
Two bullets matching the rows above verbatim. 'hours or days', in the first bullet, is highlighted yellow.
The highlight singles out the timing clause of the definition as the point to remember.
Lines up each RIFLE tier against its AKIN counterpart on the same two measurements so a threshold match or a gap is visible stage by stage.
| Criteria | RIFLE | AKIN |
|---|---|---|
| Risk / Stage 1 — sCreatinine | ↑sCrea × 1.5 | ↑ sCrea × 1.5 or ↑≥0.3 mg/dl in sCrea |
| Risk / Stage 1 — Urine output | < 0.5 ml/kg per h × 6 h | < 0.5 ml/kg per h × 6 h |
| Injury / Stage 2 — sCreatinine | ↑sCrea × 2 | ↑sCrea × 2 |
| Injury / Stage 2 — Urine output | < 0.5 ml/kg per h × 12 h | < 0.5 ml/kg per h × 12 h |
| Failure / Stage 3 — sCreatinine | ↑sCrea × 3 or ≥ 0.5 mg/dl if baseline sCrea ↑ > 4.0 mg/dl | ↑sCrea × 3 or ↑≥0.5 mg/dl if baseline sCrea > 4.0 mg/dl |
| Failure / Stage 3 — Urine output | < 0.3 ml/kg per h × 24 h or anuria × 12 h | < 0.3 ml/kg per h × 24 h or anuria × 12 h |
| Loss | Complete loss of renal function > 4 weeks | source silent |
| End-stage | End-stage renal disease | source silent |
| Initiation of renal replacement therapy | source silent | Patients who receive RRT are considered to have met stage 3 criteria, irrespective of the stage they are in at the time of RRT. |
Why this matters: AKIN's Stage 1 also fires on a smaller absolute creatinine rise (≥0.3 mg/dl) than RIFLE's Risk tier states, and RIFLE keeps two tiers past Failure (Loss, End-stage) that AKIN never names — reading a stage number across systems without this table risks under- or over-grading severity.

A staged severity chart: RIFLE's five tiers (Risk, Injury, Failure, Loss, End-stage) and AKIN's three tiers (Stage 1, Stage 2, Stage 3) each set against an sCreatinine threshold and a urine-output threshold, arranged least to most severe under an 'Increasing severity' label with an 'Outcome' marker.
The stepped shape ranks the tiers by severity at a glance and shows RIFLE running two tiers past where AKIN stops — a fact no single text line states outright.
The RIFLE stages are read low to high severity: Risk is mildest, End-stage is worst.
Why this matters: Without the ranking stated, the five names read as a category list rather than a severity scale, which changes what a stage number is supposed to communicate.
RIFLE and AKIN both grade AKI severity from the same two measurements — the rise in creatinine and the fall in urine output — but RIFLE keeps two tiers AKIN does not have.
AKIN stops at Stage 3; RIFLE continues to Loss and End-stage.
Why this matters: A reported stage doesn't carry its system with it — Loss and End-stage have no AKIN number to map to, so a stage read off one system cannot be assumed to mean the same severity on the other.

Stage 1: SCr 1.5–1.9 times baseline OR ≥26.5 μmol/L (0.3 mg/dL) increase | Urine output <0.5 mL/kg/h for 6–12 h. Stage 2: SCr 2–2.9 times baseline | Urine output <0.5 mL/kg/h for 6–12 h. Stage 3: SCr 3 times baseline OR initiation of renal replacement therapy OR (in patients <18 years) decrease in eGFR to <35 mL/min per 1.73 m² | Urine output: anuria for ≥12 h.
The KDIGO table itself, in full — the numeric SCr multiples, the absolute μmol/L/mg/dL threshold, the paediatric eGFR clause, and the RRT-initiation clause for Stage 3 — none of which exist as text anywhere else in the deck. The only text row for this slide was the bare heading.
AKI incidence rises with how severe the infection is: sepsis versus septic shock, same measure.
Why this matters: The two figures come from different populations in the same sentence — sepsis alone versus septic shock — so citing '25%' or '50%' without saying which group it describes over- or understates the other group's risk.

Three bullets matching the rows above verbatim. '1 in 5 adults and 1 in 3 children', '25% of patients with sepsis' and '50% of patients with septic shock' are highlighted yellow.
Highlighting picks out the four numbers she wants remembered from the three bullets; the 5% UK community-acquired figure is left unhighlighted.
This Outline slide repeats, word for word, the same bullet list already given at the row above.
Why this matters: Recognising the repeat as a section marker, not new content, stops the same bullet list from being read twice as if it were two different facts.

