
Inflammation — PAMPs/DAMPs signalling through tubular TLRs; leukocyte adhesion
Adaptive metabolic downregulation — tubular cells switch off energy-costly transport to survive; a defence, not death
Venous congestion — the right-sided contribution nobody measures
The clinical consequence
More MAP and more fluid do not automatically mean more filtration. Once perfusion is adequate, additional fluid is congestive, not restorative — this is the physiology behind Lecture 2 and 3.
Takasu O et al. Am J Respir Crit Care Med 2013;187:509 · Gomez H, Kellum JA. Crit Care Clin 2016 · Langenberg C, Bellomo R. Crit Care 2005 · Ronco Ch 45
Intrinsic AKI — acute tubular injury (ATN)
Ischemic ATN
Shock of any type, cardiac arrest, prolonged clamping, CPB
Outer medulla (S3 segment, thick ascending limb) is the watershed
Prostate, pelvic or retroperitoneal malignancy, retroperitoneal fibrosis
Stones (bilateral, or single functioning kidney), papillary necrosis
Clot retention, neurogenic bladder, blocked or kinked catheter
Intratubular: crystals, myeloma cast nephropathy
How it presents
Anuria alternating with polyuria is classic but uncommon
Partial obstruction can present with normal urine output
Post-obstructive diuresis after relief — replace, but do not chase
Common pitfall
A Foley in place is not proof of patency — flush it. And early or volume-depleted obstruction can show no hydronephrosis on ultrasound: if the story fits, image again or get a CT.
Koyner Ch 5, 18
Nephrotoxins — the part of the differential you can actually change
The vancomycin + piperacillin-tazobactam AKI signal comes from observational data. The randomised ACORN trial (cefepime vs piperacillin-tazobactam, 2023) found no difference in AKI — much of the signal is probably creatinine-secretion interference, not injury. Do not let it drive antibiotic choice alone.
Koyner Ch 5, 8 · Qian ET et al. JAMA 2023;330:1557 (ACORN) · Perazella MA. Clin J Am Soc Nephrol 2019
Organ crosstalk syndromes — when the kidney is the messenger
Cardiorenal syndrome (Ronco types 1–5)
Type 1 acute cardiac → renal · Type 2 chronic HF → CKD
Type 3 acute renal → cardiac · Type 4 CKD → cardiac
Type 5 systemic (sepsis, amyloid) → both
Congestion, not low output, is the dominant driver in most type-1 patients
Hepatorenal syndrome — AKI (HRS-AKI)
ICA 2019: diagnose by KDIGO criteria — the old fixed Cr ≥2.5 mg/dL threshold is gone
Requires: cirrhosis + ascites, no shock, no nephrotoxins, no response to albumin 1 g/kg × 2 d, no structural disease
Treat with terlipressin + albumin (CONFIRM, NEJM 2021) — watch for respiratory failure
Ronco C et al. J Am Coll Cardiol 2008;52:1527 · Angeli P et al. J Hepatol 2019;71:811 (ICA) · Wong F et al. N Engl J Med 2021;384:818 · Koyner Ch 40
04
The first 24 hours of the consult
A reproducible sequence: exposure history, the bedside, the urine, the ultrasound — then a decision about biopsy.
Koyner Ch 5, 18
A consult checklist that never fails
History & exposure
Volume losses: diarrhoea, bleeding, burns, drains, third spacing
Every hypotensive episode — read the flowsheet, not the summary
Contrast, surgery, CPB time, IABP/ECMO cannulation
Full medication reconciliation including pre-admission NSAIDs and herbals
Baseline kidney function — ask, then verify against a real laboratory value
FeNa and FeUrea are only interpretable before diuretics
UOsm, urine Na/K/Cl, spot protein-to-creatinine ratio
Urine dipstick blood positive but no RBCs → myoglobin or haemoglobin
Urine anion gap when a non-gap acidosis appears (Lecture 7)
Koyner Ch 5 · Perazella MA et al. Clin J Am Soc Nephrol 2010;5:402 (cast scoring)
Urine chemistries: prerenal vs ATN — and their limits
Index
Prerenal
ATN
Caveat that ruins it
FeNa
<1%
>2%
Useless after any diuretic; low in contrast AKI, pigment AKI, HRS and early GN
FeUrea
<35%
>50%
Better after diuretics, but low in HRS and with urea recirculation
UOsm
>500
<350
Needs concentrating ability — meaningless in CKD, DI or osmotic diuresis
Urine Na
<20
>40
Tracks sodium intake and diuretics more than tubular health
BUN/Cr
>20:1
10–15:1
Raised by GI bleeding, steroids, catabolism; lowered by liver disease, malnutrition
Key point
These indices are supporting evidence, never a verdict. In the right patient, a carefully monitored fluid challenge with a dynamic endpoint answers the question faster than any ratio.
