The seven objective bullets, red-bulleted, matching the rows above verbatim. The last bullet, 'Appreciate the importance of prompt action to reverse AKI', is highlighted yellow.

The yellow highlight singles out that last objective as the one she wants emphasised — no text row records this emphasis.

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.

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.

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.

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.

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.

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.

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.

Organisation chart: a top box 'Renal Parenchymal' connects via a horizontal bar down to three boxes - 'Glomerular / Acute rapidly progressive GN', 'Acute Tubulointerstitial' (no example text in its box), 'Vascular / vasculitis accelerated hypertension, cholesterol embolism, HUS'.

Visually confirms all three are siblings under one parent and that only two of the three carry a worked example - matches the text hierarchy already captured in rows, no new fact.

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.

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.

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.

Closes the RRT indications slide; its five indications (symptomatic uraemia, refractory hyperkalaemia, refractory pulmonary oedema, severe acidosis, drug removal) are already extracted above this marker.

No content beyond the bullets already converted to text.