Three red circles name the three categories on one urinary tract: A - Pre-Renal obstruction around the renal artery where it leaves the aorta; C - Intra-renal obstruction around the left kidney; B - Post Renal obstruction around the upper ureters. Small uncircled hatch-marks then repeat the letters at every level the type can occur - A on both renal arteries, C on both kidneys, B on both ureters and again at the prostate and urethra.
The picture puts all three categories on one drawing, so post-renal is visibly the only one with several possible levels - ureter, bladder outlet, prostate, urethra - while pre-renal and intra-renal each have one.

Top node reads ↓GFR — the falling arrow is the diagram's subject. One branch, 'Changes in the circulation', lists three drivers: hypovolaemia, hypotension without hypovolaemia, and low cardiac output. The other branch, 'Intra-renal causes (disturbed renal autoregulation)', names NSAIDs and ACE inhibitors.
The diagram's connecting arrows from GFR to each branch were not captured as text — the rows list the same content as separate lines with no arrow between them.
Both lower GFR. One is a whole-body circulation problem, the other is the kidney's own autoregulation being disturbed. The items inside each branch are alternatives, not a sequence.
Same effect, two different starting points.
Why this matters: Both branches are grouped under one heading (pre-renal) and produce the same fall in GFR from different starting points — a whole-body circulation problem versus a drug disturbing the kidney's own autoregulation — so conflating them hides which mechanism is driving the injury.
The Pre-renal slide names 'disturbed renal autoregulation' as an intra-renal cause; this slide gives the three substances that do the regulating.
Same mechanism, unpacked one slide later.
Why this matters: Without this slide, 'disturbed renal autoregulation' on the earlier slide names a mechanism with no stated substances behind it.

A Normal labels the afferent arteriole, the efferent arteriole, the smooth muscle and the glomerulus, with a legend separating glomerular filtration from blood flow. B Stimulus: reduced renal perfusion → ↓transglomerular pressure → ↓GFR. C Response: intrarenal activation of the renin-angiotensin system → efferent arteriolar vasoconstriction → increases transglomerular pressure → restores GFR. A fourth panel draws Renin → A I → A II with the constriction marked on the efferent arteriole.
The picture carries the step the bullet list does not: the arteriole angiotensin constricts to rescue GFR is the efferent one. Squeezing the outflow raises pressure across the filter; squeezing the inflow would lower it.
The cutoff is not just an association — the lecture states the hormonal mechanism behind it.
Hypovolaemia is almost always associated with high…→>20:1 (BUN:C) or >40:1 (U:C) suggests pre-renal cause…
Why this matters: Knowing the ADH-driven mechanism, not just the cutoff number, is what lets the ratio be read as pre-renal evidence rather than an isolated lab value.
Full text-slide screenshot, not a separate diagram: the same BUN:creatinine text already in the rows above. Her own emphasis: 20:1 and pre-renal are printed in red, along with the word Explanation:, while >40:1 stays plain black — she marks the BUN:C ratio (20:1) as the one to remember, not the U:C ratio (40:1).The lecture gives a diagnostic cutoff for the BUN:creatinine ratio in the text and gives the FENa cutoff on the slide 17 table rather than in the text rows.
Why this matters: Both cutoffs are part of the lecture, but only one is in the extracted text rows — missing the slide table would wrongly read FENa as a formula with no stated threshold.

Table, 4 rows x 2 columns (Pre-renal | Intrinsic): Urine specific gravity — >1.020 | <1.010. Urine osmolality (mOsm/kg) — >500 | <350. Urine sodium (mmol/L) — <10 | >20. FeNa — <1% | >1%. A boxed note below repeats the FeNa formula text already in the rows.
The full pre-renal vs intrinsic lab cutoff table — specific gravity, osmolality, urine sodium and FeNa thresholds — none of which appear anywhere in the extracted text rows.
A blue IV fluid-bag clipart icon beside the heading; no labels or values on it. Body text matches the fluid-resuscitation bullets already in the rows, highlighted in yellow. Her own emphasis: three phrases are highlighted in yellow on the slide - fluid resuscitation, fluid challenge of 250 mL crystalloid, and Crystalloids and particularly balanced solutions such as plasmalyte and Ringer’s lactate. The text conversion keeps the words and drops the emphasis.AKI needs the whole outflow blocked. Count the tubes at each level.
Block one ureter and the other kidney carries on; below the bladder there is nothing to carry on with.
Why this matters: The word 'bilateral' only makes sense once the tube count at each level is counted — without it, the ureter case and the urethra case look like the same kind of blockage.