Koyner Ch 5 · Ronco Ch 55
Renal ultrasound — fast, cheap, bedside
Hydronephrosis → obstruction; false negatives in early, volume-deplete and encasing retroperitoneal disease
Size & echogenicity — kidneys <9 cm with thin cortex mean this is not a new problem
Bladder — the two most useful minutes of the study
Doppler resistive index — RI >0.75 suggests persistent AKI, but it is confounded by age, heart rate, pulse pressure and pressors
Renal vein flow pattern — the congestion signal (VExUS, Lecture 4)
What ultrasound cannot do
It cannot distinguish prerenal from ATN, cannot exclude early obstruction, and cannot diagnose glomerular disease. Order it to answer a specific question, not as a reflex.
Koyner Ch 18 · Ronco Ch 33 · Darmon M et al. Intensive Care Med 2011;37:68 (RI)
Putting it together: prerenal vs ATN
Feature
Prerenal
Acute tubular injury
Response to volume
Creatinine falls in 24–72 h
No immediate response; may worsen with more fluid
Urine chemistry
FeNa <1%, UOsm >500, BUN/Cr >20
FeNa >2%, UOsm <350, BUN/Cr 10–15
Sediment
Bland, hyaline casts
Muddy-brown granular casts, tubular cells
Damage biomarkers
Negative
Positive (NGAL, [TIMP-2]·[IGFBP7]) — Lecture 4
Course
Days
1–3 weeks; a third will need KRT
Koyner Ch 5, 16
When does an ICU patient need a kidney biopsy?
Biopsy changes management when…
Active urinary sediment: RBC casts, dysmorphic haematuria, heavy proteinuria
Suspected RPGN, vasculitis, anti-GBM — days matter
AKI without a plausible haemodynamic or toxic explanation
No recovery beyond 3–4 weeks with an unclear cause
Suspected AIN where the culprit drug cannot be stopped empirically
Weigh against
Uncorrectable coagulopathy or platelets <50 ×10⁹/L
Uncontrolled hypertension, single kidney, hydronephrosis, active infection
Clinically significant bleeding ~1–2%; transfusion or intervention rarer
The transjugular route is an option when bleeding risk is high or the patient is ventilated and cannot be positioned
Key point
Ask one question before booking: "If the biopsy shows what I suspect, will I start immunosuppression tonight?" If the answer is no, the biopsy can usually wait.
Koyner Ch 5 · Ronco Ch 56 · Corapi KM et al. Am J Kidney Dis 2012;60:62
05
Epidemiology & outcomes
The numbers to quote when the team says "the creatinine is only a little up".
Severity of illness, emergency vs elective surgery
Genetic: APOL1 risk variants in patients of African ancestry
Exposure (modifiable — today)
Hypotension: cumulative time below MAP 65 predicts AKI dose-dependently
Nephrotoxin burden — count them, stop what you can
Fluid overload and raised intra-abdominal pressure
Hyperglycaemia, anaemia, hypoxaemia
Timing of contrast and elective procedures
Key point
KDIGO risk stratification exists so that the bundle (stop nephrotoxins, optimise haemodynamics, monitor creatinine and UO, avoid hyperglycaemia) can be applied before stage 3 arrives — see Lecture 3.
Koyner Ch 6, 8 · Walsh M et al. Anesthesiology 2013;119:507 (MAP thresholds) · KDIGO 2012
Dose–response: stage and duration both predict death
Stage 3mortality several-fold higher, independent of severity score
>7 dayspersistent AKI adds risk on top of peak stage
Severity and duration are independent — a brief stage 3 may fare better than a fortnight of stage 2
Repeat episodes compound the risk of CKD progression
Fluid overload at KRT initiation independently predicts death (PICARD, PICARD-era cohorts)
Koyner Ch 6 · Bouchard J et al. Kidney Int 2009;76:422 · Mehta RL et al. Kidney Int 2011 · Coca SG et al. Kidney Int 2009
AKI-D: the sickest subgroup you will follow for years
~13% of ICU patients receive KRT; in the BEST Kidney cohort hospital mortality reached 60%
Modern trial cohorts: 90-day mortality ≈ 44% (STARRT-AKI, both arms)
Among survivors, 10–30% remain dialysis-dependent at hospital discharge
KRT dependence at 90 days is now a co-primary trial endpoint — and it was higher with accelerated initiation (10.4% vs 6.0%)
Most recovery happens in the first 1–4 weeks: wean deliberately (Lecture 9)
What to tell the family on day 1
"Dialysis here is usually temporary support while the kidney recovers, but it is also a marker of how sick the whole body is. We will know much more in two weeks."
Uchino S et al. JAMA 2005;294:813 · STARRT-AKI Investigators. N Engl J Med 2020;383:240 · Koyner Ch 6
Beyond discharge: post-AKI care is a clinical duty
What the survivor carries
Higher risk of CKD, ESKD, heart failure, hypertension and death
Risk is graded by stage, duration and number of episodes
Present even when creatinine returns to "normal" — the reserve is gone
What the discharge summary must contain
Peak stage, cause, whether KRT was used, discharge creatinine
Medication list reconciled: which nephrotoxins were stopped and whether to restart
A creatinine and urine-protein check within 3 months
Named follow-up: nephrology for stage 3, KRT-treated, or unrecovered patients
Koyner Ch 51 · See EJ et al. Kidney Int 2019;95:160 · KDIGO 2012 (Section 3.5)
06
Cases & special hosts
Contexts where the same criteria describe a completely different differential.
Koyner Ch 38–39
Case 1 · 68 M, septic shock from urinary source
ICU day 2. Norepinephrine 0.4 µg/kg/min, MAP 62. Receiving piperacillin-tazobactam and vancomycin. Abdomen distended.
What KDIGO stage — and what are the four mechanisms operating simultaneously?
Think 45 seconds · answer on the next slide
Case 1 — four mechanisms, one creatinine
Stage 2
Cr 2.2× baseline. The UO criterion at 8 h does not yet qualify — reassess at 12 h.
Sepsis
Microcirculatory heterogeneity and inflammation — the dominant driver, and not fixed by more fluid.
Nephrotoxins
Check the vancomycin AUC; ask whether the combination is still needed once cultures return.
Congestion
IAP 19 mmHg with CVP 16 — renal perfusion pressure is MAP − IAP ≈ 43 mmHg. Decompress, do not fill.
Key point
Treat the whole picture: source control, restore perfusion pressure, stop what you can stop, and relieve the abdomen. No single intervention here is "the" treatment.
Koyner Ch 5, 8, 36 · Ronco Ch 45
Cardiac surgery-associated AKI
Incidence 20–30% by KDIGO; 1–2% need dialysis — but that 1–2% has mortality above 40%
Mechanisms: low output, haemolysis with free haemoglobin, systemic inflammation from bypass, atheroemboli, contrast from recent angiography, nephrotoxins
Preoperative risk scores (Cleveland Clinic / Thakar, Mehta) stratify before the incision
Bypass time and re-exploration are the strongest intraoperative predictors
What actually prevents it
Delay elective surgery ≥24–48 h after contrast, avoid intraoperative hypotension, restrictive transfusion, and apply the KDIGO bundle to biomarker-positive patients (PrevAKI). Not: "renal-dose" dopamine, mannitol, or fenoldopam.