Hydronephrosis diagram, Healthy Kidney vs Hydronephrosis side by side. Labels: Kidney, Ureter, Full bladder, Urethra. An arrow runs upward from the bladder toward the kidney, numbered: 1. The bladder is unable to empty; 2. The pressure is transmitted to the kidney; 3. There is a build-up of fluid in the kidney.
Her own emphasis: Ultrasound must be done is highlighted in yellow - the action she marks as non-optional on this slide.
Acute tubular necrosis, 80-90% of renal parenchymal AKI, arises from either of two named causes.
One route has a stated mechanism; the other doesn't.
Why this matters: Same endpoint (ATN), different action: prolonged prerenal AKI is addressed by restoring perfusion (fluid resuscitation, the rows above); the nephrotoxin route is addressed by withholding/avoiding the drug (the rows below) or, if it caused the AKI, RRT to remove it (the row below).

Two curved arrows drop from the '80-90% Acute tubular necrosis' header at top-centre: one down-left, arrowhead into 'nephrotoxins causing direct injury and cell death in renal tubules (Drugs, e.g. aminoglycosides)'; one down-right, arrowhead into 'Prolonged prerenal'.
Confirms these are two parallel, independent routes into ATN - both arrows originate from the same ATN header and neither points to the other - the same two causes already listed in the text, drawn as a branching diagram rather than stated as new.
Renal parenchymal (intrinsic) AKI is split into three categories by which kidney structure is damaged.
Three sites named; only two given worked examples.
Why this matters: Which structure is damaged sets the workup for at least one branch — glomerular disease points to the immune profile ordered when GN is suspected — but the deck names no corresponding test for the vascular or tubulointerstitial categories, so treating 'renal parenchymal AKI' as one bucket loses that distinction.
The bullet lists vasoconstriction, a drop in oxygen, then tubular hypoxia in sequence; the arrows that joined them were dropped when the slide converted to text.
The sequence survives; the connecting symbols do not.
Why this matters: The slide draws vasoconstriction, falling oxygen and tubular hypoxia as one causal chain with arrows; naming the lost arrows keeps the three terms from being read as an unordered list.

Only the first bullet carries arrows: 'Intrarenal microvascular vasoconstriction' [arrow] a downward arrow before 'O2' [arrow] 'tubular hypoxia' - one straight left-to-right chain of three terms. The second bullet ('Increased endothelial and vascular smooth muscle cell structural damage') and third bullet ('Tubular cell injury') sit below as separate, unconnected bullet points - no arrows link them to the first bullet or to each other.
Restores the exact arrows the text conversion lost: vasoconstriction causes decreased O2, which causes tubular hypoxia - one causal chain, not three independent labels. The other two bullets are NOT drawn as later steps in that chain; they stand alone with no arrow, so the diagram does not support reading this as a four-step ordered pathogenesis.

A single nephron drawn top to bottom. An afferent arteriole enters a glomerular loop labelled 'Decreased glomerular filtration rate', with 'Afferent arteriolar constriction' at the entering vessel. The tube runs down into a tubule labelled 'Ischemic/toxic insult', where two arrows point to 'Back-leak' and 'Tubular injury'. The tubule lumen at the bottom is filled with debris labelled 'Obstruction'.
The image sites each of the six terms at a specific point on one nephron and its arrows show flow/leak direction, not one term causing another - the flat text list gives no such order or link between them.
A red 'EMERGENCY' alarm-bell clipart icon top-right; body text matches the rows already transcribed (pre/renal/post-renal question, bladder-outflow-obstruction bullets), with 'assessing the volume status is vital' highlighted yellow. Her own emphasis: assessing the volume status is vital is highlighted in yellow on the slide. The words survive the conversion; the emphasis does not.A prior creatinine reading, certain chronic biochemical changes, and kidney size on ultrasound each help tell a new kidney injury from long-standing kidney disease.
| Point of comparison | Acute Kidney Injury (AKI) | Chronic Kidney Disease (CKD) |
|---|---|---|
| Previous serum creatinine | Previous recent normal serum creatinine | Previous abnormal high serum creatinine |
| Anemia, high PTH hyperphosphatemia, hypocalcaemia, | Less common | More common |
| Kidney size on ultrasound abdomen | Kidney is normal in size | Kidney is small except in patients with diabetes who have normal or large sized kidneys |
| Chronicity of symptoms | Acute illness with acute/sudden onset of symptoms e.g. dyspnea, nausea, vomiting, diarrhea | Long previous history of symptoms e.g. fatigue, nausea, nocturia, itching |
| Oliguria (anuria) | Common | Common |
Why this matters: This table is how AKI is told from CKD before treatment: the deck's recovery statements (ATN recovering in 7–21 days, post-renal AKI returning to baseline) are made only about AKI, never about CKD.
Chronicity of symptoms splits the two conditions: AKI's symptoms start suddenly, CKD's have built up over a long history.
Why this matters: Symptom timing is one of the ways this lecture tells acute injury apart from chronic disease.
Oliguria/anuria is marked common for both AKI and CKD — the one row in this comparison where the two conditions don't separate.
Why this matters: Shows this finding does not help distinguish acute from chronic kidney disease.

Closes the acute-vs-chronic comparison slide; its rows in this slice — chronicity of symptoms and oliguria/anuria — are already extracted as separate table_row lines above this marker.
Her own emphasis: every discriminating phrase in the table is underlined on the slide - the previous-creatinine pair, the kidney-size pair, and the oliguria pair that reads Common on both sides.

Closes the general-measures Management slide; its four bullets (fluid balance, daily weight/BP, medication review, collateral history) are already extracted as list items above this marker.
Her own emphasis: withhold nephrotoxins is highlighted in yellow among the general measures.
Avoiding nephrotoxic drugs is stated twice: first as a general measure (medication review to withhold nephrotoxins), then again here with day-by-day dose adjustment and anticoagulants named as a particular risk.
Why this matters: Repetition across both Management slides marks nephrotoxin avoidance as a recurring priority, not a one-off point.

Closes the second Management slide; its six bullets (hyperkalaemia, acid-base balance, pulmonary oedema, sepsis, drug use, nutrition) are already extracted above this marker.
Her own emphasis: Nephrotoxins must be avoided is highlighted in yellow - the same instruction she highlighted on the previous slide, marked twice.
CRRT is not one technique but an umbrella term; the next two lines name its two specific forms.
Why this matters: Reading 'CRRT' as one specific technique rather than an umbrella would blur it with the two named forms underneath it (HDF, CVVHF), which are what actually gets ordered and run.
This Outline slide repeats the same bullet list shown on the lecture's earlier Outline slides, adding one line the earlier copies do not have: Acute Hyperuricemic nephropathy.
Why this matters: Spotting the repeat and its one addition marks Acute Hyperuricemic nephropathy as the new topic about to be covered, rather than reading the whole list as freshly introduced content.
The lecture gives two names for one entity here: rhabdomyolysis and "crush syndrome."
Why this matters: A question or report using either term is asking about the same condition — treating them as two separate entities would double-count one topic.

Slide repeats the row text verbatim, but highlights URIC ACID in yellow within the sentence listing released products (uric acid, potassium, phosphate).
The yellow highlight singles out uric acid as the emphasised product among the three released — a visual cue the plain text does not carry, and it foreshadows the next three slides, all on acute hyperuricaemic nephropathy specifically.
Tumour lysis raises uric acid production, and the excess uric acid then crystallises and blocks the urinary tract, causing renal failure.
tumour cells lyse in response to chemotherapy, large…→Renal failure is due to intrarenal and extrarenal…
Why this matters: Naming the two-step chain — overproduction then crystallisation and obstruction — is what makes prevention (lowering uric acid before it crystallises) the logical target, rather than treating the renal failure as unrelated to the tumour lysis.
Plain text slide; every line already appears as its own row above. Her own emphasis: Allopurinol is printed in bold italic inside its bullet, distinct from the plain surrounding sentence — she is calling out the drug name itself, not just the sub-heading.
Plain text slide; every line already appears as its own row above. Her own emphasis: Rasburicase is printed in bold italic inside its bullet, the same treatment given to Allopurinol on the previous slide — Febuxostat in the bullet above it is left plain.AKI's mortality risk is not fixed: it rises with how complicated the case is, worst with ITU-level non-renal organ failure. Separately, the lecture states sepsis-related AKI carries a worse prognosis than AKI without sepsis — it is not benchmarked against the ITU figure.
Why this matters: Prognosis in AKI depends on context, but the source makes two separate comparisons here, not one ranked scale of three: uncomplicated AKI vs ITU-level organ failure by percentage, and sepsis-related AKI vs non-sepsis AKI with no percentage given — the sepsis line is not stated to beat the ITU figure.