Koyner Ch 39 · Thakar CV et al. J Am Soc Nephrol 2005;16:162 · Meersch M et al. Intensive Care Med 2017;43:1551 (PrevAKI)
Obstetric AKI
Pregnancy-specific causes
Preeclampsia / eclampsia / HELLP — the commonest
Haemorrhage: abruption, atony, previa; acute cortical necrosis in severe cases
Normal pregnancy creatinine is lower (≈0.4–0.8) — a "normal" 1.0 is already abnormal
Delivery is often the definitive therapy in preeclampsia/HELLP
Magnesium for seizure prophylaxis — dose-adjust in AKI, follow levels
Dialysis is safe in pregnancy; start earlier and dialyse longer (target BUN <45 mg/dL)
Do not forget obstruction — gravid uterus, stones
Koyner Ch 38 · Ronco Ch 40 · Fakhouri F et al. J Am Soc Nephrol 2017
07
Pitfalls & wrap-up
The two cognitive errors that account for most missed diagnoses on the consult service.
Koyner Ch 5
Two errors that cost kidneys
Pitfall 1 — premature closure on "ATN"
Glomerulonephritis, TMA, interstitial nephritis and obstruction all hide inside ICU AKI. Before writing "ATN", confirm you have looked at the sediment, checked platelets and LDH, reviewed every new drug, and imaged the bladder.
Pitfall 2 — trusting derived ratios in the wrong host
Liver disease and malnutrition lower BUN (a false "intrinsic" pattern); GI bleeding and steroids raise it (a false "prerenal" pattern). Sarcopenia flattens creatinine. Trimethoprim, cimetidine and cobicistat raise creatinine without touching GFR.
A 74 M, day 6 of ceftriaxone for pneumonia. Cr 1.0 → 3.1 mg/dL, urine output preserved at 1.1 mL/kg/h, bladder scan 30 mL, BP 145/85. Maculopapular rash on both legs. WBC 12 ×10⁹/L with 6% eosinophils; urine shows sterile pyuria and WBC casts.
A. Prerenal · B. Acute interstitial nephritis · C. Postrenal · D. Ischaemic ATN
Hands up — then justify your answer with one finding
Key takeaways
Stage with KDIGO using both creatinine and urine output — and write down which baseline you used.
Ask "will this reverse?" — transient versus persistent AKI predicts outcome better than the stage alone.
Expect ICU AKI to be multifactorial; septic AKI is inflammatory and microcirculatory, not simple ischaemia.
Sediment, urine chemistries and a bedside ultrasound belong in the first 24 hours — every time.
~57% of ICU patients develop AKI and ~13% receive KRT; act with the urgency those numbers deserve.
AKI is a doorway to CKD: name the follow-up before the patient leaves your service.
References & further reading
Where to go deeper
KDIGO AKI Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl. 2012;2:1–138.
Hoste EAJ, Bagshaw SM, Bellomo R, et al. Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Med. 2015;41:1411–1423.
Uchino S, Kellum JA, Bellomo R, et al. Acute renal failure in critically ill patients (BEST Kidney). JAMA. 2005;294:813–818.
Chawla LS, Bellomo R, Bihorac A, et al. Acute kidney disease and renal recovery: consensus report of the ADQI 16 Workgroup. Nat Rev Nephrol. 2017;13:241–257.
See EJ, Jayasinghe K, Glassford N, et al. Long-term risk of adverse outcomes after AKI: a systematic review and meta-analysis. Kidney Int. 2019;95:160–172.
Takasu O, Gaut JP, Watanabe E, et al. Mechanisms of cardiac and renal dysfunction in patients dying of sepsis. Am J Respir Crit Care Med. 2013;187:509–517.
Koyner JL, Topf JM, Lerma EV, eds. Handbook of Critical Care Nephrology. Wolters Kluwer; 2021 (Ch 5–7, 38–40, 51).
Critical Care Nephrology · Two-Week Intensive
Thank you
Questions & discussion — bring a consult from this week and we will stage it together.